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A reflection on Ghana’s mental health system
In recent years, the delivery of mental health services in Ghana has expanded substantially, especially since the passing of the Mental Health Act in 2012. In this article, I reflect on my experience as a visiting psychiatry resident in August 2018 at 2 Ghanaian hospitals located in Accra and Navrongo. Evident strengths of the mental health system were family support for patients and the scope of psychiatrists, while the most prominent weakness was the inadequate funding. As treatment of mental illness expands, more funding, psychiatrists, and mental health workers will be critical for the continued success of Ghana’s mental health system.
Psychiatric treatment in Ghana
Ghana has a population of approximately 28 million people, yet the country has an estimated 18 to 25 psychiatrists, up from 11 psychiatrists in 2011.1-3 Compared with the United States, which has 10.54 psychiatrists per 100,000 people (approximately 1 psychiatrist per 9,500 people), Ghana has .058 psychiatrists per 100,000 people (approximately 1 psychiatrist per 1.7 million people).4 In Ghana, most psychiatric care is delivered by mental health nurses, community mental health officers (CMHOs), and clinical psychiatric officers; supervision by psychiatrists is limited.3 Due to low public awareness, a scarcity of clinicians, and limited access to diagnostic services and medications, individuals with psychiatric illness in Ghana are often stigmatized, undertreated, and mistreated. To address this, in March 2012, Ghana passed Mental Health Act 846, which established a mental health commission and outlined protections for individuals with mental health needs.5 Since then, the number of people seeking treatment and the number of clinicians have expanded, but there are still significant challenges, such as a lack of funding for medications and facilities, and limited clinicians.6
During my last year of psychiatry residency at Mount Sinai Hospital in New York, I spent several weeks in Ghana at 2 institutions, observing and supervising the provision of psychiatric services. This was my first experience with the country’s health care system; therefore, my objectives were to:
- assess the current state of psychiatric services through observation and interviews with clinical staff
- provide instruction to clinicians in areas of need.
Two-thirds of my time was spent at the Accra Psychiatric Hospital, 1 of only 3 psychiatric hospitals in Ghana, all of which are located in the southern region of the country. The remainder of my time was spent at the Navrongo War Memorial Hospital in Ghana’s Northern Region.
The Accra Psychiatric Hospital is a sprawling complex near the center of the capital city. Every morning I walked through a large outdoor waiting area to the examination room, which was filled with at least 30 patients by 9
Navrongo War Memorial Hospital. There are no practicing psychiatrists in the northern region of the country; therefore, all mental health care is delivered by mental health nurses and CMHOs. CMHOs have 1 year of training plus a minimum of 2 years of service. They focus on identifying psychiatric cases in the community and coordinating treatment. Nurses have prescribing rights. A psychiatrist should be scheduled to visit the various districts in the region every 6 months to provide supervision, but this is not always feasible.
When I visited, I was the only psychiatrist who had been to this hospital in more than 1 year. During my time there, I reviewed the treatment protocols and gave lectures on the management of psychiatric emergencies and motivational interviewing, because addiction to alcohol and tramadol are 2 of the most pressing mental health problems in the country.7 I also saw patients with nurses, and supervised them on their assessment and treatment.
Continue to: In Ghana...
In Ghana, psychiatric services are often delivered using the community mental health model, in which many patients are visited in their homes. One morning, we went to a prayer camp to see if there were any individuals who would benefit from psychiatric services. There were no cases that day, but during the visit I sat under a tree where a few years before it was not uncommon to find a person who was psychotic or agitated chained to the tree. Several years of outreach by the local nurses has resulted in the camp leaders better recognizing mental illness early and contacting the nurses, as opposed to locking a person in chains for an extended period.
On one occasion, we answered a crisis call where a person experiencing a psychotic episode had locked himself in his house. The team talked with the individual through a locked screen door for 30 minutes, after which he eventually came out of the home to speak with us. A few days later, the patient accepted fluphenazine decanoate injection at his home. Two weeks later, he came to the outpatient clinic to continue treatment. Four months later, the patient was still in treatment and had started an apprenticeship for repairing cars.
As I was walking out of the hospital on my last day, I was called back to see a woman with a seizure who had been brought to the hospital. Unfortunately, there was no more diazepam in stock with which to treat her. This event highlighted the lack of resources available in this setting.
3 Take-home messages
My experience at both hospitals led me to reflect on 3 important factors impacting the mental health system in Ghana:
Family support. For at least 80% of appointments, patients were accompanied by family members or friends. The family hierarchy is still dominant in the Ghanaian culture, and clinicians often need the buy-in of the family, especially when financial support is required. More often than not, families enhanced patients’ treatment, but in some instances, they were a barrier.
Continue to: The types of cases
The types of cases. Most of the patients coming to both hospitals had diagnoses of bipolar disorder, schizophrenia, substance use disorder, or epilepsy. My impression was that patients or family members sought treatment for disorders that were conspicuous. I saw <5 cases of depression or anxiety. I wonder if this was because:
- patients with these disorders were referred to psychologists
- patients sought out faith-based treatment
- there was a lower incidence of these disorders, or these disorders were detected less frequently.
Inadequate funding. Despite the clinicians’ astute observations and diagnoses, they faced challenges, including a lack of access to medications because pharmacies were out of stock, or the patient or hospital could not afford the medication. At times, these challenges resulted in patients admitted to the hospital not receiving medications. When Mental Health Act 846 was implemented, it was widely purported that mental health care would be available to everyone, but the funding mechanism was not firmly established.8,9 Currently, laboratory workup, mental health treatment, and medications are not covered by health insurance, and government funding for mental health is insufficient. Therefore, in most areas, the entire cost burden of psychiatric care falls on patients and their families, or on hospitals.
Making progress despite barriers
In her inaugural address, former American Psychiatric Association President Altha J. Stewart, MD, named expanding the organization’s work in global mental health as one of her 3 primary goals.10 There are several means by which American psychiatrists can support the work of psychiatrists in Ghana and elsewhere. One way is by helping the mental health commission and other entities within the country petition the government and health insurance companies to expand coverage for mental health services. Teleconferencing, in which psychiatrists in Ghana or other parts of the world provide supervision to mid-level clinicians, has been piloted in other countries such as Liberia and could be implemented to address the critical shortages of psychiatrists in certain regions.11
In the past 7 years, Ghana has made significant strides in destigmatizing mental illness, and as a result more individuals are seeking treatment and more clinicians at all levels are being trained. Despite significant barriers, physicians, nurses, and other mental health workers deliver empathic and evidence-based treatment in a manner that defies the mental health system’s current limitations.
1. Ofori-Atta A, Attafuah J, Jack H, et al. Joining psychiatric care and faith healing in a prayer camp in Ghana: randomised trial. Br J Psychiatry. 2018;212(1):34-41.
2. Ghana has only 18 psychiatrists; experts beg government for more funds. GhanaWeb. https://www.ghanaweb.com/GhanaHomePage/NewsArchive/Ghana-has-only-18-psychiatrists-experts-beg-government-for-more-funds-591732. Published October 17, 2017. Accessed July 24, 2019.
3. Agyapong VIO, Farren C, McAuliffe E. Improving Ghana’s mental healthcare through task-shifting-psychiatrists and health policy directors perceptions about government’s commitment and the role of community mental health workers. Global Health. 2016;12:57.
4. World Health Organization. Global Health Observatory data repository. http://apps.who.int/gho/data/node.main.MHHR?lang=en. Published April 25, 2019. Accessed July 24, 2019.
5. Walker GH, Osei A. Mental health law in Ghana. BJPsych Int. 2017;14(2):38-39.
6. Doku VC, Wusu-Takyi A, Awakame J. Implementing the Mental Health Act in Ghana: any challenges ahead? Ghana Med J. 2012;46(4):241-250.
7. Kissiedu E. High dose Tramadol floods market. Business Day. http://businessdayghana.com/high-dose-tramadol-floods-market/. Published September 25, 2017. Accessed July 24, 2019.
8. Badu E, O’Brien AP, Mitchell R. An integrative review of potential enablers and barriers to accessing mental health services in Ghana. Health Res Policy Syst. 2018;16(1):110.
9. Ghana mental health care delivery risks collapse for lack of funds. News Ghana. https://www.newsghana.com.gh/ghana-mental-health-care-delivery-risks-collapse-for-lack-of-funds/. Published May 29, 2018. Accessed July 24, 2019.
10. Stewart AJ. Response to the Presidential Address. Am J Psychiatry. 2018;175(8):726-727.
11. Katz, CL, Washington FB, Sacco M, et al. A resident-based telepsychiatry supervision pilot program in Liberia. Psychiatr Serv. 2018;70(3):243-246.
In recent years, the delivery of mental health services in Ghana has expanded substantially, especially since the passing of the Mental Health Act in 2012. In this article, I reflect on my experience as a visiting psychiatry resident in August 2018 at 2 Ghanaian hospitals located in Accra and Navrongo. Evident strengths of the mental health system were family support for patients and the scope of psychiatrists, while the most prominent weakness was the inadequate funding. As treatment of mental illness expands, more funding, psychiatrists, and mental health workers will be critical for the continued success of Ghana’s mental health system.
Psychiatric treatment in Ghana
Ghana has a population of approximately 28 million people, yet the country has an estimated 18 to 25 psychiatrists, up from 11 psychiatrists in 2011.1-3 Compared with the United States, which has 10.54 psychiatrists per 100,000 people (approximately 1 psychiatrist per 9,500 people), Ghana has .058 psychiatrists per 100,000 people (approximately 1 psychiatrist per 1.7 million people).4 In Ghana, most psychiatric care is delivered by mental health nurses, community mental health officers (CMHOs), and clinical psychiatric officers; supervision by psychiatrists is limited.3 Due to low public awareness, a scarcity of clinicians, and limited access to diagnostic services and medications, individuals with psychiatric illness in Ghana are often stigmatized, undertreated, and mistreated. To address this, in March 2012, Ghana passed Mental Health Act 846, which established a mental health commission and outlined protections for individuals with mental health needs.5 Since then, the number of people seeking treatment and the number of clinicians have expanded, but there are still significant challenges, such as a lack of funding for medications and facilities, and limited clinicians.6
During my last year of psychiatry residency at Mount Sinai Hospital in New York, I spent several weeks in Ghana at 2 institutions, observing and supervising the provision of psychiatric services. This was my first experience with the country’s health care system; therefore, my objectives were to:
- assess the current state of psychiatric services through observation and interviews with clinical staff
- provide instruction to clinicians in areas of need.
Two-thirds of my time was spent at the Accra Psychiatric Hospital, 1 of only 3 psychiatric hospitals in Ghana, all of which are located in the southern region of the country. The remainder of my time was spent at the Navrongo War Memorial Hospital in Ghana’s Northern Region.
The Accra Psychiatric Hospital is a sprawling complex near the center of the capital city. Every morning I walked through a large outdoor waiting area to the examination room, which was filled with at least 30 patients by 9
Navrongo War Memorial Hospital. There are no practicing psychiatrists in the northern region of the country; therefore, all mental health care is delivered by mental health nurses and CMHOs. CMHOs have 1 year of training plus a minimum of 2 years of service. They focus on identifying psychiatric cases in the community and coordinating treatment. Nurses have prescribing rights. A psychiatrist should be scheduled to visit the various districts in the region every 6 months to provide supervision, but this is not always feasible.
When I visited, I was the only psychiatrist who had been to this hospital in more than 1 year. During my time there, I reviewed the treatment protocols and gave lectures on the management of psychiatric emergencies and motivational interviewing, because addiction to alcohol and tramadol are 2 of the most pressing mental health problems in the country.7 I also saw patients with nurses, and supervised them on their assessment and treatment.
Continue to: In Ghana...
In Ghana, psychiatric services are often delivered using the community mental health model, in which many patients are visited in their homes. One morning, we went to a prayer camp to see if there were any individuals who would benefit from psychiatric services. There were no cases that day, but during the visit I sat under a tree where a few years before it was not uncommon to find a person who was psychotic or agitated chained to the tree. Several years of outreach by the local nurses has resulted in the camp leaders better recognizing mental illness early and contacting the nurses, as opposed to locking a person in chains for an extended period.
On one occasion, we answered a crisis call where a person experiencing a psychotic episode had locked himself in his house. The team talked with the individual through a locked screen door for 30 minutes, after which he eventually came out of the home to speak with us. A few days later, the patient accepted fluphenazine decanoate injection at his home. Two weeks later, he came to the outpatient clinic to continue treatment. Four months later, the patient was still in treatment and had started an apprenticeship for repairing cars.
As I was walking out of the hospital on my last day, I was called back to see a woman with a seizure who had been brought to the hospital. Unfortunately, there was no more diazepam in stock with which to treat her. This event highlighted the lack of resources available in this setting.
3 Take-home messages
My experience at both hospitals led me to reflect on 3 important factors impacting the mental health system in Ghana:
Family support. For at least 80% of appointments, patients were accompanied by family members or friends. The family hierarchy is still dominant in the Ghanaian culture, and clinicians often need the buy-in of the family, especially when financial support is required. More often than not, families enhanced patients’ treatment, but in some instances, they were a barrier.
Continue to: The types of cases
The types of cases. Most of the patients coming to both hospitals had diagnoses of bipolar disorder, schizophrenia, substance use disorder, or epilepsy. My impression was that patients or family members sought treatment for disorders that were conspicuous. I saw <5 cases of depression or anxiety. I wonder if this was because:
- patients with these disorders were referred to psychologists
- patients sought out faith-based treatment
- there was a lower incidence of these disorders, or these disorders were detected less frequently.
Inadequate funding. Despite the clinicians’ astute observations and diagnoses, they faced challenges, including a lack of access to medications because pharmacies were out of stock, or the patient or hospital could not afford the medication. At times, these challenges resulted in patients admitted to the hospital not receiving medications. When Mental Health Act 846 was implemented, it was widely purported that mental health care would be available to everyone, but the funding mechanism was not firmly established.8,9 Currently, laboratory workup, mental health treatment, and medications are not covered by health insurance, and government funding for mental health is insufficient. Therefore, in most areas, the entire cost burden of psychiatric care falls on patients and their families, or on hospitals.
Making progress despite barriers
In her inaugural address, former American Psychiatric Association President Altha J. Stewart, MD, named expanding the organization’s work in global mental health as one of her 3 primary goals.10 There are several means by which American psychiatrists can support the work of psychiatrists in Ghana and elsewhere. One way is by helping the mental health commission and other entities within the country petition the government and health insurance companies to expand coverage for mental health services. Teleconferencing, in which psychiatrists in Ghana or other parts of the world provide supervision to mid-level clinicians, has been piloted in other countries such as Liberia and could be implemented to address the critical shortages of psychiatrists in certain regions.11
In the past 7 years, Ghana has made significant strides in destigmatizing mental illness, and as a result more individuals are seeking treatment and more clinicians at all levels are being trained. Despite significant barriers, physicians, nurses, and other mental health workers deliver empathic and evidence-based treatment in a manner that defies the mental health system’s current limitations.
In recent years, the delivery of mental health services in Ghana has expanded substantially, especially since the passing of the Mental Health Act in 2012. In this article, I reflect on my experience as a visiting psychiatry resident in August 2018 at 2 Ghanaian hospitals located in Accra and Navrongo. Evident strengths of the mental health system were family support for patients and the scope of psychiatrists, while the most prominent weakness was the inadequate funding. As treatment of mental illness expands, more funding, psychiatrists, and mental health workers will be critical for the continued success of Ghana’s mental health system.
Psychiatric treatment in Ghana
Ghana has a population of approximately 28 million people, yet the country has an estimated 18 to 25 psychiatrists, up from 11 psychiatrists in 2011.1-3 Compared with the United States, which has 10.54 psychiatrists per 100,000 people (approximately 1 psychiatrist per 9,500 people), Ghana has .058 psychiatrists per 100,000 people (approximately 1 psychiatrist per 1.7 million people).4 In Ghana, most psychiatric care is delivered by mental health nurses, community mental health officers (CMHOs), and clinical psychiatric officers; supervision by psychiatrists is limited.3 Due to low public awareness, a scarcity of clinicians, and limited access to diagnostic services and medications, individuals with psychiatric illness in Ghana are often stigmatized, undertreated, and mistreated. To address this, in March 2012, Ghana passed Mental Health Act 846, which established a mental health commission and outlined protections for individuals with mental health needs.5 Since then, the number of people seeking treatment and the number of clinicians have expanded, but there are still significant challenges, such as a lack of funding for medications and facilities, and limited clinicians.6
During my last year of psychiatry residency at Mount Sinai Hospital in New York, I spent several weeks in Ghana at 2 institutions, observing and supervising the provision of psychiatric services. This was my first experience with the country’s health care system; therefore, my objectives were to:
- assess the current state of psychiatric services through observation and interviews with clinical staff
- provide instruction to clinicians in areas of need.
Two-thirds of my time was spent at the Accra Psychiatric Hospital, 1 of only 3 psychiatric hospitals in Ghana, all of which are located in the southern region of the country. The remainder of my time was spent at the Navrongo War Memorial Hospital in Ghana’s Northern Region.
The Accra Psychiatric Hospital is a sprawling complex near the center of the capital city. Every morning I walked through a large outdoor waiting area to the examination room, which was filled with at least 30 patients by 9
Navrongo War Memorial Hospital. There are no practicing psychiatrists in the northern region of the country; therefore, all mental health care is delivered by mental health nurses and CMHOs. CMHOs have 1 year of training plus a minimum of 2 years of service. They focus on identifying psychiatric cases in the community and coordinating treatment. Nurses have prescribing rights. A psychiatrist should be scheduled to visit the various districts in the region every 6 months to provide supervision, but this is not always feasible.
When I visited, I was the only psychiatrist who had been to this hospital in more than 1 year. During my time there, I reviewed the treatment protocols and gave lectures on the management of psychiatric emergencies and motivational interviewing, because addiction to alcohol and tramadol are 2 of the most pressing mental health problems in the country.7 I also saw patients with nurses, and supervised them on their assessment and treatment.
Continue to: In Ghana...
In Ghana, psychiatric services are often delivered using the community mental health model, in which many patients are visited in their homes. One morning, we went to a prayer camp to see if there were any individuals who would benefit from psychiatric services. There were no cases that day, but during the visit I sat under a tree where a few years before it was not uncommon to find a person who was psychotic or agitated chained to the tree. Several years of outreach by the local nurses has resulted in the camp leaders better recognizing mental illness early and contacting the nurses, as opposed to locking a person in chains for an extended period.
On one occasion, we answered a crisis call where a person experiencing a psychotic episode had locked himself in his house. The team talked with the individual through a locked screen door for 30 minutes, after which he eventually came out of the home to speak with us. A few days later, the patient accepted fluphenazine decanoate injection at his home. Two weeks later, he came to the outpatient clinic to continue treatment. Four months later, the patient was still in treatment and had started an apprenticeship for repairing cars.
As I was walking out of the hospital on my last day, I was called back to see a woman with a seizure who had been brought to the hospital. Unfortunately, there was no more diazepam in stock with which to treat her. This event highlighted the lack of resources available in this setting.
3 Take-home messages
My experience at both hospitals led me to reflect on 3 important factors impacting the mental health system in Ghana:
Family support. For at least 80% of appointments, patients were accompanied by family members or friends. The family hierarchy is still dominant in the Ghanaian culture, and clinicians often need the buy-in of the family, especially when financial support is required. More often than not, families enhanced patients’ treatment, but in some instances, they were a barrier.
Continue to: The types of cases
The types of cases. Most of the patients coming to both hospitals had diagnoses of bipolar disorder, schizophrenia, substance use disorder, or epilepsy. My impression was that patients or family members sought treatment for disorders that were conspicuous. I saw <5 cases of depression or anxiety. I wonder if this was because:
- patients with these disorders were referred to psychologists
- patients sought out faith-based treatment
- there was a lower incidence of these disorders, or these disorders were detected less frequently.
Inadequate funding. Despite the clinicians’ astute observations and diagnoses, they faced challenges, including a lack of access to medications because pharmacies were out of stock, or the patient or hospital could not afford the medication. At times, these challenges resulted in patients admitted to the hospital not receiving medications. When Mental Health Act 846 was implemented, it was widely purported that mental health care would be available to everyone, but the funding mechanism was not firmly established.8,9 Currently, laboratory workup, mental health treatment, and medications are not covered by health insurance, and government funding for mental health is insufficient. Therefore, in most areas, the entire cost burden of psychiatric care falls on patients and their families, or on hospitals.
Making progress despite barriers
In her inaugural address, former American Psychiatric Association President Altha J. Stewart, MD, named expanding the organization’s work in global mental health as one of her 3 primary goals.10 There are several means by which American psychiatrists can support the work of psychiatrists in Ghana and elsewhere. One way is by helping the mental health commission and other entities within the country petition the government and health insurance companies to expand coverage for mental health services. Teleconferencing, in which psychiatrists in Ghana or other parts of the world provide supervision to mid-level clinicians, has been piloted in other countries such as Liberia and could be implemented to address the critical shortages of psychiatrists in certain regions.11
In the past 7 years, Ghana has made significant strides in destigmatizing mental illness, and as a result more individuals are seeking treatment and more clinicians at all levels are being trained. Despite significant barriers, physicians, nurses, and other mental health workers deliver empathic and evidence-based treatment in a manner that defies the mental health system’s current limitations.
1. Ofori-Atta A, Attafuah J, Jack H, et al. Joining psychiatric care and faith healing in a prayer camp in Ghana: randomised trial. Br J Psychiatry. 2018;212(1):34-41.
2. Ghana has only 18 psychiatrists; experts beg government for more funds. GhanaWeb. https://www.ghanaweb.com/GhanaHomePage/NewsArchive/Ghana-has-only-18-psychiatrists-experts-beg-government-for-more-funds-591732. Published October 17, 2017. Accessed July 24, 2019.
3. Agyapong VIO, Farren C, McAuliffe E. Improving Ghana’s mental healthcare through task-shifting-psychiatrists and health policy directors perceptions about government’s commitment and the role of community mental health workers. Global Health. 2016;12:57.
4. World Health Organization. Global Health Observatory data repository. http://apps.who.int/gho/data/node.main.MHHR?lang=en. Published April 25, 2019. Accessed July 24, 2019.
5. Walker GH, Osei A. Mental health law in Ghana. BJPsych Int. 2017;14(2):38-39.
6. Doku VC, Wusu-Takyi A, Awakame J. Implementing the Mental Health Act in Ghana: any challenges ahead? Ghana Med J. 2012;46(4):241-250.
7. Kissiedu E. High dose Tramadol floods market. Business Day. http://businessdayghana.com/high-dose-tramadol-floods-market/. Published September 25, 2017. Accessed July 24, 2019.
8. Badu E, O’Brien AP, Mitchell R. An integrative review of potential enablers and barriers to accessing mental health services in Ghana. Health Res Policy Syst. 2018;16(1):110.
9. Ghana mental health care delivery risks collapse for lack of funds. News Ghana. https://www.newsghana.com.gh/ghana-mental-health-care-delivery-risks-collapse-for-lack-of-funds/. Published May 29, 2018. Accessed July 24, 2019.
10. Stewart AJ. Response to the Presidential Address. Am J Psychiatry. 2018;175(8):726-727.
11. Katz, CL, Washington FB, Sacco M, et al. A resident-based telepsychiatry supervision pilot program in Liberia. Psychiatr Serv. 2018;70(3):243-246.
1. Ofori-Atta A, Attafuah J, Jack H, et al. Joining psychiatric care and faith healing in a prayer camp in Ghana: randomised trial. Br J Psychiatry. 2018;212(1):34-41.
2. Ghana has only 18 psychiatrists; experts beg government for more funds. GhanaWeb. https://www.ghanaweb.com/GhanaHomePage/NewsArchive/Ghana-has-only-18-psychiatrists-experts-beg-government-for-more-funds-591732. Published October 17, 2017. Accessed July 24, 2019.
3. Agyapong VIO, Farren C, McAuliffe E. Improving Ghana’s mental healthcare through task-shifting-psychiatrists and health policy directors perceptions about government’s commitment and the role of community mental health workers. Global Health. 2016;12:57.
4. World Health Organization. Global Health Observatory data repository. http://apps.who.int/gho/data/node.main.MHHR?lang=en. Published April 25, 2019. Accessed July 24, 2019.
5. Walker GH, Osei A. Mental health law in Ghana. BJPsych Int. 2017;14(2):38-39.
6. Doku VC, Wusu-Takyi A, Awakame J. Implementing the Mental Health Act in Ghana: any challenges ahead? Ghana Med J. 2012;46(4):241-250.
7. Kissiedu E. High dose Tramadol floods market. Business Day. http://businessdayghana.com/high-dose-tramadol-floods-market/. Published September 25, 2017. Accessed July 24, 2019.
8. Badu E, O’Brien AP, Mitchell R. An integrative review of potential enablers and barriers to accessing mental health services in Ghana. Health Res Policy Syst. 2018;16(1):110.
9. Ghana mental health care delivery risks collapse for lack of funds. News Ghana. https://www.newsghana.com.gh/ghana-mental-health-care-delivery-risks-collapse-for-lack-of-funds/. Published May 29, 2018. Accessed July 24, 2019.
10. Stewart AJ. Response to the Presidential Address. Am J Psychiatry. 2018;175(8):726-727.
11. Katz, CL, Washington FB, Sacco M, et al. A resident-based telepsychiatry supervision pilot program in Liberia. Psychiatr Serv. 2018;70(3):243-246.
Recognizing and treating ketamine abuse
The N-methyl-
Physicians need to be aware, however, that many patients use illicit ketamine, either for recreational purposes or as self-treatment to control depressive symptoms. To help clinicians identify the signs of ketamine abuse, we discuss the adverse effects of illicit use, and suggest treatment approaches.
Ad verse effects of ketamine abuse
Ketamine can be consumed in various ways; snorting it in a powder form is a preferred route for recreational use.2 The primary disadvantage of oral use is that it increases the likelihood of nausea and vomiting.2
While ketamine is generally safe in a supervised clinical setting, approximately 2.5 million individuals use various illicit forms of ketamine—which is known as Special K and by other names—in recreational settings (eg, dance clubs) where it might be used with other substances.3 Alcohol, in particular, compounds the sedative effects of ketamine and can lead to death by overdose.
At a subanesthetic dose, ketamine can induce dissociative and/or transcendental states that are particularly attractive to those intrigued by mystical experiences, pronounced changes in perception, or euphoria.4 High doses of ketamine—relative to a commonly used recreational dose—can produce a unique “K-hole” state in which a user is unable to control his/her body and could lose consciousness.5 A K-hole state may trigger a cycle of delirium that warrants immediate clinical attention.3
Researchers have postulated that NMDA antagonism may negatively impact memory consolidation.3,6 Even more troubling is the potential for systemic injuries because illicit ketamine use may contribute to ulcerative cystitis, severely disturbed kidney function (eg, hydronephrosis), or epigastric pain.3 Chronic abuse tends to result in more systemic sequelae, affecting the bladder, kidneys, and heart. Adverse effects that require emergent care include blood in urine, changes in vision (eg, nystagmus), chest discomfort, labored breathing, agitation, seizures, and/or altered consciousness.6
Treating ketamine abuse
Treatment should be tailored to the patient’s symptoms. If the patient presents with “K-bladder” (ie, ketamine bladder syndrome), he/she may need surgical intervention or a cystectomy.4,7 Therapeutic management of K-bladder entails recognizing bladder symptoms that are specific to ketamine use, such as interstitial or ulcerative cystitis and lower urinary tract symptoms.7 Clinicians should monitor patients for increased voiding episodes during the day, voiding urgency, or a general sense of bladder fullness. Patients with K-bladder also may complain of suprapubic pain or blood in the urine.7
Continue to: Consider referring patients to...
Consider referring patients to an individualized, ketamine-specific rehabilitation program that is modeled after other substance-specific rehabilitation programs. It is critical to address withdrawal symptoms (eg, anorexia, fatigue, tremors, chills, tachycardia, nightmares, etc.). Patients undergoing ketamine withdrawal may develop anxiety and depression, with or without suicidal ideation, that might persist during a 4- to 5-day withdrawal period.8
‘Self-medicating’ ketamine users
Clinicians need to be particularly vigilant for situations in which a patient has used ketamine in an attempt to control his/her depressive symptoms. Some researchers have described ketamine as a revolutionary drug for TRD, and it is reasonable to suspect that some patients with depressive symptoms may have consulted Internet sources to learn how to self-medicate using ketamine. Patients who have consumed smaller doses of ketamine recreationally may have developed a tolerance in which the receptors are no longer responsive to the effects at that dose, and therefore might not respond when given ketamine in a clinical setting. Proper history taking and patient education are essential for these users, and clinicians may need to develop a personalized therapeutic plan for ketamine administration. If, on the other hand, a patient has a history of chronic ketamine use (perhaps at high doses), depression may occur secondary to this type of ketamine abuse. For such patients, clinicians should explore alternative treatment modalities, such as transcranial magnetic stimulation.
1. Kurdi MS, Theerth KA, Deva RS. Ketamine: current applications in anesthesia, pain, and critical care. Anesth Essays Res. 2014;8(3):283-290.
2. Davis K. What are the uses of ketamine? Medical News Today. https://www.medicalnewstoday.com/articles/302663.php. Updated October 12, 2017. Published October 11, 2019.
3. Chaverneff F. Ketamine: mechanisms of action, uses in pain medicine, and side effects. Clinical Pain Advisor. https://www.clinicalpainadvisor.com/home/conference-highlights/painweek-2018/ketamine-mechanisms-of-action-uses-in-pain-medicine-and-side-effects/. Published 2018. Accessed October 11, 2019.
4. Gao M, Rejaei D, Liu H. Ketamine use in current clinical practice. Acta Pharmacol Sin. 2016;37(7):865-872.
5. Orhurhu VJ, Claus LE, Cohen SP. Ketamine toxicity. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK541087. Updated April 11, 2019. Accessed October 18, 2019.
6. Pai A, Heining M. Ketamine. Continuing Education in Anaesthesia Critical Care & Pain. 20071;7(2):59-63.
7. Logan K. Addressing ketamine bladder syndrome. Nursing Times. https://www.nursingtimes.net/clinical-archive/medicine-management/addressing-ketamine-bladder-syndrome-19-06-2011/. Published June 19, 2011. Accessed October 11, 2019.
8. Lin PC, Lane HY, Lin CH. Spontaneous remission of ketamine withdrawal-related depression. Clin Neuropharmacol. 2016;39(1):51-52.
The N-methyl-
Physicians need to be aware, however, that many patients use illicit ketamine, either for recreational purposes or as self-treatment to control depressive symptoms. To help clinicians identify the signs of ketamine abuse, we discuss the adverse effects of illicit use, and suggest treatment approaches.
Ad verse effects of ketamine abuse
Ketamine can be consumed in various ways; snorting it in a powder form is a preferred route for recreational use.2 The primary disadvantage of oral use is that it increases the likelihood of nausea and vomiting.2
While ketamine is generally safe in a supervised clinical setting, approximately 2.5 million individuals use various illicit forms of ketamine—which is known as Special K and by other names—in recreational settings (eg, dance clubs) where it might be used with other substances.3 Alcohol, in particular, compounds the sedative effects of ketamine and can lead to death by overdose.
At a subanesthetic dose, ketamine can induce dissociative and/or transcendental states that are particularly attractive to those intrigued by mystical experiences, pronounced changes in perception, or euphoria.4 High doses of ketamine—relative to a commonly used recreational dose—can produce a unique “K-hole” state in which a user is unable to control his/her body and could lose consciousness.5 A K-hole state may trigger a cycle of delirium that warrants immediate clinical attention.3
Researchers have postulated that NMDA antagonism may negatively impact memory consolidation.3,6 Even more troubling is the potential for systemic injuries because illicit ketamine use may contribute to ulcerative cystitis, severely disturbed kidney function (eg, hydronephrosis), or epigastric pain.3 Chronic abuse tends to result in more systemic sequelae, affecting the bladder, kidneys, and heart. Adverse effects that require emergent care include blood in urine, changes in vision (eg, nystagmus), chest discomfort, labored breathing, agitation, seizures, and/or altered consciousness.6
Treating ketamine abuse
Treatment should be tailored to the patient’s symptoms. If the patient presents with “K-bladder” (ie, ketamine bladder syndrome), he/she may need surgical intervention or a cystectomy.4,7 Therapeutic management of K-bladder entails recognizing bladder symptoms that are specific to ketamine use, such as interstitial or ulcerative cystitis and lower urinary tract symptoms.7 Clinicians should monitor patients for increased voiding episodes during the day, voiding urgency, or a general sense of bladder fullness. Patients with K-bladder also may complain of suprapubic pain or blood in the urine.7
Continue to: Consider referring patients to...
Consider referring patients to an individualized, ketamine-specific rehabilitation program that is modeled after other substance-specific rehabilitation programs. It is critical to address withdrawal symptoms (eg, anorexia, fatigue, tremors, chills, tachycardia, nightmares, etc.). Patients undergoing ketamine withdrawal may develop anxiety and depression, with or without suicidal ideation, that might persist during a 4- to 5-day withdrawal period.8
‘Self-medicating’ ketamine users
Clinicians need to be particularly vigilant for situations in which a patient has used ketamine in an attempt to control his/her depressive symptoms. Some researchers have described ketamine as a revolutionary drug for TRD, and it is reasonable to suspect that some patients with depressive symptoms may have consulted Internet sources to learn how to self-medicate using ketamine. Patients who have consumed smaller doses of ketamine recreationally may have developed a tolerance in which the receptors are no longer responsive to the effects at that dose, and therefore might not respond when given ketamine in a clinical setting. Proper history taking and patient education are essential for these users, and clinicians may need to develop a personalized therapeutic plan for ketamine administration. If, on the other hand, a patient has a history of chronic ketamine use (perhaps at high doses), depression may occur secondary to this type of ketamine abuse. For such patients, clinicians should explore alternative treatment modalities, such as transcranial magnetic stimulation.
The N-methyl-
Physicians need to be aware, however, that many patients use illicit ketamine, either for recreational purposes or as self-treatment to control depressive symptoms. To help clinicians identify the signs of ketamine abuse, we discuss the adverse effects of illicit use, and suggest treatment approaches.
Ad verse effects of ketamine abuse
Ketamine can be consumed in various ways; snorting it in a powder form is a preferred route for recreational use.2 The primary disadvantage of oral use is that it increases the likelihood of nausea and vomiting.2
While ketamine is generally safe in a supervised clinical setting, approximately 2.5 million individuals use various illicit forms of ketamine—which is known as Special K and by other names—in recreational settings (eg, dance clubs) where it might be used with other substances.3 Alcohol, in particular, compounds the sedative effects of ketamine and can lead to death by overdose.
At a subanesthetic dose, ketamine can induce dissociative and/or transcendental states that are particularly attractive to those intrigued by mystical experiences, pronounced changes in perception, or euphoria.4 High doses of ketamine—relative to a commonly used recreational dose—can produce a unique “K-hole” state in which a user is unable to control his/her body and could lose consciousness.5 A K-hole state may trigger a cycle of delirium that warrants immediate clinical attention.3
Researchers have postulated that NMDA antagonism may negatively impact memory consolidation.3,6 Even more troubling is the potential for systemic injuries because illicit ketamine use may contribute to ulcerative cystitis, severely disturbed kidney function (eg, hydronephrosis), or epigastric pain.3 Chronic abuse tends to result in more systemic sequelae, affecting the bladder, kidneys, and heart. Adverse effects that require emergent care include blood in urine, changes in vision (eg, nystagmus), chest discomfort, labored breathing, agitation, seizures, and/or altered consciousness.6
Treating ketamine abuse
Treatment should be tailored to the patient’s symptoms. If the patient presents with “K-bladder” (ie, ketamine bladder syndrome), he/she may need surgical intervention or a cystectomy.4,7 Therapeutic management of K-bladder entails recognizing bladder symptoms that are specific to ketamine use, such as interstitial or ulcerative cystitis and lower urinary tract symptoms.7 Clinicians should monitor patients for increased voiding episodes during the day, voiding urgency, or a general sense of bladder fullness. Patients with K-bladder also may complain of suprapubic pain or blood in the urine.7
Continue to: Consider referring patients to...
Consider referring patients to an individualized, ketamine-specific rehabilitation program that is modeled after other substance-specific rehabilitation programs. It is critical to address withdrawal symptoms (eg, anorexia, fatigue, tremors, chills, tachycardia, nightmares, etc.). Patients undergoing ketamine withdrawal may develop anxiety and depression, with or without suicidal ideation, that might persist during a 4- to 5-day withdrawal period.8
‘Self-medicating’ ketamine users
Clinicians need to be particularly vigilant for situations in which a patient has used ketamine in an attempt to control his/her depressive symptoms. Some researchers have described ketamine as a revolutionary drug for TRD, and it is reasonable to suspect that some patients with depressive symptoms may have consulted Internet sources to learn how to self-medicate using ketamine. Patients who have consumed smaller doses of ketamine recreationally may have developed a tolerance in which the receptors are no longer responsive to the effects at that dose, and therefore might not respond when given ketamine in a clinical setting. Proper history taking and patient education are essential for these users, and clinicians may need to develop a personalized therapeutic plan for ketamine administration. If, on the other hand, a patient has a history of chronic ketamine use (perhaps at high doses), depression may occur secondary to this type of ketamine abuse. For such patients, clinicians should explore alternative treatment modalities, such as transcranial magnetic stimulation.
1. Kurdi MS, Theerth KA, Deva RS. Ketamine: current applications in anesthesia, pain, and critical care. Anesth Essays Res. 2014;8(3):283-290.
2. Davis K. What are the uses of ketamine? Medical News Today. https://www.medicalnewstoday.com/articles/302663.php. Updated October 12, 2017. Published October 11, 2019.
3. Chaverneff F. Ketamine: mechanisms of action, uses in pain medicine, and side effects. Clinical Pain Advisor. https://www.clinicalpainadvisor.com/home/conference-highlights/painweek-2018/ketamine-mechanisms-of-action-uses-in-pain-medicine-and-side-effects/. Published 2018. Accessed October 11, 2019.
4. Gao M, Rejaei D, Liu H. Ketamine use in current clinical practice. Acta Pharmacol Sin. 2016;37(7):865-872.
5. Orhurhu VJ, Claus LE, Cohen SP. Ketamine toxicity. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK541087. Updated April 11, 2019. Accessed October 18, 2019.
6. Pai A, Heining M. Ketamine. Continuing Education in Anaesthesia Critical Care & Pain. 20071;7(2):59-63.
7. Logan K. Addressing ketamine bladder syndrome. Nursing Times. https://www.nursingtimes.net/clinical-archive/medicine-management/addressing-ketamine-bladder-syndrome-19-06-2011/. Published June 19, 2011. Accessed October 11, 2019.
8. Lin PC, Lane HY, Lin CH. Spontaneous remission of ketamine withdrawal-related depression. Clin Neuropharmacol. 2016;39(1):51-52.
1. Kurdi MS, Theerth KA, Deva RS. Ketamine: current applications in anesthesia, pain, and critical care. Anesth Essays Res. 2014;8(3):283-290.
2. Davis K. What are the uses of ketamine? Medical News Today. https://www.medicalnewstoday.com/articles/302663.php. Updated October 12, 2017. Published October 11, 2019.
3. Chaverneff F. Ketamine: mechanisms of action, uses in pain medicine, and side effects. Clinical Pain Advisor. https://www.clinicalpainadvisor.com/home/conference-highlights/painweek-2018/ketamine-mechanisms-of-action-uses-in-pain-medicine-and-side-effects/. Published 2018. Accessed October 11, 2019.
4. Gao M, Rejaei D, Liu H. Ketamine use in current clinical practice. Acta Pharmacol Sin. 2016;37(7):865-872.
5. Orhurhu VJ, Claus LE, Cohen SP. Ketamine toxicity. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK541087. Updated April 11, 2019. Accessed October 18, 2019.
6. Pai A, Heining M. Ketamine. Continuing Education in Anaesthesia Critical Care & Pain. 20071;7(2):59-63.
7. Logan K. Addressing ketamine bladder syndrome. Nursing Times. https://www.nursingtimes.net/clinical-archive/medicine-management/addressing-ketamine-bladder-syndrome-19-06-2011/. Published June 19, 2011. Accessed October 11, 2019.
8. Lin PC, Lane HY, Lin CH. Spontaneous remission of ketamine withdrawal-related depression. Clin Neuropharmacol. 2016;39(1):51-52.
Neuropsychological testing: A useful but underutilized resource
We have all treated a patient for whom you know you had the diagnosis correct, the medication regimen was working, and the patient adhered to treatment, but something was still “off.” There was something cognitively that wasn’t right, and you had identified subtle (and some overt) errors in the standard psychiatric cognitive assessment that didn’t seem amenable to psychotropic medications. Perhaps what was needed was neuropsychological testing, one of the most useful but underutilized resources available to help fine-tune diagnosis and treatment. Finding a neuropsychologist who is sensitive to the unique needs of patients with psychiatric disorders, and knowing what and how to communicate the clinical picture and need for the referral, can be challenging due to the limited availability, time, and cost of a full battery of standardized tests.
This article describes the purpose of neuropsychological testing, why it is an important part of psychiatry, and how to make the best use of it.
What is neuropsychological testing?
Neuropsychological testing is a comprehensive evaluation designed to assess cognitive functioning, such as attention, language, learning, memory, and visuospatial and executive functioning. Neuropsychology has its own vocabulary and lexicon that are important for psychiatric clinicians to understand. Some terms, such as aphasia, working memory, and dementia, are familiar to many clinicians. However, others, such as information processing speed, performance validity testing, and semantic memory, might not be. Common neuropsychological terms are defined in Table 1.
The neuropsychologist’s role
A neuropsychologist is a psychologist with advanced training in brain-behavior relationships who can help determine if cognitive problems are related to neurologic, medical, or psychiatric factors. A neuropsychological evaluation can identify the etiology of a patient’s cognitive difficulties, such as stroke, poorly controlled diabetes, or mental health symptoms, to help guide treatment. It can be difficult to determine if a patient who is experiencing significant cognitive, functional, or behavioral changes has an underlying cognitive disorder (eg, dementia or major neurocognitive disorder) or something else, such as a psychiatric condition. Indeed, many psychiatric conditions, including schizophrenia, bipolar disorder, posttraumatic stress disorder (PTSD), and major depressive disorder (MDD), can present with significant cognitive difficulties. Thus, when patients report an increase in forgetfulness or changes in their ability to care for themselves, neuropsychological testing can help determine the cause.
How to refer to a neuropsychologist
Developing a referral network with a neuropsychologist should be a component of establishing a psychiatric practice. A neuropsychologist can help identify deficits that may interfere with the patient’s ability to adhere to a treatment plan, monitor medications, or actively participate in treatment and therapy. When making a referral for neuropsychological testing, it is important to be clear about the specific concerns so the neuropsychologist knows how to best evaluate the patient. A psychiatric clinician does not order specific neuropsychological tests, but thoroughly describes the problem so the neuropsychologist can determine the appropriate tests after interviewing the patient. For example, if a patient reports memory problems, it is essential to give the neuropsychologist specific clinical data so he/she can determine if the symptoms are due to a neurodegenerative or psychiatric condition. Then, after interviewing the patient (and, possibly, a family member), the neuropsychologist can construct a battery of tests to best answer the question.
Which neuropsychological tests are available?
There is a large battery of neuropsychological tests that require a licensed psychologist to administer and interpret.1 Those commonly used in research and practice to differentiate neurologically-based cognitive deficits associated with psychiatric disorders include the Wechsler Adult Intelligence Scale-4th edition (WAIS-IV) for assessing intelligence, the California Verbal Learning Test-Third Edition (CVLT-3) for verbal memory and learning, the Brief Visuospatial Memory Test-Revised for visual memory, the Wisconsin Card Sorting Test (WCST) for executive functions, and the Ruff 2&7 Selective Attention Test for sustained attention.2 These and other commonly used tests are described in Table 2.1
Neuropsychological testing vs psychological testing
The neuropsychologist will use psychometric properties (such as the validity and reliability of the test) and available normative data to pick the most appropriate tests. To date, there are no specific tests that clearly delineate psychiatric from nonpsychiatric etiologies, although the Screen for Cognitive Impairment in Psychiatry (SCIP)3 was developed in 2013 to explore cognitive abilities in the functional psychoses; it is beginning to be used in other studies.4,5 The neuropsychologist will consider the patient’s current concerns, the onset and progression of these concerns, and the pattern in testing behavior to help determine if psychiatric conditions are the most likely etiology.
Continue to: In addition to cognitive tests...
In addition to cognitive tests, the neuropsychologist might also administer psychological tests. These might include commonly used screening tools such as the Patient Health Questionnaire-9 (PHQ-9)6 or Geriatric Depression Scale (GDS),7 or more comprehensive objective personality measures, such as the Minnesota Multiphasic Personality Inventory-2-Restructured Format (MMPI-2-RF)8 or Personality Assessment Inventory (PAI).9 These tests, along with a thorough clinical history, can help identify if a psychiatric condition is present. In addition, for the more extensive tests such as the MMPI-2-RF or PAI, there are certain neuropsychological profiles that are consistent with a psychiatric etiology for cognitive difficulties. These profiles are formulated based on specific test scores in combination with complex patient variables.
Understanding the report
While there will be stylistic differences in reports depending on the neuropsychologist’s setting, referral source, and personal preferences, most will include discussion of why the patient was referred for evaluation and a description of the onset and progression of the problem.10 Reports often also include pertinent medical and psychiatric history, substance use history, and family medical history. A section on social history is important to help establish premorbid functioning, and might include information about prenatal/birth complications, developmental milestones, educational history, and occupational history. Information about current psychosocial support or stressors, including marital status or current/past legal issues, can be helpful. In addition to this history, there is often a section on behavioral observations, especially if anything stood out or might have affected the validity of the data.
There are also objective measures of validity that the neuropsychologist might administer to evaluate whether the results are valid. Issues of validity are monitored through the evaluation, and are used to determine if the results are consistent with known neurologic patterns. If the results are deemed not valid, then low scores cannot be reliably interpreted as evidence of impairment. This is akin to an arm moving during an X-ray, thereby blurring the results. If valid, the results of objective testing are include in the neuropsychologist’s report; this can range from providing raw scores, standard scores, and/or percentiles to a general description of how the patient did on testing.
The section that is usually of most interest to psychiatric clinicians is the summary, which explains the results, might offer a diagnosis, and discusses possible etiologies. This might be where the neuropsychologist discusses if the findings are due to a neurologic or psychiatric condition. From this comes the neuropsychologist’s recommendations. When a psychiatric condition is determined to be the underlying etiology, the neuropsychologist might recommend psychotherapy or some other psychiatric treatment.
Why is neuropsychological testing important?
Schizophrenia, MDD, bipolar disorder, and PTSD produce significant neurobiologic changes that often result in deterioration of a patient’s global cognitive function. Increased emphasis and attention in psychiatric research have yielded more clues to the neurobiology of cognition. However, even though many psychiatric clinicians are trained in cognitive assessments, such as the “clock test,” “serial sevens,” “numbers forward and backward,” “proverb,” and “word recall,” and common scenarios to evaluate judgment and insight, such as “mailing a letter” and “smoke in a movie theatre,” most of these components are not completed during a standard psychiatric evaluation. Because the time allotted to completing a psychiatric evaluation continues to be shortened, it is sometimes difficult to complete the “6 bullets” required by the Centers for Medicare & Medicaid Services as part of the mental status exam (Table 311).
Continue to: To date, the best evidence...
To date, the best evidence for neuropsychological deficits exists for patients with schizophrenia, bipolar disorder, MDD, and PTSD.12,13 The Box2,14-24 describes the findings of studies of neuropsychological deficits in patients with schizophrenia and bipolar disorder.
Box
Patients with schizophrenia have been the subjects of neuropsychological testing for decades. The results have shown deficits on many standardized tests, including those of attention, memory, and executive functioning, although some patients might perform within normal limits.15
A federal initiative through the National Institute of Mental Health (NIMH) known as MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia) was developed in the late 1990s to develop consensus on the underlying cognitive deficits in schizophrenia. MATRICS was created with the hopes that it would allow the FDA to approve treatments for those cognitive deficits independent of psychosis because current psychotropic medications have minimal efficacy on cognition.16,17 The MATRICS group identified working memory, attention/vigilance, verbal learning and memory, visual learning and memory, speed of processing, reasoning and problem solving, and social cognition as the key cognitive domains most affected in schizophrenia.14 The initial program has since evolved into 3 distinct NIMH programs: CNTRICS18 (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia), TURNS19 (Treatment Units for Research on Neurocognition in Schizophrenia), and TENETS20 (Treatment and Evaluation Network for Trials in Schizophrenia). The combination of neuropsychological testing and neuroimaging has led to the conceptualization of schizophrenia as a neurodevelopmental disorder.
Individuals at risk for psychosis
As clinicians, we have long heard from parents of children with schizophrenia a standard trajectory of functional decline: early premorbid changes, a fairly measurable prodromal period marked by subtle deterioration in cognitive functioning, followed by the actual illness trajectory. In a recent meta-analysis, researchers compared the results of 60 neuropsychological tests comprising 9 domains in people who were at clinical high risk for psychosis who eventually converted to a psychotic disorder (CHR-P), those at clinical high risk who did not convert to psychosis (CHR-NP), and healthy controls.21 They found that neuropsychological performance deficits were greater in CHR-P individuals than in those in the CHR-NP group, and both had greater deficits than healthy controls.
For many patients with schizophrenia, full cognitive maturation is never reached.22 In general, decreased motivation in schizophrenia has been correlated with neurocognitive deficits.23
Schizophrenia vs bipolar disorder
In a study comparing neuropsychological functioning in patients with schizophrenia and bipolar disorder with psychotic features (BP-P), researchers found greater deficits in schizophrenia, including immediate verbal recall, working memory, processing speed, and verbal fluency.22 Patients with BP-P demonstrated impairment consistent with generalized impairment in verbal learning and memory, working memory, and processing speed.22
Children/adolescents
In a recent study comparing child and adolescent offspring of patients with schizophrenia (n = 41) and bipolar disorder (n = 90), researchers identified neuropsychological deficits in visual memory for both groups, suggesting common genetic linkages. The schizophrenia offspring scored lower in verbal memory and word memory, while bipolar offspring scored lower on the processing speed index and visual memory.2
Information processing
Another study compared the results of neuropsychological testing and the P300 component of auditory event-related potential (an electrophysiological measure) in 30 patients with schizophrenia, siblings without illness, and normal controls.24 The battery of neuropsychological tests included the Digit Symbol Substitution Test, Digit Vigilance Test, Trail Making Test-B, and Stroop test. The P300 is well correlated with information processing. Researchers found decreased P300 amplitude and latency in the patients and normal levels in the controls; siblings scored somewhere in between.24 Scores on the neuropsychological tests were consistently below normal in both patients and their siblings, with patients scoring the lowest.24
Continue to: Neuropsychological testing
Neuropsychological testing: 2 Case studies
The following 2 cases illustrate the pivotal role of neuropsychological testing in formulating an accurate differential diagnosis, and facilitating improved outcomes.
Case 1
A veteran with PTSD and memory complaints
Mr. J, age 70, is a married man who spent his career in the military, including combat service in the Vietnam War. His service in Vietnam included an event in which he couldn’t save platoon members from an ambush and death in a firefight, after which he developed PTSD. He retired after 25 years of service.
Mr. J’s psychiatrist refers him to a neuropsychologist for complaints of memory difficulties, including a fear that he’s developing Alzheimer’s disease (AD). Because of the concern for AD, he undergoes tests of learning and memory, such as the CVLT-3, the Brief Visuospatial Memory Test-Revised, and the Logical Memory subtest from the Wechsler Memory Scale–4th Edition. Other tests include a measure of confrontation naming, verbal fluency (phonemic and semantic fluency), construction, attention, processing speed, and problem solving. In addition, a measure of psychiatric and emotional functioning is also administered (the MMPI-2-RF).
The results determined that Mr. J’s subjective experience of recall deficits is better explained by anxiety resulting from the cumulative impact of day-to-day emotional stress in the setting of chronic PTSD.25 Mr. J was experiencing cognitive sequelae from a complicated emotional dynamic, comprised of situational stress, amplified by coping difficulties that were rooted in older posttraumatic symptoms. These emotions, and the cognitive load they generated, interfered with the normal processes of attention and organization necessary for the encoding of information to be remembered.26 He described being visibly angered by the clutter in his home (the result of multiple people living there, including a young grandchild), having his efforts to get things done interrupted by the needs of others, and a perceived loss of control gradually generalized to even mundane circumstances, as often occurs with traumatic responses. In short, he was chronically overwhelmed and not experiencing the beginnings of dementia.
For Mr. J, neuropsychological testing helped define the focus and course of therapy. If he had been diagnosed with a major neurocognitive disorder, therapy might have taken a more acceptance and grief-based approach, to help him adjust to a chronic, potentially life-limiting condition. Because this diagnosis was ruled out, and his cognitive complaints were determined to be secondary to a core diagnosis of PTSD, therapy instead focused on treating PTSD.
Continue to: Case 2
Case 2
A 55-year-old with bipolar I disorder
Mr. S, age 55, is taken to the emergency department (ED) because of his complaints of a severe headache. While undergoing brain MRI, Mr. S becomes highly agitated and aggressive to the radiology staff and is transferred to the psychiatric inpatient unit. He has a history of bipolar disorder that was treated with lithium approximately 20 years ago. Due to continued agitation, he is transferred to the state hospital and prescribed multiple medications, including an unspecified first-generation antipsychotic (FGA) that results in drooling and causes him to stoop and shuffle.
Mr. S’s wife contacts a community psychiatrist after becoming frustrated by her inability to communicate with the staff at the state hospital. During a 1-hour consult, she reveals that Mr. S was a competitive speedboat racer and had suffered numerous concussions due to accidents; at least 3 of these concussions that occurred when he was in his 20s and 30s had included a loss of consciousness. Mr. S had always been treated in the ED, and never required hospitalization. He had a previous marriage, was estranged from his ex-wife and 3 children, and has a history of alcohol abuse.
The MRI taken in the ED reveals numerous patches of scar tissue throughout the cortex, most notably in the striatum areas. The psychiatrist suspects that Mr. S’s agitation and irritation were related to focal seizure activity. He encourages Mr. S’s wife to speak with the attending psychiatrist at the state hospital and ask for him to be discharged home under her care.
Eventually, Mr. S is referred for a neurologic consult and neuropsychological testing. The testing included measures of attention and working, learning and memory, and executive functioning. The results reveal numerous deficits that Mr. S had been able to compensate for when he was younger, including problems with recall of newly learned information and difficulty modifying his behavior according to feedback. Mr. S is weaned from high doses of the FGA and is stabilized on 2 antiepileptic agents, sertraline, and low-dose olanzapine. A rehabilitation plan is developed, and Mr. S remains out of the hospital.
A team-based approach
Psychiatric clinicians need to recognize the subtle as well as overt cognitive deficits present in patients with many of the illnesses that we treat on a daily basis. In this era of performance- and value-based care, it is important to understand the common neuropsychological tests available to assist in providing patient-centered care tailored to specific cognitive deficits. Including a neuropsychologist is essential to implementing a team-based approach.
Continue to: Bottom Line
Bottom Line
Neuropsychological testing can help pinpoint key cognitive deficits that interfere with the potential for optimal patient outcomes. Psychiatric clinicians need to be knowledgeable about the common tests used and how to incorporate the results into their diagnosis and treatment plans.
Related Resources
- The American Academy of Clinical Neuropsychology. www.theaacn.org.
- Schwarz L. Answers to 7 questions about using neuropsychological testing in your practice. Current Psychiatry. 2014;13(3):33-39.
Drug Brand Names
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Sertraline • Zoloft
1. Zucchella C, Federico A, Martini A, et al. Neuropsychological testing: how to understand it. Practical Neurology. 2018;18(3):227-237.
2. de la Serna E, Sugranyes G, Sanchez-Gistau V, et al. Neuropsychological characteristics of child and adolescent offspring of patients with schizophrenia or bipolar disorder. Schizophr Res. 2017;183:110-115.
3. Gómez-Benito J, Guilera G, Pino Ó, et al. The screen for cognitive impairment in psychiatry: diagnostic-specific standardization in psychiatric ill patients. BMC Psychiatry. 2013;13:127.
4. Fuente-Tomas L, Arranz B, Safont G, et al. Classification of patients with bipolar disorder using k-means clustering. PLoS One. 2019;14(1):e0210314.
5. Kronbichler L, Stelzig-Schöler R, Pearce BG, et al. Schizophrenia and category-selectivity in the brain: Normal for faces but abnormal for houses. Front Psychiatry. 2018;9:47.
6. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med. 2001;16(9):606-613.
7. Yesavage A, Brink TL, Rose TL, et al. Development and validation of a geriatric depression screening scale: a preliminary report. J Psychiatr Res. 1983;17(1):37-49.
8. Ben-Porath YS, Tellegen A. Minnesota multi-phasic personality inventory-2 restructured form: MMPI-2-RF. San Antonio, TX: NCS Pearson; 2008.
9. Morey LC. Personality assessment inventory. Odessa, FL: Psychological Assessment Resources; 1991.
10. Donder J, ed. Neuropsychological report writing. New York, NY: The Guilford Press; 2016.
11. Department of Health and Human Services, Centers for Medicare and Medicaid Services. Evaluation and management services. https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/eval-mgmt-serv-guide-ICN006764.pdf. Published August 2017. Accessed October 10, 2019.
12. Hunt S, Root JC, Bascetta BL. Effort testing in schizophrenia and schizoaffective disorder: validity indicator profile and test of memory malingering performance characteristics. Arch Clin Neuropsychol. 2014;29(2):164-172.
13. Gorlyn M, Keilp J, Burke A, et al. Treatment-related improvement in neuropsychological functioning in suicidal depressed patients: paroxetine vs. bupropion. Psychiatry Res. 2015;225(3):407-412.
14. Pettersson R, Söderström S, Nilsson KW. Diagnosing ADHD in adults: an examination of the discriminative validity of neuropsychological tests and diagnostic assessment instruments. J Atten Disord. 2018;22(11):1019-1031.
15. Urfer-Parnas, A, Mortensen EL, Parnas J. Core of schizophrenia: estrangement, dementia or neurocognitive disorder? Psychopathology. 2010;43(5):300-311.
16. Green MF, Nuechterlein KH, Gold JM, et al. Approaching a consensus cognitive battery for clinical trials in schizophrenia: the NIMH-MATRICS conference to select cognitive domains and test criteria. Biolog Psych. 2004;56(5):301-307.
17. Green MF, Nuechterlein KH. The MATRICS initiative: developing a consensus cognitive battery for clinical trials. Schizophr Res. 2004;72(1):1-3.
18. Kern RS, Green MF, Nuechterlein KH, et al. NIMH-MATRICS survey on assessment of neurocognition in schizophrenia. Schizophr Res. 2004;72(1):11-19.
19. Carter CS, Barch DM. Cognitive neuroscience-based approaches to measuring and improving treatment effects on cognition in schizophrenia: the CNTRICS initiative. Schizophr Bull. 2007;33(5):1131-1137.
20. Geyer M. New opportunities in the treatment of cognitive impairments associated with schizophrenia. Curr Dir Psych Sci. 2010;19(4):264-269.
21. Hauser M, Zhang JP, Sheridan EM, et al. Neuropsychological test performance to enhance identification of subjects at clinical high risk for psychosis and to be most promising for predictive algorithms for conversion to psychosis: a meta-analysis. J Clin Psych. 2017;78(1):e28-e40. doi: 10.4088/JCP.15r10197.
22. Menkes MW, Armstrong K, Blackford JU, et al. Neuropsychological functioning in early and chronic stages of schizophrenia and psychotic bipolar disorder. Schizophr Res. 2019;206:413-419.
23. Najas-Garcia A, Gomez-Benito J, Hueda-Medina T. The relationship of motivation and neurocognition with functionality in schizophrenia: a meta-analytic review. Community Ment Health J. 2018;54(7):1019-1049.
24. Raghavan DV, Shanmugiah A, Bharathi P, et al. P300 and neuropsychological measurements in patients with schizophrenia and their healthy biological siblings. Indian J Psychiatry. 2016;58(4):454-458.
25. Mozzambani A, Fuso S, Malta S, et al. Long-term follow-up of attentional and executive functions of PTSD patients. Psychol Neurosci. 2017;10(2):215-224.
26. Woon F, Farrer T, Braman C, et al A meta-analysis of the relationship between symptom severity of posttraumatic stress disorder and executive function. Cogn Neuropsychiatry. 2017;22(1):1-16.
We have all treated a patient for whom you know you had the diagnosis correct, the medication regimen was working, and the patient adhered to treatment, but something was still “off.” There was something cognitively that wasn’t right, and you had identified subtle (and some overt) errors in the standard psychiatric cognitive assessment that didn’t seem amenable to psychotropic medications. Perhaps what was needed was neuropsychological testing, one of the most useful but underutilized resources available to help fine-tune diagnosis and treatment. Finding a neuropsychologist who is sensitive to the unique needs of patients with psychiatric disorders, and knowing what and how to communicate the clinical picture and need for the referral, can be challenging due to the limited availability, time, and cost of a full battery of standardized tests.
This article describes the purpose of neuropsychological testing, why it is an important part of psychiatry, and how to make the best use of it.
What is neuropsychological testing?
Neuropsychological testing is a comprehensive evaluation designed to assess cognitive functioning, such as attention, language, learning, memory, and visuospatial and executive functioning. Neuropsychology has its own vocabulary and lexicon that are important for psychiatric clinicians to understand. Some terms, such as aphasia, working memory, and dementia, are familiar to many clinicians. However, others, such as information processing speed, performance validity testing, and semantic memory, might not be. Common neuropsychological terms are defined in Table 1.
The neuropsychologist’s role
A neuropsychologist is a psychologist with advanced training in brain-behavior relationships who can help determine if cognitive problems are related to neurologic, medical, or psychiatric factors. A neuropsychological evaluation can identify the etiology of a patient’s cognitive difficulties, such as stroke, poorly controlled diabetes, or mental health symptoms, to help guide treatment. It can be difficult to determine if a patient who is experiencing significant cognitive, functional, or behavioral changes has an underlying cognitive disorder (eg, dementia or major neurocognitive disorder) or something else, such as a psychiatric condition. Indeed, many psychiatric conditions, including schizophrenia, bipolar disorder, posttraumatic stress disorder (PTSD), and major depressive disorder (MDD), can present with significant cognitive difficulties. Thus, when patients report an increase in forgetfulness or changes in their ability to care for themselves, neuropsychological testing can help determine the cause.
How to refer to a neuropsychologist
Developing a referral network with a neuropsychologist should be a component of establishing a psychiatric practice. A neuropsychologist can help identify deficits that may interfere with the patient’s ability to adhere to a treatment plan, monitor medications, or actively participate in treatment and therapy. When making a referral for neuropsychological testing, it is important to be clear about the specific concerns so the neuropsychologist knows how to best evaluate the patient. A psychiatric clinician does not order specific neuropsychological tests, but thoroughly describes the problem so the neuropsychologist can determine the appropriate tests after interviewing the patient. For example, if a patient reports memory problems, it is essential to give the neuropsychologist specific clinical data so he/she can determine if the symptoms are due to a neurodegenerative or psychiatric condition. Then, after interviewing the patient (and, possibly, a family member), the neuropsychologist can construct a battery of tests to best answer the question.
Which neuropsychological tests are available?
There is a large battery of neuropsychological tests that require a licensed psychologist to administer and interpret.1 Those commonly used in research and practice to differentiate neurologically-based cognitive deficits associated with psychiatric disorders include the Wechsler Adult Intelligence Scale-4th edition (WAIS-IV) for assessing intelligence, the California Verbal Learning Test-Third Edition (CVLT-3) for verbal memory and learning, the Brief Visuospatial Memory Test-Revised for visual memory, the Wisconsin Card Sorting Test (WCST) for executive functions, and the Ruff 2&7 Selective Attention Test for sustained attention.2 These and other commonly used tests are described in Table 2.1
Neuropsychological testing vs psychological testing
The neuropsychologist will use psychometric properties (such as the validity and reliability of the test) and available normative data to pick the most appropriate tests. To date, there are no specific tests that clearly delineate psychiatric from nonpsychiatric etiologies, although the Screen for Cognitive Impairment in Psychiatry (SCIP)3 was developed in 2013 to explore cognitive abilities in the functional psychoses; it is beginning to be used in other studies.4,5 The neuropsychologist will consider the patient’s current concerns, the onset and progression of these concerns, and the pattern in testing behavior to help determine if psychiatric conditions are the most likely etiology.
Continue to: In addition to cognitive tests...
In addition to cognitive tests, the neuropsychologist might also administer psychological tests. These might include commonly used screening tools such as the Patient Health Questionnaire-9 (PHQ-9)6 or Geriatric Depression Scale (GDS),7 or more comprehensive objective personality measures, such as the Minnesota Multiphasic Personality Inventory-2-Restructured Format (MMPI-2-RF)8 or Personality Assessment Inventory (PAI).9 These tests, along with a thorough clinical history, can help identify if a psychiatric condition is present. In addition, for the more extensive tests such as the MMPI-2-RF or PAI, there are certain neuropsychological profiles that are consistent with a psychiatric etiology for cognitive difficulties. These profiles are formulated based on specific test scores in combination with complex patient variables.
Understanding the report
While there will be stylistic differences in reports depending on the neuropsychologist’s setting, referral source, and personal preferences, most will include discussion of why the patient was referred for evaluation and a description of the onset and progression of the problem.10 Reports often also include pertinent medical and psychiatric history, substance use history, and family medical history. A section on social history is important to help establish premorbid functioning, and might include information about prenatal/birth complications, developmental milestones, educational history, and occupational history. Information about current psychosocial support or stressors, including marital status or current/past legal issues, can be helpful. In addition to this history, there is often a section on behavioral observations, especially if anything stood out or might have affected the validity of the data.
There are also objective measures of validity that the neuropsychologist might administer to evaluate whether the results are valid. Issues of validity are monitored through the evaluation, and are used to determine if the results are consistent with known neurologic patterns. If the results are deemed not valid, then low scores cannot be reliably interpreted as evidence of impairment. This is akin to an arm moving during an X-ray, thereby blurring the results. If valid, the results of objective testing are include in the neuropsychologist’s report; this can range from providing raw scores, standard scores, and/or percentiles to a general description of how the patient did on testing.
The section that is usually of most interest to psychiatric clinicians is the summary, which explains the results, might offer a diagnosis, and discusses possible etiologies. This might be where the neuropsychologist discusses if the findings are due to a neurologic or psychiatric condition. From this comes the neuropsychologist’s recommendations. When a psychiatric condition is determined to be the underlying etiology, the neuropsychologist might recommend psychotherapy or some other psychiatric treatment.
Why is neuropsychological testing important?
Schizophrenia, MDD, bipolar disorder, and PTSD produce significant neurobiologic changes that often result in deterioration of a patient’s global cognitive function. Increased emphasis and attention in psychiatric research have yielded more clues to the neurobiology of cognition. However, even though many psychiatric clinicians are trained in cognitive assessments, such as the “clock test,” “serial sevens,” “numbers forward and backward,” “proverb,” and “word recall,” and common scenarios to evaluate judgment and insight, such as “mailing a letter” and “smoke in a movie theatre,” most of these components are not completed during a standard psychiatric evaluation. Because the time allotted to completing a psychiatric evaluation continues to be shortened, it is sometimes difficult to complete the “6 bullets” required by the Centers for Medicare & Medicaid Services as part of the mental status exam (Table 311).
Continue to: To date, the best evidence...
To date, the best evidence for neuropsychological deficits exists for patients with schizophrenia, bipolar disorder, MDD, and PTSD.12,13 The Box2,14-24 describes the findings of studies of neuropsychological deficits in patients with schizophrenia and bipolar disorder.
Box
Patients with schizophrenia have been the subjects of neuropsychological testing for decades. The results have shown deficits on many standardized tests, including those of attention, memory, and executive functioning, although some patients might perform within normal limits.15
A federal initiative through the National Institute of Mental Health (NIMH) known as MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia) was developed in the late 1990s to develop consensus on the underlying cognitive deficits in schizophrenia. MATRICS was created with the hopes that it would allow the FDA to approve treatments for those cognitive deficits independent of psychosis because current psychotropic medications have minimal efficacy on cognition.16,17 The MATRICS group identified working memory, attention/vigilance, verbal learning and memory, visual learning and memory, speed of processing, reasoning and problem solving, and social cognition as the key cognitive domains most affected in schizophrenia.14 The initial program has since evolved into 3 distinct NIMH programs: CNTRICS18 (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia), TURNS19 (Treatment Units for Research on Neurocognition in Schizophrenia), and TENETS20 (Treatment and Evaluation Network for Trials in Schizophrenia). The combination of neuropsychological testing and neuroimaging has led to the conceptualization of schizophrenia as a neurodevelopmental disorder.
Individuals at risk for psychosis
As clinicians, we have long heard from parents of children with schizophrenia a standard trajectory of functional decline: early premorbid changes, a fairly measurable prodromal period marked by subtle deterioration in cognitive functioning, followed by the actual illness trajectory. In a recent meta-analysis, researchers compared the results of 60 neuropsychological tests comprising 9 domains in people who were at clinical high risk for psychosis who eventually converted to a psychotic disorder (CHR-P), those at clinical high risk who did not convert to psychosis (CHR-NP), and healthy controls.21 They found that neuropsychological performance deficits were greater in CHR-P individuals than in those in the CHR-NP group, and both had greater deficits than healthy controls.
For many patients with schizophrenia, full cognitive maturation is never reached.22 In general, decreased motivation in schizophrenia has been correlated with neurocognitive deficits.23
Schizophrenia vs bipolar disorder
In a study comparing neuropsychological functioning in patients with schizophrenia and bipolar disorder with psychotic features (BP-P), researchers found greater deficits in schizophrenia, including immediate verbal recall, working memory, processing speed, and verbal fluency.22 Patients with BP-P demonstrated impairment consistent with generalized impairment in verbal learning and memory, working memory, and processing speed.22
Children/adolescents
In a recent study comparing child and adolescent offspring of patients with schizophrenia (n = 41) and bipolar disorder (n = 90), researchers identified neuropsychological deficits in visual memory for both groups, suggesting common genetic linkages. The schizophrenia offspring scored lower in verbal memory and word memory, while bipolar offspring scored lower on the processing speed index and visual memory.2
Information processing
Another study compared the results of neuropsychological testing and the P300 component of auditory event-related potential (an electrophysiological measure) in 30 patients with schizophrenia, siblings without illness, and normal controls.24 The battery of neuropsychological tests included the Digit Symbol Substitution Test, Digit Vigilance Test, Trail Making Test-B, and Stroop test. The P300 is well correlated with information processing. Researchers found decreased P300 amplitude and latency in the patients and normal levels in the controls; siblings scored somewhere in between.24 Scores on the neuropsychological tests were consistently below normal in both patients and their siblings, with patients scoring the lowest.24
Continue to: Neuropsychological testing
Neuropsychological testing: 2 Case studies
The following 2 cases illustrate the pivotal role of neuropsychological testing in formulating an accurate differential diagnosis, and facilitating improved outcomes.
Case 1
A veteran with PTSD and memory complaints
Mr. J, age 70, is a married man who spent his career in the military, including combat service in the Vietnam War. His service in Vietnam included an event in which he couldn’t save platoon members from an ambush and death in a firefight, after which he developed PTSD. He retired after 25 years of service.
Mr. J’s psychiatrist refers him to a neuropsychologist for complaints of memory difficulties, including a fear that he’s developing Alzheimer’s disease (AD). Because of the concern for AD, he undergoes tests of learning and memory, such as the CVLT-3, the Brief Visuospatial Memory Test-Revised, and the Logical Memory subtest from the Wechsler Memory Scale–4th Edition. Other tests include a measure of confrontation naming, verbal fluency (phonemic and semantic fluency), construction, attention, processing speed, and problem solving. In addition, a measure of psychiatric and emotional functioning is also administered (the MMPI-2-RF).
The results determined that Mr. J’s subjective experience of recall deficits is better explained by anxiety resulting from the cumulative impact of day-to-day emotional stress in the setting of chronic PTSD.25 Mr. J was experiencing cognitive sequelae from a complicated emotional dynamic, comprised of situational stress, amplified by coping difficulties that were rooted in older posttraumatic symptoms. These emotions, and the cognitive load they generated, interfered with the normal processes of attention and organization necessary for the encoding of information to be remembered.26 He described being visibly angered by the clutter in his home (the result of multiple people living there, including a young grandchild), having his efforts to get things done interrupted by the needs of others, and a perceived loss of control gradually generalized to even mundane circumstances, as often occurs with traumatic responses. In short, he was chronically overwhelmed and not experiencing the beginnings of dementia.
For Mr. J, neuropsychological testing helped define the focus and course of therapy. If he had been diagnosed with a major neurocognitive disorder, therapy might have taken a more acceptance and grief-based approach, to help him adjust to a chronic, potentially life-limiting condition. Because this diagnosis was ruled out, and his cognitive complaints were determined to be secondary to a core diagnosis of PTSD, therapy instead focused on treating PTSD.
Continue to: Case 2
Case 2
A 55-year-old with bipolar I disorder
Mr. S, age 55, is taken to the emergency department (ED) because of his complaints of a severe headache. While undergoing brain MRI, Mr. S becomes highly agitated and aggressive to the radiology staff and is transferred to the psychiatric inpatient unit. He has a history of bipolar disorder that was treated with lithium approximately 20 years ago. Due to continued agitation, he is transferred to the state hospital and prescribed multiple medications, including an unspecified first-generation antipsychotic (FGA) that results in drooling and causes him to stoop and shuffle.
Mr. S’s wife contacts a community psychiatrist after becoming frustrated by her inability to communicate with the staff at the state hospital. During a 1-hour consult, she reveals that Mr. S was a competitive speedboat racer and had suffered numerous concussions due to accidents; at least 3 of these concussions that occurred when he was in his 20s and 30s had included a loss of consciousness. Mr. S had always been treated in the ED, and never required hospitalization. He had a previous marriage, was estranged from his ex-wife and 3 children, and has a history of alcohol abuse.
The MRI taken in the ED reveals numerous patches of scar tissue throughout the cortex, most notably in the striatum areas. The psychiatrist suspects that Mr. S’s agitation and irritation were related to focal seizure activity. He encourages Mr. S’s wife to speak with the attending psychiatrist at the state hospital and ask for him to be discharged home under her care.
Eventually, Mr. S is referred for a neurologic consult and neuropsychological testing. The testing included measures of attention and working, learning and memory, and executive functioning. The results reveal numerous deficits that Mr. S had been able to compensate for when he was younger, including problems with recall of newly learned information and difficulty modifying his behavior according to feedback. Mr. S is weaned from high doses of the FGA and is stabilized on 2 antiepileptic agents, sertraline, and low-dose olanzapine. A rehabilitation plan is developed, and Mr. S remains out of the hospital.
A team-based approach
Psychiatric clinicians need to recognize the subtle as well as overt cognitive deficits present in patients with many of the illnesses that we treat on a daily basis. In this era of performance- and value-based care, it is important to understand the common neuropsychological tests available to assist in providing patient-centered care tailored to specific cognitive deficits. Including a neuropsychologist is essential to implementing a team-based approach.
Continue to: Bottom Line
Bottom Line
Neuropsychological testing can help pinpoint key cognitive deficits that interfere with the potential for optimal patient outcomes. Psychiatric clinicians need to be knowledgeable about the common tests used and how to incorporate the results into their diagnosis and treatment plans.
Related Resources
- The American Academy of Clinical Neuropsychology. www.theaacn.org.
- Schwarz L. Answers to 7 questions about using neuropsychological testing in your practice. Current Psychiatry. 2014;13(3):33-39.
Drug Brand Names
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Sertraline • Zoloft
We have all treated a patient for whom you know you had the diagnosis correct, the medication regimen was working, and the patient adhered to treatment, but something was still “off.” There was something cognitively that wasn’t right, and you had identified subtle (and some overt) errors in the standard psychiatric cognitive assessment that didn’t seem amenable to psychotropic medications. Perhaps what was needed was neuropsychological testing, one of the most useful but underutilized resources available to help fine-tune diagnosis and treatment. Finding a neuropsychologist who is sensitive to the unique needs of patients with psychiatric disorders, and knowing what and how to communicate the clinical picture and need for the referral, can be challenging due to the limited availability, time, and cost of a full battery of standardized tests.
This article describes the purpose of neuropsychological testing, why it is an important part of psychiatry, and how to make the best use of it.
What is neuropsychological testing?
Neuropsychological testing is a comprehensive evaluation designed to assess cognitive functioning, such as attention, language, learning, memory, and visuospatial and executive functioning. Neuropsychology has its own vocabulary and lexicon that are important for psychiatric clinicians to understand. Some terms, such as aphasia, working memory, and dementia, are familiar to many clinicians. However, others, such as information processing speed, performance validity testing, and semantic memory, might not be. Common neuropsychological terms are defined in Table 1.
The neuropsychologist’s role
A neuropsychologist is a psychologist with advanced training in brain-behavior relationships who can help determine if cognitive problems are related to neurologic, medical, or psychiatric factors. A neuropsychological evaluation can identify the etiology of a patient’s cognitive difficulties, such as stroke, poorly controlled diabetes, or mental health symptoms, to help guide treatment. It can be difficult to determine if a patient who is experiencing significant cognitive, functional, or behavioral changes has an underlying cognitive disorder (eg, dementia or major neurocognitive disorder) or something else, such as a psychiatric condition. Indeed, many psychiatric conditions, including schizophrenia, bipolar disorder, posttraumatic stress disorder (PTSD), and major depressive disorder (MDD), can present with significant cognitive difficulties. Thus, when patients report an increase in forgetfulness or changes in their ability to care for themselves, neuropsychological testing can help determine the cause.
How to refer to a neuropsychologist
Developing a referral network with a neuropsychologist should be a component of establishing a psychiatric practice. A neuropsychologist can help identify deficits that may interfere with the patient’s ability to adhere to a treatment plan, monitor medications, or actively participate in treatment and therapy. When making a referral for neuropsychological testing, it is important to be clear about the specific concerns so the neuropsychologist knows how to best evaluate the patient. A psychiatric clinician does not order specific neuropsychological tests, but thoroughly describes the problem so the neuropsychologist can determine the appropriate tests after interviewing the patient. For example, if a patient reports memory problems, it is essential to give the neuropsychologist specific clinical data so he/she can determine if the symptoms are due to a neurodegenerative or psychiatric condition. Then, after interviewing the patient (and, possibly, a family member), the neuropsychologist can construct a battery of tests to best answer the question.
Which neuropsychological tests are available?
There is a large battery of neuropsychological tests that require a licensed psychologist to administer and interpret.1 Those commonly used in research and practice to differentiate neurologically-based cognitive deficits associated with psychiatric disorders include the Wechsler Adult Intelligence Scale-4th edition (WAIS-IV) for assessing intelligence, the California Verbal Learning Test-Third Edition (CVLT-3) for verbal memory and learning, the Brief Visuospatial Memory Test-Revised for visual memory, the Wisconsin Card Sorting Test (WCST) for executive functions, and the Ruff 2&7 Selective Attention Test for sustained attention.2 These and other commonly used tests are described in Table 2.1
Neuropsychological testing vs psychological testing
The neuropsychologist will use psychometric properties (such as the validity and reliability of the test) and available normative data to pick the most appropriate tests. To date, there are no specific tests that clearly delineate psychiatric from nonpsychiatric etiologies, although the Screen for Cognitive Impairment in Psychiatry (SCIP)3 was developed in 2013 to explore cognitive abilities in the functional psychoses; it is beginning to be used in other studies.4,5 The neuropsychologist will consider the patient’s current concerns, the onset and progression of these concerns, and the pattern in testing behavior to help determine if psychiatric conditions are the most likely etiology.
Continue to: In addition to cognitive tests...
In addition to cognitive tests, the neuropsychologist might also administer psychological tests. These might include commonly used screening tools such as the Patient Health Questionnaire-9 (PHQ-9)6 or Geriatric Depression Scale (GDS),7 or more comprehensive objective personality measures, such as the Minnesota Multiphasic Personality Inventory-2-Restructured Format (MMPI-2-RF)8 or Personality Assessment Inventory (PAI).9 These tests, along with a thorough clinical history, can help identify if a psychiatric condition is present. In addition, for the more extensive tests such as the MMPI-2-RF or PAI, there are certain neuropsychological profiles that are consistent with a psychiatric etiology for cognitive difficulties. These profiles are formulated based on specific test scores in combination with complex patient variables.
Understanding the report
While there will be stylistic differences in reports depending on the neuropsychologist’s setting, referral source, and personal preferences, most will include discussion of why the patient was referred for evaluation and a description of the onset and progression of the problem.10 Reports often also include pertinent medical and psychiatric history, substance use history, and family medical history. A section on social history is important to help establish premorbid functioning, and might include information about prenatal/birth complications, developmental milestones, educational history, and occupational history. Information about current psychosocial support or stressors, including marital status or current/past legal issues, can be helpful. In addition to this history, there is often a section on behavioral observations, especially if anything stood out or might have affected the validity of the data.
There are also objective measures of validity that the neuropsychologist might administer to evaluate whether the results are valid. Issues of validity are monitored through the evaluation, and are used to determine if the results are consistent with known neurologic patterns. If the results are deemed not valid, then low scores cannot be reliably interpreted as evidence of impairment. This is akin to an arm moving during an X-ray, thereby blurring the results. If valid, the results of objective testing are include in the neuropsychologist’s report; this can range from providing raw scores, standard scores, and/or percentiles to a general description of how the patient did on testing.
The section that is usually of most interest to psychiatric clinicians is the summary, which explains the results, might offer a diagnosis, and discusses possible etiologies. This might be where the neuropsychologist discusses if the findings are due to a neurologic or psychiatric condition. From this comes the neuropsychologist’s recommendations. When a psychiatric condition is determined to be the underlying etiology, the neuropsychologist might recommend psychotherapy or some other psychiatric treatment.
Why is neuropsychological testing important?
Schizophrenia, MDD, bipolar disorder, and PTSD produce significant neurobiologic changes that often result in deterioration of a patient’s global cognitive function. Increased emphasis and attention in psychiatric research have yielded more clues to the neurobiology of cognition. However, even though many psychiatric clinicians are trained in cognitive assessments, such as the “clock test,” “serial sevens,” “numbers forward and backward,” “proverb,” and “word recall,” and common scenarios to evaluate judgment and insight, such as “mailing a letter” and “smoke in a movie theatre,” most of these components are not completed during a standard psychiatric evaluation. Because the time allotted to completing a psychiatric evaluation continues to be shortened, it is sometimes difficult to complete the “6 bullets” required by the Centers for Medicare & Medicaid Services as part of the mental status exam (Table 311).
Continue to: To date, the best evidence...
To date, the best evidence for neuropsychological deficits exists for patients with schizophrenia, bipolar disorder, MDD, and PTSD.12,13 The Box2,14-24 describes the findings of studies of neuropsychological deficits in patients with schizophrenia and bipolar disorder.
Box
Patients with schizophrenia have been the subjects of neuropsychological testing for decades. The results have shown deficits on many standardized tests, including those of attention, memory, and executive functioning, although some patients might perform within normal limits.15
A federal initiative through the National Institute of Mental Health (NIMH) known as MATRICS (Measurement and Treatment Research to Improve Cognition in Schizophrenia) was developed in the late 1990s to develop consensus on the underlying cognitive deficits in schizophrenia. MATRICS was created with the hopes that it would allow the FDA to approve treatments for those cognitive deficits independent of psychosis because current psychotropic medications have minimal efficacy on cognition.16,17 The MATRICS group identified working memory, attention/vigilance, verbal learning and memory, visual learning and memory, speed of processing, reasoning and problem solving, and social cognition as the key cognitive domains most affected in schizophrenia.14 The initial program has since evolved into 3 distinct NIMH programs: CNTRICS18 (Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia), TURNS19 (Treatment Units for Research on Neurocognition in Schizophrenia), and TENETS20 (Treatment and Evaluation Network for Trials in Schizophrenia). The combination of neuropsychological testing and neuroimaging has led to the conceptualization of schizophrenia as a neurodevelopmental disorder.
Individuals at risk for psychosis
As clinicians, we have long heard from parents of children with schizophrenia a standard trajectory of functional decline: early premorbid changes, a fairly measurable prodromal period marked by subtle deterioration in cognitive functioning, followed by the actual illness trajectory. In a recent meta-analysis, researchers compared the results of 60 neuropsychological tests comprising 9 domains in people who were at clinical high risk for psychosis who eventually converted to a psychotic disorder (CHR-P), those at clinical high risk who did not convert to psychosis (CHR-NP), and healthy controls.21 They found that neuropsychological performance deficits were greater in CHR-P individuals than in those in the CHR-NP group, and both had greater deficits than healthy controls.
For many patients with schizophrenia, full cognitive maturation is never reached.22 In general, decreased motivation in schizophrenia has been correlated with neurocognitive deficits.23
Schizophrenia vs bipolar disorder
In a study comparing neuropsychological functioning in patients with schizophrenia and bipolar disorder with psychotic features (BP-P), researchers found greater deficits in schizophrenia, including immediate verbal recall, working memory, processing speed, and verbal fluency.22 Patients with BP-P demonstrated impairment consistent with generalized impairment in verbal learning and memory, working memory, and processing speed.22
Children/adolescents
In a recent study comparing child and adolescent offspring of patients with schizophrenia (n = 41) and bipolar disorder (n = 90), researchers identified neuropsychological deficits in visual memory for both groups, suggesting common genetic linkages. The schizophrenia offspring scored lower in verbal memory and word memory, while bipolar offspring scored lower on the processing speed index and visual memory.2
Information processing
Another study compared the results of neuropsychological testing and the P300 component of auditory event-related potential (an electrophysiological measure) in 30 patients with schizophrenia, siblings without illness, and normal controls.24 The battery of neuropsychological tests included the Digit Symbol Substitution Test, Digit Vigilance Test, Trail Making Test-B, and Stroop test. The P300 is well correlated with information processing. Researchers found decreased P300 amplitude and latency in the patients and normal levels in the controls; siblings scored somewhere in between.24 Scores on the neuropsychological tests were consistently below normal in both patients and their siblings, with patients scoring the lowest.24
Continue to: Neuropsychological testing
Neuropsychological testing: 2 Case studies
The following 2 cases illustrate the pivotal role of neuropsychological testing in formulating an accurate differential diagnosis, and facilitating improved outcomes.
Case 1
A veteran with PTSD and memory complaints
Mr. J, age 70, is a married man who spent his career in the military, including combat service in the Vietnam War. His service in Vietnam included an event in which he couldn’t save platoon members from an ambush and death in a firefight, after which he developed PTSD. He retired after 25 years of service.
Mr. J’s psychiatrist refers him to a neuropsychologist for complaints of memory difficulties, including a fear that he’s developing Alzheimer’s disease (AD). Because of the concern for AD, he undergoes tests of learning and memory, such as the CVLT-3, the Brief Visuospatial Memory Test-Revised, and the Logical Memory subtest from the Wechsler Memory Scale–4th Edition. Other tests include a measure of confrontation naming, verbal fluency (phonemic and semantic fluency), construction, attention, processing speed, and problem solving. In addition, a measure of psychiatric and emotional functioning is also administered (the MMPI-2-RF).
The results determined that Mr. J’s subjective experience of recall deficits is better explained by anxiety resulting from the cumulative impact of day-to-day emotional stress in the setting of chronic PTSD.25 Mr. J was experiencing cognitive sequelae from a complicated emotional dynamic, comprised of situational stress, amplified by coping difficulties that were rooted in older posttraumatic symptoms. These emotions, and the cognitive load they generated, interfered with the normal processes of attention and organization necessary for the encoding of information to be remembered.26 He described being visibly angered by the clutter in his home (the result of multiple people living there, including a young grandchild), having his efforts to get things done interrupted by the needs of others, and a perceived loss of control gradually generalized to even mundane circumstances, as often occurs with traumatic responses. In short, he was chronically overwhelmed and not experiencing the beginnings of dementia.
For Mr. J, neuropsychological testing helped define the focus and course of therapy. If he had been diagnosed with a major neurocognitive disorder, therapy might have taken a more acceptance and grief-based approach, to help him adjust to a chronic, potentially life-limiting condition. Because this diagnosis was ruled out, and his cognitive complaints were determined to be secondary to a core diagnosis of PTSD, therapy instead focused on treating PTSD.
Continue to: Case 2
Case 2
A 55-year-old with bipolar I disorder
Mr. S, age 55, is taken to the emergency department (ED) because of his complaints of a severe headache. While undergoing brain MRI, Mr. S becomes highly agitated and aggressive to the radiology staff and is transferred to the psychiatric inpatient unit. He has a history of bipolar disorder that was treated with lithium approximately 20 years ago. Due to continued agitation, he is transferred to the state hospital and prescribed multiple medications, including an unspecified first-generation antipsychotic (FGA) that results in drooling and causes him to stoop and shuffle.
Mr. S’s wife contacts a community psychiatrist after becoming frustrated by her inability to communicate with the staff at the state hospital. During a 1-hour consult, she reveals that Mr. S was a competitive speedboat racer and had suffered numerous concussions due to accidents; at least 3 of these concussions that occurred when he was in his 20s and 30s had included a loss of consciousness. Mr. S had always been treated in the ED, and never required hospitalization. He had a previous marriage, was estranged from his ex-wife and 3 children, and has a history of alcohol abuse.
The MRI taken in the ED reveals numerous patches of scar tissue throughout the cortex, most notably in the striatum areas. The psychiatrist suspects that Mr. S’s agitation and irritation were related to focal seizure activity. He encourages Mr. S’s wife to speak with the attending psychiatrist at the state hospital and ask for him to be discharged home under her care.
Eventually, Mr. S is referred for a neurologic consult and neuropsychological testing. The testing included measures of attention and working, learning and memory, and executive functioning. The results reveal numerous deficits that Mr. S had been able to compensate for when he was younger, including problems with recall of newly learned information and difficulty modifying his behavior according to feedback. Mr. S is weaned from high doses of the FGA and is stabilized on 2 antiepileptic agents, sertraline, and low-dose olanzapine. A rehabilitation plan is developed, and Mr. S remains out of the hospital.
A team-based approach
Psychiatric clinicians need to recognize the subtle as well as overt cognitive deficits present in patients with many of the illnesses that we treat on a daily basis. In this era of performance- and value-based care, it is important to understand the common neuropsychological tests available to assist in providing patient-centered care tailored to specific cognitive deficits. Including a neuropsychologist is essential to implementing a team-based approach.
Continue to: Bottom Line
Bottom Line
Neuropsychological testing can help pinpoint key cognitive deficits that interfere with the potential for optimal patient outcomes. Psychiatric clinicians need to be knowledgeable about the common tests used and how to incorporate the results into their diagnosis and treatment plans.
Related Resources
- The American Academy of Clinical Neuropsychology. www.theaacn.org.
- Schwarz L. Answers to 7 questions about using neuropsychological testing in your practice. Current Psychiatry. 2014;13(3):33-39.
Drug Brand Names
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Sertraline • Zoloft
1. Zucchella C, Federico A, Martini A, et al. Neuropsychological testing: how to understand it. Practical Neurology. 2018;18(3):227-237.
2. de la Serna E, Sugranyes G, Sanchez-Gistau V, et al. Neuropsychological characteristics of child and adolescent offspring of patients with schizophrenia or bipolar disorder. Schizophr Res. 2017;183:110-115.
3. Gómez-Benito J, Guilera G, Pino Ó, et al. The screen for cognitive impairment in psychiatry: diagnostic-specific standardization in psychiatric ill patients. BMC Psychiatry. 2013;13:127.
4. Fuente-Tomas L, Arranz B, Safont G, et al. Classification of patients with bipolar disorder using k-means clustering. PLoS One. 2019;14(1):e0210314.
5. Kronbichler L, Stelzig-Schöler R, Pearce BG, et al. Schizophrenia and category-selectivity in the brain: Normal for faces but abnormal for houses. Front Psychiatry. 2018;9:47.
6. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med. 2001;16(9):606-613.
7. Yesavage A, Brink TL, Rose TL, et al. Development and validation of a geriatric depression screening scale: a preliminary report. J Psychiatr Res. 1983;17(1):37-49.
8. Ben-Porath YS, Tellegen A. Minnesota multi-phasic personality inventory-2 restructured form: MMPI-2-RF. San Antonio, TX: NCS Pearson; 2008.
9. Morey LC. Personality assessment inventory. Odessa, FL: Psychological Assessment Resources; 1991.
10. Donder J, ed. Neuropsychological report writing. New York, NY: The Guilford Press; 2016.
11. Department of Health and Human Services, Centers for Medicare and Medicaid Services. Evaluation and management services. https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/eval-mgmt-serv-guide-ICN006764.pdf. Published August 2017. Accessed October 10, 2019.
12. Hunt S, Root JC, Bascetta BL. Effort testing in schizophrenia and schizoaffective disorder: validity indicator profile and test of memory malingering performance characteristics. Arch Clin Neuropsychol. 2014;29(2):164-172.
13. Gorlyn M, Keilp J, Burke A, et al. Treatment-related improvement in neuropsychological functioning in suicidal depressed patients: paroxetine vs. bupropion. Psychiatry Res. 2015;225(3):407-412.
14. Pettersson R, Söderström S, Nilsson KW. Diagnosing ADHD in adults: an examination of the discriminative validity of neuropsychological tests and diagnostic assessment instruments. J Atten Disord. 2018;22(11):1019-1031.
15. Urfer-Parnas, A, Mortensen EL, Parnas J. Core of schizophrenia: estrangement, dementia or neurocognitive disorder? Psychopathology. 2010;43(5):300-311.
16. Green MF, Nuechterlein KH, Gold JM, et al. Approaching a consensus cognitive battery for clinical trials in schizophrenia: the NIMH-MATRICS conference to select cognitive domains and test criteria. Biolog Psych. 2004;56(5):301-307.
17. Green MF, Nuechterlein KH. The MATRICS initiative: developing a consensus cognitive battery for clinical trials. Schizophr Res. 2004;72(1):1-3.
18. Kern RS, Green MF, Nuechterlein KH, et al. NIMH-MATRICS survey on assessment of neurocognition in schizophrenia. Schizophr Res. 2004;72(1):11-19.
19. Carter CS, Barch DM. Cognitive neuroscience-based approaches to measuring and improving treatment effects on cognition in schizophrenia: the CNTRICS initiative. Schizophr Bull. 2007;33(5):1131-1137.
20. Geyer M. New opportunities in the treatment of cognitive impairments associated with schizophrenia. Curr Dir Psych Sci. 2010;19(4):264-269.
21. Hauser M, Zhang JP, Sheridan EM, et al. Neuropsychological test performance to enhance identification of subjects at clinical high risk for psychosis and to be most promising for predictive algorithms for conversion to psychosis: a meta-analysis. J Clin Psych. 2017;78(1):e28-e40. doi: 10.4088/JCP.15r10197.
22. Menkes MW, Armstrong K, Blackford JU, et al. Neuropsychological functioning in early and chronic stages of schizophrenia and psychotic bipolar disorder. Schizophr Res. 2019;206:413-419.
23. Najas-Garcia A, Gomez-Benito J, Hueda-Medina T. The relationship of motivation and neurocognition with functionality in schizophrenia: a meta-analytic review. Community Ment Health J. 2018;54(7):1019-1049.
24. Raghavan DV, Shanmugiah A, Bharathi P, et al. P300 and neuropsychological measurements in patients with schizophrenia and their healthy biological siblings. Indian J Psychiatry. 2016;58(4):454-458.
25. Mozzambani A, Fuso S, Malta S, et al. Long-term follow-up of attentional and executive functions of PTSD patients. Psychol Neurosci. 2017;10(2):215-224.
26. Woon F, Farrer T, Braman C, et al A meta-analysis of the relationship between symptom severity of posttraumatic stress disorder and executive function. Cogn Neuropsychiatry. 2017;22(1):1-16.
1. Zucchella C, Federico A, Martini A, et al. Neuropsychological testing: how to understand it. Practical Neurology. 2018;18(3):227-237.
2. de la Serna E, Sugranyes G, Sanchez-Gistau V, et al. Neuropsychological characteristics of child and adolescent offspring of patients with schizophrenia or bipolar disorder. Schizophr Res. 2017;183:110-115.
3. Gómez-Benito J, Guilera G, Pino Ó, et al. The screen for cognitive impairment in psychiatry: diagnostic-specific standardization in psychiatric ill patients. BMC Psychiatry. 2013;13:127.
4. Fuente-Tomas L, Arranz B, Safont G, et al. Classification of patients with bipolar disorder using k-means clustering. PLoS One. 2019;14(1):e0210314.
5. Kronbichler L, Stelzig-Schöler R, Pearce BG, et al. Schizophrenia and category-selectivity in the brain: Normal for faces but abnormal for houses. Front Psychiatry. 2018;9:47.
6. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med. 2001;16(9):606-613.
7. Yesavage A, Brink TL, Rose TL, et al. Development and validation of a geriatric depression screening scale: a preliminary report. J Psychiatr Res. 1983;17(1):37-49.
8. Ben-Porath YS, Tellegen A. Minnesota multi-phasic personality inventory-2 restructured form: MMPI-2-RF. San Antonio, TX: NCS Pearson; 2008.
9. Morey LC. Personality assessment inventory. Odessa, FL: Psychological Assessment Resources; 1991.
10. Donder J, ed. Neuropsychological report writing. New York, NY: The Guilford Press; 2016.
11. Department of Health and Human Services, Centers for Medicare and Medicaid Services. Evaluation and management services. https://www.cms.gov/Outreach-and-Education/Medicare-Learning-Network-MLN/MLNProducts/Downloads/eval-mgmt-serv-guide-ICN006764.pdf. Published August 2017. Accessed October 10, 2019.
12. Hunt S, Root JC, Bascetta BL. Effort testing in schizophrenia and schizoaffective disorder: validity indicator profile and test of memory malingering performance characteristics. Arch Clin Neuropsychol. 2014;29(2):164-172.
13. Gorlyn M, Keilp J, Burke A, et al. Treatment-related improvement in neuropsychological functioning in suicidal depressed patients: paroxetine vs. bupropion. Psychiatry Res. 2015;225(3):407-412.
14. Pettersson R, Söderström S, Nilsson KW. Diagnosing ADHD in adults: an examination of the discriminative validity of neuropsychological tests and diagnostic assessment instruments. J Atten Disord. 2018;22(11):1019-1031.
15. Urfer-Parnas, A, Mortensen EL, Parnas J. Core of schizophrenia: estrangement, dementia or neurocognitive disorder? Psychopathology. 2010;43(5):300-311.
16. Green MF, Nuechterlein KH, Gold JM, et al. Approaching a consensus cognitive battery for clinical trials in schizophrenia: the NIMH-MATRICS conference to select cognitive domains and test criteria. Biolog Psych. 2004;56(5):301-307.
17. Green MF, Nuechterlein KH. The MATRICS initiative: developing a consensus cognitive battery for clinical trials. Schizophr Res. 2004;72(1):1-3.
18. Kern RS, Green MF, Nuechterlein KH, et al. NIMH-MATRICS survey on assessment of neurocognition in schizophrenia. Schizophr Res. 2004;72(1):11-19.
19. Carter CS, Barch DM. Cognitive neuroscience-based approaches to measuring and improving treatment effects on cognition in schizophrenia: the CNTRICS initiative. Schizophr Bull. 2007;33(5):1131-1137.
20. Geyer M. New opportunities in the treatment of cognitive impairments associated with schizophrenia. Curr Dir Psych Sci. 2010;19(4):264-269.
21. Hauser M, Zhang JP, Sheridan EM, et al. Neuropsychological test performance to enhance identification of subjects at clinical high risk for psychosis and to be most promising for predictive algorithms for conversion to psychosis: a meta-analysis. J Clin Psych. 2017;78(1):e28-e40. doi: 10.4088/JCP.15r10197.
22. Menkes MW, Armstrong K, Blackford JU, et al. Neuropsychological functioning in early and chronic stages of schizophrenia and psychotic bipolar disorder. Schizophr Res. 2019;206:413-419.
23. Najas-Garcia A, Gomez-Benito J, Hueda-Medina T. The relationship of motivation and neurocognition with functionality in schizophrenia: a meta-analytic review. Community Ment Health J. 2018;54(7):1019-1049.
24. Raghavan DV, Shanmugiah A, Bharathi P, et al. P300 and neuropsychological measurements in patients with schizophrenia and their healthy biological siblings. Indian J Psychiatry. 2016;58(4):454-458.
25. Mozzambani A, Fuso S, Malta S, et al. Long-term follow-up of attentional and executive functions of PTSD patients. Psychol Neurosci. 2017;10(2):215-224.
26. Woon F, Farrer T, Braman C, et al A meta-analysis of the relationship between symptom severity of posttraumatic stress disorder and executive function. Cogn Neuropsychiatry. 2017;22(1):1-16.
Bipolar disorder or borderline personality disorder?
Although evidence suggests that bipolar disorder (BD) and borderline personality disorder (BPD) are distinct entities, their differential diagnosis is often challenging as a result of considerable overlap of phenotypical features. Moreover, BD and BPD frequently co-occur, which makes it even more difficult to differentiate these 2 conditions. Strategies for improving diagnostic accuracy are critical to optimizing patients’ clinical outcomes and long-term prognosis. Misdiagnosing these 2 conditions can be particularly deleterious, and failure to recognize their co-occurrence can result in additional burden to typically complex and severe clinical presentations.
This article describes key aspects of the differential diagnosis between BD and BPD, emphasizing core features and major dissimilarities between these 2 conditions, and discusses the implications of misdiagnosis. The goal is to highlight the clinical and psychopathological aspects of BD and BPD to help clinicians properly distinguish these 2 disorders.
Psychopathological and sociodemographic correlates
Bipolar disorder is a chronic and severe mental illness that is classified based on clusters of symptoms—manic, hypomanic, and depressive.1 It is among the 10 leading causes of disability worldwide, with significant morbidity arising from acute affective episodes and subacute states.2 Data suggest the lifetime prevalence of BPD is 2.1%, and subthreshold forms may affect an additional 2.4% of the US population.3 The onset of symptoms typically occurs during late adolescence or early adulthood, and mood lability and cyclothymic temperament are the most common prodromal features.4
In contrast, personality disorders, such as BPD, are characteristically pervasive and maladaptive patterns of emotional responses that usually deviate from an individual’s stage of development and cultural background.1 These disorders tend to cause significant impairment, particularly in personal, occupational, and social domains. Environmental factors, such as early childhood trauma, seem to play an important role in the genesis of personality disorders, which may be particularly relevant in BPD, a disorder characterized by marked impulsivity and a pattern of instability in personal relationships, self-image, and affect.1,5,6 Similarly to BD, BPD is also chronic and highly disabling.
According to the National Survey on Alcohol and Related Conditions (NESARC), approximately 15% of US adults were found to have at least one type of personality disorder, and 6% met criteria for a cluster B personality disorder (antisocial, borderline, narcissistic, and histrionic).7 The lifetime prevalence of BPD is nearly 2%, with higher estimates observed in psychiatric settings.7,8
As a result of the phenotypical resemblance between BD and BPD (Figure), the differential diagnosis is often difficult. Recent studies suggest that co-occurrence of BD and BPD is common, with rates of comorbid BPD as high as 29% in BD I and 24% in BD II.8,9 On the other hand, nearly 20% of individuals with BPD seem to have comorbid BD.8,9 Several studies suggest that comorbid personality disorders represent a negative prognostic factor in the course of mood disorders, and the presence of BPD in patients with BD seems to be associated with more severe clinical presentations, greater treatment complexity, a higher number of depressive episodes, poor inter-episode functioning, and higher rates of other comorbidities, such as substance use disorders (SUDs).8-11 The effect of BD on the course of BPD is unclear and fairly unexplored, although it has been suggested that better control of mood symptoms may lead to more stable psychosocial functioning in BPD.9
Whether BD and BPD are part of the same spectrum is a matter for debate.12-14 Multidimensional approaches have been proposed to better characterize these disorders in at-risk populations, based on structured interviews, self-administered and clinician-rated clinical scales (Table 1), neuroimaging studies, biological markers, and machine-learning models.15,16 Compelling evidence suggests that BD and BPD have distinct underlying neurobiological and psychopathological mechanisms12,13; however, the differential diagnosis still relies on phenotypical features, since the search for biological markers has not yet identified specific biomarkers that can be used in clinical practice.
Continue to: Core features of BPD...
Core features of BPD, such as mood lability, impulsivity, and risk-taking behaviors, are also part of the diagnostic criteria for BD (Table 2).1 Similarly, depressive symptoms prevail in the course of BD.17,18 This adds complexity to the differential because “depressivity” is also part of the diagnostic criteria for BPD.1 Therefore, comprehensive psychiatric assessments and longitudinal observations are critical to diagnostic accuracy and treatment planning. Further characterization of symptoms, such as onset patterns, clinical course, phenomenology of symptoms (eg, timing, frequency, duration, triggers), and personality traits, will provide information to properly distinguish these 2 syndromes when, for example, it is unclear if the “mood swings” and impulsivity are part of a mood or a personality disorder (Table 3).
Clinical features: A closer look
Borderline personality disorder. Affect dysregulation, emotional instability, impoverished and unstable self-image, and chronic feelings of emptiness are core features of BPD.1,5,19 These characteristics, when combined with a fear of abandonment or rejection, a compromised ability to recognize the feelings and needs of others, and extremes of idealization-devaluation, tend to culminate in problematic and chaotic relationships.6,19 Individuals with BPD may become suspicious or paranoid under stressful situations. Under these circumstances, individuals with BPD may also experience depersonalization and other dissociative symptoms.6,20 The mood lability and emotional instability observed in patients with BPD usually are in response to environmental factors, and although generally intense and out of proportion, they tend to be ephemeral and short-lived, typically lasting a few hours.1,5 The anxiety and depressive symptoms reported by patients with BPD frequently are associated with feelings of “falling apart” or “losing control,” pessimism, shame, and low self-esteem. Coping strategies tend to be poorly developed and/or maladaptive, and individuals with BPD usually display a hostile and antagonistic demeanor and engage in suicidal or nonsuicidal self-injury (NSSI) behaviors as means to alleviate overwhelming emotional distress. Impulsivity, disinhibition, poor tolerance to frustration, and risk-taking behaviors are also characteristic of BPD.1,5 As a result, BPD is usually associated with significant impairment in functioning, multiple hospitalizations, and high rates of comorbid mood disorders, posttraumatic stress disorder (PTSD), SUDs, and death by suicide.
Bipolar disorder. Conversely, the fluctuations in mood and affect observed in patients with BD are usually episodic rather than pervasive, and tend to last longer (typically days to weeks) compared with the transient mood shifts observed in patients with BPD.4,17,18 The impulsivity, psychomotor agitation, and increased goal-directed activity reported by patients with BD are usually seen in the context of an acute affective episode, and are far less common during periods of stability or euthymic affect.4,17,18 Grandiosity and inflated self-esteem—hallmarks of a manic or hypomanic state—seem to oppose the unstable self-image observed in BPD, although indecisiveness and low self-worth may be observed in individuals with BD during depressive episodes. Antidepressant-induced mania or hypomania, atypical depressive episodes, and disruptions in sleep and circadian rhythms may be predictors of BD.4,21 Furthermore, although psychosocial stressors may be associated with acute affective episodes in early stages of bipolar illness, over time minimal stressors are necessary to ignite new affective episodes.22,23 Although BD is associated with high rates of suicide, suicide attempts are usually seen in the context of an acute depressive episode, and NSSI behaviors are less common among patients with BD.24
Lastly, other biographical data, such as a history of early life trauma, comorbidity, and a family history of psychiatric illnesses, can be particularly helpful in establishing the differential diagnosis between BD and BPD.25 For instance, evidence suggests that the heritability of BD may be as high as 70%, which usually translates into an extensive family history of bipolar and related disorders.26 In addition, studies suggest a high co-occurrence of anxiety disorders, attention-deficit/hyperactivity disorder, and SUDs in patients with BD, whereas PTSD, SUDs, and eating disorders tend to be highly comorbid with BPD.27 Childhood adversity (ie, a history of physical, sexual, or emotional abuse, or neglect) seems to be pivotal in the genesis of BPD and may predispose these individuals to psychotic and dissociative symptoms, particularly those with a history of sexual abuse, while playing a more secondary role in BD.28-31
Implications of misdiagnosis
In the view of the limitations of the existing models, multidimensional approaches are necessary to improve diagnostic accuracy. Presently, the differential diagnosis of BD and BPD continues to rely on clinical findings and syndromic classifications. Misdiagnosing BD and BPD has adverse therapeutic and prognostic implications.32 For instance, while psychotropic medications and neuromodulatory therapies (eg, electroconvulsive therapy, repetitive transcranial magnetic stimulation) are considered first-line treatments for patients with BD, psychosocial interventions tend to be adjunctive treatments in BD.33 Conversely, although pharmacotherapy might be helpful for patients with BPD, psychosocial and behavioral interventions are the mainstay treatment for this disorder, with the strongest evidence supporting cognitive-behavioral therapy, dialectical behavioral therapy, mentalization-based therapy, and transference-focused therapy.34-36 Thus, misdiagnosing BD as BPD with comorbid depression may result in the use of antidepressants, which can be detrimental in BD. Antidepressant treatment of BD, particularly as monotherapy, has been associated with manic or hypomanic switch, mixed states, and frequent cycling.21 Moreover, delays in diagnosis and proper treatment of BD may result in protracted mood symptoms, prolonged affective episodes, higher rates of disability, functional impairment, and overall worse clinical outcomes.24 In addition, because behavioral and psychosocial interventions are usually adjunctive therapies rather than first-line interventions for patients with BD, misdiagnosing BPD as BD may ultimately prevent these individuals from receiving proper treatment, likely resulting in more severe functional impairment, multiple hospitalizations, self-inflicted injuries, and suicide attempts, since psychotropic medications are not particularly effective for improving self-efficacy and coping strategies, nor for correcting cognitive distortions, particularly in self-image, and pathological personality traits, all of which are critical aspects of BPD treatment.
Continue to: Several factors might...
Several factors might make clinicians reluctant to diagnose BPD, or bias them to diagnose BD more frequently. These include a lack of familiarity with the diagnostic criteria for BPD, the phenotypical resemblance between BP and BPD, or even concerns about the stigma and negative implications that are associated with a BPD diagnosis.32,37,38
Whereas BD is currently perceived as a condition with a strong biological basis, there are considerable misconceptions regarding BPD and its nature.4-6,22,26 As a consequence, individuals with BPD tend to be perceived as “difficult-to-treat,” “uncooperative,” or “attention-seeking.” These misconceptions may result in poor clinician-patient relationships, unmet clinical and psychiatric needs, and frustration for both clinicians and patients.37
Through advances in biological psychiatry, precision medicine may someday be a part of psychiatric practice. Biological “signatures” may eventually help clinicians in diagnosing and treating psychiatric disorders. Presently, however, rigorous history-taking and comprehensive clinical assessments are still the most powerful tools a clinician can use to accomplish these goals. Finally, destigmatizing psychiatric disorders and educating patients and clinicians are also critical to improving clinical outcomes and promoting mental health in a compassionate and empathetic fashion.
Bottom Line
Despite the phenotypical resemblance between bipolar disorder (BP) and borderline personality disorder (BPD), the 2 are independent conditions with distinct neurobiological and psychopathological underpinnings. Clinicians can use a rigorous assessment of pathological personality traits and characterization of symptoms, such as onset patterns, clinical course, and phenomenology, to properly distinguish between BP and BPD.
Related Resources
- Fiedorowicz JG, Black DW. Borderline, bipolar, or both? Frame your diagnosis on the patient history. Current Psychiatry. 2010; 9(1):21-24,29-32.
- Zimmerman M. Improving the recognition of borderline personality disorder. Current Psychiatry. 2017;16(10):13-19.
- National Institute of Mental Health. Overview on bipolar disorder. www.nimh.nih.gov/health/publications/bipolar-disorder/index.shtml. Revised October 2018.
- National Institute of Mental Health. Overview on borderline personality disorder. www.nimh.nih.gov/health/publications/borderline-personality-disorder-fact-sheet/index.shtml.
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Whiteford HA, Degenhardt L, Rehm J, et al. Global burden of disease attributable to mental and substance use disorders: findings from the Global Burden of Disease Study 2010. Lancet. 2013;382(9904):1575-1586.
3. Merikangas KR, Akiskal HS, Angst J, et al. Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Arch Gen Psychiatry. 2007;64(5):543-552.
4. Malhi GS, Bargh DM, Coulston CM, et al. Predicting bipolar disorder on the basis of phenomenology: implications for prevention and early intervention. Bipolar Disord. 2014;16(5):455-470.
5. Skodol AE, Gunderson JG, Pfohl B, et al. The borderline diagnosis I: psychopathology. Biol Psychiatry. 2002;51(12):936-950.
6. Skodol AE, Siever LJ, Livesley WJ, et al. The borderline diagnosis II: biology, genetics, and clinical course. Biol Psychiatry. 2002;51(12):951-963.
7. Hasin DS, Grant BF. The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Waves 1 and 2: review and summary of findings. Soc Psychiatry Psychiatr Epidemiol. 2015;50(11):1609-1640.
8. McDermid J, Sareen J, El-Gabalawy R, et al. Co-morbidity of bipolar disorder and borderline personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Compr Psychiatry. 2015;58:18-28.
9. Gunderson JG, Weinberg I, Daversa MT, et al. Descriptive and longitudinal observations on the relationship of borderline personality disorder and bipolar disorder. Am J Psychiatry. 2006;163(7):1173-1178.
10. Swartz HA, Pilkonis PA, Frank E, et al. Acute treatment outcomes in patients with bipolar I disorder and co-morbid borderline personality disorder receiving medication and psychotherapy. Bipolar Disord. 2005;7(2):192-197.
11. Riemann G, Weisscher N, Post RM, et al. The relationship between self-reported borderline personality features and prospective illness course in bipolar disorder. Int J Bipolar Disord. 2017;5(1):31.
12. de la Rosa I, Oquendo MA, García G, et al. Determining if borderline personality disorder and bipolar disorder are alternative expressions of the same disorder. J Clin Psychiatry. 2017;778(8):e994-e999. doi: 10.4088/JCP.16m11190.
13. di Giacomo E, Aspesi F, Fotiadou M, et al. Unblending borderline personality and bipolar disorders. J Psychiatr Res. 2017;91:90-97.
14. Parker G, Bayes A, McClure G, et al. Clinical status of comorbid bipolar disorder and borderline personality disorder. Br J Psychiatry. 2016;209(3):209-215.
15. Perez Arribas I, Goodwin GM, Geddes JR, et al. A signature-based machine learning model for distinguishing bipolar disorder and borderline personality disorder. Transl Psychiatry. 2018;8(1):274.
16. Insel T, Cuthbert B, Garvey M, et al. Research Domain Criteria (RDoC): toward a new classification framework for research on mental disorders. Am J Psychiatry. 2010;167(7):748-751.
17. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of the weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry. 2002;59(6):530-537.
18. Judd LL, Akiskal HS, Schettler PJ, et al. A prospective investigation of the natural history of the long-term weekly symptomatic status of bipolar II disorder. Arch Gen Psychiatry. 2003;60(3):261-269.
19. Oldham JM, Skodol AE, Bender DS. A current integrative perspective on personality disorders. American Psychiatric Publishing, Inc. 2005.
20. Herzog JI, Schmahl C. Adverse childhood experiences and the consequences on neurobiological, psychosocial, and somatic conditions across the lifespan. Front Psychiatry. 2018;9:420.
21. Barbuti M, Pacchiarotti I, Vieta E, et al. Antidepressant-induced hypomania/mania in patients with major depression: evidence from the BRIDGE-II-MIX study. J Affect Disord. 2017;219:187-192.
22. Post RM. Mechanisms of illness progression in the recurrent affective disorders. Neurotox Res. 2010;18(3-4):256-271.
23. da Costa SC, Passos IC, Lowri C, et al. Refractory bipolar disorder and neuroprogression. Prog Neuro-Psychopharmacology Biol Psychiatry. 2016;70:103-110.
24. Crump C, Sundquist K, Winkleby MA, et al. Comorbidities and mortality in bipolar disorder: a Swedish national cohort study. JAMA Psychiatry. 2013;70(9):931-939.
25. Zimmerman M, Martinez JH, Morgan TA, et al. Distinguishing bipolar II depression from major depressive disorder with comorbid borderline personality disorder: demographic, clinical, and family history differences. J Clin Psychiatry. 2013;74(9):880-886.
26. Hasler G, Drevets WC, Gould TD, et al. Toward constructing an endophenotype strategy for bipolar disorders. Biol Psychiatry. 2006;60(2):93-105.
27. Brieger P, Ehrt U, Marneros A. Frequency of comorbid personality disorders in bipolar and unipolar affective disorders. Compr Psychiatry. 2003;44(1):28-34.
28. Leverich GS, McElroy SL, Suppes T, et al. Early physical and sexual abuse associated with an adverse course of bipolar illness. Biol Psychiatry. 2002;51(4):288-297.
29. Leverich GS, Post RM. Course of bipolar illness after history of childhood trauma. Lancet. 2006;367(9516):1040-1042.
30. Golier JA, Yehuda R, Bierer LM, et al. The relationship of borderline personality disorder to posttraumatic stress disorder and traumatic events. Am J Psychiatry. 2003;160(11):2018-2024.
31. Nicol K, Pope M, Romaniuk L, et al. Childhood trauma, midbrain activation and psychotic symptoms in borderline personality disorder. Transl Psychiatry. 2015;5:e559. doi:10.1038/tp.2015.53.
32. Ruggero CJ, Zimmerman M, Chelminski I, et al. Borderline personality disorder and the misdiagnosis of bipolar disorder. J Psychiatr Res. 2010;44(6):405-408.
33. Geddes JR, Miklowitz DJ. Treatment of bipolar disorder. Lancet. 2013;381(9878):1672-1682.
34. McMain S, Korman LM, Dimeff L. Dialectical behavior therapy and the treatment of emotion dysregulation. J Clin Psychol. 2001;57(2):183-196.
35. Cristea IA, Gentili C, Cotet CD, et al. Efficacy of psychotherapies for borderline personality disorder: a systematic review and meta-analysis. JAMA Psychiatry. 2017;74(4):319-328.
36. Linehan MM, Korslund KE, Harned MS, et al. Dialectical behavior therapy for high suicide risk in individuals with borderline personality disorder. JAMA Psychiatry. 2015;72(75);475-482.
37. LeQuesne ER, Hersh RG. Disclosure of a diagnosis of borderline personality disorder. J Psychiatr Pract. 2004:10(3):170-176.
38. Young AH. Bipolar disorder: diagnostic conundrums and associated comorbidities. J Clin Psychiatry. 2009;70(8):e26. doi:10.4088/jcp.7067br6c.
Although evidence suggests that bipolar disorder (BD) and borderline personality disorder (BPD) are distinct entities, their differential diagnosis is often challenging as a result of considerable overlap of phenotypical features. Moreover, BD and BPD frequently co-occur, which makes it even more difficult to differentiate these 2 conditions. Strategies for improving diagnostic accuracy are critical to optimizing patients’ clinical outcomes and long-term prognosis. Misdiagnosing these 2 conditions can be particularly deleterious, and failure to recognize their co-occurrence can result in additional burden to typically complex and severe clinical presentations.
This article describes key aspects of the differential diagnosis between BD and BPD, emphasizing core features and major dissimilarities between these 2 conditions, and discusses the implications of misdiagnosis. The goal is to highlight the clinical and psychopathological aspects of BD and BPD to help clinicians properly distinguish these 2 disorders.
Psychopathological and sociodemographic correlates
Bipolar disorder is a chronic and severe mental illness that is classified based on clusters of symptoms—manic, hypomanic, and depressive.1 It is among the 10 leading causes of disability worldwide, with significant morbidity arising from acute affective episodes and subacute states.2 Data suggest the lifetime prevalence of BPD is 2.1%, and subthreshold forms may affect an additional 2.4% of the US population.3 The onset of symptoms typically occurs during late adolescence or early adulthood, and mood lability and cyclothymic temperament are the most common prodromal features.4
In contrast, personality disorders, such as BPD, are characteristically pervasive and maladaptive patterns of emotional responses that usually deviate from an individual’s stage of development and cultural background.1 These disorders tend to cause significant impairment, particularly in personal, occupational, and social domains. Environmental factors, such as early childhood trauma, seem to play an important role in the genesis of personality disorders, which may be particularly relevant in BPD, a disorder characterized by marked impulsivity and a pattern of instability in personal relationships, self-image, and affect.1,5,6 Similarly to BD, BPD is also chronic and highly disabling.
According to the National Survey on Alcohol and Related Conditions (NESARC), approximately 15% of US adults were found to have at least one type of personality disorder, and 6% met criteria for a cluster B personality disorder (antisocial, borderline, narcissistic, and histrionic).7 The lifetime prevalence of BPD is nearly 2%, with higher estimates observed in psychiatric settings.7,8
As a result of the phenotypical resemblance between BD and BPD (Figure), the differential diagnosis is often difficult. Recent studies suggest that co-occurrence of BD and BPD is common, with rates of comorbid BPD as high as 29% in BD I and 24% in BD II.8,9 On the other hand, nearly 20% of individuals with BPD seem to have comorbid BD.8,9 Several studies suggest that comorbid personality disorders represent a negative prognostic factor in the course of mood disorders, and the presence of BPD in patients with BD seems to be associated with more severe clinical presentations, greater treatment complexity, a higher number of depressive episodes, poor inter-episode functioning, and higher rates of other comorbidities, such as substance use disorders (SUDs).8-11 The effect of BD on the course of BPD is unclear and fairly unexplored, although it has been suggested that better control of mood symptoms may lead to more stable psychosocial functioning in BPD.9
Whether BD and BPD are part of the same spectrum is a matter for debate.12-14 Multidimensional approaches have been proposed to better characterize these disorders in at-risk populations, based on structured interviews, self-administered and clinician-rated clinical scales (Table 1), neuroimaging studies, biological markers, and machine-learning models.15,16 Compelling evidence suggests that BD and BPD have distinct underlying neurobiological and psychopathological mechanisms12,13; however, the differential diagnosis still relies on phenotypical features, since the search for biological markers has not yet identified specific biomarkers that can be used in clinical practice.
Continue to: Core features of BPD...
Core features of BPD, such as mood lability, impulsivity, and risk-taking behaviors, are also part of the diagnostic criteria for BD (Table 2).1 Similarly, depressive symptoms prevail in the course of BD.17,18 This adds complexity to the differential because “depressivity” is also part of the diagnostic criteria for BPD.1 Therefore, comprehensive psychiatric assessments and longitudinal observations are critical to diagnostic accuracy and treatment planning. Further characterization of symptoms, such as onset patterns, clinical course, phenomenology of symptoms (eg, timing, frequency, duration, triggers), and personality traits, will provide information to properly distinguish these 2 syndromes when, for example, it is unclear if the “mood swings” and impulsivity are part of a mood or a personality disorder (Table 3).
Clinical features: A closer look
Borderline personality disorder. Affect dysregulation, emotional instability, impoverished and unstable self-image, and chronic feelings of emptiness are core features of BPD.1,5,19 These characteristics, when combined with a fear of abandonment or rejection, a compromised ability to recognize the feelings and needs of others, and extremes of idealization-devaluation, tend to culminate in problematic and chaotic relationships.6,19 Individuals with BPD may become suspicious or paranoid under stressful situations. Under these circumstances, individuals with BPD may also experience depersonalization and other dissociative symptoms.6,20 The mood lability and emotional instability observed in patients with BPD usually are in response to environmental factors, and although generally intense and out of proportion, they tend to be ephemeral and short-lived, typically lasting a few hours.1,5 The anxiety and depressive symptoms reported by patients with BPD frequently are associated with feelings of “falling apart” or “losing control,” pessimism, shame, and low self-esteem. Coping strategies tend to be poorly developed and/or maladaptive, and individuals with BPD usually display a hostile and antagonistic demeanor and engage in suicidal or nonsuicidal self-injury (NSSI) behaviors as means to alleviate overwhelming emotional distress. Impulsivity, disinhibition, poor tolerance to frustration, and risk-taking behaviors are also characteristic of BPD.1,5 As a result, BPD is usually associated with significant impairment in functioning, multiple hospitalizations, and high rates of comorbid mood disorders, posttraumatic stress disorder (PTSD), SUDs, and death by suicide.
Bipolar disorder. Conversely, the fluctuations in mood and affect observed in patients with BD are usually episodic rather than pervasive, and tend to last longer (typically days to weeks) compared with the transient mood shifts observed in patients with BPD.4,17,18 The impulsivity, psychomotor agitation, and increased goal-directed activity reported by patients with BD are usually seen in the context of an acute affective episode, and are far less common during periods of stability or euthymic affect.4,17,18 Grandiosity and inflated self-esteem—hallmarks of a manic or hypomanic state—seem to oppose the unstable self-image observed in BPD, although indecisiveness and low self-worth may be observed in individuals with BD during depressive episodes. Antidepressant-induced mania or hypomania, atypical depressive episodes, and disruptions in sleep and circadian rhythms may be predictors of BD.4,21 Furthermore, although psychosocial stressors may be associated with acute affective episodes in early stages of bipolar illness, over time minimal stressors are necessary to ignite new affective episodes.22,23 Although BD is associated with high rates of suicide, suicide attempts are usually seen in the context of an acute depressive episode, and NSSI behaviors are less common among patients with BD.24
Lastly, other biographical data, such as a history of early life trauma, comorbidity, and a family history of psychiatric illnesses, can be particularly helpful in establishing the differential diagnosis between BD and BPD.25 For instance, evidence suggests that the heritability of BD may be as high as 70%, which usually translates into an extensive family history of bipolar and related disorders.26 In addition, studies suggest a high co-occurrence of anxiety disorders, attention-deficit/hyperactivity disorder, and SUDs in patients with BD, whereas PTSD, SUDs, and eating disorders tend to be highly comorbid with BPD.27 Childhood adversity (ie, a history of physical, sexual, or emotional abuse, or neglect) seems to be pivotal in the genesis of BPD and may predispose these individuals to psychotic and dissociative symptoms, particularly those with a history of sexual abuse, while playing a more secondary role in BD.28-31
Implications of misdiagnosis
In the view of the limitations of the existing models, multidimensional approaches are necessary to improve diagnostic accuracy. Presently, the differential diagnosis of BD and BPD continues to rely on clinical findings and syndromic classifications. Misdiagnosing BD and BPD has adverse therapeutic and prognostic implications.32 For instance, while psychotropic medications and neuromodulatory therapies (eg, electroconvulsive therapy, repetitive transcranial magnetic stimulation) are considered first-line treatments for patients with BD, psychosocial interventions tend to be adjunctive treatments in BD.33 Conversely, although pharmacotherapy might be helpful for patients with BPD, psychosocial and behavioral interventions are the mainstay treatment for this disorder, with the strongest evidence supporting cognitive-behavioral therapy, dialectical behavioral therapy, mentalization-based therapy, and transference-focused therapy.34-36 Thus, misdiagnosing BD as BPD with comorbid depression may result in the use of antidepressants, which can be detrimental in BD. Antidepressant treatment of BD, particularly as monotherapy, has been associated with manic or hypomanic switch, mixed states, and frequent cycling.21 Moreover, delays in diagnosis and proper treatment of BD may result in protracted mood symptoms, prolonged affective episodes, higher rates of disability, functional impairment, and overall worse clinical outcomes.24 In addition, because behavioral and psychosocial interventions are usually adjunctive therapies rather than first-line interventions for patients with BD, misdiagnosing BPD as BD may ultimately prevent these individuals from receiving proper treatment, likely resulting in more severe functional impairment, multiple hospitalizations, self-inflicted injuries, and suicide attempts, since psychotropic medications are not particularly effective for improving self-efficacy and coping strategies, nor for correcting cognitive distortions, particularly in self-image, and pathological personality traits, all of which are critical aspects of BPD treatment.
Continue to: Several factors might...
Several factors might make clinicians reluctant to diagnose BPD, or bias them to diagnose BD more frequently. These include a lack of familiarity with the diagnostic criteria for BPD, the phenotypical resemblance between BP and BPD, or even concerns about the stigma and negative implications that are associated with a BPD diagnosis.32,37,38
Whereas BD is currently perceived as a condition with a strong biological basis, there are considerable misconceptions regarding BPD and its nature.4-6,22,26 As a consequence, individuals with BPD tend to be perceived as “difficult-to-treat,” “uncooperative,” or “attention-seeking.” These misconceptions may result in poor clinician-patient relationships, unmet clinical and psychiatric needs, and frustration for both clinicians and patients.37
Through advances in biological psychiatry, precision medicine may someday be a part of psychiatric practice. Biological “signatures” may eventually help clinicians in diagnosing and treating psychiatric disorders. Presently, however, rigorous history-taking and comprehensive clinical assessments are still the most powerful tools a clinician can use to accomplish these goals. Finally, destigmatizing psychiatric disorders and educating patients and clinicians are also critical to improving clinical outcomes and promoting mental health in a compassionate and empathetic fashion.
Bottom Line
Despite the phenotypical resemblance between bipolar disorder (BP) and borderline personality disorder (BPD), the 2 are independent conditions with distinct neurobiological and psychopathological underpinnings. Clinicians can use a rigorous assessment of pathological personality traits and characterization of symptoms, such as onset patterns, clinical course, and phenomenology, to properly distinguish between BP and BPD.
Related Resources
- Fiedorowicz JG, Black DW. Borderline, bipolar, or both? Frame your diagnosis on the patient history. Current Psychiatry. 2010; 9(1):21-24,29-32.
- Zimmerman M. Improving the recognition of borderline personality disorder. Current Psychiatry. 2017;16(10):13-19.
- National Institute of Mental Health. Overview on bipolar disorder. www.nimh.nih.gov/health/publications/bipolar-disorder/index.shtml. Revised October 2018.
- National Institute of Mental Health. Overview on borderline personality disorder. www.nimh.nih.gov/health/publications/borderline-personality-disorder-fact-sheet/index.shtml.
Although evidence suggests that bipolar disorder (BD) and borderline personality disorder (BPD) are distinct entities, their differential diagnosis is often challenging as a result of considerable overlap of phenotypical features. Moreover, BD and BPD frequently co-occur, which makes it even more difficult to differentiate these 2 conditions. Strategies for improving diagnostic accuracy are critical to optimizing patients’ clinical outcomes and long-term prognosis. Misdiagnosing these 2 conditions can be particularly deleterious, and failure to recognize their co-occurrence can result in additional burden to typically complex and severe clinical presentations.
This article describes key aspects of the differential diagnosis between BD and BPD, emphasizing core features and major dissimilarities between these 2 conditions, and discusses the implications of misdiagnosis. The goal is to highlight the clinical and psychopathological aspects of BD and BPD to help clinicians properly distinguish these 2 disorders.
Psychopathological and sociodemographic correlates
Bipolar disorder is a chronic and severe mental illness that is classified based on clusters of symptoms—manic, hypomanic, and depressive.1 It is among the 10 leading causes of disability worldwide, with significant morbidity arising from acute affective episodes and subacute states.2 Data suggest the lifetime prevalence of BPD is 2.1%, and subthreshold forms may affect an additional 2.4% of the US population.3 The onset of symptoms typically occurs during late adolescence or early adulthood, and mood lability and cyclothymic temperament are the most common prodromal features.4
In contrast, personality disorders, such as BPD, are characteristically pervasive and maladaptive patterns of emotional responses that usually deviate from an individual’s stage of development and cultural background.1 These disorders tend to cause significant impairment, particularly in personal, occupational, and social domains. Environmental factors, such as early childhood trauma, seem to play an important role in the genesis of personality disorders, which may be particularly relevant in BPD, a disorder characterized by marked impulsivity and a pattern of instability in personal relationships, self-image, and affect.1,5,6 Similarly to BD, BPD is also chronic and highly disabling.
According to the National Survey on Alcohol and Related Conditions (NESARC), approximately 15% of US adults were found to have at least one type of personality disorder, and 6% met criteria for a cluster B personality disorder (antisocial, borderline, narcissistic, and histrionic).7 The lifetime prevalence of BPD is nearly 2%, with higher estimates observed in psychiatric settings.7,8
As a result of the phenotypical resemblance between BD and BPD (Figure), the differential diagnosis is often difficult. Recent studies suggest that co-occurrence of BD and BPD is common, with rates of comorbid BPD as high as 29% in BD I and 24% in BD II.8,9 On the other hand, nearly 20% of individuals with BPD seem to have comorbid BD.8,9 Several studies suggest that comorbid personality disorders represent a negative prognostic factor in the course of mood disorders, and the presence of BPD in patients with BD seems to be associated with more severe clinical presentations, greater treatment complexity, a higher number of depressive episodes, poor inter-episode functioning, and higher rates of other comorbidities, such as substance use disorders (SUDs).8-11 The effect of BD on the course of BPD is unclear and fairly unexplored, although it has been suggested that better control of mood symptoms may lead to more stable psychosocial functioning in BPD.9
Whether BD and BPD are part of the same spectrum is a matter for debate.12-14 Multidimensional approaches have been proposed to better characterize these disorders in at-risk populations, based on structured interviews, self-administered and clinician-rated clinical scales (Table 1), neuroimaging studies, biological markers, and machine-learning models.15,16 Compelling evidence suggests that BD and BPD have distinct underlying neurobiological and psychopathological mechanisms12,13; however, the differential diagnosis still relies on phenotypical features, since the search for biological markers has not yet identified specific biomarkers that can be used in clinical practice.
Continue to: Core features of BPD...
Core features of BPD, such as mood lability, impulsivity, and risk-taking behaviors, are also part of the diagnostic criteria for BD (Table 2).1 Similarly, depressive symptoms prevail in the course of BD.17,18 This adds complexity to the differential because “depressivity” is also part of the diagnostic criteria for BPD.1 Therefore, comprehensive psychiatric assessments and longitudinal observations are critical to diagnostic accuracy and treatment planning. Further characterization of symptoms, such as onset patterns, clinical course, phenomenology of symptoms (eg, timing, frequency, duration, triggers), and personality traits, will provide information to properly distinguish these 2 syndromes when, for example, it is unclear if the “mood swings” and impulsivity are part of a mood or a personality disorder (Table 3).
Clinical features: A closer look
Borderline personality disorder. Affect dysregulation, emotional instability, impoverished and unstable self-image, and chronic feelings of emptiness are core features of BPD.1,5,19 These characteristics, when combined with a fear of abandonment or rejection, a compromised ability to recognize the feelings and needs of others, and extremes of idealization-devaluation, tend to culminate in problematic and chaotic relationships.6,19 Individuals with BPD may become suspicious or paranoid under stressful situations. Under these circumstances, individuals with BPD may also experience depersonalization and other dissociative symptoms.6,20 The mood lability and emotional instability observed in patients with BPD usually are in response to environmental factors, and although generally intense and out of proportion, they tend to be ephemeral and short-lived, typically lasting a few hours.1,5 The anxiety and depressive symptoms reported by patients with BPD frequently are associated with feelings of “falling apart” or “losing control,” pessimism, shame, and low self-esteem. Coping strategies tend to be poorly developed and/or maladaptive, and individuals with BPD usually display a hostile and antagonistic demeanor and engage in suicidal or nonsuicidal self-injury (NSSI) behaviors as means to alleviate overwhelming emotional distress. Impulsivity, disinhibition, poor tolerance to frustration, and risk-taking behaviors are also characteristic of BPD.1,5 As a result, BPD is usually associated with significant impairment in functioning, multiple hospitalizations, and high rates of comorbid mood disorders, posttraumatic stress disorder (PTSD), SUDs, and death by suicide.
Bipolar disorder. Conversely, the fluctuations in mood and affect observed in patients with BD are usually episodic rather than pervasive, and tend to last longer (typically days to weeks) compared with the transient mood shifts observed in patients with BPD.4,17,18 The impulsivity, psychomotor agitation, and increased goal-directed activity reported by patients with BD are usually seen in the context of an acute affective episode, and are far less common during periods of stability or euthymic affect.4,17,18 Grandiosity and inflated self-esteem—hallmarks of a manic or hypomanic state—seem to oppose the unstable self-image observed in BPD, although indecisiveness and low self-worth may be observed in individuals with BD during depressive episodes. Antidepressant-induced mania or hypomania, atypical depressive episodes, and disruptions in sleep and circadian rhythms may be predictors of BD.4,21 Furthermore, although psychosocial stressors may be associated with acute affective episodes in early stages of bipolar illness, over time minimal stressors are necessary to ignite new affective episodes.22,23 Although BD is associated with high rates of suicide, suicide attempts are usually seen in the context of an acute depressive episode, and NSSI behaviors are less common among patients with BD.24
Lastly, other biographical data, such as a history of early life trauma, comorbidity, and a family history of psychiatric illnesses, can be particularly helpful in establishing the differential diagnosis between BD and BPD.25 For instance, evidence suggests that the heritability of BD may be as high as 70%, which usually translates into an extensive family history of bipolar and related disorders.26 In addition, studies suggest a high co-occurrence of anxiety disorders, attention-deficit/hyperactivity disorder, and SUDs in patients with BD, whereas PTSD, SUDs, and eating disorders tend to be highly comorbid with BPD.27 Childhood adversity (ie, a history of physical, sexual, or emotional abuse, or neglect) seems to be pivotal in the genesis of BPD and may predispose these individuals to psychotic and dissociative symptoms, particularly those with a history of sexual abuse, while playing a more secondary role in BD.28-31
Implications of misdiagnosis
In the view of the limitations of the existing models, multidimensional approaches are necessary to improve diagnostic accuracy. Presently, the differential diagnosis of BD and BPD continues to rely on clinical findings and syndromic classifications. Misdiagnosing BD and BPD has adverse therapeutic and prognostic implications.32 For instance, while psychotropic medications and neuromodulatory therapies (eg, electroconvulsive therapy, repetitive transcranial magnetic stimulation) are considered first-line treatments for patients with BD, psychosocial interventions tend to be adjunctive treatments in BD.33 Conversely, although pharmacotherapy might be helpful for patients with BPD, psychosocial and behavioral interventions are the mainstay treatment for this disorder, with the strongest evidence supporting cognitive-behavioral therapy, dialectical behavioral therapy, mentalization-based therapy, and transference-focused therapy.34-36 Thus, misdiagnosing BD as BPD with comorbid depression may result in the use of antidepressants, which can be detrimental in BD. Antidepressant treatment of BD, particularly as monotherapy, has been associated with manic or hypomanic switch, mixed states, and frequent cycling.21 Moreover, delays in diagnosis and proper treatment of BD may result in protracted mood symptoms, prolonged affective episodes, higher rates of disability, functional impairment, and overall worse clinical outcomes.24 In addition, because behavioral and psychosocial interventions are usually adjunctive therapies rather than first-line interventions for patients with BD, misdiagnosing BPD as BD may ultimately prevent these individuals from receiving proper treatment, likely resulting in more severe functional impairment, multiple hospitalizations, self-inflicted injuries, and suicide attempts, since psychotropic medications are not particularly effective for improving self-efficacy and coping strategies, nor for correcting cognitive distortions, particularly in self-image, and pathological personality traits, all of which are critical aspects of BPD treatment.
Continue to: Several factors might...
Several factors might make clinicians reluctant to diagnose BPD, or bias them to diagnose BD more frequently. These include a lack of familiarity with the diagnostic criteria for BPD, the phenotypical resemblance between BP and BPD, or even concerns about the stigma and negative implications that are associated with a BPD diagnosis.32,37,38
Whereas BD is currently perceived as a condition with a strong biological basis, there are considerable misconceptions regarding BPD and its nature.4-6,22,26 As a consequence, individuals with BPD tend to be perceived as “difficult-to-treat,” “uncooperative,” or “attention-seeking.” These misconceptions may result in poor clinician-patient relationships, unmet clinical and psychiatric needs, and frustration for both clinicians and patients.37
Through advances in biological psychiatry, precision medicine may someday be a part of psychiatric practice. Biological “signatures” may eventually help clinicians in diagnosing and treating psychiatric disorders. Presently, however, rigorous history-taking and comprehensive clinical assessments are still the most powerful tools a clinician can use to accomplish these goals. Finally, destigmatizing psychiatric disorders and educating patients and clinicians are also critical to improving clinical outcomes and promoting mental health in a compassionate and empathetic fashion.
Bottom Line
Despite the phenotypical resemblance between bipolar disorder (BP) and borderline personality disorder (BPD), the 2 are independent conditions with distinct neurobiological and psychopathological underpinnings. Clinicians can use a rigorous assessment of pathological personality traits and characterization of symptoms, such as onset patterns, clinical course, and phenomenology, to properly distinguish between BP and BPD.
Related Resources
- Fiedorowicz JG, Black DW. Borderline, bipolar, or both? Frame your diagnosis on the patient history. Current Psychiatry. 2010; 9(1):21-24,29-32.
- Zimmerman M. Improving the recognition of borderline personality disorder. Current Psychiatry. 2017;16(10):13-19.
- National Institute of Mental Health. Overview on bipolar disorder. www.nimh.nih.gov/health/publications/bipolar-disorder/index.shtml. Revised October 2018.
- National Institute of Mental Health. Overview on borderline personality disorder. www.nimh.nih.gov/health/publications/borderline-personality-disorder-fact-sheet/index.shtml.
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Whiteford HA, Degenhardt L, Rehm J, et al. Global burden of disease attributable to mental and substance use disorders: findings from the Global Burden of Disease Study 2010. Lancet. 2013;382(9904):1575-1586.
3. Merikangas KR, Akiskal HS, Angst J, et al. Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Arch Gen Psychiatry. 2007;64(5):543-552.
4. Malhi GS, Bargh DM, Coulston CM, et al. Predicting bipolar disorder on the basis of phenomenology: implications for prevention and early intervention. Bipolar Disord. 2014;16(5):455-470.
5. Skodol AE, Gunderson JG, Pfohl B, et al. The borderline diagnosis I: psychopathology. Biol Psychiatry. 2002;51(12):936-950.
6. Skodol AE, Siever LJ, Livesley WJ, et al. The borderline diagnosis II: biology, genetics, and clinical course. Biol Psychiatry. 2002;51(12):951-963.
7. Hasin DS, Grant BF. The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Waves 1 and 2: review and summary of findings. Soc Psychiatry Psychiatr Epidemiol. 2015;50(11):1609-1640.
8. McDermid J, Sareen J, El-Gabalawy R, et al. Co-morbidity of bipolar disorder and borderline personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Compr Psychiatry. 2015;58:18-28.
9. Gunderson JG, Weinberg I, Daversa MT, et al. Descriptive and longitudinal observations on the relationship of borderline personality disorder and bipolar disorder. Am J Psychiatry. 2006;163(7):1173-1178.
10. Swartz HA, Pilkonis PA, Frank E, et al. Acute treatment outcomes in patients with bipolar I disorder and co-morbid borderline personality disorder receiving medication and psychotherapy. Bipolar Disord. 2005;7(2):192-197.
11. Riemann G, Weisscher N, Post RM, et al. The relationship between self-reported borderline personality features and prospective illness course in bipolar disorder. Int J Bipolar Disord. 2017;5(1):31.
12. de la Rosa I, Oquendo MA, García G, et al. Determining if borderline personality disorder and bipolar disorder are alternative expressions of the same disorder. J Clin Psychiatry. 2017;778(8):e994-e999. doi: 10.4088/JCP.16m11190.
13. di Giacomo E, Aspesi F, Fotiadou M, et al. Unblending borderline personality and bipolar disorders. J Psychiatr Res. 2017;91:90-97.
14. Parker G, Bayes A, McClure G, et al. Clinical status of comorbid bipolar disorder and borderline personality disorder. Br J Psychiatry. 2016;209(3):209-215.
15. Perez Arribas I, Goodwin GM, Geddes JR, et al. A signature-based machine learning model for distinguishing bipolar disorder and borderline personality disorder. Transl Psychiatry. 2018;8(1):274.
16. Insel T, Cuthbert B, Garvey M, et al. Research Domain Criteria (RDoC): toward a new classification framework for research on mental disorders. Am J Psychiatry. 2010;167(7):748-751.
17. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of the weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry. 2002;59(6):530-537.
18. Judd LL, Akiskal HS, Schettler PJ, et al. A prospective investigation of the natural history of the long-term weekly symptomatic status of bipolar II disorder. Arch Gen Psychiatry. 2003;60(3):261-269.
19. Oldham JM, Skodol AE, Bender DS. A current integrative perspective on personality disorders. American Psychiatric Publishing, Inc. 2005.
20. Herzog JI, Schmahl C. Adverse childhood experiences and the consequences on neurobiological, psychosocial, and somatic conditions across the lifespan. Front Psychiatry. 2018;9:420.
21. Barbuti M, Pacchiarotti I, Vieta E, et al. Antidepressant-induced hypomania/mania in patients with major depression: evidence from the BRIDGE-II-MIX study. J Affect Disord. 2017;219:187-192.
22. Post RM. Mechanisms of illness progression in the recurrent affective disorders. Neurotox Res. 2010;18(3-4):256-271.
23. da Costa SC, Passos IC, Lowri C, et al. Refractory bipolar disorder and neuroprogression. Prog Neuro-Psychopharmacology Biol Psychiatry. 2016;70:103-110.
24. Crump C, Sundquist K, Winkleby MA, et al. Comorbidities and mortality in bipolar disorder: a Swedish national cohort study. JAMA Psychiatry. 2013;70(9):931-939.
25. Zimmerman M, Martinez JH, Morgan TA, et al. Distinguishing bipolar II depression from major depressive disorder with comorbid borderline personality disorder: demographic, clinical, and family history differences. J Clin Psychiatry. 2013;74(9):880-886.
26. Hasler G, Drevets WC, Gould TD, et al. Toward constructing an endophenotype strategy for bipolar disorders. Biol Psychiatry. 2006;60(2):93-105.
27. Brieger P, Ehrt U, Marneros A. Frequency of comorbid personality disorders in bipolar and unipolar affective disorders. Compr Psychiatry. 2003;44(1):28-34.
28. Leverich GS, McElroy SL, Suppes T, et al. Early physical and sexual abuse associated with an adverse course of bipolar illness. Biol Psychiatry. 2002;51(4):288-297.
29. Leverich GS, Post RM. Course of bipolar illness after history of childhood trauma. Lancet. 2006;367(9516):1040-1042.
30. Golier JA, Yehuda R, Bierer LM, et al. The relationship of borderline personality disorder to posttraumatic stress disorder and traumatic events. Am J Psychiatry. 2003;160(11):2018-2024.
31. Nicol K, Pope M, Romaniuk L, et al. Childhood trauma, midbrain activation and psychotic symptoms in borderline personality disorder. Transl Psychiatry. 2015;5:e559. doi:10.1038/tp.2015.53.
32. Ruggero CJ, Zimmerman M, Chelminski I, et al. Borderline personality disorder and the misdiagnosis of bipolar disorder. J Psychiatr Res. 2010;44(6):405-408.
33. Geddes JR, Miklowitz DJ. Treatment of bipolar disorder. Lancet. 2013;381(9878):1672-1682.
34. McMain S, Korman LM, Dimeff L. Dialectical behavior therapy and the treatment of emotion dysregulation. J Clin Psychol. 2001;57(2):183-196.
35. Cristea IA, Gentili C, Cotet CD, et al. Efficacy of psychotherapies for borderline personality disorder: a systematic review and meta-analysis. JAMA Psychiatry. 2017;74(4):319-328.
36. Linehan MM, Korslund KE, Harned MS, et al. Dialectical behavior therapy for high suicide risk in individuals with borderline personality disorder. JAMA Psychiatry. 2015;72(75);475-482.
37. LeQuesne ER, Hersh RG. Disclosure of a diagnosis of borderline personality disorder. J Psychiatr Pract. 2004:10(3):170-176.
38. Young AH. Bipolar disorder: diagnostic conundrums and associated comorbidities. J Clin Psychiatry. 2009;70(8):e26. doi:10.4088/jcp.7067br6c.
1. Diagnostic and statistical manual of mental disorders, 5th ed. Washington, DC: American Psychiatric Association; 2013.
2. Whiteford HA, Degenhardt L, Rehm J, et al. Global burden of disease attributable to mental and substance use disorders: findings from the Global Burden of Disease Study 2010. Lancet. 2013;382(9904):1575-1586.
3. Merikangas KR, Akiskal HS, Angst J, et al. Lifetime and 12-month prevalence of bipolar spectrum disorder in the National Comorbidity Survey replication. Arch Gen Psychiatry. 2007;64(5):543-552.
4. Malhi GS, Bargh DM, Coulston CM, et al. Predicting bipolar disorder on the basis of phenomenology: implications for prevention and early intervention. Bipolar Disord. 2014;16(5):455-470.
5. Skodol AE, Gunderson JG, Pfohl B, et al. The borderline diagnosis I: psychopathology. Biol Psychiatry. 2002;51(12):936-950.
6. Skodol AE, Siever LJ, Livesley WJ, et al. The borderline diagnosis II: biology, genetics, and clinical course. Biol Psychiatry. 2002;51(12):951-963.
7. Hasin DS, Grant BF. The National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) Waves 1 and 2: review and summary of findings. Soc Psychiatry Psychiatr Epidemiol. 2015;50(11):1609-1640.
8. McDermid J, Sareen J, El-Gabalawy R, et al. Co-morbidity of bipolar disorder and borderline personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Compr Psychiatry. 2015;58:18-28.
9. Gunderson JG, Weinberg I, Daversa MT, et al. Descriptive and longitudinal observations on the relationship of borderline personality disorder and bipolar disorder. Am J Psychiatry. 2006;163(7):1173-1178.
10. Swartz HA, Pilkonis PA, Frank E, et al. Acute treatment outcomes in patients with bipolar I disorder and co-morbid borderline personality disorder receiving medication and psychotherapy. Bipolar Disord. 2005;7(2):192-197.
11. Riemann G, Weisscher N, Post RM, et al. The relationship between self-reported borderline personality features and prospective illness course in bipolar disorder. Int J Bipolar Disord. 2017;5(1):31.
12. de la Rosa I, Oquendo MA, García G, et al. Determining if borderline personality disorder and bipolar disorder are alternative expressions of the same disorder. J Clin Psychiatry. 2017;778(8):e994-e999. doi: 10.4088/JCP.16m11190.
13. di Giacomo E, Aspesi F, Fotiadou M, et al. Unblending borderline personality and bipolar disorders. J Psychiatr Res. 2017;91:90-97.
14. Parker G, Bayes A, McClure G, et al. Clinical status of comorbid bipolar disorder and borderline personality disorder. Br J Psychiatry. 2016;209(3):209-215.
15. Perez Arribas I, Goodwin GM, Geddes JR, et al. A signature-based machine learning model for distinguishing bipolar disorder and borderline personality disorder. Transl Psychiatry. 2018;8(1):274.
16. Insel T, Cuthbert B, Garvey M, et al. Research Domain Criteria (RDoC): toward a new classification framework for research on mental disorders. Am J Psychiatry. 2010;167(7):748-751.
17. Judd LL, Akiskal HS, Schettler PJ, et al. The long-term natural history of the weekly symptomatic status of bipolar I disorder. Arch Gen Psychiatry. 2002;59(6):530-537.
18. Judd LL, Akiskal HS, Schettler PJ, et al. A prospective investigation of the natural history of the long-term weekly symptomatic status of bipolar II disorder. Arch Gen Psychiatry. 2003;60(3):261-269.
19. Oldham JM, Skodol AE, Bender DS. A current integrative perspective on personality disorders. American Psychiatric Publishing, Inc. 2005.
20. Herzog JI, Schmahl C. Adverse childhood experiences and the consequences on neurobiological, psychosocial, and somatic conditions across the lifespan. Front Psychiatry. 2018;9:420.
21. Barbuti M, Pacchiarotti I, Vieta E, et al. Antidepressant-induced hypomania/mania in patients with major depression: evidence from the BRIDGE-II-MIX study. J Affect Disord. 2017;219:187-192.
22. Post RM. Mechanisms of illness progression in the recurrent affective disorders. Neurotox Res. 2010;18(3-4):256-271.
23. da Costa SC, Passos IC, Lowri C, et al. Refractory bipolar disorder and neuroprogression. Prog Neuro-Psychopharmacology Biol Psychiatry. 2016;70:103-110.
24. Crump C, Sundquist K, Winkleby MA, et al. Comorbidities and mortality in bipolar disorder: a Swedish national cohort study. JAMA Psychiatry. 2013;70(9):931-939.
25. Zimmerman M, Martinez JH, Morgan TA, et al. Distinguishing bipolar II depression from major depressive disorder with comorbid borderline personality disorder: demographic, clinical, and family history differences. J Clin Psychiatry. 2013;74(9):880-886.
26. Hasler G, Drevets WC, Gould TD, et al. Toward constructing an endophenotype strategy for bipolar disorders. Biol Psychiatry. 2006;60(2):93-105.
27. Brieger P, Ehrt U, Marneros A. Frequency of comorbid personality disorders in bipolar and unipolar affective disorders. Compr Psychiatry. 2003;44(1):28-34.
28. Leverich GS, McElroy SL, Suppes T, et al. Early physical and sexual abuse associated with an adverse course of bipolar illness. Biol Psychiatry. 2002;51(4):288-297.
29. Leverich GS, Post RM. Course of bipolar illness after history of childhood trauma. Lancet. 2006;367(9516):1040-1042.
30. Golier JA, Yehuda R, Bierer LM, et al. The relationship of borderline personality disorder to posttraumatic stress disorder and traumatic events. Am J Psychiatry. 2003;160(11):2018-2024.
31. Nicol K, Pope M, Romaniuk L, et al. Childhood trauma, midbrain activation and psychotic symptoms in borderline personality disorder. Transl Psychiatry. 2015;5:e559. doi:10.1038/tp.2015.53.
32. Ruggero CJ, Zimmerman M, Chelminski I, et al. Borderline personality disorder and the misdiagnosis of bipolar disorder. J Psychiatr Res. 2010;44(6):405-408.
33. Geddes JR, Miklowitz DJ. Treatment of bipolar disorder. Lancet. 2013;381(9878):1672-1682.
34. McMain S, Korman LM, Dimeff L. Dialectical behavior therapy and the treatment of emotion dysregulation. J Clin Psychol. 2001;57(2):183-196.
35. Cristea IA, Gentili C, Cotet CD, et al. Efficacy of psychotherapies for borderline personality disorder: a systematic review and meta-analysis. JAMA Psychiatry. 2017;74(4):319-328.
36. Linehan MM, Korslund KE, Harned MS, et al. Dialectical behavior therapy for high suicide risk in individuals with borderline personality disorder. JAMA Psychiatry. 2015;72(75);475-482.
37. LeQuesne ER, Hersh RG. Disclosure of a diagnosis of borderline personality disorder. J Psychiatr Pract. 2004:10(3):170-176.
38. Young AH. Bipolar disorder: diagnostic conundrums and associated comorbidities. J Clin Psychiatry. 2009;70(8):e26. doi:10.4088/jcp.7067br6c.
Losing a patient to suicide: Navigating the aftermath
At some point during their career, many mental health professionals will lose a patient to suicide, but few will be prepared for the experience and its aftermath. As I described in Part 1 of this article (
A chance for growth
Traumatic experiences such as a suicide loss can paradoxically present a multitude of opportunities for new growth and profound personal transformation.1 Such transformation is primarily fostered by social support in the aftermath of the trauma.2
Virtually all of the models of the clinician’s suicide grief trajectory I described in Part 1 not only assume the eventual resolution of the distressing reactions accompanying the original loss, but also suggest that mastery of these reactions can be a catalyst for both personal and professional growth. Clearly, not everyone who experiences such a loss will experience subsequent growth; there are many reports of clinicians leaving the field3 or becoming “burned out” after this occurs. Yet most clinicians who have described this loss in the literature and in discussion groups (including those I’ve conducted) have reported more positive eventual outcomes. It is difficult to establish whether this is due to a cohort effect—clinicians who are most likely to write about their experiences, be interviewed for research studies, and/or to seek out and participate in discussion/support groups may be more prone to find benefits in this experience, either by virtue of their nature or through the subsequent process of sharing these experiences in a supportive atmosphere.
The literature on patient suicide loss, as well as anecdotal reports, confirms that clinicians who experience optimal support are able to identify many retrospective benefits of their experience.4-6 Clinicians generally report that they are better able to identify potential risk and protective factors for suicide, and are more knowledgeable about optimal interventions with individuals who are suicidal. They also describe an increased sensitivity towards patients who are suicidal and those bereaved by suicide. In addition, clinicians report a reduction in therapeutic grandiosity/omnipotence, and more realistic appraisals and expectations in relation to their clinical competence. In their effort to understand the “whys” of their patient’s suicide, they are likely to retrospectively identify errors in treatment, “missed cues,” or things they might subsequently do differently,7 and to learn from these mistakes. Optimally, clinicians become more aware of their own therapeutic limitations, both in the short- and the long-term, and can use this knowledge to better determine how they will continue their clinical work. They also become much more aware of the issues involved in the aftermath of a patient suicide, including perceived gaps in the clinical and institutional systems that could optimally offer support to families and clinicians.
In addition to the positive changes related to knowledge and clinical skills, many clinicians also note deeper personal changes subsequent to their patient’s suicide, consistent with the literature on posttraumatic growth.1 Munson8 explored internal changes in clinicians following a patient suicide and found that in the aftermath, clinicians experienced both posttraumatic growth and compassion fatigue. He also found that the amount of time that elapsed since the patient’s suicide predicted posttraumatic growth, and the seemingly counterintuitive result that the number of years of clinical experience prior to the suicide was negatively correlated with posttraumatic growth.
Huhra et al4 described some of the existential issues that a clinician is likely to confront following a patient suicide. A clinician’s attempt to find a way to meaningfully understand the circumstances around this loss often prompts reflection on mortality, freedom, choice and personal autonomy, and the scope and limits of one’s responsibility toward others. The suicide challenges one’s previous conceptions and expectations around these professional issues, and the clinician must construct new paradigms that serve to integrate these new experiences and perspectives in a coherent way.
One of the most notable sequelae of this (and to other traumatic) experience is a subsequent desire to make use of the learning inherent in these experiences and to “give back.” Once they feel that they have resolved their own grief process, many clinicians express the desire to support others with similar experiences. Even when their experiences have been quite distressing, many clinicians are able to view the suicide as an opportunity to learn about ongoing limitations in the systems of support, and to work toward changing these in a way that ensures that future clinician-survivors will have more supportive experiences. Many view these new perspectives, and their consequent ability to be more helpful, as “unexpected gifts.” They often express gratitude toward the people and resources that have allowed them to make these transformations. Jones5 noted “the tragedy of patient suicide can also be an opportunity for us as therapists to grow in our skills at assessing and intervening in a suicidal crisis, to broaden and deepen the support we give and receive, to grow in our appreciation of the precious gift that life is, and to help each other live it more fully.”
Continue to: Guidelines for postvention
Guidelines for postvention
When a patient suicide occurs in the context of an agency setting, Grad9 recommends prompt responses on 4 levels:
- administrative
- institutional
- educational
- emotional.
Numerous authors5,10-21 have developed suggestions, guidelines, and detailed postvention protocols to help agencies and clinicians in various mental health settings navigate the often-complicated sequelae to a patient’s suicide. The Table highlights a few of these. Most emphasize that information about suicide loss, including both its statistical likelihood and its potential aftermath, should integrated into clinicians’ general education and training. They also suggest that suicide postvention policies and protocols be in place from the outset, and that such information be incorporated into institutional policy and procedure manuals. In addition, they stress that legal, institutional, and administrative needs be balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Institutional and administrative procedures
The following are some of the recommended procedures that should take place following a suicide loss. The postvention protocols listed in the Table provide more detailed recommendations.
Legal/ethical. It is essential to consult with a legal representative/risk management specialist associated with the affected agency (ideally, one with specific expertise in suicide litigation.). It is also crucial to clarify who holds privilege after a patient’s death (varies by state), what may and may not be shared under the restrictions of confidentiality and Health Insurance Portability and Accountability Act (HIPAA) laws, and to clarify procedures for chart completion and review. It is also important to clarify the specific information to be shared both within and outside of the agency, and how to address the needs of current patients in the agency settings.
Case review. The optimal purpose of the case review (also known as a psychological autopsy) is to facilitate learning, identify gaps in agency procedures and training, improve pre- and postvention procedures, and help clinicians cope with the loss.22 Again, the legal and administrative needs of the agency need to be balanced with the attention to the emotional impact on the treating clinician.17 Ellis and Patel18 recommend delaying this procedure until the treating clinician is no longer in the “shock” phase of the loss, and is able to think and process events more objectively.
Continue to: Family contact
Family contact. Most authors have recommended that clinicians and/or agencies reach out to surviving families. Although some legal representatives will advise against this, experts in the field of suicide litigation have noted that compassionate family contact reduces liability and facilitates healing for both parties. In a personal communication (May 2008), Eric Harris, of the American Psychological Association Trust, recommended “compassion over caution” when considering these issues. Again, it is important to clarify who holds privilege after a patient’s death in determining when and with whom the patient’s confidential information may be shared. When confidentiality may be broken, clinical judgment should be used to determine how best to present the information to grieving family members.
Even if surviving family members do not hold privilege, there are many things that clinicians can do to be helpful.23 Inevitably, families will want any information that will help them make sense of the loss, and general psychoeducation about mental illness and suicide can be helpful in this regard. In addition, providing information about “Survivors After Suicide” support groups, reading materials, etc., can be helpful. Both support groups and survivor-related bibliographies are available on the web sites of the American Association of Suicidology (www.suicidology.org) and The American Foundation for Suicide Prevention (www.afsp.org).
In addition, clinicians should ask the family if it would be helpful if they were to attend the funeral/memorial services, and how to introduce themselves if asked by other attendees.
Patients in clinics/hospitals. When a patient suicide occurs in a clinic or hospital setting, it is likely to impact other patients in that setting to the extent that they have heard, about the event, even from outside sources.According to Hodgkinson,24 in addition to being overwhelmed with intense feelings about the suicide loss (particularly if they had known the patient), affected patients are likely to be at increased risk for suicidal behaviors. This is consistent with the considerable literature on suicide contagion.
Thus, it is important to clarify information to be shared with patients; however, avoid describing details of the method, because this can foster contagion and “copycat” suicides. In addition, Kaye and Soreff22 noted that these patients may now be concerned about the staff’s ability to be helpful to them, because they were unable to help the deceased. In light of this, take extra care to attend to the impact of the suicide on current patients, and to monitor both pre-existing and new suicidality.
Continue to: Helping affected clinicians
Helping affected clinicians
Suggestions for optimally supporting affected clinicians include:
- clear communication about the nature of upcoming administrative procedures (including chart and institutional reviews)
- consultation from supervisors and/or colleagues that is supportive and reassuring, rather than blaming
- opportunities for the clinician to talk openly about the experience of the loss, either individually or in group settings, without fear of judgment or censure
- recognition that the loss is likely to impact clinical work, support in monitoring this impact, and the provision of medical leaves and/or modified caseloads (ie, fewer high-risk patients) as necessary.
Box 1
Frank Jones and Judy Meade founded the Clinical Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss…to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”7 Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www.cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and links to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Both researchers and clinician-survivors in my practice and support groups have noted that speaking with other clinicians who have experienced suicide loss can be particularly reassuring and validating. If none are available on staff, the listserve and online support groups of the American Association of Suicidology’s Clinician Survivor Task Force may be helpful (Box 17). In addition, the film “Collateral Damages: The Impact of Patient Suicide on the Physician” features physicians describing their experience of losing a patient to suicide (Box 2).
Box 2
“Collateral Damages: The Impact of Patient Suicide on the Physician” is a film that features several physicians speaking about their experience of losing a patient to suicide, as well as a group discussion. Psychiatrists in this educational film include Drs. Glen Gabbard, Sidney Zisook, and Jim Lomax. This resource can be used to facilitate an educational session for physicians, psychologists, residents, or other trainees. Please contact [email protected] to request a DVD of this film and a copy of a related article, Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-430.
Schultz14 offered suggestions for staff in supervisory positions, noting that they may bear at least some clinical and legal responsibility for the treatments that they supervise. She encouraged supervisors to take an active stance in advocating for trainees, to encourage colleagues to express their support, and to discourage rumors and other stigmatizing reactions. Schultz also urges supervisors to14:
- allow extra time for the clinician to engage in the normative exploration of the “whys” that are unique to suicide survivors
- use education about suicide to help the clinician gain a more realistic perspective on their relative culpability
- become aware of and provide education about normative grief reactions following a suicide.
Continue to: Because a suicide loss...
Because a suicide loss is likely to affect a clinician’s subsequent clinical activity, Schultz encourages supervisors to help clinicians monitor this impact on their work.14
A supportive environment is key
Losing a patient to suicide is a complicated, potentially traumatic process that many mental health clinicians will face. Yet with comprehensive and supportive postvention policies in place, clinicians who are impacted are more likely to experience healing and posttraumatic growth in both personal and professional domains.
Bottom Line
Although often traumatic, losing a patient to suicide presents clinicians with an opportunity for personal and professional growth. Following established postvention protocols can help ensure that legal, institutional, and administrative needs are balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Dotinga R. Coping when a patient commits suicide. July 21, 2017. www.mdedge.com/psychiatry/article/142975/depression/coping-when-patient-commits-suicide.
- Gutin N. Losing a patent to suicide: What we know. Part 1. 2019;18(10):14-16,19-22,30-32.
1. Tedeschi RG, Calhoun LG. Beyond the concept of recovery: Growth and the experience of loss. Death Stud. 2008;32(1):27-39.
2. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
3. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
4. Huhra R, Hunka N, Rogers J, et al. Finding meaning: theoretical perspectives on patient suicide. Paper presented at: 2004 Annual Conference of the American Association of Suicidology; April 2004; Miami, FL.
5. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
6. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
7. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
8. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainesville, Florida: University of Florida; 2009.
9. Grad OT. Therapists as survivors of suicide loss. In: Wasserman D, Wasserman C, eds. Oxford textbook of suicidology and suicide prevention. Oxford, UK: Oxford University Press; 2009:609-615.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
13. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. www.cliniciansurvivor.org (under Postvention tab). Published September 21, 2009. Accessed August 26, 2019.
14. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
15. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
16. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information. http://cliniciansurvivor.org. Published May 16, 2016. Accessed January 13, 2019.
17. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
18. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
19. Figueroa S, Dalack GW. Exploring the impact of suicide on clinicians: a multidisciplinary retreat model. J Psychiatr Pract. 2013;19(1):72-77.
20. Lerner U, Brooks, K, McNeil DE, et al. Coping with a patient’s suicide: a curriculum for psychiatry residency training programs. Acad Psychiatry. 2012;36(1):29-33.
21. Prabhakar D, Balon R, Anzia J, et al. Helping psychiatry residents cope with patient suicide. Acad Psychiatry. 2014;38(5):593-597.
22. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
23. McGann VL, Gutin N, Jordan JR. Guidelines for postvention care with survivor families after the suicide of a client. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:133-155.
24. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
At some point during their career, many mental health professionals will lose a patient to suicide, but few will be prepared for the experience and its aftermath. As I described in Part 1 of this article (
A chance for growth
Traumatic experiences such as a suicide loss can paradoxically present a multitude of opportunities for new growth and profound personal transformation.1 Such transformation is primarily fostered by social support in the aftermath of the trauma.2
Virtually all of the models of the clinician’s suicide grief trajectory I described in Part 1 not only assume the eventual resolution of the distressing reactions accompanying the original loss, but also suggest that mastery of these reactions can be a catalyst for both personal and professional growth. Clearly, not everyone who experiences such a loss will experience subsequent growth; there are many reports of clinicians leaving the field3 or becoming “burned out” after this occurs. Yet most clinicians who have described this loss in the literature and in discussion groups (including those I’ve conducted) have reported more positive eventual outcomes. It is difficult to establish whether this is due to a cohort effect—clinicians who are most likely to write about their experiences, be interviewed for research studies, and/or to seek out and participate in discussion/support groups may be more prone to find benefits in this experience, either by virtue of their nature or through the subsequent process of sharing these experiences in a supportive atmosphere.
The literature on patient suicide loss, as well as anecdotal reports, confirms that clinicians who experience optimal support are able to identify many retrospective benefits of their experience.4-6 Clinicians generally report that they are better able to identify potential risk and protective factors for suicide, and are more knowledgeable about optimal interventions with individuals who are suicidal. They also describe an increased sensitivity towards patients who are suicidal and those bereaved by suicide. In addition, clinicians report a reduction in therapeutic grandiosity/omnipotence, and more realistic appraisals and expectations in relation to their clinical competence. In their effort to understand the “whys” of their patient’s suicide, they are likely to retrospectively identify errors in treatment, “missed cues,” or things they might subsequently do differently,7 and to learn from these mistakes. Optimally, clinicians become more aware of their own therapeutic limitations, both in the short- and the long-term, and can use this knowledge to better determine how they will continue their clinical work. They also become much more aware of the issues involved in the aftermath of a patient suicide, including perceived gaps in the clinical and institutional systems that could optimally offer support to families and clinicians.
In addition to the positive changes related to knowledge and clinical skills, many clinicians also note deeper personal changes subsequent to their patient’s suicide, consistent with the literature on posttraumatic growth.1 Munson8 explored internal changes in clinicians following a patient suicide and found that in the aftermath, clinicians experienced both posttraumatic growth and compassion fatigue. He also found that the amount of time that elapsed since the patient’s suicide predicted posttraumatic growth, and the seemingly counterintuitive result that the number of years of clinical experience prior to the suicide was negatively correlated with posttraumatic growth.
Huhra et al4 described some of the existential issues that a clinician is likely to confront following a patient suicide. A clinician’s attempt to find a way to meaningfully understand the circumstances around this loss often prompts reflection on mortality, freedom, choice and personal autonomy, and the scope and limits of one’s responsibility toward others. The suicide challenges one’s previous conceptions and expectations around these professional issues, and the clinician must construct new paradigms that serve to integrate these new experiences and perspectives in a coherent way.
One of the most notable sequelae of this (and to other traumatic) experience is a subsequent desire to make use of the learning inherent in these experiences and to “give back.” Once they feel that they have resolved their own grief process, many clinicians express the desire to support others with similar experiences. Even when their experiences have been quite distressing, many clinicians are able to view the suicide as an opportunity to learn about ongoing limitations in the systems of support, and to work toward changing these in a way that ensures that future clinician-survivors will have more supportive experiences. Many view these new perspectives, and their consequent ability to be more helpful, as “unexpected gifts.” They often express gratitude toward the people and resources that have allowed them to make these transformations. Jones5 noted “the tragedy of patient suicide can also be an opportunity for us as therapists to grow in our skills at assessing and intervening in a suicidal crisis, to broaden and deepen the support we give and receive, to grow in our appreciation of the precious gift that life is, and to help each other live it more fully.”
Continue to: Guidelines for postvention
Guidelines for postvention
When a patient suicide occurs in the context of an agency setting, Grad9 recommends prompt responses on 4 levels:
- administrative
- institutional
- educational
- emotional.
Numerous authors5,10-21 have developed suggestions, guidelines, and detailed postvention protocols to help agencies and clinicians in various mental health settings navigate the often-complicated sequelae to a patient’s suicide. The Table highlights a few of these. Most emphasize that information about suicide loss, including both its statistical likelihood and its potential aftermath, should integrated into clinicians’ general education and training. They also suggest that suicide postvention policies and protocols be in place from the outset, and that such information be incorporated into institutional policy and procedure manuals. In addition, they stress that legal, institutional, and administrative needs be balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Institutional and administrative procedures
The following are some of the recommended procedures that should take place following a suicide loss. The postvention protocols listed in the Table provide more detailed recommendations.
Legal/ethical. It is essential to consult with a legal representative/risk management specialist associated with the affected agency (ideally, one with specific expertise in suicide litigation.). It is also crucial to clarify who holds privilege after a patient’s death (varies by state), what may and may not be shared under the restrictions of confidentiality and Health Insurance Portability and Accountability Act (HIPAA) laws, and to clarify procedures for chart completion and review. It is also important to clarify the specific information to be shared both within and outside of the agency, and how to address the needs of current patients in the agency settings.
Case review. The optimal purpose of the case review (also known as a psychological autopsy) is to facilitate learning, identify gaps in agency procedures and training, improve pre- and postvention procedures, and help clinicians cope with the loss.22 Again, the legal and administrative needs of the agency need to be balanced with the attention to the emotional impact on the treating clinician.17 Ellis and Patel18 recommend delaying this procedure until the treating clinician is no longer in the “shock” phase of the loss, and is able to think and process events more objectively.
Continue to: Family contact
Family contact. Most authors have recommended that clinicians and/or agencies reach out to surviving families. Although some legal representatives will advise against this, experts in the field of suicide litigation have noted that compassionate family contact reduces liability and facilitates healing for both parties. In a personal communication (May 2008), Eric Harris, of the American Psychological Association Trust, recommended “compassion over caution” when considering these issues. Again, it is important to clarify who holds privilege after a patient’s death in determining when and with whom the patient’s confidential information may be shared. When confidentiality may be broken, clinical judgment should be used to determine how best to present the information to grieving family members.
Even if surviving family members do not hold privilege, there are many things that clinicians can do to be helpful.23 Inevitably, families will want any information that will help them make sense of the loss, and general psychoeducation about mental illness and suicide can be helpful in this regard. In addition, providing information about “Survivors After Suicide” support groups, reading materials, etc., can be helpful. Both support groups and survivor-related bibliographies are available on the web sites of the American Association of Suicidology (www.suicidology.org) and The American Foundation for Suicide Prevention (www.afsp.org).
In addition, clinicians should ask the family if it would be helpful if they were to attend the funeral/memorial services, and how to introduce themselves if asked by other attendees.
Patients in clinics/hospitals. When a patient suicide occurs in a clinic or hospital setting, it is likely to impact other patients in that setting to the extent that they have heard, about the event, even from outside sources.According to Hodgkinson,24 in addition to being overwhelmed with intense feelings about the suicide loss (particularly if they had known the patient), affected patients are likely to be at increased risk for suicidal behaviors. This is consistent with the considerable literature on suicide contagion.
Thus, it is important to clarify information to be shared with patients; however, avoid describing details of the method, because this can foster contagion and “copycat” suicides. In addition, Kaye and Soreff22 noted that these patients may now be concerned about the staff’s ability to be helpful to them, because they were unable to help the deceased. In light of this, take extra care to attend to the impact of the suicide on current patients, and to monitor both pre-existing and new suicidality.
Continue to: Helping affected clinicians
Helping affected clinicians
Suggestions for optimally supporting affected clinicians include:
- clear communication about the nature of upcoming administrative procedures (including chart and institutional reviews)
- consultation from supervisors and/or colleagues that is supportive and reassuring, rather than blaming
- opportunities for the clinician to talk openly about the experience of the loss, either individually or in group settings, without fear of judgment or censure
- recognition that the loss is likely to impact clinical work, support in monitoring this impact, and the provision of medical leaves and/or modified caseloads (ie, fewer high-risk patients) as necessary.
Box 1
Frank Jones and Judy Meade founded the Clinical Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss…to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”7 Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www.cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and links to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Both researchers and clinician-survivors in my practice and support groups have noted that speaking with other clinicians who have experienced suicide loss can be particularly reassuring and validating. If none are available on staff, the listserve and online support groups of the American Association of Suicidology’s Clinician Survivor Task Force may be helpful (Box 17). In addition, the film “Collateral Damages: The Impact of Patient Suicide on the Physician” features physicians describing their experience of losing a patient to suicide (Box 2).
Box 2
“Collateral Damages: The Impact of Patient Suicide on the Physician” is a film that features several physicians speaking about their experience of losing a patient to suicide, as well as a group discussion. Psychiatrists in this educational film include Drs. Glen Gabbard, Sidney Zisook, and Jim Lomax. This resource can be used to facilitate an educational session for physicians, psychologists, residents, or other trainees. Please contact [email protected] to request a DVD of this film and a copy of a related article, Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-430.
Schultz14 offered suggestions for staff in supervisory positions, noting that they may bear at least some clinical and legal responsibility for the treatments that they supervise. She encouraged supervisors to take an active stance in advocating for trainees, to encourage colleagues to express their support, and to discourage rumors and other stigmatizing reactions. Schultz also urges supervisors to14:
- allow extra time for the clinician to engage in the normative exploration of the “whys” that are unique to suicide survivors
- use education about suicide to help the clinician gain a more realistic perspective on their relative culpability
- become aware of and provide education about normative grief reactions following a suicide.
Continue to: Because a suicide loss...
Because a suicide loss is likely to affect a clinician’s subsequent clinical activity, Schultz encourages supervisors to help clinicians monitor this impact on their work.14
A supportive environment is key
Losing a patient to suicide is a complicated, potentially traumatic process that many mental health clinicians will face. Yet with comprehensive and supportive postvention policies in place, clinicians who are impacted are more likely to experience healing and posttraumatic growth in both personal and professional domains.
Bottom Line
Although often traumatic, losing a patient to suicide presents clinicians with an opportunity for personal and professional growth. Following established postvention protocols can help ensure that legal, institutional, and administrative needs are balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Dotinga R. Coping when a patient commits suicide. July 21, 2017. www.mdedge.com/psychiatry/article/142975/depression/coping-when-patient-commits-suicide.
- Gutin N. Losing a patent to suicide: What we know. Part 1. 2019;18(10):14-16,19-22,30-32.
At some point during their career, many mental health professionals will lose a patient to suicide, but few will be prepared for the experience and its aftermath. As I described in Part 1 of this article (
A chance for growth
Traumatic experiences such as a suicide loss can paradoxically present a multitude of opportunities for new growth and profound personal transformation.1 Such transformation is primarily fostered by social support in the aftermath of the trauma.2
Virtually all of the models of the clinician’s suicide grief trajectory I described in Part 1 not only assume the eventual resolution of the distressing reactions accompanying the original loss, but also suggest that mastery of these reactions can be a catalyst for both personal and professional growth. Clearly, not everyone who experiences such a loss will experience subsequent growth; there are many reports of clinicians leaving the field3 or becoming “burned out” after this occurs. Yet most clinicians who have described this loss in the literature and in discussion groups (including those I’ve conducted) have reported more positive eventual outcomes. It is difficult to establish whether this is due to a cohort effect—clinicians who are most likely to write about their experiences, be interviewed for research studies, and/or to seek out and participate in discussion/support groups may be more prone to find benefits in this experience, either by virtue of their nature or through the subsequent process of sharing these experiences in a supportive atmosphere.
The literature on patient suicide loss, as well as anecdotal reports, confirms that clinicians who experience optimal support are able to identify many retrospective benefits of their experience.4-6 Clinicians generally report that they are better able to identify potential risk and protective factors for suicide, and are more knowledgeable about optimal interventions with individuals who are suicidal. They also describe an increased sensitivity towards patients who are suicidal and those bereaved by suicide. In addition, clinicians report a reduction in therapeutic grandiosity/omnipotence, and more realistic appraisals and expectations in relation to their clinical competence. In their effort to understand the “whys” of their patient’s suicide, they are likely to retrospectively identify errors in treatment, “missed cues,” or things they might subsequently do differently,7 and to learn from these mistakes. Optimally, clinicians become more aware of their own therapeutic limitations, both in the short- and the long-term, and can use this knowledge to better determine how they will continue their clinical work. They also become much more aware of the issues involved in the aftermath of a patient suicide, including perceived gaps in the clinical and institutional systems that could optimally offer support to families and clinicians.
In addition to the positive changes related to knowledge and clinical skills, many clinicians also note deeper personal changes subsequent to their patient’s suicide, consistent with the literature on posttraumatic growth.1 Munson8 explored internal changes in clinicians following a patient suicide and found that in the aftermath, clinicians experienced both posttraumatic growth and compassion fatigue. He also found that the amount of time that elapsed since the patient’s suicide predicted posttraumatic growth, and the seemingly counterintuitive result that the number of years of clinical experience prior to the suicide was negatively correlated with posttraumatic growth.
Huhra et al4 described some of the existential issues that a clinician is likely to confront following a patient suicide. A clinician’s attempt to find a way to meaningfully understand the circumstances around this loss often prompts reflection on mortality, freedom, choice and personal autonomy, and the scope and limits of one’s responsibility toward others. The suicide challenges one’s previous conceptions and expectations around these professional issues, and the clinician must construct new paradigms that serve to integrate these new experiences and perspectives in a coherent way.
One of the most notable sequelae of this (and to other traumatic) experience is a subsequent desire to make use of the learning inherent in these experiences and to “give back.” Once they feel that they have resolved their own grief process, many clinicians express the desire to support others with similar experiences. Even when their experiences have been quite distressing, many clinicians are able to view the suicide as an opportunity to learn about ongoing limitations in the systems of support, and to work toward changing these in a way that ensures that future clinician-survivors will have more supportive experiences. Many view these new perspectives, and their consequent ability to be more helpful, as “unexpected gifts.” They often express gratitude toward the people and resources that have allowed them to make these transformations. Jones5 noted “the tragedy of patient suicide can also be an opportunity for us as therapists to grow in our skills at assessing and intervening in a suicidal crisis, to broaden and deepen the support we give and receive, to grow in our appreciation of the precious gift that life is, and to help each other live it more fully.”
Continue to: Guidelines for postvention
Guidelines for postvention
When a patient suicide occurs in the context of an agency setting, Grad9 recommends prompt responses on 4 levels:
- administrative
- institutional
- educational
- emotional.
Numerous authors5,10-21 have developed suggestions, guidelines, and detailed postvention protocols to help agencies and clinicians in various mental health settings navigate the often-complicated sequelae to a patient’s suicide. The Table highlights a few of these. Most emphasize that information about suicide loss, including both its statistical likelihood and its potential aftermath, should integrated into clinicians’ general education and training. They also suggest that suicide postvention policies and protocols be in place from the outset, and that such information be incorporated into institutional policy and procedure manuals. In addition, they stress that legal, institutional, and administrative needs be balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Institutional and administrative procedures
The following are some of the recommended procedures that should take place following a suicide loss. The postvention protocols listed in the Table provide more detailed recommendations.
Legal/ethical. It is essential to consult with a legal representative/risk management specialist associated with the affected agency (ideally, one with specific expertise in suicide litigation.). It is also crucial to clarify who holds privilege after a patient’s death (varies by state), what may and may not be shared under the restrictions of confidentiality and Health Insurance Portability and Accountability Act (HIPAA) laws, and to clarify procedures for chart completion and review. It is also important to clarify the specific information to be shared both within and outside of the agency, and how to address the needs of current patients in the agency settings.
Case review. The optimal purpose of the case review (also known as a psychological autopsy) is to facilitate learning, identify gaps in agency procedures and training, improve pre- and postvention procedures, and help clinicians cope with the loss.22 Again, the legal and administrative needs of the agency need to be balanced with the attention to the emotional impact on the treating clinician.17 Ellis and Patel18 recommend delaying this procedure until the treating clinician is no longer in the “shock” phase of the loss, and is able to think and process events more objectively.
Continue to: Family contact
Family contact. Most authors have recommended that clinicians and/or agencies reach out to surviving families. Although some legal representatives will advise against this, experts in the field of suicide litigation have noted that compassionate family contact reduces liability and facilitates healing for both parties. In a personal communication (May 2008), Eric Harris, of the American Psychological Association Trust, recommended “compassion over caution” when considering these issues. Again, it is important to clarify who holds privilege after a patient’s death in determining when and with whom the patient’s confidential information may be shared. When confidentiality may be broken, clinical judgment should be used to determine how best to present the information to grieving family members.
Even if surviving family members do not hold privilege, there are many things that clinicians can do to be helpful.23 Inevitably, families will want any information that will help them make sense of the loss, and general psychoeducation about mental illness and suicide can be helpful in this regard. In addition, providing information about “Survivors After Suicide” support groups, reading materials, etc., can be helpful. Both support groups and survivor-related bibliographies are available on the web sites of the American Association of Suicidology (www.suicidology.org) and The American Foundation for Suicide Prevention (www.afsp.org).
In addition, clinicians should ask the family if it would be helpful if they were to attend the funeral/memorial services, and how to introduce themselves if asked by other attendees.
Patients in clinics/hospitals. When a patient suicide occurs in a clinic or hospital setting, it is likely to impact other patients in that setting to the extent that they have heard, about the event, even from outside sources.According to Hodgkinson,24 in addition to being overwhelmed with intense feelings about the suicide loss (particularly if they had known the patient), affected patients are likely to be at increased risk for suicidal behaviors. This is consistent with the considerable literature on suicide contagion.
Thus, it is important to clarify information to be shared with patients; however, avoid describing details of the method, because this can foster contagion and “copycat” suicides. In addition, Kaye and Soreff22 noted that these patients may now be concerned about the staff’s ability to be helpful to them, because they were unable to help the deceased. In light of this, take extra care to attend to the impact of the suicide on current patients, and to monitor both pre-existing and new suicidality.
Continue to: Helping affected clinicians
Helping affected clinicians
Suggestions for optimally supporting affected clinicians include:
- clear communication about the nature of upcoming administrative procedures (including chart and institutional reviews)
- consultation from supervisors and/or colleagues that is supportive and reassuring, rather than blaming
- opportunities for the clinician to talk openly about the experience of the loss, either individually or in group settings, without fear of judgment or censure
- recognition that the loss is likely to impact clinical work, support in monitoring this impact, and the provision of medical leaves and/or modified caseloads (ie, fewer high-risk patients) as necessary.
Box 1
Frank Jones and Judy Meade founded the Clinical Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss…to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”7 Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www.cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and links to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Both researchers and clinician-survivors in my practice and support groups have noted that speaking with other clinicians who have experienced suicide loss can be particularly reassuring and validating. If none are available on staff, the listserve and online support groups of the American Association of Suicidology’s Clinician Survivor Task Force may be helpful (Box 17). In addition, the film “Collateral Damages: The Impact of Patient Suicide on the Physician” features physicians describing their experience of losing a patient to suicide (Box 2).
Box 2
“Collateral Damages: The Impact of Patient Suicide on the Physician” is a film that features several physicians speaking about their experience of losing a patient to suicide, as well as a group discussion. Psychiatrists in this educational film include Drs. Glen Gabbard, Sidney Zisook, and Jim Lomax. This resource can be used to facilitate an educational session for physicians, psychologists, residents, or other trainees. Please contact [email protected] to request a DVD of this film and a copy of a related article, Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-430.
Schultz14 offered suggestions for staff in supervisory positions, noting that they may bear at least some clinical and legal responsibility for the treatments that they supervise. She encouraged supervisors to take an active stance in advocating for trainees, to encourage colleagues to express their support, and to discourage rumors and other stigmatizing reactions. Schultz also urges supervisors to14:
- allow extra time for the clinician to engage in the normative exploration of the “whys” that are unique to suicide survivors
- use education about suicide to help the clinician gain a more realistic perspective on their relative culpability
- become aware of and provide education about normative grief reactions following a suicide.
Continue to: Because a suicide loss...
Because a suicide loss is likely to affect a clinician’s subsequent clinical activity, Schultz encourages supervisors to help clinicians monitor this impact on their work.14
A supportive environment is key
Losing a patient to suicide is a complicated, potentially traumatic process that many mental health clinicians will face. Yet with comprehensive and supportive postvention policies in place, clinicians who are impacted are more likely to experience healing and posttraumatic growth in both personal and professional domains.
Bottom Line
Although often traumatic, losing a patient to suicide presents clinicians with an opportunity for personal and professional growth. Following established postvention protocols can help ensure that legal, institutional, and administrative needs are balanced with the emotional needs of affected clinicians and staff, as well as those of the surviving family.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Dotinga R. Coping when a patient commits suicide. July 21, 2017. www.mdedge.com/psychiatry/article/142975/depression/coping-when-patient-commits-suicide.
- Gutin N. Losing a patent to suicide: What we know. Part 1. 2019;18(10):14-16,19-22,30-32.
1. Tedeschi RG, Calhoun LG. Beyond the concept of recovery: Growth and the experience of loss. Death Stud. 2008;32(1):27-39.
2. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
3. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
4. Huhra R, Hunka N, Rogers J, et al. Finding meaning: theoretical perspectives on patient suicide. Paper presented at: 2004 Annual Conference of the American Association of Suicidology; April 2004; Miami, FL.
5. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
6. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
7. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
8. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainesville, Florida: University of Florida; 2009.
9. Grad OT. Therapists as survivors of suicide loss. In: Wasserman D, Wasserman C, eds. Oxford textbook of suicidology and suicide prevention. Oxford, UK: Oxford University Press; 2009:609-615.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
13. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. www.cliniciansurvivor.org (under Postvention tab). Published September 21, 2009. Accessed August 26, 2019.
14. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
15. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
16. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information. http://cliniciansurvivor.org. Published May 16, 2016. Accessed January 13, 2019.
17. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
18. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
19. Figueroa S, Dalack GW. Exploring the impact of suicide on clinicians: a multidisciplinary retreat model. J Psychiatr Pract. 2013;19(1):72-77.
20. Lerner U, Brooks, K, McNeil DE, et al. Coping with a patient’s suicide: a curriculum for psychiatry residency training programs. Acad Psychiatry. 2012;36(1):29-33.
21. Prabhakar D, Balon R, Anzia J, et al. Helping psychiatry residents cope with patient suicide. Acad Psychiatry. 2014;38(5):593-597.
22. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
23. McGann VL, Gutin N, Jordan JR. Guidelines for postvention care with survivor families after the suicide of a client. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:133-155.
24. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
1. Tedeschi RG, Calhoun LG. Beyond the concept of recovery: Growth and the experience of loss. Death Stud. 2008;32(1):27-39.
2. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
3. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
4. Huhra R, Hunka N, Rogers J, et al. Finding meaning: theoretical perspectives on patient suicide. Paper presented at: 2004 Annual Conference of the American Association of Suicidology; April 2004; Miami, FL.
5. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
6. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
7. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
8. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainesville, Florida: University of Florida; 2009.
9. Grad OT. Therapists as survivors of suicide loss. In: Wasserman D, Wasserman C, eds. Oxford textbook of suicidology and suicide prevention. Oxford, UK: Oxford University Press; 2009:609-615.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
13. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. www.cliniciansurvivor.org (under Postvention tab). Published September 21, 2009. Accessed August 26, 2019.
14. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
15. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
16. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information. http://cliniciansurvivor.org. Published May 16, 2016. Accessed January 13, 2019.
17. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
18. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
19. Figueroa S, Dalack GW. Exploring the impact of suicide on clinicians: a multidisciplinary retreat model. J Psychiatr Pract. 2013;19(1):72-77.
20. Lerner U, Brooks, K, McNeil DE, et al. Coping with a patient’s suicide: a curriculum for psychiatry residency training programs. Acad Psychiatry. 2012;36(1):29-33.
21. Prabhakar D, Balon R, Anzia J, et al. Helping psychiatry residents cope with patient suicide. Acad Psychiatry. 2014;38(5):593-597.
22. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
23. McGann VL, Gutin N, Jordan JR. Guidelines for postvention care with survivor families after the suicide of a client. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:133-155.
24. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
Losing a patient to suicide: What we know
Studies have found that 1 in 2 psychiatrists,1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,5 will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.
This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:
- the impact of losing a patient to suicide
- confidentiality-related constraints on the ability to discuss and process the loss
- legal and ethical issues
- colleagues’ reactions and stigma
- the effects of a suicide loss on one’s clinical work.
Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide.
A neglected topic
For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.1-5 Despite this, coping with a patient’s suicide is a “neglected topic”8 in residency and general mental health training.
There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh9), and several authors10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale20 found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.
A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.
Grief and other emotional effects
In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.21 Chemtob et al2 found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.
Continue to: Jordan and McIntosh have detailed...
Jordan and McIntosh22 have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher23 term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.
Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.24-27
Clinicians’ unique reactions
For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman13 have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.
Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.28,29
These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.11
Continue to: Hendin et al found...
Hendin et al30 found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al4 similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft31 describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.32
Many clinicians have noted that they considered leaving the field after such a loss,33,34 and it is hypothesized that many may have done so.35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.29,35
Box 1
Several authors have proposed general models for describing the suicide grief trajectories of clinicians after a suicide loss. Tillman38 identified distinct groups of responses to this event: traumatic, affective, those related to the treatment, those related to interactions with colleagues, liability concerns, and the impact on one’s professional philosophy. She also found that Erikson’s stages of identity39 provided an uncannily similar trajectory to the ways in which those who participated in her research—clinicians at a mental hospital—had attempted to cope with their patients’ deaths, noting that the “suicide of a patient may provoke a revisiting of Erikson’s psychosocial crises in a telescoped and accelerated fashion.”38
Maltsberger40 offered a detailed psychoanalytic analysis of the responses clinicians may manifest in relation to a suicide loss, including the initial narcissistic injury sustained in relation to their patient’s actions; the subsequent potential for melancholic, atonement, or avoidance reactions; and the eventual capacity for the resolution of these reactions.
Al-Mateen et al33 described 3 phases of the clinician’s reaction after losing a patient who was a child to suicide:
- initial, which includes trauma and shock
- turmoil, which includes emotional flooding and functional impairments
- new growth, in which clinicians are able to reflect on their experiences and implications for training and policy.
For each phase, they also described staff activities that would foster forward movement through the trajectory.
In a 1981 study, Bissell41 found that psychiatric nurses who had experienced patient completed suicides progressed through several developmental stages (naïveté, recognition, responsibility, individual choice) that enabled them to come to terms with their personal reactions and place the ultimate responsibility for the suicide with the patient.
After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 133,38-41). Box 22-4,6,16,24,29,30,33,34,40,42-45 describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.
Box 2
There are many factors that make the experience of losing a patient to suicide unique and variable for individual clinicians. These include the amount of a clinician’s professional training and experience, both in general and in working with potentially suicidal individuals. Chemtob et al2 found that trainees were more likely to experience patient suicide loss than more seasoned clinicians, and to experience more distress.4,30,42 Brown24 noted that many training programs were likely to assign the most “extraordinarily sick patients to inexperienced trainees.” He noted that because the skill level of trainees has not yet tempered their personal aspirations, they are likely to experience a patient’s suicide as a personal failure. However, in contrast to the findings of Kleespies,42 Hendin,30 Ruskin et al,4 and Brown24 suggested that the overall impact of a patient’s suicide may be greater for seasoned clinicians, when the “protective advantage” or “explanation” of being in training is no longer applicable. This appears consistent with Munson’s study,43 which found that a greater number of years of clinical experience prior to a suicide loss was negatively correlated with posttraumatic growth.
Other factors affecting a clinician’s grief response include the context in which the treatment occurred, such as inpatient, outpatient, clinic, private practice, etc.44; the presence and involvement of supportive mentors or supervisors16; the length and intensity of the clinical relationship6,29; countertransference issues40; whether the patient was a child33; and the time elapsed since the suicide occurred.
In addition, each clinician’s set of personal and life experiences can affect the way he/ she moves through the grieving process. Any previous trauma or losses, particularly prior exposure to suicide, will likely impact a clinician’s reaction to his/her current loss, as will any susceptibility to anxiety or depression. Gorkin45 has suggested that the degree of omnipotence in the clinician’s therapeutic strivings will affect his/her ability to accept the inherent ambiguity involved in suicide loss. Gender may also play a role: Henry et al34 found that female clinicians had higher levels of stress reactions, and Grad et al3 found that female clinicians felt more shame and guilt and professed more doubts about their professional competence than male clinicians, and were more than twice as likely as men to identify talking with colleagues as an effective coping strategy.
Continue to: Implications of confidentiality restrictions
Implications of confidentiality restrictions
Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.46
The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 312).
Box 3
Frank Jones and Judy Meade founded the Clinician Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss … to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”12
Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It now supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www. cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and a link to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Continue to: Doka has described...
Doka47 has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.
Other legal/ethical issues
The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,48 the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al49 found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.
In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”
Other studies29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth17 also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.
Professional relationships/colleagues’ reactions
Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,52 “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al30 noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.
Continue to: Negative reactions from professional colleagues...
Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al53 found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.
Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.
Stigma around suicide is well documented.25 In The Surgeon General’s Call to Action to Prevent Suicide,54 former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al26 found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.
In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.
Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.
Continue to: Effects on clinical work
Effects on clinical work
A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al30 noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.
In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”15 In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.
In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.68 Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.69
Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”40 some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson70 noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz16 described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.
Working toward a supportive solution
In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (
Bottom Line
For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.
1. Alexander D, Klein S, Gray NM, et al. Suicide by patients: questionnaire study of its effect on consultant psychiatrists. BMJ. 2000;320(7249):1571-1574.
2. Chemtob CM, Hamada RS, Bauer G, et al. Patients’ suicides: frequency and impact on psychiatrists. Am J Psychiatry. 1988;145(2):224-228.
3. Grad OT, Zavasnik A, Groleger U. Suicide of a patient: gender differences in bereavement reactions of therapists. Suicide Life Threat Behav. 1997;27(4):379-386.
4. Ruskin R, Sakinofsky I, Bagby RM, et al. Impact of patient suicide on psychiatrists and psychiatric trainees. Acad Psychiatry. 2004;28(2):104-110.
5. Bersoff DN. Ethical conflicts in psychology, 2nd ed. Washington, DC: American Psychological Association; 1999.
6. Chemtob CM, Bauer GB, Hamada RS, et al. Patient suicide: occupational hazard for psychologists and psychiatrists. Prof Psychol Res Pr. 1989;20(5):294-300.
7. Rubin HL. Surviving a suicide in your practice. In: Blumenthal SJ, Kupfer DJ, eds. Suicide over the life cycle: risk factors, assessment, and treatment of suicidal patients. Washington, DC: American Psychiatric Press; 1990:619-636.
8. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
9. McIntosh JL. Clinicians as survivors of suicide: bibliography. American Association of Suicidology Clinician Survivor Task Force. http://pages.iu.edu/~jmcintos/Surv.Ther.bib.htm. Updated May 19, 2019. Accessed August 26, 2019.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
13. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
14. Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-30.
15. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. http://pages.iu.edu/~jmcintos/postvention.htm. Published September 21, 2009. Accessed August 26, 2019.
16. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
17. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
18. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information.
19. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
20. Melton B, Coverdale J. What do we teach psychiatric residents about suicide? A national survey of chief residents. Acad Psychiatry. 2009;33(1):47-50.
21. Valente SM. Psychotherapist reactions to the suicide of a patient. Am J Orthopsychiatry. 1994;64(4):614-621.
22. Jordan JR, McIntosh JL. Is suicide bereavement different? A framework for rethinking the question. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:19-42.
23. Jordan JR, Baugher B. After suicide loss: coping with your grief, 2nd ed. Newcastle, WA: Caring People Press; 2016.
24. Brown HB. The impact of suicide on therapists in training. Compr Psychiatry. 1987;28(2):101-112.
25. Cvinar JG. Do suicide survivors suffer social stigma: a review of the literature. Perspect Psychiatr Care. 2005;41(1):14-21.
26. Feigelman W, Gorman BS, Jordan JR. Stigmatization and suicide bereavement. Death Stud. 2009;33(7):591-608.
27. Goffman E. Stigma: notes on the management of spoiled identity. New York, NY: Simon & Schuster; 1963.
28. Goldney RD. The privilege and responsibility of suicide prevention. Crisis. 2000;21(1):8-15.
29. Litman RE. When patients commit suicide. Am J Psychother. 1965;19(4):570-576.
30. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
31. Rycroft P. Touching the heart and soul of therapy: surviving client suicide. Women Ther. 2004;28(1):83-94.
32. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
33. Al-Mateen CS, Jones K, Linker J, et al. Clinician response to a child who completes suicide. Child Adolesc Psychiatric Clin N Am. 2018;27(4):621-635.
34. Henry M, Séguin M, Drouin M-S. Mental health professionals’ response to the suicide of their patients [in French]. Revue Québécoise de Psychologie. 2004;25:241-257.
35. Carter RE. Some effects of client suicide on the therapist. Psychother Theory Res Practice. 1971;8(4):287-289.
36. Dewar I, Eagles J, Klein S, et al. Psychiatric trainees’ experiences of, and reactions to, patient suicide. Psychiatr Bull. 2000;24(1):20-23.
37. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
38. Tillman JG. When a patient commits suicide: an empirical study of psychoanalytic clinicians. Inter J Psychoanal. 2006;87(1):159-177.
39. Erikson EH. Identity and the life cycle. New York, NY: International Universities Press, Inc.; 1959.
40. Maltsberger JT. The implications of patient suicide for the surviving psychotherapist. In: Jacobs D, ed. Suicide and clinical practice. Washington, DC: American Psychiatric Press; 1992:169-182.
41. Bissell BPH. The experience of the nurse therapist working with suicidal cases: a developmental study [dissertation]. Boston, MA: Boston University School of Education; 1981.
42. Kleespies PM. The stress of patient suicidal behavior: Implications for interns and training programs in psychology. Prof Psychol Res Pract. 1993;24(4):477-482.
43. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainsville, Florida: University of Florida; 2009.
44. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
45. Gorkin M. On the suicide of one’s patient. Bull Menninger Clin. 1985;49(1):1-9.
46. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
47. Doka KJ. Disenfranchised grief: new Directions, challenges, and strategies for practice. Champaign, IL: Research Press; 2002.
48. Bongar B. The suicidal patient: clinical and legal standards of care, 2nd ed. Washington, DC: American Psychological Association; 2002.
49. Peterson EM, Luoma JB, Dunne E. Suicide survivors’ perceptions of the treating clinician. Suicide Life Threat Behav. 2002;32(2):158-166.
50. Kolodny S, Binder RL, Bronstein AA, et al. The working through of patients’ suicides by four therapists. Suicide Life Threat Behav. 1979;9(1):33-46.
51. Marshall KA. When a patient commits suicide. Suicide Life Threat Behav. 1980;10(1):29-40.
52. Jobes DA, Maltsberger JT. The hazards of treating suicidal patients. In: Sussman MB, ed. A perilous calling: the hazards of psychotherapy practice. New York, NY: Wiley & Sons; 1995:200-214.
53. Castelli-Dransart DA, Gutjahr E, Gulfi A, et al. Patient suicide in institutions: emotional responses and traumatic impact on Swiss mental health professionals. Death Stud. 2014;38(1-5):315-321.
54. US Public Health Service. The Surgeon General’s call to action to prevent suicide. Washington, DC: Department of Health and Human Services; 1999.
55. Armour M. Violent death: understanding the context of traumatic and stigmatized grief. J Hum Behav Soc Environ. 2006;14(4):53-90.
56. Calhoun, LG, Allen BG. Social reactions to the survivor of a suicide in the family: a review of the literature. Omega (Westport). 1991;23(2):95-107.
57. Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: WW Norton & Co; 1987.
58. Harwood D, Hawton K, Hope J, et al. The grief experiences and needs of bereaved relatives and friends of older people dying through suicide: a descriptive and case-control study. J Affect Disord. 2002;72(2):185-194.
59. Jordan JR. Is suicide bereavement different? A reassessment of the literature. Suicide Life Threat Behav. 2001;31(1):91-102.
60. McIntosh JL. Control group studies of suicide survivors: a review and critique. Suicide Life Threat Behav. 2003;23(2):146-161.
61. Range LM. When a loss is due to suicide: unique aspects of bereavement. In: Harvey JH, ed. Perspectives on loss: a sourcebook. Philadelphia, PA: Brunner/Mazel; 1998:213-220.
62. Sveen CA, Walby FA. Suicide survivors’ mental health and grief reactions: a systematic review of controlled studies. Suicide Life Threat Behav. 2008;38(1):13-29.
63. Van Dongen CJ. Social context of postsuicide bereavement. Death Stud. 1993;17(2):125-141.
64. Bultema JK. The healing process for the multidisciplinary team: recovering post-inpatient suicide. J Psychosoc Nurs. 1994;32(2):19-24.
65. Cooper C. Patient suicide and assault: their impact on psychiatric hospital staff. J Psychosoc Nurs Ment Health Serv. 1995;33(6):26-29.
66. Foster VA, McAdams CR III. The impact of client suicide in counselor training: Implications for counselor education and supervision. Counselor Educ Supervision. 1999;39(1):22-33.
67. Little JD. Staff response to inpatient and outpatient suicide: what happened and what do we do? Aust N Z J Psychiatry. 1992;26(2):162-167.
68. Horn PJ. Therapists’ psychological adaptation to client suicidal behavior. Chicago, IL: Loyola University of Chicago; 1995.
69. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
70. Anderson GO. Who, what, when, where, how, and mostly why? A therapist’s grief over the suicide of a client. Women Ther. 2004;28(1):25-34.
Studies have found that 1 in 2 psychiatrists,1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,5 will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.
This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:
- the impact of losing a patient to suicide
- confidentiality-related constraints on the ability to discuss and process the loss
- legal and ethical issues
- colleagues’ reactions and stigma
- the effects of a suicide loss on one’s clinical work.
Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide.
A neglected topic
For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.1-5 Despite this, coping with a patient’s suicide is a “neglected topic”8 in residency and general mental health training.
There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh9), and several authors10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale20 found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.
A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.
Grief and other emotional effects
In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.21 Chemtob et al2 found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.
Continue to: Jordan and McIntosh have detailed...
Jordan and McIntosh22 have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher23 term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.
Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.24-27
Clinicians’ unique reactions
For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman13 have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.
Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.28,29
These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.11
Continue to: Hendin et al found...
Hendin et al30 found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al4 similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft31 describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.32
Many clinicians have noted that they considered leaving the field after such a loss,33,34 and it is hypothesized that many may have done so.35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.29,35
Box 1
Several authors have proposed general models for describing the suicide grief trajectories of clinicians after a suicide loss. Tillman38 identified distinct groups of responses to this event: traumatic, affective, those related to the treatment, those related to interactions with colleagues, liability concerns, and the impact on one’s professional philosophy. She also found that Erikson’s stages of identity39 provided an uncannily similar trajectory to the ways in which those who participated in her research—clinicians at a mental hospital—had attempted to cope with their patients’ deaths, noting that the “suicide of a patient may provoke a revisiting of Erikson’s psychosocial crises in a telescoped and accelerated fashion.”38
Maltsberger40 offered a detailed psychoanalytic analysis of the responses clinicians may manifest in relation to a suicide loss, including the initial narcissistic injury sustained in relation to their patient’s actions; the subsequent potential for melancholic, atonement, or avoidance reactions; and the eventual capacity for the resolution of these reactions.
Al-Mateen et al33 described 3 phases of the clinician’s reaction after losing a patient who was a child to suicide:
- initial, which includes trauma and shock
- turmoil, which includes emotional flooding and functional impairments
- new growth, in which clinicians are able to reflect on their experiences and implications for training and policy.
For each phase, they also described staff activities that would foster forward movement through the trajectory.
In a 1981 study, Bissell41 found that psychiatric nurses who had experienced patient completed suicides progressed through several developmental stages (naïveté, recognition, responsibility, individual choice) that enabled them to come to terms with their personal reactions and place the ultimate responsibility for the suicide with the patient.
After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 133,38-41). Box 22-4,6,16,24,29,30,33,34,40,42-45 describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.
Box 2
There are many factors that make the experience of losing a patient to suicide unique and variable for individual clinicians. These include the amount of a clinician’s professional training and experience, both in general and in working with potentially suicidal individuals. Chemtob et al2 found that trainees were more likely to experience patient suicide loss than more seasoned clinicians, and to experience more distress.4,30,42 Brown24 noted that many training programs were likely to assign the most “extraordinarily sick patients to inexperienced trainees.” He noted that because the skill level of trainees has not yet tempered their personal aspirations, they are likely to experience a patient’s suicide as a personal failure. However, in contrast to the findings of Kleespies,42 Hendin,30 Ruskin et al,4 and Brown24 suggested that the overall impact of a patient’s suicide may be greater for seasoned clinicians, when the “protective advantage” or “explanation” of being in training is no longer applicable. This appears consistent with Munson’s study,43 which found that a greater number of years of clinical experience prior to a suicide loss was negatively correlated with posttraumatic growth.
Other factors affecting a clinician’s grief response include the context in which the treatment occurred, such as inpatient, outpatient, clinic, private practice, etc.44; the presence and involvement of supportive mentors or supervisors16; the length and intensity of the clinical relationship6,29; countertransference issues40; whether the patient was a child33; and the time elapsed since the suicide occurred.
In addition, each clinician’s set of personal and life experiences can affect the way he/ she moves through the grieving process. Any previous trauma or losses, particularly prior exposure to suicide, will likely impact a clinician’s reaction to his/her current loss, as will any susceptibility to anxiety or depression. Gorkin45 has suggested that the degree of omnipotence in the clinician’s therapeutic strivings will affect his/her ability to accept the inherent ambiguity involved in suicide loss. Gender may also play a role: Henry et al34 found that female clinicians had higher levels of stress reactions, and Grad et al3 found that female clinicians felt more shame and guilt and professed more doubts about their professional competence than male clinicians, and were more than twice as likely as men to identify talking with colleagues as an effective coping strategy.
Continue to: Implications of confidentiality restrictions
Implications of confidentiality restrictions
Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.46
The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 312).
Box 3
Frank Jones and Judy Meade founded the Clinician Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss … to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”12
Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It now supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www. cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and a link to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Continue to: Doka has described...
Doka47 has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.
Other legal/ethical issues
The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,48 the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al49 found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.
In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”
Other studies29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth17 also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.
Professional relationships/colleagues’ reactions
Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,52 “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al30 noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.
Continue to: Negative reactions from professional colleagues...
Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al53 found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.
Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.
Stigma around suicide is well documented.25 In The Surgeon General’s Call to Action to Prevent Suicide,54 former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al26 found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.
In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.
Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.
Continue to: Effects on clinical work
Effects on clinical work
A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al30 noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.
In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”15 In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.
In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.68 Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.69
Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”40 some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson70 noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz16 described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.
Working toward a supportive solution
In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (
Bottom Line
For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.
Studies have found that 1 in 2 psychiatrists,1-4 and 1 in 5 psychologists, clinical social workers, and other mental health professionals,5 will lose a patient to suicide in the course of their career. This statistic suggests that losing a patient to suicide constitutes a clear occupational hazard.6,7 Despite this, most mental health professionals continue to view suicide loss as an aberration. Consequently, there is often a lack of preparedness for such an event when it does occur.
This 2-part article summarizes what is currently known about the unique personal and professional issues experienced by clinician-survivors (clinicians who have lost patients and/or loved ones to suicide). In Part 1, I cover:
- the impact of losing a patient to suicide
- confidentiality-related constraints on the ability to discuss and process the loss
- legal and ethical issues
- colleagues’ reactions and stigma
- the effects of a suicide loss on one’s clinical work.
Part 2 will discuss the opportunities for personal growth that can result from experiencing a suicide loss, guidelines for optimal postventions, and steps clinicians can take to help support colleagues who have lost a patient to suicide.
A neglected topic
For psychiatrists and other mental health professionals, the loss of a patient to suicide is certainly not uncommon.1-5 Despite this, coping with a patient’s suicide is a “neglected topic”8 in residency and general mental health training.
There are many published articles on clinicians experiencing suicide loss (for a comprehensive bibliography, see McIntosh9), and several authors10-19 have developed suggestions, guidelines, and detailed postvention protocols to help clinicians navigate the often-complicated sequelae to such a loss. However, these resources have generally not been integrated into clinical training, and tend to be poorly disseminated. In a national survey of chief residents, Melton and Coverdale20 found that only 25% of residency training programs covered topics related to postvention, and 72% of chief residents felt this topic needed more attention. Thus, despite the existence of guidelines for optimal postvention and support, clinicians are often left to cope with the consequences of this difficult loss on their own, and under less-than-optimal conditions.
A patient’s suicide typically affects clinicians on multiple levels, both personally and professionally. In this article, I highlight the range of normative responses, as well as the factors that may facilitate or inhibit subsequent healing and growth, with the hope that this knowledge may be utilized to help current and future generations of clinician-survivors obtain optimal support, and that institutions who treat potentially suicidal individuals will develop optimal postvention responses following a suicide loss. Many aspects of what this article discusses also apply to clinicians who have experienced a suicide loss in their personal or family life, as this also tends to “spill over” into one’s professional roles and identity.
Grief and other emotional effects
In many ways, clinicians’ responses after a patient’s suicide are similar to those of other survivors after the loss of a loved one to suicide.21 Chemtob et al2 found that approximately one-half of psychiatrists who lost a patient to suicide had scores on the Impact of an Event Scale that were comparable to those of a clinical population seeking treatment after the death of a parent.
Continue to: Jordan and McIntosh have detailed...
Jordan and McIntosh22 have detailed several elements and themes that differentiate suicide loss and its associated reactions from other types of loss and grief. In general, suicide loss is considered traumatic, and is often accompanied by intense confusion and existential questioning, reflecting a negative impact on one’s core beliefs and assumptive world. The subsequent need to address the myriad of “why” questions left in its wake are often tinted with what Jordan and Baugher23 term the “tyranny of hindsight,” and take the form of implicit guilt for “sins of omission or commission” in relation to the lost individual.
Responses to suicide loss typically include initial shock, denial and numbness, intense sadness, anxiety, anger, and intense distress. Consistent with the traumatic nature of the loss, survivors are also likely to experience posttraumatic stress disorder symptoms such as intrusive thoughts, avoidance, and dissociation. Survivors also commonly experience significant guilt and shame, and this is likely to be socially reinforced by the general stigma associated with suicide as well as the actual blaming and avoidance responses of others.24-27
Clinicians’ unique reactions
For clinicians, there are additional components that may further complicate or exacerbate these reactions and extend their duration. First and foremost, such a loss affects clinicians on both personal and professional levels, a phenomenon that Plakun and Tillman13 have termed a “twin bereavement.” Thus, in addition to the personal grief and trauma reactions entailed in losing a patient to suicide, this loss is likely to impact clinicians’ professional identities, their relationships with colleagues, and their clinical work.
Clinicians’ professional identities are often predicated on generally shared assumptions and beliefs that, as trained professionals, they should have the power, aptitude, and competence to heal, or at least improve, the lives of patients, to reduce their distress, and to provide safety. In addition, such assumptions about clinicians’ responsibility and ability to prevent suicide are often reinforced in the clinical literature.28,29
These assumptions are often challenged, if not shattered, when patients take their own lives. A clinician’s sense of professional responsibility, the guilt and self-blame that may accompany this, self-doubts about one’s skills and clinical competence, the fear of (and actual) blame of colleagues and family members, and the real or imagined threat of litigation may all greatly exacerbate a clinician’s distress.11
Continue to: Hendin et al found...
Hendin et al30 found that mental health therapists have described losing a patient as “the most profoundly disturbing event of their professional careers,” noting that one-third of these clinicians experienced severe distress that lasted at least 1 year beyond the initial loss. In a 2004 study, Ruskin et al4 similarly found that one-quarter of psychiatrists and psychiatric trainees noted that losing a patient had a “profound and enduring effect on them.” In her article on surviving a patient’s suicide, Rycroft31 describes a “professional void” following the loss of her patient, in which “the world had changed, nothing was predictable any more, and it was no longer safe to assume anything.” Additionally, many clinicians experience an “acute sense of aloneness and isolation” subsequent to the loss.32
Many clinicians have noted that they considered leaving the field after such a loss,33,34 and it is hypothesized that many may have done so.35-37 Others have noted that, at least temporarily, they stopped treating patients who were potentially suicidal.29,35
Box 1
Several authors have proposed general models for describing the suicide grief trajectories of clinicians after a suicide loss. Tillman38 identified distinct groups of responses to this event: traumatic, affective, those related to the treatment, those related to interactions with colleagues, liability concerns, and the impact on one’s professional philosophy. She also found that Erikson’s stages of identity39 provided an uncannily similar trajectory to the ways in which those who participated in her research—clinicians at a mental hospital—had attempted to cope with their patients’ deaths, noting that the “suicide of a patient may provoke a revisiting of Erikson’s psychosocial crises in a telescoped and accelerated fashion.”38
Maltsberger40 offered a detailed psychoanalytic analysis of the responses clinicians may manifest in relation to a suicide loss, including the initial narcissistic injury sustained in relation to their patient’s actions; the subsequent potential for melancholic, atonement, or avoidance reactions; and the eventual capacity for the resolution of these reactions.
Al-Mateen et al33 described 3 phases of the clinician’s reaction after losing a patient who was a child to suicide:
- initial, which includes trauma and shock
- turmoil, which includes emotional flooding and functional impairments
- new growth, in which clinicians are able to reflect on their experiences and implications for training and policy.
For each phase, they also described staff activities that would foster forward movement through the trajectory.
In a 1981 study, Bissell41 found that psychiatric nurses who had experienced patient completed suicides progressed through several developmental stages (naïveté, recognition, responsibility, individual choice) that enabled them to come to terms with their personal reactions and place the ultimate responsibility for the suicide with the patient.
After losing a patient to suicide, a clinician may experience grief that proceeds through specific stages (Box 133,38-41). Box 22-4,6,16,24,29,30,33,34,40,42-45 describes a wide range of factors that affect each clinician’s unique response to losing a patient to suicide.
Box 2
There are many factors that make the experience of losing a patient to suicide unique and variable for individual clinicians. These include the amount of a clinician’s professional training and experience, both in general and in working with potentially suicidal individuals. Chemtob et al2 found that trainees were more likely to experience patient suicide loss than more seasoned clinicians, and to experience more distress.4,30,42 Brown24 noted that many training programs were likely to assign the most “extraordinarily sick patients to inexperienced trainees.” He noted that because the skill level of trainees has not yet tempered their personal aspirations, they are likely to experience a patient’s suicide as a personal failure. However, in contrast to the findings of Kleespies,42 Hendin,30 Ruskin et al,4 and Brown24 suggested that the overall impact of a patient’s suicide may be greater for seasoned clinicians, when the “protective advantage” or “explanation” of being in training is no longer applicable. This appears consistent with Munson’s study,43 which found that a greater number of years of clinical experience prior to a suicide loss was negatively correlated with posttraumatic growth.
Other factors affecting a clinician’s grief response include the context in which the treatment occurred, such as inpatient, outpatient, clinic, private practice, etc.44; the presence and involvement of supportive mentors or supervisors16; the length and intensity of the clinical relationship6,29; countertransference issues40; whether the patient was a child33; and the time elapsed since the suicide occurred.
In addition, each clinician’s set of personal and life experiences can affect the way he/ she moves through the grieving process. Any previous trauma or losses, particularly prior exposure to suicide, will likely impact a clinician’s reaction to his/her current loss, as will any susceptibility to anxiety or depression. Gorkin45 has suggested that the degree of omnipotence in the clinician’s therapeutic strivings will affect his/her ability to accept the inherent ambiguity involved in suicide loss. Gender may also play a role: Henry et al34 found that female clinicians had higher levels of stress reactions, and Grad et al3 found that female clinicians felt more shame and guilt and professed more doubts about their professional competence than male clinicians, and were more than twice as likely as men to identify talking with colleagues as an effective coping strategy.
Continue to: Implications of confidentiality restrictions
Implications of confidentiality restrictions
Confidentiality issues, as well as advice from attorneys to limit the disclosure of information about a patient, are likely to preclude a clinician’s ability to talk freely about the patient, the therapeutic relationship, and his/her reactions to the loss, all of which are known to facilitate movement through the grief process.46
The development of trust and the sharing of pain are just 2 factors that can make the clinical encounter an intense emotional experience for both parties. Recent trends in the psychodynamic literature acknowledge the profundity and depth of the personal impact that patients have on the clinician, an impact that is neither pathological nor an indication of poor boundaries in the therapy dyad, but instead a recognition of how all aspects of the clinician’s person, whether consciously or not, are used within the context of a therapeutic relationship. Yet when clinicians lose a patient, confidentiality restrictions often leave them wondering if and where any aspects of their experiences can be shared. Legal counsel may advise a clinician against speaking to consultants or supervisors or even surviving family members for fear that these non-privileged communications are subject to discovery should any legal proceedings ensue. Furthermore, the usual grief rituals that facilitate the healing of loss and the processing of grief (eg, gathering with others who knew the deceased, sharing feelings and memories, attending memorials) are usually denied to the clinician, and are often compounded by the reactions of one’s professional colleagues, who tend not to view the therapist’s grief as “legitimate.” Thus, clinician-survivors, despite having experienced a profound and traumatic loss, have very few places where this may be processed or even validated. As one clinician in a clinician-survivors support group stated, “I felt like I was grieving in a vacuum, that I wasn’t allowed to talk about how much my patient meant to me or how I’m feeling about it.” The isolation of grieving alone is likely to be compounded by the general lack of resources for supporting clinicians after such a loss. In contrast to the general suicide “survivor” network of support groups for family members who have experienced a suicide loss, there is an almost complete lack of supportive resources for clinicians following such a loss, and most clinicians are not aware of the resources that are available, such as the Clinician Survivor Task Force of the American Association of Suicidology (Box 312).
Box 3
Frank Jones and Judy Meade founded the Clinician Survivor Task Force (CSTF) of the American Association of Suicidology (AAS) in 1987. As Jones noted, “clinicians who have lost patients to suicide need a place to acknowledge and carry forward their personal loss … to benefit both personally and professionally from the opportunity to talk with other therapists who have survived the loss of a patient through suicide.”12
Nina Gutin, PhD, and Vanessa McGann, PhD, have co-chaired the CSTF since 2003. It now supports clinicians who have lost patients and/or loved ones, with the recognition that both types of losses carry implications within clinical and professional domains. The CSTF provides a listserve, opportunities to participate in video support groups, and a web site (www. cliniciansurvivor.org) that provides information about the clinician-survivor experience, the opportunity to read and post narratives about one’s experience with suicide loss, an updated bibliography maintained by John McIntosh, PhD, a list of clinical contacts, and a link to several excellent postvention protocols. In addition, Drs. Gutin and McGann conduct clinician-survivor support activities at the annual AAS conference, and in their respective geographic areas.
Continue to: Doka has described...
Doka47 has described “disenfranchised grief” in which the bereaved person does not receive the type and quality of support accorded to other bereaved persons, and thus is likely to internalize the view that his/her grief is not legitimate, and to believe that sharing related distress is a shame-ridden liability. This clearly relates to the sense of profound isolation and distress often described by clinician-survivors.
Other legal/ethical issues
The clinician-survivor’s concern about litigation, or an actual lawsuit, is likely to produce intense anxiety. This common fear is both understandable and credible. According to Bongar,48 the most common malpractice lawsuits filed against clinicians are those that involve a patient’s suicide. Peterson et al49 found that 34% of surviving family members considered bringing a lawsuit against the clinician, and of these, 57% consulted a lawyer.
In addition, an institution’s concern about protecting itself from liability may compromise its ability to support the clinician or trainee who sustained the loss. As noted above, the potential prohibitions around discussing the case can compromise the grief process. Additionally, the fear of (or actual) legal reprisals against supervisors and the larger institution may engender angry and blaming responses toward the treating clinician. In a personal communication (April 2008), Quinnett described an incident in which a supervising psychologist stomped into the grieving therapist’s office unannounced and shouted, “Now look what you’ve done! You’re going to get me sued!”
Other studies29,50,51 note that clinician-survivors fear losing their job, and that their colleagues and supervisors will be reluctant to assign new patients to them. Spiegleman and Werth17 also note that trainees grapple with additional concerns over negative evaluations, suspension or termination from clinical sites or training programs, and a potential interruption of obtaining a degree. Such supervisory and institutional reactions are likely to intensify a clinician’s sense of shame and distress, and are antithetical to postvention responses that promote optimal personal and professional growth. Such negative reactions are also likely to contribute to a clinician or trainee’s subsequent reluctance to work with suicidal individuals, or their decision to discontinue their clinical work altogether. Lastly, other ethical issues, such as contact with the patient’s family following the suicide, attending the funeral, etc., are likely to be a source of additional anxiety and distress, particularly if the clinician needs to address these issues in isolation.
Professional relationships/colleagues’ reactions
Many clinician-survivors have described reactions from colleagues and supervisors that are hurtful and unsupportive. According to Jobes and Maltsberger,52 “the suicide death of a patient in active treatment is commonly taken as prima facie evidence that the therapist, somehow or another, has mismanaged the case,” and thus the clinician often faces unwarranted blame and censure from colleagues and supervisors. Hendin et al30 noted that many trainees found reactions by their institutions to be insensitive and unsupportive, one noting that the department’s review of the case “felt more like a tribunal or inquest.” In a personal communication (April 2008), Quinnett noted that many clinicians he interviewed following a suicide loss reported a pattern of isolation and interpersonal discomfort with their colleagues, who implicitly or explicitly expressed concerns about their competence. He described how a respected colleague received “no understanding, no support, only abuse” from her supervisors. Such responses, while perhaps surprising from mental health professionals, probably reflect the long-standing cultural attitude of social condemnation of suicide, and of those who are associated with it.
Continue to: Negative reactions from professional colleagues...
Negative reactions from professional colleagues are most likely to occur immediately after the suicide loss and/or during the course of a subsequent investigation or psychological autopsy. Castelli-Dransart et al53 found that the lack of institutional support after a clinician experiences a suicide loss contributed to significantly higher stress responses for impacted clinicians, and may lead to a well-founded ambivalence about disclosure to colleagues, and consequent resistance to seeking out optimal supervision/consultation or even personal therapy that could help the clinician gain clarity on the effects of these issues. Many mental health professionals have described how, after the distressing experience of losing a patient to suicide, they moved through this process in relative isolation and loneliness, feeling abandoned by their colleagues and by their own hopes and expectations for support.
Stigmatization. In clinical settings, when a patient in treatment completes suicide, the treating clinician becomes an easy scapegoat for family members and colleagues. To the extent that mental health professionals are not immune from the effects and imposition of stigma, this might also affect their previously mentioned tendency to project judgment, overtly or covertly, onto the treating clinician.
Stigma around suicide is well documented.25 In The Surgeon General’s Call to Action to Prevent Suicide,54 former Surgeon General David Satcher specifically described stigma around suicide as one of the biggest barriers to prevention. Studies have shown that individuals bereaved by suicide are also stigmatized, and that those who were in caregiving roles (parents, clinicians) are believed to be more psychologically disturbed, less likable, more blameworthy, and less worthy of receiving support than other bereaved individuals.25,55-63 These judgments often mirror survivors’ self-punitive assessments, which then become exacerbated by and intertwined with both externally imposed and internalized stigma. Hence, it is not uncommon for suicide survivors to question their own right to grieve, to report low expectations of social support, and to feel compelled to deny or hide the mode of death. Feigelman et al26 found that stigmatization after a suicide loss was specifically associated with ongoing grief difficulties, depression, and suicidal thinking.
In my long-term work with clinician-survivors, I’ve come to believe that in addition to stigma around suicide, there may also be stigma projected by colleagues in relation to a clinician’s perceived emotional vulnerability. A traumatized clinician potentially challenges the notion of the implicit dichotomy/power imbalance between professionals and the patients we treat: “Us”—the professional, competent, healthy, and benevolent clinicians who have the care to offer, and “Them”—our patients, being needy, pathological, looking to us for care. This “us/them” distinction may serve to bolster a clinician’s professional esteem and identity. But when one of “us” becomes one of “them”—when a professional colleague is perceived as being emotionally vulnerable—this can be threatening to the predicates of this distinction, leading to the need to put the affected clinician firmly into the “them” camp. Thus, unwarranted condemnations of the clinician-survivor’s handling of the case, and/or the pathologizing of their normative grief reactions after the suicide loss, can seem justified.
Stigma associated both with suicide and with professional vulnerability is likely to be internalized and to have a profound effect on the clinician’s decisions about disclosure, asking for support, and ultimately on one’s ability to integrate the loss. When this occurs, it is likely to lead to even more isolation, shame, and self-blame. It is not surprising that many clinicians consider leaving the profession after this type of experience.
Continue to: Effects on clinical work
Effects on clinical work
A suicide loss is also likely to affect a clinician’s therapeutic work. Many authors12,52,64-67 have found that this commonly leads therapists to question their abilities as clinicians, and to experience a sharp loss of confidence in their work with patients. The shattered beliefs and assumptions around the efficacy of the therapeutic process, a sense of guilt or self-blame, and any perceived or actual negative judgment from colleagues can dramatically compromise a clinician’s sense of competence. Hendin et al30 noted that even the most experienced therapists expressed difficulty in trusting their own clinical judgment, or accurately assessing risk after a suicide loss.
In addition, the common grief and trauma-related responses to a suicide loss (including shock, numbness, sadness, anxiety, and generalized distress) are likely to result in at least some temporary disruption of a clinician’s optimal functioning. If trauma-related symptoms are more pronounced, the effect and longevity of such impairment may be exacerbated, and are likely to “impair clinical response and therapeutic judgment.”15 In addition, because such symptoms and states may be triggered by exposure to other potentially suicidal patients, they are more likely to impact clinical functioning when the clinician works with suicidal individuals. Thus, the normative responses to a suicide loss are likely to impact a clinician’s work, just as they are likely to impact the personal and occupational functioning of any survivor of suicide loss.
In clinician-survivor discussions and support groups I’ve led, participants have identified many common areas of clinical impact. Perhaps one of the most common early responses reported by clinician-survivors who continued to work with potentially suicidal individuals was to become hypervigilant in relation to any perceived suicide risk, to interpret such risk in such a way as to warrant more conservative interventions than are necessary, and to consequently minimize the patient’s own capacities for self-care.68 Conversely, others reported a tendency to minimize or deny suicidal potential by, for example, avoiding asking patients directly about suicidal ideation, even when they later realized that such questioning was indicated.69
Suicide loss may also lead to more subtle clinical reactions that have been observed not only with suicidal patients, but also in relation to patients who struggle with loss or grief. These include avoidant or even dissociative reactions in relation to their patient’s pain, which in turn can impact the clinician’s ability to “be fully present” or empathic in clinical encounters.50,69 Still, other clinicians noted that they tended to project residual feelings of anger onto their current suicidal patients, or envied patients who seemed to have mastered their grief. Consistent with Maltsberger’s description of “atonement reactions,”40 some clinicians found themselves doing more than should be expected for their patients, even losing their sense of professional boundaries in the process. Anderson70 noted that in pushing herself beyond what she knew were her optimal clinical boundaries, she was “punishing herself” for failing to prevent her patient’s suicide because, as she realized, “doing ‘penance’ was better than feeling helpless and powerless.” And Schultz16 described how therapists may have subsequent difficulty in trusting other patients, especially if patients who completed suicide did not disclose or denied their suicidal intent.
Working toward a supportive solution
In summary, unless clinicians who lose a patient to suicide have more supportive experiences, the combination of confidentiality-related restrictions, confusion about legal/ethical repercussions, unsupportive reactions from colleagues, and unexpected impairments in clinical work are likely to lead to intensified distress, isolation, the perceived need to “hide” the impact in professional settings, and consideration of leaving the profession. However, as I will describe in Part 2 (
Bottom Line
For mental health clinicians, losing a patient to suicide is a clear occupational hazard. After a suicide loss, clinicians often experience unique personal and professional challenges, including the impact of the loss on clinical work and professional identity, legal/ethical issues, and confidentiality-related constraints on the ability to discuss and process the loss.
Related Resources
- American Association of Suicidology Clinician Survivor Task Force. www.cliniciansurvivor.org.
- Gutin N. Helping survivors in the aftermath of suicide loss. Current Psychiatry. 2018;17(8):27-33.
1. Alexander D, Klein S, Gray NM, et al. Suicide by patients: questionnaire study of its effect on consultant psychiatrists. BMJ. 2000;320(7249):1571-1574.
2. Chemtob CM, Hamada RS, Bauer G, et al. Patients’ suicides: frequency and impact on psychiatrists. Am J Psychiatry. 1988;145(2):224-228.
3. Grad OT, Zavasnik A, Groleger U. Suicide of a patient: gender differences in bereavement reactions of therapists. Suicide Life Threat Behav. 1997;27(4):379-386.
4. Ruskin R, Sakinofsky I, Bagby RM, et al. Impact of patient suicide on psychiatrists and psychiatric trainees. Acad Psychiatry. 2004;28(2):104-110.
5. Bersoff DN. Ethical conflicts in psychology, 2nd ed. Washington, DC: American Psychological Association; 1999.
6. Chemtob CM, Bauer GB, Hamada RS, et al. Patient suicide: occupational hazard for psychologists and psychiatrists. Prof Psychol Res Pr. 1989;20(5):294-300.
7. Rubin HL. Surviving a suicide in your practice. In: Blumenthal SJ, Kupfer DJ, eds. Suicide over the life cycle: risk factors, assessment, and treatment of suicidal patients. Washington, DC: American Psychiatric Press; 1990:619-636.
8. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
9. McIntosh JL. Clinicians as survivors of suicide: bibliography. American Association of Suicidology Clinician Survivor Task Force. http://pages.iu.edu/~jmcintos/Surv.Ther.bib.htm. Updated May 19, 2019. Accessed August 26, 2019.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
13. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
14. Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-30.
15. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. http://pages.iu.edu/~jmcintos/postvention.htm. Published September 21, 2009. Accessed August 26, 2019.
16. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
17. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
18. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information.
19. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
20. Melton B, Coverdale J. What do we teach psychiatric residents about suicide? A national survey of chief residents. Acad Psychiatry. 2009;33(1):47-50.
21. Valente SM. Psychotherapist reactions to the suicide of a patient. Am J Orthopsychiatry. 1994;64(4):614-621.
22. Jordan JR, McIntosh JL. Is suicide bereavement different? A framework for rethinking the question. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:19-42.
23. Jordan JR, Baugher B. After suicide loss: coping with your grief, 2nd ed. Newcastle, WA: Caring People Press; 2016.
24. Brown HB. The impact of suicide on therapists in training. Compr Psychiatry. 1987;28(2):101-112.
25. Cvinar JG. Do suicide survivors suffer social stigma: a review of the literature. Perspect Psychiatr Care. 2005;41(1):14-21.
26. Feigelman W, Gorman BS, Jordan JR. Stigmatization and suicide bereavement. Death Stud. 2009;33(7):591-608.
27. Goffman E. Stigma: notes on the management of spoiled identity. New York, NY: Simon & Schuster; 1963.
28. Goldney RD. The privilege and responsibility of suicide prevention. Crisis. 2000;21(1):8-15.
29. Litman RE. When patients commit suicide. Am J Psychother. 1965;19(4):570-576.
30. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
31. Rycroft P. Touching the heart and soul of therapy: surviving client suicide. Women Ther. 2004;28(1):83-94.
32. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
33. Al-Mateen CS, Jones K, Linker J, et al. Clinician response to a child who completes suicide. Child Adolesc Psychiatric Clin N Am. 2018;27(4):621-635.
34. Henry M, Séguin M, Drouin M-S. Mental health professionals’ response to the suicide of their patients [in French]. Revue Québécoise de Psychologie. 2004;25:241-257.
35. Carter RE. Some effects of client suicide on the therapist. Psychother Theory Res Practice. 1971;8(4):287-289.
36. Dewar I, Eagles J, Klein S, et al. Psychiatric trainees’ experiences of, and reactions to, patient suicide. Psychiatr Bull. 2000;24(1):20-23.
37. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
38. Tillman JG. When a patient commits suicide: an empirical study of psychoanalytic clinicians. Inter J Psychoanal. 2006;87(1):159-177.
39. Erikson EH. Identity and the life cycle. New York, NY: International Universities Press, Inc.; 1959.
40. Maltsberger JT. The implications of patient suicide for the surviving psychotherapist. In: Jacobs D, ed. Suicide and clinical practice. Washington, DC: American Psychiatric Press; 1992:169-182.
41. Bissell BPH. The experience of the nurse therapist working with suicidal cases: a developmental study [dissertation]. Boston, MA: Boston University School of Education; 1981.
42. Kleespies PM. The stress of patient suicidal behavior: Implications for interns and training programs in psychology. Prof Psychol Res Pract. 1993;24(4):477-482.
43. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainsville, Florida: University of Florida; 2009.
44. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
45. Gorkin M. On the suicide of one’s patient. Bull Menninger Clin. 1985;49(1):1-9.
46. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
47. Doka KJ. Disenfranchised grief: new Directions, challenges, and strategies for practice. Champaign, IL: Research Press; 2002.
48. Bongar B. The suicidal patient: clinical and legal standards of care, 2nd ed. Washington, DC: American Psychological Association; 2002.
49. Peterson EM, Luoma JB, Dunne E. Suicide survivors’ perceptions of the treating clinician. Suicide Life Threat Behav. 2002;32(2):158-166.
50. Kolodny S, Binder RL, Bronstein AA, et al. The working through of patients’ suicides by four therapists. Suicide Life Threat Behav. 1979;9(1):33-46.
51. Marshall KA. When a patient commits suicide. Suicide Life Threat Behav. 1980;10(1):29-40.
52. Jobes DA, Maltsberger JT. The hazards of treating suicidal patients. In: Sussman MB, ed. A perilous calling: the hazards of psychotherapy practice. New York, NY: Wiley & Sons; 1995:200-214.
53. Castelli-Dransart DA, Gutjahr E, Gulfi A, et al. Patient suicide in institutions: emotional responses and traumatic impact on Swiss mental health professionals. Death Stud. 2014;38(1-5):315-321.
54. US Public Health Service. The Surgeon General’s call to action to prevent suicide. Washington, DC: Department of Health and Human Services; 1999.
55. Armour M. Violent death: understanding the context of traumatic and stigmatized grief. J Hum Behav Soc Environ. 2006;14(4):53-90.
56. Calhoun, LG, Allen BG. Social reactions to the survivor of a suicide in the family: a review of the literature. Omega (Westport). 1991;23(2):95-107.
57. Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: WW Norton & Co; 1987.
58. Harwood D, Hawton K, Hope J, et al. The grief experiences and needs of bereaved relatives and friends of older people dying through suicide: a descriptive and case-control study. J Affect Disord. 2002;72(2):185-194.
59. Jordan JR. Is suicide bereavement different? A reassessment of the literature. Suicide Life Threat Behav. 2001;31(1):91-102.
60. McIntosh JL. Control group studies of suicide survivors: a review and critique. Suicide Life Threat Behav. 2003;23(2):146-161.
61. Range LM. When a loss is due to suicide: unique aspects of bereavement. In: Harvey JH, ed. Perspectives on loss: a sourcebook. Philadelphia, PA: Brunner/Mazel; 1998:213-220.
62. Sveen CA, Walby FA. Suicide survivors’ mental health and grief reactions: a systematic review of controlled studies. Suicide Life Threat Behav. 2008;38(1):13-29.
63. Van Dongen CJ. Social context of postsuicide bereavement. Death Stud. 1993;17(2):125-141.
64. Bultema JK. The healing process for the multidisciplinary team: recovering post-inpatient suicide. J Psychosoc Nurs. 1994;32(2):19-24.
65. Cooper C. Patient suicide and assault: their impact on psychiatric hospital staff. J Psychosoc Nurs Ment Health Serv. 1995;33(6):26-29.
66. Foster VA, McAdams CR III. The impact of client suicide in counselor training: Implications for counselor education and supervision. Counselor Educ Supervision. 1999;39(1):22-33.
67. Little JD. Staff response to inpatient and outpatient suicide: what happened and what do we do? Aust N Z J Psychiatry. 1992;26(2):162-167.
68. Horn PJ. Therapists’ psychological adaptation to client suicidal behavior. Chicago, IL: Loyola University of Chicago; 1995.
69. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
70. Anderson GO. Who, what, when, where, how, and mostly why? A therapist’s grief over the suicide of a client. Women Ther. 2004;28(1):25-34.
1. Alexander D, Klein S, Gray NM, et al. Suicide by patients: questionnaire study of its effect on consultant psychiatrists. BMJ. 2000;320(7249):1571-1574.
2. Chemtob CM, Hamada RS, Bauer G, et al. Patients’ suicides: frequency and impact on psychiatrists. Am J Psychiatry. 1988;145(2):224-228.
3. Grad OT, Zavasnik A, Groleger U. Suicide of a patient: gender differences in bereavement reactions of therapists. Suicide Life Threat Behav. 1997;27(4):379-386.
4. Ruskin R, Sakinofsky I, Bagby RM, et al. Impact of patient suicide on psychiatrists and psychiatric trainees. Acad Psychiatry. 2004;28(2):104-110.
5. Bersoff DN. Ethical conflicts in psychology, 2nd ed. Washington, DC: American Psychological Association; 1999.
6. Chemtob CM, Bauer GB, Hamada RS, et al. Patient suicide: occupational hazard for psychologists and psychiatrists. Prof Psychol Res Pr. 1989;20(5):294-300.
7. Rubin HL. Surviving a suicide in your practice. In: Blumenthal SJ, Kupfer DJ, eds. Suicide over the life cycle: risk factors, assessment, and treatment of suicidal patients. Washington, DC: American Psychiatric Press; 1990:619-636.
8. Kaye NS, Soreff SM. The psychiatrist’s role, responses, and responsibilities when a patient commits suicide. Am J Psychiatry. 1991;148(6):739-743.
9. McIntosh JL. Clinicians as survivors of suicide: bibliography. American Association of Suicidology Clinician Survivor Task Force. http://pages.iu.edu/~jmcintos/Surv.Ther.bib.htm. Updated May 19, 2019. Accessed August 26, 2019.
10. Douglas J, Brown HN. Suicide: understanding and responding: Harvard Medical School perspectives. Madison, CT: International Universities Press; 1989.
11. Farberow NL. The mental health professional as suicide survivor. Clin Neuropsychiatry. 2005;2(1):13-20.
12. Jones FA Jr. Therapists as survivors of patient suicide. In: Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: W.W. Norton; 1987;126-141.
13. Plakun EM, Tillman JG. Responding to clinicians after loss of a patient to suicide. Dir Psychiatry. 2005;25:301-310.
14. Prabhakar D, Anzia JM, Balon R, et al. “Collateral damages”: preparing residents for coping with patient suicide. Acad Psychiatry. 2013;37(6):429-30.
15. Quinnett P. QPR: for suicide prevention. QPR Institute, Inc. http://pages.iu.edu/~jmcintos/postvention.htm. Published September 21, 2009. Accessed August 26, 2019.
16. Schultz, D. Suggestions for supervisors when a therapist experiences a client’s suicide. Women Ther. 2005;28(1):59-69.
17. Spiegelman JS Jr, Werth JL Jr. Don’t forget about me: the experiences of therapists-in-training after a patient has attempted or died by suicide. Women Ther. 2005;28(1):35-57.
18. American Association of Suicidology. Clinician Survivor Task Force. Clinicians as survivors of suicide: postvention information.
19. Whitmore CA, Cook J, Salg L. Supporting residents in the wake of patient suicide. The American Journal of Psychiatry Residents’ Journal. 2017;12(1):5-7.
20. Melton B, Coverdale J. What do we teach psychiatric residents about suicide? A national survey of chief residents. Acad Psychiatry. 2009;33(1):47-50.
21. Valente SM. Psychotherapist reactions to the suicide of a patient. Am J Orthopsychiatry. 1994;64(4):614-621.
22. Jordan JR, McIntosh JL. Is suicide bereavement different? A framework for rethinking the question. In: Jordan JR, McIntosh JL, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:19-42.
23. Jordan JR, Baugher B. After suicide loss: coping with your grief, 2nd ed. Newcastle, WA: Caring People Press; 2016.
24. Brown HB. The impact of suicide on therapists in training. Compr Psychiatry. 1987;28(2):101-112.
25. Cvinar JG. Do suicide survivors suffer social stigma: a review of the literature. Perspect Psychiatr Care. 2005;41(1):14-21.
26. Feigelman W, Gorman BS, Jordan JR. Stigmatization and suicide bereavement. Death Stud. 2009;33(7):591-608.
27. Goffman E. Stigma: notes on the management of spoiled identity. New York, NY: Simon & Schuster; 1963.
28. Goldney RD. The privilege and responsibility of suicide prevention. Crisis. 2000;21(1):8-15.
29. Litman RE. When patients commit suicide. Am J Psychother. 1965;19(4):570-576.
30. Hendin H, Lipschitz A, Maltsberger JT, et al. Therapists’ reactions to patients’ suicides. Am J Psychiatry. 2000;157(12):2022-2027.
31. Rycroft P. Touching the heart and soul of therapy: surviving client suicide. Women Ther. 2004;28(1):83-94.
32. Ellis TE, Patel AB. Client suicide: what now? Cogn Behav Pract. 2012;19(2):277-287.
33. Al-Mateen CS, Jones K, Linker J, et al. Clinician response to a child who completes suicide. Child Adolesc Psychiatric Clin N Am. 2018;27(4):621-635.
34. Henry M, Séguin M, Drouin M-S. Mental health professionals’ response to the suicide of their patients [in French]. Revue Québécoise de Psychologie. 2004;25:241-257.
35. Carter RE. Some effects of client suicide on the therapist. Psychother Theory Res Practice. 1971;8(4):287-289.
36. Dewar I, Eagles J, Klein S, et al. Psychiatric trainees’ experiences of, and reactions to, patient suicide. Psychiatr Bull. 2000;24(1):20-23.
37. Gitlin M. Aftermath of a tragedy: reaction of psychiatrists to patient suicides. Psychiatr Ann. 2007;37(10):684-687.
38. Tillman JG. When a patient commits suicide: an empirical study of psychoanalytic clinicians. Inter J Psychoanal. 2006;87(1):159-177.
39. Erikson EH. Identity and the life cycle. New York, NY: International Universities Press, Inc.; 1959.
40. Maltsberger JT. The implications of patient suicide for the surviving psychotherapist. In: Jacobs D, ed. Suicide and clinical practice. Washington, DC: American Psychiatric Press; 1992:169-182.
41. Bissell BPH. The experience of the nurse therapist working with suicidal cases: a developmental study [dissertation]. Boston, MA: Boston University School of Education; 1981.
42. Kleespies PM. The stress of patient suicidal behavior: Implications for interns and training programs in psychology. Prof Psychol Res Pract. 1993;24(4):477-482.
43. Munson JS. Impact of client suicide on practitioner posttraumatic growth [dissertation]. Gainsville, Florida: University of Florida; 2009.
44. Hodgkinson PE. Responding to in-patient suicide. Br J Med Psychol. 1987;60(4):387-392.
45. Gorkin M. On the suicide of one’s patient. Bull Menninger Clin. 1985;49(1):1-9.
46. Fuentes MA, Cruz D. Posttraumatic growth: positive psychological changes after trauma. Mental Health News. 2009;11(1):31,37.
47. Doka KJ. Disenfranchised grief: new Directions, challenges, and strategies for practice. Champaign, IL: Research Press; 2002.
48. Bongar B. The suicidal patient: clinical and legal standards of care, 2nd ed. Washington, DC: American Psychological Association; 2002.
49. Peterson EM, Luoma JB, Dunne E. Suicide survivors’ perceptions of the treating clinician. Suicide Life Threat Behav. 2002;32(2):158-166.
50. Kolodny S, Binder RL, Bronstein AA, et al. The working through of patients’ suicides by four therapists. Suicide Life Threat Behav. 1979;9(1):33-46.
51. Marshall KA. When a patient commits suicide. Suicide Life Threat Behav. 1980;10(1):29-40.
52. Jobes DA, Maltsberger JT. The hazards of treating suicidal patients. In: Sussman MB, ed. A perilous calling: the hazards of psychotherapy practice. New York, NY: Wiley & Sons; 1995:200-214.
53. Castelli-Dransart DA, Gutjahr E, Gulfi A, et al. Patient suicide in institutions: emotional responses and traumatic impact on Swiss mental health professionals. Death Stud. 2014;38(1-5):315-321.
54. US Public Health Service. The Surgeon General’s call to action to prevent suicide. Washington, DC: Department of Health and Human Services; 1999.
55. Armour M. Violent death: understanding the context of traumatic and stigmatized grief. J Hum Behav Soc Environ. 2006;14(4):53-90.
56. Calhoun, LG, Allen BG. Social reactions to the survivor of a suicide in the family: a review of the literature. Omega (Westport). 1991;23(2):95-107.
57. Dunne EJ, McIntosh JL, Dunne-Maxim K, eds. Suicide and its aftermath: understanding and counseling the survivors. New York, NY: WW Norton & Co; 1987.
58. Harwood D, Hawton K, Hope J, et al. The grief experiences and needs of bereaved relatives and friends of older people dying through suicide: a descriptive and case-control study. J Affect Disord. 2002;72(2):185-194.
59. Jordan JR. Is suicide bereavement different? A reassessment of the literature. Suicide Life Threat Behav. 2001;31(1):91-102.
60. McIntosh JL. Control group studies of suicide survivors: a review and critique. Suicide Life Threat Behav. 2003;23(2):146-161.
61. Range LM. When a loss is due to suicide: unique aspects of bereavement. In: Harvey JH, ed. Perspectives on loss: a sourcebook. Philadelphia, PA: Brunner/Mazel; 1998:213-220.
62. Sveen CA, Walby FA. Suicide survivors’ mental health and grief reactions: a systematic review of controlled studies. Suicide Life Threat Behav. 2008;38(1):13-29.
63. Van Dongen CJ. Social context of postsuicide bereavement. Death Stud. 1993;17(2):125-141.
64. Bultema JK. The healing process for the multidisciplinary team: recovering post-inpatient suicide. J Psychosoc Nurs. 1994;32(2):19-24.
65. Cooper C. Patient suicide and assault: their impact on psychiatric hospital staff. J Psychosoc Nurs Ment Health Serv. 1995;33(6):26-29.
66. Foster VA, McAdams CR III. The impact of client suicide in counselor training: Implications for counselor education and supervision. Counselor Educ Supervision. 1999;39(1):22-33.
67. Little JD. Staff response to inpatient and outpatient suicide: what happened and what do we do? Aust N Z J Psychiatry. 1992;26(2):162-167.
68. Horn PJ. Therapists’ psychological adaptation to client suicidal behavior. Chicago, IL: Loyola University of Chicago; 1995.
69. Gutin N, McGann VM, Jordan JR. The impact of suicide on professional caregivers. In: Jordan J, McIntosh J, eds. Grief after suicide: understanding the consequences and caring for the survivors. New York, NY: Routledge; 2011:93-111.
70. Anderson GO. Who, what, when, where, how, and mostly why? A therapist’s grief over the suicide of a client. Women Ther. 2004;28(1):25-34.
Assessing decisional capacity in patients with substance use disorders
Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have
How can you determine if Ms. B has the capacity to make decisions regarding her care?
Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.1 Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.
Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs2 and being admitted as inpatients in general hospitals.3 In this article, I discuss:
- the biologic basis for impaired decision-making in patients with SUDs
- common substance use–related conditions that may impact a patient’s decisional capacity
- the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
- how to assess decisional capacity in such patients.
Decisional capacity vs competence
“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.1 Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.
In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.
A biologic basis for impaired decision-making?
Jeste and Saks4 suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.
Continue to: Bechara and Damasio found...
Bechara and Damasio5 found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.
These deficits were also observed by Grant et al.6 In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.
MacDonald et al7 used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.7
Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al8 found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.
Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including9:
- consent for addiction treatment
- consistency in maintaining a choice of recovery
- changing values regarding treatment over time
- capacity to participate in addiction research involving the use of addictive substances.
Continue to: It is important to recognize...
It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.9
Substance-related disorders that affect decisional capacity
Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.
Disorders resulting from the direct effects of the substance
Temporary/reversible incapacitation
- Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.10
- Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.11,12
- Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
- Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.
Permanent incapacitation
- Dementia is associated with substance use, particularly alcohol use.13 For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
- Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
- Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).
Secondary disorders resulting from/or associated with substance use
- Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
- Human immunodeficiency virus encephalitis or dementia can result from IV drug use.
Continue to: Clinical challenges
Clinical challenges
In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.
It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box14).
Box
The legal system rarely views patients with substance use disorders (SUDs) as lacking decisional capacity in the absence of overt psychiatric or cognitive deficits. The penal system offers little if any mitigation of liability on account of addiction in civil or criminal cases. On the contrary, intoxication is an aggravating factor in such settings. Despite extensive literature that questions the “free will,” accountability, and responsibility of patients with SUDs, the legal system takes an “all-or-none” approach to this issue. It assumes free choice and accountability for patients with SUDs, except when a clear superimposed psychiatric or cognitive disorder (such as psychosis or dementia) exists. Rarely, some jurisdictions may allow for mental health commitments on account of severe and persistent addictive behaviors that clearly pose a risk to the individual or to society, implicitly recognizing that incapacitation can result from severe addiction. Nevertheless, a finding of imminent or impending dangerousness is generally required for such commitments to be justified.
In other situations, individual health care settings may resort to local hospital policies that allow impaired patients with SUDs with a clearly altered mental status to be detained for the purpose of completing medical treatment. Presumably, discharge would occur when the medical and psychiatric acuity has resolved (often under the umbrella of a “Medical Hold” policy). Jain et al14 suggested that although such commitment laws for patients with SUDs may be appealing to some people, especially family members, specific statutes and their implementation are highly variable; the deprivation of liberty raises ethical concerns; and outcome data are limited. Conversely, most states either do not have such legislation, or rarely enforce it.
How to assess decisional capacity
A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.)
- understand the decision at hand
- discuss its benefits and risks
- describe alternatives
- demonstrate an appreciation of the implications of treatment or lack thereof
- communicate a clear and consistent choice.
Continue to: While most clinicians...
While most clinicians rely on a psychiatric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).15 In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.
The Table offers a guide to assessing decisional capacity in a patient with an SUD.
Who should conduct the assessment?
Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.16 Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.
In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.
No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.
Continue to: CASE CONTINUED
CASE CONTINUED
The emergency physician requests a psychiatric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.
You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.
An increasingly common scenario
Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.
Bottom Line
Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.
Related Resources
- Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
- Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.
Drug Brand Names
Alprazolam • Xanax
Naloxone nasal spray • Narcan
1. Karlawish K. Assessment of decision-making capacity in adults. UpToDate. https://www.uptodate.com/contents/assessment-of-decision-making-capacity-in-adults. Updated July 2019. Accessed August 19, 2019.
2. Owens PL, Mutter R, Stocks C. Mental health and substance abuse-related emergency department visits among adults, 2007. HCUP Statistical Brief #92. https://www.ncbi.nlm.nih.gov/books/NBK52659/pdf/Bookshelf_NBK52659.pdf. Published July 2010. Accessed August 19, 2019.
3. Smothers BA, Yahr HT. Alcohol use disorder and illicit drug use in admissions to general hospitals in the United States. Am J Addict. 2005;14(3):256-267.
4. Jeste DV, Saks E. Decisional capacity in mental illness and substance use disorders: empirical database and policy implications. Behav Sci Law. 2006;24(4):607-628.
5. Bechara A, Damasio H. Decision-making and addiction (part I): impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequences. Neuropsychologia. 2002;40(10):1675-1689.
6. Grant S, Contoreggi C, London ED. Drug abusers show impaired performance in a laboratory test of decision making. Neuropsychologia. 2000;38(8):1180-1187.
7. MacDonald TK, Zanna MP, Fong GT. Decision making in altered states: effects of alcohol on attitudes toward drinking and driving. J Pers Soc Psychol. 1995;68(6):973-985.
8. Boettger S, Bergman M, Jenewein J, et al. Assessment of decisional capacity: prevalence of medical illness and psychiatric comorbidities. Palliat Support Care. 2015;13(5):1275-1281.
9. Charland LC. Chapter 6: Decision-making capacity and responsibility in addiction. In: Poland J, Graham G. Addiction and responsibility. Cambridge, MA: MIT Press Scholarship Online; 2011:139-158.
10. Martel ML, Klein LR, Miner JR, et al. A brief assessment of capacity to consent instrument in acutely intoxicated emergency department patients. Am J Emerg Med. 2018;36(1):18-23.
11. MacLullich AM, Beaglehole A, Hall RJ, et al. Delirium and long-term cognitive impairment. Int Rev Psychiatry. 2009;21(1):30-42.
12. Pandharipande PP, Girard TD, Jackson JC, et al. Long-term cognitive impairment after critical illness. N Engl J Med. 2013;369(14):1306-1316.
13. Rehm J, Hasan OSM, Black SE, et al. Alcohol use and dementia: a systematic scoping review. Alzheimers Res Ther. 2019;11(1):1.
14. Jain A, Christopher P, Appelbaum PS. Civil commitment for opioid and other substance use disorders: does it work? Psychiatr Serv. 2018;69(4):374-376.
15. Grisso T, Appelbaum PS. Chapter 6: Using the MacArthur competence assessment tool – treatment. In: Grisso T, Appelbaum PS. Assessing competence to consent to treatment: a guide for physicians and other health professionals. New York, NY: Oxford University Press; 1998:101-126.
16. Hazelton LD, Sterns GL, Chisholm T. Decision-making capacity and alcohol abuse: clinical and ethical considerations in personal care choices. Gen Hosp Psychiatry. 2003;25(2):130-135.
Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have
How can you determine if Ms. B has the capacity to make decisions regarding her care?
Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.1 Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.
Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs2 and being admitted as inpatients in general hospitals.3 In this article, I discuss:
- the biologic basis for impaired decision-making in patients with SUDs
- common substance use–related conditions that may impact a patient’s decisional capacity
- the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
- how to assess decisional capacity in such patients.
Decisional capacity vs competence
“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.1 Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.
In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.
A biologic basis for impaired decision-making?
Jeste and Saks4 suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.
Continue to: Bechara and Damasio found...
Bechara and Damasio5 found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.
These deficits were also observed by Grant et al.6 In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.
MacDonald et al7 used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.7
Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al8 found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.
Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including9:
- consent for addiction treatment
- consistency in maintaining a choice of recovery
- changing values regarding treatment over time
- capacity to participate in addiction research involving the use of addictive substances.
Continue to: It is important to recognize...
It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.9
Substance-related disorders that affect decisional capacity
Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.
Disorders resulting from the direct effects of the substance
Temporary/reversible incapacitation
- Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.10
- Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.11,12
- Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
- Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.
Permanent incapacitation
- Dementia is associated with substance use, particularly alcohol use.13 For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
- Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
- Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).
Secondary disorders resulting from/or associated with substance use
- Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
- Human immunodeficiency virus encephalitis or dementia can result from IV drug use.
Continue to: Clinical challenges
Clinical challenges
In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.
It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box14).
Box
The legal system rarely views patients with substance use disorders (SUDs) as lacking decisional capacity in the absence of overt psychiatric or cognitive deficits. The penal system offers little if any mitigation of liability on account of addiction in civil or criminal cases. On the contrary, intoxication is an aggravating factor in such settings. Despite extensive literature that questions the “free will,” accountability, and responsibility of patients with SUDs, the legal system takes an “all-or-none” approach to this issue. It assumes free choice and accountability for patients with SUDs, except when a clear superimposed psychiatric or cognitive disorder (such as psychosis or dementia) exists. Rarely, some jurisdictions may allow for mental health commitments on account of severe and persistent addictive behaviors that clearly pose a risk to the individual or to society, implicitly recognizing that incapacitation can result from severe addiction. Nevertheless, a finding of imminent or impending dangerousness is generally required for such commitments to be justified.
In other situations, individual health care settings may resort to local hospital policies that allow impaired patients with SUDs with a clearly altered mental status to be detained for the purpose of completing medical treatment. Presumably, discharge would occur when the medical and psychiatric acuity has resolved (often under the umbrella of a “Medical Hold” policy). Jain et al14 suggested that although such commitment laws for patients with SUDs may be appealing to some people, especially family members, specific statutes and their implementation are highly variable; the deprivation of liberty raises ethical concerns; and outcome data are limited. Conversely, most states either do not have such legislation, or rarely enforce it.
How to assess decisional capacity
A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.)
- understand the decision at hand
- discuss its benefits and risks
- describe alternatives
- demonstrate an appreciation of the implications of treatment or lack thereof
- communicate a clear and consistent choice.
Continue to: While most clinicians...
While most clinicians rely on a psychiatric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).15 In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.
The Table offers a guide to assessing decisional capacity in a patient with an SUD.
Who should conduct the assessment?
Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.16 Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.
In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.
No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.
Continue to: CASE CONTINUED
CASE CONTINUED
The emergency physician requests a psychiatric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.
You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.
An increasingly common scenario
Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.
Bottom Line
Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.
Related Resources
- Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
- Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.
Drug Brand Names
Alprazolam • Xanax
Naloxone nasal spray • Narcan
Ms. B, age 31, is brought to the emergency department (ED) via ambulance after emergency medical technicians used naloxone nasal spray to revive her following an overdose on heroin. She reports daily IV heroin use for the last 4 years as well as frequent use of other illicit substances, including marijuana and alprazolam, for which she does not have
How can you determine if Ms. B has the capacity to make decisions regarding her care?
Decisional capacity is defined as a patient’s ability to use information about an illness and the proposed treatment options to make a choice that is congruent with one’s own values and preferences.1 Determining whether a patient has adequate capacity to make decisions regarding their care is an inherent aspect of all clinician-patient interactions.
Published reports have focused on the challenges clinicians face when assessing decisional capacity in patients with psychiatric and cognitive disorders. However, there is little evidence about assessing decisional capacity in patients with substance use disorders (SUDs), even though increasing numbers of patients with SUDs are presenting to EDs2 and being admitted as inpatients in general hospitals.3 In this article, I discuss:
- the biologic basis for impaired decision-making in patients with SUDs
- common substance use–related conditions that may impact a patient’s decisional capacity
- the clinical challenges and legal considerations clinicians face when assessing decisional capacity in patients with SUDs
- how to assess decisional capacity in such patients.
Decisional capacity vs competence
“Capacity” and “competence” are not the same. Decisional capacity, which refers to the ability to make decisions, is a clinical construct that is determined by clinicians and is generally used in the acute clinical setting. Because cognition is the main determinant of capacity, conditions or treatments that affect cognition can impair an individual’s decision-making capacity.1 Decisional capacity is not a global concept but a decision-specific one, subject to fluctuations depending on the time and the nature of the decision at hand. Therefore, requests for determination of decisional capacity in the clinical setting should be specific to an individual decision or set of decisions.
In contrast, competence is an enduring legal determination of incapacitation, typically made by a probate judge. It refers to the ability of an individual to perform actions needed to put decisions into effect. Decisional capacity as assessed by a clinician often serves as the basis for petitions submitted for the purpose of competency adjudication by the judicial system.
A biologic basis for impaired decision-making?
Jeste and Saks4 suggested that addiction itself is characterized by impaired decision-making because individuals keep using a substance despite experiencing recurrent physical, psychologic, or social problems caused or worsened by the substance. Several studies suggest there may be a biologic basis for impaired decision-making in these patients, even in the absence of severe psychiatric or cognitive disorders.
Continue to: Bechara and Damasio found...
Bechara and Damasio5 found that the decision-making impairment seen in some patients with SUDs was similar to that observed in patients who have lesions of the ventromedial prefrontal cortex. In both groups of patients, the impaired decision-making was characterized by a preference to opt for high immediate reward despite even higher future losses.
These deficits were also observed by Grant et al.6 In this study, patients with SUDs displayed markedly impaired performance on the Gambling Task, which examines decisions that result in long-term losses that exceed short-term gains. However, patients with SUDs performed similarly to controls on the Wisconsin Card Sorting Test, which evaluates the ability to form abstract concepts and to shift from established response sets.
MacDonald et al7 used a laboratory experiment and 2 field studies to test the hypothesis that alcohol affects attitudes and intentions toward drinking and driving. Their findings support the concept that alcohol intoxication decreases cognitive capacity such that people are more likely to attend to only the most salient cues.7
Whether the impairment documented in such studies is a contributing factor in addiction or is a result of addiction remains uncertain. While individuals with SUDs may have some level of impairment in decision-making in general, particularly in regard to their substance use, their decisional capacity on specific clinical decisions should be assessed carefully. In a study of 300 consecutive psychiatric consultations for decisional capacity at an urban hospital, Boettger et al8 found that 41% were related to SUDs. Of these, 37% were found to have impaired decisional capacity.
Impaired decision-making in patients with SUDs may specifically pertain to choices related to their addiction, including9:
- consent for addiction treatment
- consistency in maintaining a choice of recovery
- changing values regarding treatment over time
- capacity to participate in addiction research involving the use of addictive substances.
Continue to: It is important to recognize...
It is important to recognize that this impairment may not necessarily translate into altered decisional capacity regarding other health care decisions, such as consenting to surgery or other necessary medical interventions.9
Substance-related disorders that affect decisional capacity
Substance-related syndromes can affect mood, reality testing, and/or cognitive function, thereby directly impacting a patient’s decisional capacity. Substance-related syndromes can be divided into 2 categories: 1) disorders resulting from the direct effects of the substance, and 2) secondary disorders resulting from/or associated with substance use.
Disorders resulting from the direct effects of the substance
Temporary/reversible incapacitation
- Acute intoxication or intoxication delirium may be the most frequent type of temporary incapacitation. It can result from toxic levels of licit or illicit substances; alcohol is likely the most frequent offending agent. Although some individuals who are intoxicated may appear to be alert, oriented, and able to engage in lengthy conversations, the majority do not possess adequate decisional capacity.10
- Withdrawal delirium, associated with longstanding alcohol, sedative-hypnotic, or barbiturate dependence, is typically prolonged, but usually resolves, either spontaneously or with treatment. Although most deliria resolve once the underlying etiology is corrected, vulnerable individuals may experience irreversible cognitive impairment and permanent decisional incapacitation.11,12
- Severe substance-induced depressive disorders, especially if accompanied by frank psychotic symptoms or severe depressive distortions of reality, may result in decisional incapacity. Substance abuse treatment that incorporates multiple strategies, sometimes in conjunction with pharmacotherapy to manage depression, should lead to sufficient recovery and restoration of decisional capacity.
- Transient psychotic disorders such as those associated with the use of stimulants are often treatable. Patients may recover decisional capacity spontaneously or with treatment.
Permanent incapacitation
- Dementia is associated with substance use, particularly alcohol use.13 For a patient who develops dementia, no appreciable recovery can be expected, even with prolonged abstinence.
- Persistent amnestic disorders (eg, Korsakoff syndrome) resulting from undiagnosed or untreated severe thiamine deficiency (Wernicke’s encephalopathy). Although an isolated Korsakoff syndrome consists primarily of anterograde amnesia, these patients may experience additional cognitive impairment resulting from years of alcohol consumption or associated with other neurodegenerative processes, and therefore are sufficiently impaired and lack decisional capacity. Even in the absence of such concomitant cognitive deficits, a very severe anterograde amnestic disorder directly impacts a patient’s capacity to perform the necessary tasks required to give informed consent. The inability to consolidate information about new medical developments, treatments, and procedures, even when they are thoroughly explained by the medical team, can pose serious challenges. For example, a patient may protest to being taken to surgery because he/she does not recall signing a consent form the previous day.
- Enduring severe and treatment-refractory psychotic disorders associated with drug use, specifically stimulants, can result in permanent incapacitation similar to that seen in severe primary psychotic disorders (such as treatment-resistant schizophrenia).
Secondary disorders resulting from/or associated with substance use
- Hepatic encephalopathy may be seen in patients with advanced cirrhosis of the liver (due to hepatitis C resulting from IV drug use, and/or alcohol use). In late stages of cirrhosis, the confusional state patients experience may become severe and may no longer be reversible unless liver transplantation is available and successful. This would therefore constitute a basis for permanent decisional incapacitation.
- Human immunodeficiency virus encephalitis or dementia can result from IV drug use.
Continue to: Clinical challenges
Clinical challenges
In intensive care settings, where a patient with a SUD may be treated for acute life-threatening intoxication or severe withdrawal delirium, an assumption of decisional incapacitation often exists as a result of medical acuity and impaired mentation. In these situations, treatment usually proceeds with consent obtained from next-of-kin, a guardian, or an administrative (hospital) authority when other substitute decision makers are unavailable or unwilling. In such cases, psychiatric consultation can play a dual role in documenting the patient’s decisional capacity and also in contributing to the care of patients with SUDs.
It is critical to perform a cognitive evaluation and mental status examination in a medically compromised patient with an SUD. Unfortunately, serious cognitive disorders can often be concealed by a superficially jovial or verbally skilled patient, or by an uncooperative individual who refuses to engage in a thorough conversation with his/her clinicians. These scenarios present significant challenges and may result in missed opportunities for care or premature discharges. Negative countertransference by clinicians toward patients with SUDs may also promote poor outcomes. For difficult cases, legal and ethical consultations may help mitigate risk and guide management approaches (Box14).
Box
The legal system rarely views patients with substance use disorders (SUDs) as lacking decisional capacity in the absence of overt psychiatric or cognitive deficits. The penal system offers little if any mitigation of liability on account of addiction in civil or criminal cases. On the contrary, intoxication is an aggravating factor in such settings. Despite extensive literature that questions the “free will,” accountability, and responsibility of patients with SUDs, the legal system takes an “all-or-none” approach to this issue. It assumes free choice and accountability for patients with SUDs, except when a clear superimposed psychiatric or cognitive disorder (such as psychosis or dementia) exists. Rarely, some jurisdictions may allow for mental health commitments on account of severe and persistent addictive behaviors that clearly pose a risk to the individual or to society, implicitly recognizing that incapacitation can result from severe addiction. Nevertheless, a finding of imminent or impending dangerousness is generally required for such commitments to be justified.
In other situations, individual health care settings may resort to local hospital policies that allow impaired patients with SUDs with a clearly altered mental status to be detained for the purpose of completing medical treatment. Presumably, discharge would occur when the medical and psychiatric acuity has resolved (often under the umbrella of a “Medical Hold” policy). Jain et al14 suggested that although such commitment laws for patients with SUDs may be appealing to some people, especially family members, specific statutes and their implementation are highly variable; the deprivation of liberty raises ethical concerns; and outcome data are limited. Conversely, most states either do not have such legislation, or rarely enforce it.
How to assess decisional capacity
A direct conclusion of incapacity in an individual cannot be determined solely on the knowledge of the patient having a SUD-related clinical condition. (The possible exception to this may be a patient with severe dementia.)
- understand the decision at hand
- discuss its benefits and risks
- describe alternatives
- demonstrate an appreciation of the implications of treatment or lack thereof
- communicate a clear and consistent choice.
Continue to: While most clinicians...
While most clinicians rely on a psychiatric interview (with or without a cognitive examination) to make these determinations, several instruments have been developed to aid these evaluations, such as the MacArthur Competence Assessment Tool for Treatment (Mac-CAT-T).15 In patients with potentially reversible incapacitating conditions, serial examinations over time, especially re-evaluation when a patient has achieved and maintained sobriety, may be necessary and helpful.
The Table offers a guide to assessing decisional capacity in a patient with an SUD.
Who should conduct the assessment?
Mental health professionals—usually psychiatrists or psychologists—are consulted when there is uncertainty about a patient’s decisional capacity, and when a more thorough mental status examination is warranted to formulate an informed opinion.16 Unfortunately, this typically occurs only if a patient refuses treatment or demands to be discharged before treatment has been completed, or there is a high level of risk to the patient or others after discharge.
In acute settings, when a patient consents to treatment, a psychiatric consultation regarding decisional capacity is rarely requested. While it is often tempting for medical or surgical teams to proceed with an intervention in a cooperative patient who willingly signs a consent form without a formal assessment of his/her decisional capacity, doing so raises challenging ethical and legal questions in the event of an adverse outcome. It is therefore prudent to strongly recommend that medical and surgical colleagues obtain a psychiatric consultation when an individual’s decisional capacity is uncertain, especially when a patient is known to have a psychiatric or neurocognitive disorder, or exhibits evidence of recent mental status changes. In cases of potentially reversible impairment (eg, delirium, psychosis, or acute anxiety), targeted interventions may help restore capacity and allow treatment to proceed.
No jurisdictions mandate that the determination of decisional capacity should be made exclusively by a mental health professional. Any treating health care professional (usually the attending physician) can make a determination of decisional capacity in scenarios where there is no overt evidence the patient has a mental or cognitive disorder and the patient is communicating clear and reasoned choices, or when a patient is profoundly impaired and no meaningful communication can take place.
Continue to: CASE CONTINUED
CASE CONTINUED
The emergency physician requests a psychiatric consultation. You assess Ms. B’s decisional capacity using the Mac-CAT-T along with a standard psychiatric evaluation. Her score of 14 reflects that she is able to understand the risks associated with her opioid use, and although irritated by engaging in such a discussion, is capable of reasoning through the various medical and psychosocial aspects of her addiction, and shows moderate appreciation of the impact of her choices on her future and that of significant others. The psychiatric evaluation fails to elicit any substantial mood, anxiety, or psychotic disorders associated with/or resulting from her addiction, and her cognitive examination is within normal limits. She does not exhibit severe withdrawal and is not delirious on examination. Finally, she did not harbor thoughts of intentional harm to self or others and is not deemed imminently dangerous.
You document that in your opinion, despite Ms. B’s unfortunate choices and questionable judgment, she does have the capacity to make informed decisions regarding her care and could be released against medical advice if she so chooses, while providing her with information about available resources should she decide to seek rehabilitation in the future.
An increasingly common scenario
Decisional capacity assessment in patients with SUDs is an increasingly common reason for psychiatric consultations. Primary and secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. The same principles that guide the assessment of decisional capacity in patients with other psychiatric or cognitive disorders should be applied to compromised individuals with SUDs. In challenging cases, a skilled psychiatric evaluation that is supported by a thorough cognitive examination and, when required, complemented by a legal or ethical consultation, can help clinicians make safe and judicious decisions.
Bottom Line
Assessing the decisional capacity of a patient with a substance use disorder can be challenging. Primary or secondary conditions related to substance use can affect a patient’s decisional capacity on a temporary or permanent basis. A skilled psychiatric evaluation that includes a thorough cognitive examination and is complemented by legal or ethical consultation can help in making judicious decisions.
Related Resources
- Tan SY. Determining patients’ decisional capacity. Clinical Psychiatry News. https://www.mdedge.com/psychiatry/article/137939/practice-management/determining-patients-decisional-capacity. Published May 10, 2017.
- Sorrentino R. Performing capacity evaluations: What’s expected from your consult. Current Psychiatry. 2014;13(1):41-44.
Drug Brand Names
Alprazolam • Xanax
Naloxone nasal spray • Narcan
1. Karlawish K. Assessment of decision-making capacity in adults. UpToDate. https://www.uptodate.com/contents/assessment-of-decision-making-capacity-in-adults. Updated July 2019. Accessed August 19, 2019.
2. Owens PL, Mutter R, Stocks C. Mental health and substance abuse-related emergency department visits among adults, 2007. HCUP Statistical Brief #92. https://www.ncbi.nlm.nih.gov/books/NBK52659/pdf/Bookshelf_NBK52659.pdf. Published July 2010. Accessed August 19, 2019.
3. Smothers BA, Yahr HT. Alcohol use disorder and illicit drug use in admissions to general hospitals in the United States. Am J Addict. 2005;14(3):256-267.
4. Jeste DV, Saks E. Decisional capacity in mental illness and substance use disorders: empirical database and policy implications. Behav Sci Law. 2006;24(4):607-628.
5. Bechara A, Damasio H. Decision-making and addiction (part I): impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequences. Neuropsychologia. 2002;40(10):1675-1689.
6. Grant S, Contoreggi C, London ED. Drug abusers show impaired performance in a laboratory test of decision making. Neuropsychologia. 2000;38(8):1180-1187.
7. MacDonald TK, Zanna MP, Fong GT. Decision making in altered states: effects of alcohol on attitudes toward drinking and driving. J Pers Soc Psychol. 1995;68(6):973-985.
8. Boettger S, Bergman M, Jenewein J, et al. Assessment of decisional capacity: prevalence of medical illness and psychiatric comorbidities. Palliat Support Care. 2015;13(5):1275-1281.
9. Charland LC. Chapter 6: Decision-making capacity and responsibility in addiction. In: Poland J, Graham G. Addiction and responsibility. Cambridge, MA: MIT Press Scholarship Online; 2011:139-158.
10. Martel ML, Klein LR, Miner JR, et al. A brief assessment of capacity to consent instrument in acutely intoxicated emergency department patients. Am J Emerg Med. 2018;36(1):18-23.
11. MacLullich AM, Beaglehole A, Hall RJ, et al. Delirium and long-term cognitive impairment. Int Rev Psychiatry. 2009;21(1):30-42.
12. Pandharipande PP, Girard TD, Jackson JC, et al. Long-term cognitive impairment after critical illness. N Engl J Med. 2013;369(14):1306-1316.
13. Rehm J, Hasan OSM, Black SE, et al. Alcohol use and dementia: a systematic scoping review. Alzheimers Res Ther. 2019;11(1):1.
14. Jain A, Christopher P, Appelbaum PS. Civil commitment for opioid and other substance use disorders: does it work? Psychiatr Serv. 2018;69(4):374-376.
15. Grisso T, Appelbaum PS. Chapter 6: Using the MacArthur competence assessment tool – treatment. In: Grisso T, Appelbaum PS. Assessing competence to consent to treatment: a guide for physicians and other health professionals. New York, NY: Oxford University Press; 1998:101-126.
16. Hazelton LD, Sterns GL, Chisholm T. Decision-making capacity and alcohol abuse: clinical and ethical considerations in personal care choices. Gen Hosp Psychiatry. 2003;25(2):130-135.
1. Karlawish K. Assessment of decision-making capacity in adults. UpToDate. https://www.uptodate.com/contents/assessment-of-decision-making-capacity-in-adults. Updated July 2019. Accessed August 19, 2019.
2. Owens PL, Mutter R, Stocks C. Mental health and substance abuse-related emergency department visits among adults, 2007. HCUP Statistical Brief #92. https://www.ncbi.nlm.nih.gov/books/NBK52659/pdf/Bookshelf_NBK52659.pdf. Published July 2010. Accessed August 19, 2019.
3. Smothers BA, Yahr HT. Alcohol use disorder and illicit drug use in admissions to general hospitals in the United States. Am J Addict. 2005;14(3):256-267.
4. Jeste DV, Saks E. Decisional capacity in mental illness and substance use disorders: empirical database and policy implications. Behav Sci Law. 2006;24(4):607-628.
5. Bechara A, Damasio H. Decision-making and addiction (part I): impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequences. Neuropsychologia. 2002;40(10):1675-1689.
6. Grant S, Contoreggi C, London ED. Drug abusers show impaired performance in a laboratory test of decision making. Neuropsychologia. 2000;38(8):1180-1187.
7. MacDonald TK, Zanna MP, Fong GT. Decision making in altered states: effects of alcohol on attitudes toward drinking and driving. J Pers Soc Psychol. 1995;68(6):973-985.
8. Boettger S, Bergman M, Jenewein J, et al. Assessment of decisional capacity: prevalence of medical illness and psychiatric comorbidities. Palliat Support Care. 2015;13(5):1275-1281.
9. Charland LC. Chapter 6: Decision-making capacity and responsibility in addiction. In: Poland J, Graham G. Addiction and responsibility. Cambridge, MA: MIT Press Scholarship Online; 2011:139-158.
10. Martel ML, Klein LR, Miner JR, et al. A brief assessment of capacity to consent instrument in acutely intoxicated emergency department patients. Am J Emerg Med. 2018;36(1):18-23.
11. MacLullich AM, Beaglehole A, Hall RJ, et al. Delirium and long-term cognitive impairment. Int Rev Psychiatry. 2009;21(1):30-42.
12. Pandharipande PP, Girard TD, Jackson JC, et al. Long-term cognitive impairment after critical illness. N Engl J Med. 2013;369(14):1306-1316.
13. Rehm J, Hasan OSM, Black SE, et al. Alcohol use and dementia: a systematic scoping review. Alzheimers Res Ther. 2019;11(1):1.
14. Jain A, Christopher P, Appelbaum PS. Civil commitment for opioid and other substance use disorders: does it work? Psychiatr Serv. 2018;69(4):374-376.
15. Grisso T, Appelbaum PS. Chapter 6: Using the MacArthur competence assessment tool – treatment. In: Grisso T, Appelbaum PS. Assessing competence to consent to treatment: a guide for physicians and other health professionals. New York, NY: Oxford University Press; 1998:101-126.
16. Hazelton LD, Sterns GL, Chisholm T. Decision-making capacity and alcohol abuse: clinical and ethical considerations in personal care choices. Gen Hosp Psychiatry. 2003;25(2):130-135.
The challenges of caring for a physician with a mental illness
A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.1 Physicians have higher rates of suicide than the general population.2 According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.3 Additionally, physicians also have high rates of substance use and affective disorders.1,4
Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.
CASE REPORT
Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.
At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.
On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.
Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.
Managing an extremely knowledgeable patient
During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.5
Continue to: Although his queries on medication...
Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.
We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.2 The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.
A complicated scenario
Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:
- The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
- The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.
Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.
1. Bianchi EF, Bhattacharyya MR, Meakin R. Exploring senior doctors’ beliefs and attitudes regarding mental illness within the medical profession: a qualitative study. BMJ Open. 2016;6(9):e012598. doi: 10.1136/bmjopen-2016 012598.
2. Schernhammer ES, Colditz GA. Suicide rates among physicians: a quantitative and gender assessment (meta-analysis). Am J Psychiatry. 2004;161(12):2295-2302.
3. Gold KJ, Sen A, Schwenk TL. Details on suicide among US physicians: data from the National Violent Death Reporting System. Gen Hosp Psychiatry. 2013;35(1):45-49.
4. Schneck SA. “Doctoring” doctors and their families. JAMA. 1998;280(23):2039-2042.
5. Marshall EJ. Doctors’ health and fitness to practise: treating addicted doctors. Occup Med (Lond). 2008;58(5):334-340.
A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.1 Physicians have higher rates of suicide than the general population.2 According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.3 Additionally, physicians also have high rates of substance use and affective disorders.1,4
Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.
CASE REPORT
Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.
At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.
On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.
Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.
Managing an extremely knowledgeable patient
During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.5
Continue to: Although his queries on medication...
Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.
We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.2 The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.
A complicated scenario
Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:
- The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
- The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.
Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.
A physician’s mental health is important for the delivery of quality health care to his/her patients. Early identification and treatment of physicians with mental illnesses is challenging because physicians may neglect their own mental health due to the associated stigma, time constraints, or uncertainty regarding where to seek help. Physicians often worry about whom to confide in and harbor a fear that others will doubt his/her competence after recovery.1 Physicians have higher rates of suicide than the general population.2 According to data from the National Violent Death Reporting System, a diagnosed mental illness or a job problem significantly contribute to suicide among physicians.3 Additionally, physicians also have high rates of substance use and affective disorders.1,4
Here, we present the case of a physician we treated on an inpatient psychiatry unit who stirred profound emotions in us as trainees, and discuss how we managed this complicated scenario.
CASE REPORT
Dr. P, a 35-year-old male endocrinologist, was admitted to our inpatient psychiatry unit with a diagnosis of bipolar disorder, manic, severe, with psychotic features. Earlier that day, Dr. P had walked out of his private outpatient practice where he still had several appointments. After he had been missing for several hours, he was picked up by the police. Dr. P had 2 prior psychiatric admissions; the last one had occurred >10 years ago. A few weeks before this admission, he stopped taking lithium, while continuing escitalopram. He had not been keeping his appointments with his outpatient psychiatrist.
At admission, Dr. P had pressured speech, grandiose delusions, an expansive affect, and aggressive behavior. He was responding to internal stimuli with no insight into his illness. He was evasive when asked about hallucinations. Dr. P believed he was superior in intelligence and physical prowess to everyone in the emergency department (ED), and for that reason, the ED staff was persecuting him. His urine toxicology was negative.
On the inpatient unit, because Dr. P exhibited posturing, mutism, and negativism, catatonia associated with bipolar disorder was added to his diagnosis. For the first 2 days, his catatonia was managed with oral lorazepam, 2 mg twice daily. Dr. P was also observed giving medical advice to other patients on the unit, and was told to stop. Throughout his hospitalization, he dictated his own treatment and would frequently debate with his treatment team on the pharmacologic basis for treatment decisions, asserting his expertise as a physician and claiming to have a general clinical knowledge of the acute management of bipolar disorder.
Dr. P was eventually stabilized on oral lithium, 450 mg twice daily, and aripiprazole, 10 mg/d. He also received oral clonazepam, as needed for acute agitation, which was eventually tapered and discontinued. He gradually responded to treatment, and demonstrated improved insight. The treatment team met with Dr. P’s parents, who also were physicians, to discuss treatment goals, management considerations, and an aftercare plan. After spending 8 days in the hospital, Dr. P was discharged home to the care of his immediate family, and instructed to follow up with his outpatient psychiatrist. We do not know if he resumed clinical duties.
Managing an extremely knowledgeable patient
During his hospitalization, Dr. P frequently challenged our clinical knowledge; he would repeatedly remind us that he was a physician and that we were still trainees, which caused us to second-guess ourselves. Eventually, the attending physician on our team was able to impress upon Dr. P the clearly established roles of the treatment team and the patient. It was also important to maintain open communication channels with Dr. P and his family, and to address his anxiety by discussing the treatment plan in detail.5
Continue to: Although his queries on medication...
Although his queries on medication pharmacodynamics and pharmacokinetics were daunting, we empathized with him, recognizing that his knowledge invariably contributed to his anxiety. We engaged with Dr. P and his parents and elaborated on the rationale behind treatment decisions. This earned his trust and tremendously facilitated his recovery.
We were also cautious about using benzodiazepines to treat Dr. P’s catatonia because we were concerned that his knowledge could aid him in feigning symptoms to obtain these medications. Physicians have a high rate of prescription medication abuse, mainly opiates and benzodiazepines.2 The abuse of prescription medications by physicians is related to several psychological and psychiatric factors, including anxiety, depression, stress at work, personality problems, loss of loved ones, and pain. While treating physician patients, treatment decisions that include the use of opiates and benzodiazepines should be carefully considered.
A complicated scenario
Managing a physician patient can be a rewarding experience; however, there are several factors that can impact the experience, including:
- The treating physicians’ anxiety and countertransference/transference dynamics. We repeatedly imagined ourselves in Dr. P’s position and thought long and hard about how this scenario could happen to anyone in the medical profession; these thoughts induced significant anxiety in each of us. Further, interacting with Dr. P was reminiscent of our training under senior residents and attendings. Dr. P viewed us—his treatment team—as his trainees and challenged our clinical knowledge and actions.
- The physician-patient’s emotional responses, which may include anxiety, despair, denial, and an inability to accept role reversal.
Our medical culture needs a paradigm shift. We need a model designed to encourage early self-disclosure and treatment-seeking among physicians with mental illness. This will reduce the stigma towards mental illness in our profession.
1. Bianchi EF, Bhattacharyya MR, Meakin R. Exploring senior doctors’ beliefs and attitudes regarding mental illness within the medical profession: a qualitative study. BMJ Open. 2016;6(9):e012598. doi: 10.1136/bmjopen-2016 012598.
2. Schernhammer ES, Colditz GA. Suicide rates among physicians: a quantitative and gender assessment (meta-analysis). Am J Psychiatry. 2004;161(12):2295-2302.
3. Gold KJ, Sen A, Schwenk TL. Details on suicide among US physicians: data from the National Violent Death Reporting System. Gen Hosp Psychiatry. 2013;35(1):45-49.
4. Schneck SA. “Doctoring” doctors and their families. JAMA. 1998;280(23):2039-2042.
5. Marshall EJ. Doctors’ health and fitness to practise: treating addicted doctors. Occup Med (Lond). 2008;58(5):334-340.
1. Bianchi EF, Bhattacharyya MR, Meakin R. Exploring senior doctors’ beliefs and attitudes regarding mental illness within the medical profession: a qualitative study. BMJ Open. 2016;6(9):e012598. doi: 10.1136/bmjopen-2016 012598.
2. Schernhammer ES, Colditz GA. Suicide rates among physicians: a quantitative and gender assessment (meta-analysis). Am J Psychiatry. 2004;161(12):2295-2302.
3. Gold KJ, Sen A, Schwenk TL. Details on suicide among US physicians: data from the National Violent Death Reporting System. Gen Hosp Psychiatry. 2013;35(1):45-49.
4. Schneck SA. “Doctoring” doctors and their families. JAMA. 1998;280(23):2039-2042.
5. Marshall EJ. Doctors’ health and fitness to practise: treating addicted doctors. Occup Med (Lond). 2008;58(5):334-340.
Autism, pain, and the NMDA receptor
Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”
Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-
In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.
On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).
Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.
I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.
Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.
Continue to: Implications of NMDA receptor antagonism
Implications of NMDA receptor antagonism
The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).1
Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.2 In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.3 In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.3
Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.4 Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.4
In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.
1. Vadivelu N, Schermer E, Kodumudi V, et al. Role of ketamine for analgesia in adults and children. J Anaesthesiol Clin Pharmacol. 2016;32(3):298-306.
2. Martinak B, Bolis R, Black J, et al. Dextromethorphan in cough syrup: the poor man’s psychosis. Psychopharmacol Bull. 2017;47(4):59-63.
3. Lee E, Choi S, Kim E. NMDA receptor dysfunction in autism spectrum disorders. Curr Opin Pharmacol. 2015;20:8-13.
4. Clarke C. Autism spectrum disorder and amplified pain. Case Rep Psychiatry. 2015;2015:930874. doi: 10.1155/2015/930874.
Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”
Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-
In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.
On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).
Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.
I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.
Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.
Continue to: Implications of NMDA receptor antagonism
Implications of NMDA receptor antagonism
The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).1
Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.2 In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.3 In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.3
Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.4 Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.4
In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.
Ms. G, a 36-year-old woman, presented to the emergency department (ED) requesting a neurologic evaluation. She told clinicians she had “NMDA receptor encephalitis.”
Ms. G reported successful self-treatment of “life-long” body pain that was precipitated by multiple external stimuli (food, social encounters, interpersonal conflict, etc.). Through her own research, she had learned that both ketamine and magnesium could alter nociception in rats through N-methyl-
In the ED, Ms. G had a labile affect, pressured speech, and flight of ideas. She denied any history of psychiatric treatment, suicide attempts, or substance abuse. Ms. G’s family reported she had been unusually social, talkative, and impulsive. She was admitted to the inpatient psychiatric unit with a diagnosis of mania.
On psychiatric evaluation, Ms. G was grandiose, irritable, and perseverative about her aberrant symptoms. She felt she did not experience the world as other people did, but found relief from her chronic pain after taking Delsym. She was not taking other medications. Ms. G did not report a family history of bipolar disorder or psychosis. Her laboratory results, including a comprehensive metabolic panel, complete blood count, lipid panel, thyroid studies, urine drug screening, and urinalysis, were unremarkable. Her blood pressure was mildly elevated (141/82 mm Hg).
Ms. G’s eventual diagnosis was substance-induced mania (DXM). The DXM-containing cough syrup and magnesium were discontinued in the hospital. She was stabilized on lithium extended-release, 900 mg/d (blood level 0.8 mmol/L), and olanzapine, 10 mg/d at bedtime. However, after discharge, Ms. G resumed using Delsym, which resulted in 3 subsequent psychiatric hospitalizations for mania during the next year.
I first treated Ms. G as an outpatient after her second hospitalization. At that point, she was stable. Her mental status was calm and cooperative, and she had a linear thought process. At her baseline, in the absence of mania, she had a blunted affect. She understood that DXM caused her to have manic symptoms, but she continued to believe that Delsym and magnesium cured her physical suffering and social inhibition. I noticed Ms. G would use figurative language inappropriately. I later learned she had sensitivities to food textures and a specialized interest in electronics. Because of this, I suspected Ms. G was on the autism spectrum; she met several DSM-5 criteria for autism spectrum disorder (ASD), particularly deficits in social-emotional reciprocity, highly restricted interests, and hyperreactivity to sensory input.
Upon routine lab screening, Ms. G was found to have hypothyroidism, with a thyroid-stimulating hormone level of 6.67 mcIU/mL. This resolved after discontinuing lithium. Olanzapine caused adverse metabolic effects and also was discontinued. Ms. G remained euthymic without any mood-stabilizing medication, except during periods when she abused DXM, when she would again become manic. Eventually, her motivation to avoid hospitalization would promote her abstinence.
Continue to: Implications of NMDA receptor antagonism
Implications of NMDA receptor antagonism
The use of ketamine as an NMDA receptor antagonist for treating depression and other psychiatric illnesses has gained momentum. Esketamine, the S-enantiomer of racemic ketamine, is now available as an FDA-approved intranasal formulation for treatment-resistant depression. Ketamine stops afferent nociception to the brain and is used as an analgesic (at low concentrations) and anesthetic (at high concentrations).1
Dextromethorphan is abused as a recreational drug because at high doses it works similarly to both ketamine and phencyclidine. Individuals who abuse DXM can develop psychosis, motor/cognitive impairment, agitation, fevers, hypertension, tachycardia, and death.2 In patients with ASD, researchers have identified genetic variations of NMDA receptors that are linked to dysfunction of these receptors.3 In animal models, as well as in humans, researchers have found that suppression or excitation of the NMDA receptor can ameliorate ASD symptoms, including social withdrawal and repetitive behaviors.3
Many individuals with ASD suffer from sensory abnormalities, including a reduced sensitivity to pain or a crippling sensitivity to various stimuli. Patients with ASD may have difficulty describing these abnormalities, and as a result, they may be misdiagnosed. One case report described a 15-year-old girl diagnosed with social anxiety and chronic generalized pain when in social situations.4 Pediatric rheumatologists had diagnosed her with “amplified pain syndrome.” When she presented to a mental health clinic for a neurodevelopmental evaluation, she explained to clinicians how she simply “did not ‘get’ people; they are just empty shells” and subsequently was given a diagnosis of ASD.4
In psychiatric patients who have comorbid substance use disorders, it is vital for clinicians to not only detect the presence of substance misuse, but also to understand what drives the patient toward abuse. Ms. G’s case, with its combination of substance abuse and ASD, illustrates the importance of listening to our patients for more precise diagnostic formulations, which then shape our treatment recommendations.
1. Vadivelu N, Schermer E, Kodumudi V, et al. Role of ketamine for analgesia in adults and children. J Anaesthesiol Clin Pharmacol. 2016;32(3):298-306.
2. Martinak B, Bolis R, Black J, et al. Dextromethorphan in cough syrup: the poor man’s psychosis. Psychopharmacol Bull. 2017;47(4):59-63.
3. Lee E, Choi S, Kim E. NMDA receptor dysfunction in autism spectrum disorders. Curr Opin Pharmacol. 2015;20:8-13.
4. Clarke C. Autism spectrum disorder and amplified pain. Case Rep Psychiatry. 2015;2015:930874. doi: 10.1155/2015/930874.
1. Vadivelu N, Schermer E, Kodumudi V, et al. Role of ketamine for analgesia in adults and children. J Anaesthesiol Clin Pharmacol. 2016;32(3):298-306.
2. Martinak B, Bolis R, Black J, et al. Dextromethorphan in cough syrup: the poor man’s psychosis. Psychopharmacol Bull. 2017;47(4):59-63.
3. Lee E, Choi S, Kim E. NMDA receptor dysfunction in autism spectrum disorders. Curr Opin Pharmacol. 2015;20:8-13.
4. Clarke C. Autism spectrum disorder and amplified pain. Case Rep Psychiatry. 2015;2015:930874. doi: 10.1155/2015/930874.