Current Psychiatry

I do not believe the authors of “Afraid to leave home,” (Cases That Test Your Skills, Current Psychiatry, June 2009) adequately defended their rationale for dismissing a diagnosis of obsessive-compulsive disorder (OCD) and did not consider posttraumatic stress disorder (PTSD) for Mr. B, the patient described in the article. DSM-IV clearly states that the person exhibits either obsessions or compulsions; both are not needed for a diagnosis. The patient was described as having “intense fear of bridges, upper-floor windows, express buses, subways, [and] riding in speeding vehicles,” which leads him to have intrusive, ego-dystonic thoughts that are ruminative; and he “avoids these triggers at all costs.” Clinically these sound like obsessions, which would qualify for OCD if he met other criteria, which—based on the case—he did. Furthermore, Mr. B was actively avoiding multiple situations when he felt he might harm himself. Avoidance is a common, often overlooked component of OCD that can reduce anxiety.

It would have been more helpful if Drs. Klein and Myers had described why they felt the patient did not have OCD or PTSD. It seems Mr. B would—if willing and not psychotic—have been a good candidate for exposure response prevention therapy. With such an anxious patient, this therapy could have been started as a home-based program. In addition I feel the authors did not consider the PTSD diagnosis stemming from the fear of relapse of his psychosis, which added to the clinical picture.

Megan Toufexis, DO
Child and adolescent psychiatry fellow
University of South Florida
Tampa, FL

Dr. Klein responds

OCD was the primary working diagnosis for quite some time because the thoughts did have the quality of being intrusive, ego-dystonic, and inappropriate. Furthermore, some reports associate clozapine treatment with the emergence or exacerbation of OCD symptoms.^1-3 However, OCD was ruled out after we established a strong therapeutic alliance and discovered that the thoughts did not distress him. Instead, it was the inherent fear of losing control and having no escape. The fear appeared first, and the situations in which he experienced that fear were subconsciously created because they explained the emergence of the feeling.

On a different note, Mr. B’s obsessions did not appear if he successfully avoided the situation and—most importantly—he did not find them entirely unreasonable. Mr. B felt his fear was well justified because it protected him from public humiliation or self-harm.

Regarding the PTSD diagnosis, although I would agree that Mr. B had a traumatic recollection of his illness presentation and course, he did not re-experience the events, he did not avoid the situations associated with it, and his hyper vigilance could be better explained by residual paranoia of his main disease process, which is schizophrenia, chronic paranoid type.

Carolina A. Klein, MD
Clinical assistant instructor
SUNY Downstate Medical Center
Brooklyn, NY

I do not believe the authors of “Afraid to leave home,” (Cases That Test Your Skills, Current Psychiatry, June 2009) adequately defended their rationale for dismissing a diagnosis of obsessive-compulsive disorder (OCD) and did not consider posttraumatic stress disorder (PTSD) for Mr. B, the patient described in the article. DSM-IV clearly states that the person exhibits either obsessions or compulsions; both are not needed for a diagnosis. The patient was described as having “intense fear of bridges, upper-floor windows, express buses, subways, [and] riding in speeding vehicles,” which leads him to have intrusive, ego-dystonic thoughts that are ruminative; and he “avoids these triggers at all costs.” Clinically these sound like obsessions, which would qualify for OCD if he met other criteria, which—based on the case—he did. Furthermore, Mr. B was actively avoiding multiple situations when he felt he might harm himself. Avoidance is a common, often overlooked component of OCD that can reduce anxiety.

It would have been more helpful if Drs. Klein and Myers had described why they felt the patient did not have OCD or PTSD. It seems Mr. B would—if willing and not psychotic—have been a good candidate for exposure response prevention therapy. With such an anxious patient, this therapy could have been started as a home-based program. In addition I feel the authors did not consider the PTSD diagnosis stemming from the fear of relapse of his psychosis, which added to the clinical picture.

Megan Toufexis, DO
Child and adolescent psychiatry fellow
University of South Florida
Tampa, FL

Dr. Klein responds

OCD was the primary working diagnosis for quite some time because the thoughts did have the quality of being intrusive, ego-dystonic, and inappropriate. Furthermore, some reports associate clozapine treatment with the emergence or exacerbation of OCD symptoms.^1-3 However, OCD was ruled out after we established a strong therapeutic alliance and discovered that the thoughts did not distress him. Instead, it was the inherent fear of losing control and having no escape. The fear appeared first, and the situations in which he experienced that fear were subconsciously created because they explained the emergence of the feeling.

On a different note, Mr. B’s obsessions did not appear if he successfully avoided the situation and—most importantly—he did not find them entirely unreasonable. Mr. B felt his fear was well justified because it protected him from public humiliation or self-harm.

Regarding the PTSD diagnosis, although I would agree that Mr. B had a traumatic recollection of his illness presentation and course, he did not re-experience the events, he did not avoid the situations associated with it, and his hyper vigilance could be better explained by residual paranoia of his main disease process, which is schizophrenia, chronic paranoid type.

Carolina A. Klein, MD
Clinical assistant instructor
SUNY Downstate Medical Center
Brooklyn, NY

I do not believe the authors of “Afraid to leave home,” (Cases That Test Your Skills, Current Psychiatry, June 2009) adequately defended their rationale for dismissing a diagnosis of obsessive-compulsive disorder (OCD) and did not consider posttraumatic stress disorder (PTSD) for Mr. B, the patient described in the article. DSM-IV clearly states that the person exhibits either obsessions or compulsions; both are not needed for a diagnosis. The patient was described as having “intense fear of bridges, upper-floor windows, express buses, subways, [and] riding in speeding vehicles,” which leads him to have intrusive, ego-dystonic thoughts that are ruminative; and he “avoids these triggers at all costs.” Clinically these sound like obsessions, which would qualify for OCD if he met other criteria, which—based on the case—he did. Furthermore, Mr. B was actively avoiding multiple situations when he felt he might harm himself. Avoidance is a common, often overlooked component of OCD that can reduce anxiety.

It would have been more helpful if Drs. Klein and Myers had described why they felt the patient did not have OCD or PTSD. It seems Mr. B would—if willing and not psychotic—have been a good candidate for exposure response prevention therapy. With such an anxious patient, this therapy could have been started as a home-based program. In addition I feel the authors did not consider the PTSD diagnosis stemming from the fear of relapse of his psychosis, which added to the clinical picture.

Megan Toufexis, DO
Child and adolescent psychiatry fellow
University of South Florida
Tampa, FL

Dr. Klein responds

OCD was the primary working diagnosis for quite some time because the thoughts did have the quality of being intrusive, ego-dystonic, and inappropriate. Furthermore, some reports associate clozapine treatment with the emergence or exacerbation of OCD symptoms.^1-3 However, OCD was ruled out after we established a strong therapeutic alliance and discovered that the thoughts did not distress him. Instead, it was the inherent fear of losing control and having no escape. The fear appeared first, and the situations in which he experienced that fear were subconsciously created because they explained the emergence of the feeling.

On a different note, Mr. B’s obsessions did not appear if he successfully avoided the situation and—most importantly—he did not find them entirely unreasonable. Mr. B felt his fear was well justified because it protected him from public humiliation or self-harm.

Regarding the PTSD diagnosis, although I would agree that Mr. B had a traumatic recollection of his illness presentation and course, he did not re-experience the events, he did not avoid the situations associated with it, and his hyper vigilance could be better explained by residual paranoia of his main disease process, which is schizophrenia, chronic paranoid type.

Carolina A. Klein, MD
Clinical assistant instructor
SUNY Downstate Medical Center
Brooklyn, NY

Every psychiatrist and mental health professional encourages patients to “express your feelings.” Venting produces a cathartic effect, especially if frustrations have been harbored for a while. So I thought I should practice what I preach and tell you some things that annoy me about the contemporary state of psychiatry, which might bother some of you as well.

• Why have we allowed our patients to be relocated from hospitals to jails and prisons? How were the mentally ill transformed from “patients” to “felons?” State hospitals have been shuttered, but correctional facilities are a growth industry.
• Why have community-based mentally ill patients become “clients,” as if mental healthcare was a business transaction? Would cardiologists or oncologists accept labeling their patients as “clients?” No chance!
• Why did psychiatrists shed their white coats and psychiatric nurses replace their professional uniforms with street clothes? Medical attire used to serve as an important environmental cue that an inpatient ward was a “therapeutic facility.” Nowadays, hospitalized psychotic and bipolar patients think they are in a hotel (or, as one of my psychotic patients said recently, in a spaceship).
• Why is it that the more powerful the evidence that mental illnesses are brain disorders with neurobiological roots, the more “demedicalized” the community mental health system has become?
• Why don’t practitioners actively support research when they know that every treatment in clinical practice today was once a research project? The breakthrough treatments of tomorrow are being researched today. One simple way clinicians can help accelerate treatment discoveries is to refer patients to therapeutic clinical trials at local academic institutions.
• When are we going to overcome bureaucratic obstacles and give our public sector seriously mentally ill patients the continuity of care they need and deserve? Changing psychiatrists frequently puts patients at risk for diagnostic and treatment errors, repeated mistakes, and difficulties building rapport and therapeutic alliances.
• Why aren’t more psychiatrists collaborating actively with primary care providers? Up to 50% of chronically mentally ill individuals have serious medical conditions,¹ and up to 50% of primary care patients have mental health problems.² We desperately need an integrated, collaborative approach to mind-body illnesses.
• Why have psychiatrists in community mental health settings been reduced to writing prescriptions and doing “med checks” during sessions too brief to allow for the optimal approach of integrating psychotherapy with psychopharmacology?
• Why are politicians so callous about citizens’ health that they even consider granting the privilege to prescribe powerful, sometimes high-risk psychotropics to persons who have had no professional medical training?
• Why is there so much criticism about off-label use of antidepressants, mood stabilizers, and atypical antipsychotics, when 85% of DSM-IV-TR psychiatric disorders do not have any FDA-approved drug treatment?³ Do “armchair critics” have a better idea for treating serious psychiatric disorders?
• Why is there such a scarcity of long-term psychiatric beds for patients who need that type of supervised care? And why do we psychiatrists tolerate managed care policies that dictate discharging psychotic or suicidal inpatients after only 5 or 6 days of treatment?
• Why does the stigma of mental illness persist, even though 75 million (1 in 4) Americans has a diagnosable mental disorder in any given year?⁴
• Finally, why are we standing still when the dysfunctional public mental health system was declared “in shambles” in 2003 by the final report of the President’s New Freedom Commission on Mental Health?⁵

So there, I feel better sharing a few things that bug me. Feel free to share your gripes with me. Better still, let’s try to develop some solutions to these problems.

Every psychiatrist and mental health professional encourages patients to “express your feelings.” Venting produces a cathartic effect, especially if frustrations have been harbored for a while. So I thought I should practice what I preach and tell you some things that annoy me about the contemporary state of psychiatry, which might bother some of you as well.

• Why have we allowed our patients to be relocated from hospitals to jails and prisons? How were the mentally ill transformed from “patients” to “felons?” State hospitals have been shuttered, but correctional facilities are a growth industry.
• Why have community-based mentally ill patients become “clients,” as if mental healthcare was a business transaction? Would cardiologists or oncologists accept labeling their patients as “clients?” No chance!
• Why did psychiatrists shed their white coats and psychiatric nurses replace their professional uniforms with street clothes? Medical attire used to serve as an important environmental cue that an inpatient ward was a “therapeutic facility.” Nowadays, hospitalized psychotic and bipolar patients think they are in a hotel (or, as one of my psychotic patients said recently, in a spaceship).
• Why is it that the more powerful the evidence that mental illnesses are brain disorders with neurobiological roots, the more “demedicalized” the community mental health system has become?
• Why don’t practitioners actively support research when they know that every treatment in clinical practice today was once a research project? The breakthrough treatments of tomorrow are being researched today. One simple way clinicians can help accelerate treatment discoveries is to refer patients to therapeutic clinical trials at local academic institutions.
• When are we going to overcome bureaucratic obstacles and give our public sector seriously mentally ill patients the continuity of care they need and deserve? Changing psychiatrists frequently puts patients at risk for diagnostic and treatment errors, repeated mistakes, and difficulties building rapport and therapeutic alliances.
• Why aren’t more psychiatrists collaborating actively with primary care providers? Up to 50% of chronically mentally ill individuals have serious medical conditions,¹ and up to 50% of primary care patients have mental health problems.² We desperately need an integrated, collaborative approach to mind-body illnesses.
• Why have psychiatrists in community mental health settings been reduced to writing prescriptions and doing “med checks” during sessions too brief to allow for the optimal approach of integrating psychotherapy with psychopharmacology?
• Why are politicians so callous about citizens’ health that they even consider granting the privilege to prescribe powerful, sometimes high-risk psychotropics to persons who have had no professional medical training?
• Why is there so much criticism about off-label use of antidepressants, mood stabilizers, and atypical antipsychotics, when 85% of DSM-IV-TR psychiatric disorders do not have any FDA-approved drug treatment?³ Do “armchair critics” have a better idea for treating serious psychiatric disorders?
• Why is there such a scarcity of long-term psychiatric beds for patients who need that type of supervised care? And why do we psychiatrists tolerate managed care policies that dictate discharging psychotic or suicidal inpatients after only 5 or 6 days of treatment?
• Why does the stigma of mental illness persist, even though 75 million (1 in 4) Americans has a diagnosable mental disorder in any given year?⁴
• Finally, why are we standing still when the dysfunctional public mental health system was declared “in shambles” in 2003 by the final report of the President’s New Freedom Commission on Mental Health?⁵

So there, I feel better sharing a few things that bug me. Feel free to share your gripes with me. Better still, let’s try to develop some solutions to these problems.

Every psychiatrist and mental health professional encourages patients to “express your feelings.” Venting produces a cathartic effect, especially if frustrations have been harbored for a while. So I thought I should practice what I preach and tell you some things that annoy me about the contemporary state of psychiatry, which might bother some of you as well.

• Why have we allowed our patients to be relocated from hospitals to jails and prisons? How were the mentally ill transformed from “patients” to “felons?” State hospitals have been shuttered, but correctional facilities are a growth industry.
• Why have community-based mentally ill patients become “clients,” as if mental healthcare was a business transaction? Would cardiologists or oncologists accept labeling their patients as “clients?” No chance!
• Why did psychiatrists shed their white coats and psychiatric nurses replace their professional uniforms with street clothes? Medical attire used to serve as an important environmental cue that an inpatient ward was a “therapeutic facility.” Nowadays, hospitalized psychotic and bipolar patients think they are in a hotel (or, as one of my psychotic patients said recently, in a spaceship).
• Why is it that the more powerful the evidence that mental illnesses are brain disorders with neurobiological roots, the more “demedicalized” the community mental health system has become?
• Why don’t practitioners actively support research when they know that every treatment in clinical practice today was once a research project? The breakthrough treatments of tomorrow are being researched today. One simple way clinicians can help accelerate treatment discoveries is to refer patients to therapeutic clinical trials at local academic institutions.
• When are we going to overcome bureaucratic obstacles and give our public sector seriously mentally ill patients the continuity of care they need and deserve? Changing psychiatrists frequently puts patients at risk for diagnostic and treatment errors, repeated mistakes, and difficulties building rapport and therapeutic alliances.
• Why aren’t more psychiatrists collaborating actively with primary care providers? Up to 50% of chronically mentally ill individuals have serious medical conditions,¹ and up to 50% of primary care patients have mental health problems.² We desperately need an integrated, collaborative approach to mind-body illnesses.
• Why have psychiatrists in community mental health settings been reduced to writing prescriptions and doing “med checks” during sessions too brief to allow for the optimal approach of integrating psychotherapy with psychopharmacology?
• Why are politicians so callous about citizens’ health that they even consider granting the privilege to prescribe powerful, sometimes high-risk psychotropics to persons who have had no professional medical training?
• Why is there so much criticism about off-label use of antidepressants, mood stabilizers, and atypical antipsychotics, when 85% of DSM-IV-TR psychiatric disorders do not have any FDA-approved drug treatment?³ Do “armchair critics” have a better idea for treating serious psychiatric disorders?
• Why is there such a scarcity of long-term psychiatric beds for patients who need that type of supervised care? And why do we psychiatrists tolerate managed care policies that dictate discharging psychotic or suicidal inpatients after only 5 or 6 days of treatment?
• Why does the stigma of mental illness persist, even though 75 million (1 in 4) Americans has a diagnosable mental disorder in any given year?⁴
• Finally, why are we standing still when the dysfunctional public mental health system was declared “in shambles” in 2003 by the final report of the President’s New Freedom Commission on Mental Health?⁵

So there, I feel better sharing a few things that bug me. Feel free to share your gripes with me. Better still, let’s try to develop some solutions to these problems.

CASE: Spirits replacing body parts

Mrs. P, age 63, is admitted involuntarily to our inpatient unit after elopement from another emergency room the prior day. For several weeks she had been leaving her house multiple times and wandering the streets in the middle of each night.

Mrs. P is experiencing auditory and visual hallucinations of evil spirits and religious and hypersexual delusions. She cannot recognize her face and believes her voice has been replaced by another’s. She also thinks that her face, nose, lips, voice, and abdomen are not her own. She believes evil spirits that reside within her body are continuously replacing her body parts. She claims these spirits inhabit her left vaginal wall, deposit money there, and are sexually assaulting her each night. She feels that a constant battle between good and evil spirits occurs within her body. She is very angry and states she does not need medication but rather an exorcism.

During her admission, Mrs. P continues to display psychomotor agitation, pressured speech, disorganized thought, religious and hypersexual delusions, grandiosity, and auditory and visual hallucinations. A workup that included a basic metabolic panel, complete blood count, thyroid tests, and abdominal/pelvic CT finds no medical causes for her symptoms. Ob/Gyn is consulted, but Mrs. P refuses a vaginal ultrasound.

The author’s observations

Mrs. P demonstrated symptoms consistent with both mood and thought disorders. Her symptoms of pressured speech, grandiosity, hypersexuality, and decreased need for sleep suggest a manic episode in bipolar disorder. The thought disorganization, delusions, and hallucinations were in line with psychosis.

HISTORY: Failed medications

Mrs. P was first hospitalized at age 29 and has had multiple inpatient admissions for mania, depression, and psychosis. As an outpatient, she was noncompliant with her medications and regularly decompensated and required acute inpatient admission.

Past failed medication trials include risperidone, risperidone long-acting injection, paliperidone, ziprasidone, quetiapine, haloperidol, lamotrigine, and valproic acid. These trials failed because of intolerable side effects or lack of efficacy. She takes lithium, 600 mg every morning and 900 mg at bedtime, for mood stabilization but refuses to try antipsychotics again because she feels the devil is going to attack her through the medications.

The authors’ observations

During her initial hospitalization at age 29, Mrs. P was diagnosed with schizophrenia. In subsequent years she appeared more manic, so her diagnosis was changed to schizoaffective disorder-bipolar type.

Based on our clinical interview, we decide that Mrs. P exhibits a variant of Capgras syndrome, a type of delusional misidentification syndrome in which a person believes other people are not their true selves but have been replaced by identical imposters ( Table ).¹ Patients will at some level recognize a person, but they cannot experience the familiarity that is usually felt when seeing that person. Mrs. P’s case was unusual because instead of believing her loved ones were imposters, she could not recognize herself—her body, face, and voice were foreign to her.

We consider and rule out other misidentification syndromes, including mirrored-self misidentification, a condition in which patients cannot recognize themselves (and sometimes others) in a mirror. Mrs. P’s inability to recognize herself is not limited to her reflection. She is adamant that her hands and a part of her abdomen are not her own but another woman’s. She maintains this delusion even when looking directly at herself.

Breen² argued that a face-processing deficit alone may not account for a mirror delusion; an inability to understand mirror spatial relations in reflections also may be present. Similar to Capgras, in mirrored-self misidentification there may be a perceptual deficit as well as a reasoning deficit that allows the patient to hold on to the delusion. In both delusions, there is a failure of reality testing.³

Table

4 types of delusional misidentification syndromes

Capgras syndrome

Capgras syndrome can be triggered by systemic infections, thyroid dysfunction, concussion, or intoxication. It is seen with head injury, toxic encephalopathy, and dementia.⁵

Joseph Capgras first described this syndrome in 1923. He discovered it by studying brain-injured patients who had prosopagnosia—the inability to recognize familiar faces. Patients with prosopagnosia are not delusional and understand that their inability to recognize faces is an impairment. Brain-injured patients with prosopagnosia had an autonomic arousal (measured by galvanic skin response) with familiar faces and thus unconscious face recognition was intact.⁵

Ellis et al⁶ described Capgras syndrome as being a “reverse” of prosopagnosia. They felt that in patients with Capgras, the conscious ability to recognize a face is intact, but the patient cannot produce an emotional response that usually occurs when seeing a familiar face. Thus, patients can recognize a person but feel that something is “off” or “wrong” and believe that the person must be an “imposter.” This hypothesis was supported by a 1997 study of 5 patients with schizophrenia who had Capgras.⁷

Breen² reviewed 69 case reports of Capgras that had brain imaging results. Twenty-seven had normal brain imaging, 31 had global atrophy or bilateral brain damage, 2 had global atrophy and a right focal lesion, and 6 had a right hemispheric lesion. Thus, Capgras can occur in patients with normal or abnormal brain imaging.

Young⁹ developed an interactionist model of Capgras syndrome, in which a patient’s delusional belief allows the patient to explain his or her confusion and give the experience meaning. The experience then validates the belief, which makes the belief resistant to revision.

The main treatment of Capgras syndrome is pharmacotherapy with antipsychotics and cognitive-behavioral therapy (CBT) to help with fixed delusions.

Box

TREATMENT: Pharmacotherapy

At admission, Mrs. P was taking only lithium for mood stabilization because she refused to take antipsychotics. During her stay, she reluctantly agrees to start haloperidol, which is titrated up to 20 mg bid. She experiences delusions related to the Devil attacking her via the haloperidol and thus is switched to fluphenazine, titrated up to 20 mg bid. She feels that liquid fluphenazine agrees with her the most, so she is stabilized and eventually discharged with this formulation. Switching to a depot formulation would have improved compliance, but Mrs. P adamantly resists this.

As her psychotic symptoms begin to resolve, Mrs. P begins to feel she is getting her body parts back. For example, she feels her face is her own but her nose is still not hers. During Mrs. P’s hospitalization, these bodily delusions lessen and eventually clear.

Other aspects of her psychosis and mania also resolve. She has some residual religious delusions at discharge but feels she has her body back and overall is much improved. Upon discharge Mrs. P is encouraged to follow up with a therapist for CBT, but she feels she does not need therapy and wants only to speak with her priest, even after most of her symptoms resolve. She also declines neuropsychological counseling.

Related resources

• Denes G. Capgras delusion. Neurol Sci. 2007;28:163-164.
  
• Coltheart M, Langdon R, McKay R. Schizophrenia and monothematic delusions. Schizophr Bull. 2007;33:642-647. http://schizophreniabulletin.oxfordjournals.org/cgi/content/full/33/3/642.
  

• Fluphenazine • Prolixin
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Eskalith, Lithobid
  
• Paliperidone • Invega
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Risperidone long-acting injection • Risperdal Consta
  
• Valproic acid • Depakote
  
• Ziprasidone • Geodon
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Spirits replacing body parts

Mrs. P, age 63, is admitted involuntarily to our inpatient unit after elopement from another emergency room the prior day. For several weeks she had been leaving her house multiple times and wandering the streets in the middle of each night.

Mrs. P is experiencing auditory and visual hallucinations of evil spirits and religious and hypersexual delusions. She cannot recognize her face and believes her voice has been replaced by another’s. She also thinks that her face, nose, lips, voice, and abdomen are not her own. She believes evil spirits that reside within her body are continuously replacing her body parts. She claims these spirits inhabit her left vaginal wall, deposit money there, and are sexually assaulting her each night. She feels that a constant battle between good and evil spirits occurs within her body. She is very angry and states she does not need medication but rather an exorcism.

During her admission, Mrs. P continues to display psychomotor agitation, pressured speech, disorganized thought, religious and hypersexual delusions, grandiosity, and auditory and visual hallucinations. A workup that included a basic metabolic panel, complete blood count, thyroid tests, and abdominal/pelvic CT finds no medical causes for her symptoms. Ob/Gyn is consulted, but Mrs. P refuses a vaginal ultrasound.

The author’s observations

Mrs. P demonstrated symptoms consistent with both mood and thought disorders. Her symptoms of pressured speech, grandiosity, hypersexuality, and decreased need for sleep suggest a manic episode in bipolar disorder. The thought disorganization, delusions, and hallucinations were in line with psychosis.

HISTORY: Failed medications

Mrs. P was first hospitalized at age 29 and has had multiple inpatient admissions for mania, depression, and psychosis. As an outpatient, she was noncompliant with her medications and regularly decompensated and required acute inpatient admission.

Past failed medication trials include risperidone, risperidone long-acting injection, paliperidone, ziprasidone, quetiapine, haloperidol, lamotrigine, and valproic acid. These trials failed because of intolerable side effects or lack of efficacy. She takes lithium, 600 mg every morning and 900 mg at bedtime, for mood stabilization but refuses to try antipsychotics again because she feels the devil is going to attack her through the medications.

The authors’ observations

During her initial hospitalization at age 29, Mrs. P was diagnosed with schizophrenia. In subsequent years she appeared more manic, so her diagnosis was changed to schizoaffective disorder-bipolar type.

Based on our clinical interview, we decide that Mrs. P exhibits a variant of Capgras syndrome, a type of delusional misidentification syndrome in which a person believes other people are not their true selves but have been replaced by identical imposters ( Table ).¹ Patients will at some level recognize a person, but they cannot experience the familiarity that is usually felt when seeing that person. Mrs. P’s case was unusual because instead of believing her loved ones were imposters, she could not recognize herself—her body, face, and voice were foreign to her.

We consider and rule out other misidentification syndromes, including mirrored-self misidentification, a condition in which patients cannot recognize themselves (and sometimes others) in a mirror. Mrs. P’s inability to recognize herself is not limited to her reflection. She is adamant that her hands and a part of her abdomen are not her own but another woman’s. She maintains this delusion even when looking directly at herself.

Breen² argued that a face-processing deficit alone may not account for a mirror delusion; an inability to understand mirror spatial relations in reflections also may be present. Similar to Capgras, in mirrored-self misidentification there may be a perceptual deficit as well as a reasoning deficit that allows the patient to hold on to the delusion. In both delusions, there is a failure of reality testing.³

Table

4 types of delusional misidentification syndromes

Capgras syndrome

Capgras syndrome can be triggered by systemic infections, thyroid dysfunction, concussion, or intoxication. It is seen with head injury, toxic encephalopathy, and dementia.⁵

Joseph Capgras first described this syndrome in 1923. He discovered it by studying brain-injured patients who had prosopagnosia—the inability to recognize familiar faces. Patients with prosopagnosia are not delusional and understand that their inability to recognize faces is an impairment. Brain-injured patients with prosopagnosia had an autonomic arousal (measured by galvanic skin response) with familiar faces and thus unconscious face recognition was intact.⁵

Ellis et al⁶ described Capgras syndrome as being a “reverse” of prosopagnosia. They felt that in patients with Capgras, the conscious ability to recognize a face is intact, but the patient cannot produce an emotional response that usually occurs when seeing a familiar face. Thus, patients can recognize a person but feel that something is “off” or “wrong” and believe that the person must be an “imposter.” This hypothesis was supported by a 1997 study of 5 patients with schizophrenia who had Capgras.⁷

Breen² reviewed 69 case reports of Capgras that had brain imaging results. Twenty-seven had normal brain imaging, 31 had global atrophy or bilateral brain damage, 2 had global atrophy and a right focal lesion, and 6 had a right hemispheric lesion. Thus, Capgras can occur in patients with normal or abnormal brain imaging.

Young⁹ developed an interactionist model of Capgras syndrome, in which a patient’s delusional belief allows the patient to explain his or her confusion and give the experience meaning. The experience then validates the belief, which makes the belief resistant to revision.

The main treatment of Capgras syndrome is pharmacotherapy with antipsychotics and cognitive-behavioral therapy (CBT) to help with fixed delusions.

Box

TREATMENT: Pharmacotherapy

At admission, Mrs. P was taking only lithium for mood stabilization because she refused to take antipsychotics. During her stay, she reluctantly agrees to start haloperidol, which is titrated up to 20 mg bid. She experiences delusions related to the Devil attacking her via the haloperidol and thus is switched to fluphenazine, titrated up to 20 mg bid. She feels that liquid fluphenazine agrees with her the most, so she is stabilized and eventually discharged with this formulation. Switching to a depot formulation would have improved compliance, but Mrs. P adamantly resists this.

As her psychotic symptoms begin to resolve, Mrs. P begins to feel she is getting her body parts back. For example, she feels her face is her own but her nose is still not hers. During Mrs. P’s hospitalization, these bodily delusions lessen and eventually clear.

Other aspects of her psychosis and mania also resolve. She has some residual religious delusions at discharge but feels she has her body back and overall is much improved. Upon discharge Mrs. P is encouraged to follow up with a therapist for CBT, but she feels she does not need therapy and wants only to speak with her priest, even after most of her symptoms resolve. She also declines neuropsychological counseling.

Related resources

• Denes G. Capgras delusion. Neurol Sci. 2007;28:163-164.
  
• Coltheart M, Langdon R, McKay R. Schizophrenia and monothematic delusions. Schizophr Bull. 2007;33:642-647. http://schizophreniabulletin.oxfordjournals.org/cgi/content/full/33/3/642.
  

• Fluphenazine • Prolixin
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Eskalith, Lithobid
  
• Paliperidone • Invega
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Risperidone long-acting injection • Risperdal Consta
  
• Valproic acid • Depakote
  
• Ziprasidone • Geodon
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

CASE: Spirits replacing body parts

Mrs. P, age 63, is admitted involuntarily to our inpatient unit after elopement from another emergency room the prior day. For several weeks she had been leaving her house multiple times and wandering the streets in the middle of each night.

Mrs. P is experiencing auditory and visual hallucinations of evil spirits and religious and hypersexual delusions. She cannot recognize her face and believes her voice has been replaced by another’s. She also thinks that her face, nose, lips, voice, and abdomen are not her own. She believes evil spirits that reside within her body are continuously replacing her body parts. She claims these spirits inhabit her left vaginal wall, deposit money there, and are sexually assaulting her each night. She feels that a constant battle between good and evil spirits occurs within her body. She is very angry and states she does not need medication but rather an exorcism.

During her admission, Mrs. P continues to display psychomotor agitation, pressured speech, disorganized thought, religious and hypersexual delusions, grandiosity, and auditory and visual hallucinations. A workup that included a basic metabolic panel, complete blood count, thyroid tests, and abdominal/pelvic CT finds no medical causes for her symptoms. Ob/Gyn is consulted, but Mrs. P refuses a vaginal ultrasound.

The author’s observations

Mrs. P demonstrated symptoms consistent with both mood and thought disorders. Her symptoms of pressured speech, grandiosity, hypersexuality, and decreased need for sleep suggest a manic episode in bipolar disorder. The thought disorganization, delusions, and hallucinations were in line with psychosis.

HISTORY: Failed medications

Mrs. P was first hospitalized at age 29 and has had multiple inpatient admissions for mania, depression, and psychosis. As an outpatient, she was noncompliant with her medications and regularly decompensated and required acute inpatient admission.

Past failed medication trials include risperidone, risperidone long-acting injection, paliperidone, ziprasidone, quetiapine, haloperidol, lamotrigine, and valproic acid. These trials failed because of intolerable side effects or lack of efficacy. She takes lithium, 600 mg every morning and 900 mg at bedtime, for mood stabilization but refuses to try antipsychotics again because she feels the devil is going to attack her through the medications.

The authors’ observations

During her initial hospitalization at age 29, Mrs. P was diagnosed with schizophrenia. In subsequent years she appeared more manic, so her diagnosis was changed to schizoaffective disorder-bipolar type.

Based on our clinical interview, we decide that Mrs. P exhibits a variant of Capgras syndrome, a type of delusional misidentification syndrome in which a person believes other people are not their true selves but have been replaced by identical imposters ( Table ).¹ Patients will at some level recognize a person, but they cannot experience the familiarity that is usually felt when seeing that person. Mrs. P’s case was unusual because instead of believing her loved ones were imposters, she could not recognize herself—her body, face, and voice were foreign to her.

We consider and rule out other misidentification syndromes, including mirrored-self misidentification, a condition in which patients cannot recognize themselves (and sometimes others) in a mirror. Mrs. P’s inability to recognize herself is not limited to her reflection. She is adamant that her hands and a part of her abdomen are not her own but another woman’s. She maintains this delusion even when looking directly at herself.

Breen² argued that a face-processing deficit alone may not account for a mirror delusion; an inability to understand mirror spatial relations in reflections also may be present. Similar to Capgras, in mirrored-self misidentification there may be a perceptual deficit as well as a reasoning deficit that allows the patient to hold on to the delusion. In both delusions, there is a failure of reality testing.³

Table

4 types of delusional misidentification syndromes

Capgras syndrome

Capgras syndrome can be triggered by systemic infections, thyroid dysfunction, concussion, or intoxication. It is seen with head injury, toxic encephalopathy, and dementia.⁵

Joseph Capgras first described this syndrome in 1923. He discovered it by studying brain-injured patients who had prosopagnosia—the inability to recognize familiar faces. Patients with prosopagnosia are not delusional and understand that their inability to recognize faces is an impairment. Brain-injured patients with prosopagnosia had an autonomic arousal (measured by galvanic skin response) with familiar faces and thus unconscious face recognition was intact.⁵

Ellis et al⁶ described Capgras syndrome as being a “reverse” of prosopagnosia. They felt that in patients with Capgras, the conscious ability to recognize a face is intact, but the patient cannot produce an emotional response that usually occurs when seeing a familiar face. Thus, patients can recognize a person but feel that something is “off” or “wrong” and believe that the person must be an “imposter.” This hypothesis was supported by a 1997 study of 5 patients with schizophrenia who had Capgras.⁷

Breen² reviewed 69 case reports of Capgras that had brain imaging results. Twenty-seven had normal brain imaging, 31 had global atrophy or bilateral brain damage, 2 had global atrophy and a right focal lesion, and 6 had a right hemispheric lesion. Thus, Capgras can occur in patients with normal or abnormal brain imaging.

Young⁹ developed an interactionist model of Capgras syndrome, in which a patient’s delusional belief allows the patient to explain his or her confusion and give the experience meaning. The experience then validates the belief, which makes the belief resistant to revision.

The main treatment of Capgras syndrome is pharmacotherapy with antipsychotics and cognitive-behavioral therapy (CBT) to help with fixed delusions.

Box

TREATMENT: Pharmacotherapy

At admission, Mrs. P was taking only lithium for mood stabilization because she refused to take antipsychotics. During her stay, she reluctantly agrees to start haloperidol, which is titrated up to 20 mg bid. She experiences delusions related to the Devil attacking her via the haloperidol and thus is switched to fluphenazine, titrated up to 20 mg bid. She feels that liquid fluphenazine agrees with her the most, so she is stabilized and eventually discharged with this formulation. Switching to a depot formulation would have improved compliance, but Mrs. P adamantly resists this.

As her psychotic symptoms begin to resolve, Mrs. P begins to feel she is getting her body parts back. For example, she feels her face is her own but her nose is still not hers. During Mrs. P’s hospitalization, these bodily delusions lessen and eventually clear.

Other aspects of her psychosis and mania also resolve. She has some residual religious delusions at discharge but feels she has her body back and overall is much improved. Upon discharge Mrs. P is encouraged to follow up with a therapist for CBT, but she feels she does not need therapy and wants only to speak with her priest, even after most of her symptoms resolve. She also declines neuropsychological counseling.

Related resources

• Denes G. Capgras delusion. Neurol Sci. 2007;28:163-164.
  
• Coltheart M, Langdon R, McKay R. Schizophrenia and monothematic delusions. Schizophr Bull. 2007;33:642-647. http://schizophreniabulletin.oxfordjournals.org/cgi/content/full/33/3/642.
  

• Fluphenazine • Prolixin
  
• Haloperidol • Haldol
  
• Lamotrigine • Lamictal
  
• Lithium • Eskalith, Lithobid
  
• Paliperidone • Invega
  
• Quetiapine • Seroquel
  
• Risperidone • Risperdal
  
• Risperidone long-acting injection • Risperdal Consta
  
• Valproic acid • Depakote
  
• Ziprasidone • Geodon
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Comment on this article

Completed suicide provokes a multitude of questions: What motivated it? What interventions could have diverted it? Could anyone or anything have prevented it? The question of who dies by suicide often overshadows the question of what lessons suicide attempt (SA) survivors can teach us. Their story does not end with the attempt episode. For these patients, we have ongoing opportunities for interventions to make a difference.

A history of SA strongly predicts eventual completion, so we must try to identify which survivors will reattempt and complete suicide. This article addresses what is known about the psychiatry of suicide survivors—suicide motives and methods, clinical management, and short- and long-term outcomes—from the perspective that suicidality in this population may be a trait, with SA or deliberate self-harm (DSH) as its state-driven manifestations. When viewed in this manner, it is not just a question of who survives a suicide attempt, but who survives suicidality.

CASE REPORT: End of the game

Ms. T, age 39, was admitted to the intensive care unit after an aspirin overdose. She had been living with a man in a southern state for 8 years since the demise of her first marriage, but kept deferring remarriage. She returned to Minnesota with her teenage daughter to visit her family and stayed 6 months. Her partner phoned Ms. T every day, telling her he wanted her to come back. One day he tired of the game and said, “Fine, don’t come back.” She immediately overdosed, then called him to tell him what she’d done. He called her daughter, telling her to go check on her mother and to call 911. When later asked why she did it, Ms. T said, “So he would know how much he loved me.”

Motive for self-harm

Ms. T’s suicide attempt was nonlethal, and she reported it immediately—characteristics of parasuicidal gesturing as a motive. A useful categorization of suicidal behavior divides it into discrete categories or narratives. Gardner and Cowdry describe 4: true suicidal acts, parasuicidal gesturing, self-mutilation, and retributive rage.¹ We modify this schema with 4 additional categories: altruism, acute shame, command hallucinations, and panic ( Table 1 ).^1-3 Categories are differentiated by affective state, motivation, and goal of behavior, but all involve situations in which the individual feels a lack of other options and resorts to maladaptive strategies.

Although this classification scheme helps clinicians understand a patient’s mindset, the specific motive underpinning DSH or SA is not consistently linked to its lethality. True suicidal acts frequently are marked by careful planning and high-lethality methods that increase the risk of completed suicide, but any motive can lead to a lethal act, whether or not death was intended.^2,3

Factors that increase the risk of SA and completed suicide include male gender, age (adolescent or age >60), low socioeconomic status, and alcohol or drug abuse.⁴ An underlying mood disorder accounts for 73% of attributable risk of suicide or medically serious SA in older adults.⁵ This connection between mood and suicidality highlights the concept that emotional pain can cause so much suffering that patients seek release from distress by ending their lives.

A useful model by Shneidman⁶ casts psychological pain as 1 dimension in a 3-dimensional system that includes press and perturbation. In this model:

• Pain refers to psychological pain (from little or no pain to intolerable agony).
  
• Press means actual or imagined events in the inner or outer world that cause a person to react. It ranges from positive press (good fortune, happy events, protective factors) to negative press (stressors, failures, losses, persecution), which in turn decrease or increase the likelihood of suicide.
  
• Perturbation refers to the state of being disturbed or upset.
  

Table 1

8 categories or narratives of suicidal behavior

CASE REPORT: Caught in the act

Mrs. L, age 35, works at a nail salon and took $12 from the cash register to buy gas so she could visit her husband in the next town. She’d never done anything like that before. She planned to return the money the next day, but her act was captured by a security camera and reported before she had a chance. Her boss said she had to go to the police.

Mrs. L was so ashamed that she decided she wanted to die. She drove her car to a remote hunting area where she tried to shoot herself in the head. The gun bucked, however, and shot her in the shoulder instead. She climbed into the front seat and drove herself to the hospital.

Method of self-harm

Survival of a suicide attempt depends in part on the lethality of the suicide method. Although she survived, Mrs. L’s attempt was intended to be quite lethal and illustrates shame as a motive.

The method’s lethality does not always correlate with the intent to die.⁹ Attempters with the highest suicidal intent do not reliably choose the most lethal method, either because they overestimate the lethality of methods such as cutting or overdose or because less lethal methods were most accessible.

Firearms, which are both accessible and lethal, remain the most common and deadly method in the United States, with more suicides from gunshot than all other methods combined.¹³ Cultural factors also are involved, such as in India where poisoning (especially with readily available organophosphates) is more common than gunshot.¹⁴ Suicidality screening in psychiatric practice and in the emergency department should always include questioning about convenient access to lethal means, especially those commonly used among the local population.

Clinical management

Treatment goals for patients who have demonstrated suicidal behavior may include decreasing the occurrence of suicidal thoughts, plans, gestures, or attempts. At a population level, accepted management strategies include:

• psychotherapy (cognitive-behavioral therapy [CBT], dialectical behavioral therapy)
  
• contracts for safety (widely employed but lacking evidence of efficacy)
  
• medications that target underlying disorders (antidepressants, mood stabilizers, antipsychotics).
  

Ineffective interventions? A study examining suicide trends since 1990 in the United States¹⁸ found disheartening evidence that although treatment dramatically increased, the incidence of suicidal thoughts, plans, gestures, or attempts did not significantly decrease ( Box 1 ).^18–26 Based on a systematic review of 15 randomized controlled trials, Arensman et al¹⁹ offered 2 explanations for why studies of various psychosocial and pharmacologic interventions showed no significant effect on suicidality compared with usual care:

• the intervention had a negligible effect on patient outcomes
  
• the sample size was too small to detect clinically important differences in reattempt rates.
  

Suicide research deploys a single intervention for a diverse group of subjects rather than tailoring the approach to each particular case. A certain intervention may be highly effective for 1 patient because it is well matched to the specific blend of issues driving that patient’s suicidality, yet ineffective for another because it fails to address that individual’s underlying issues. Thus, a single treatment program standardized for research can be simultaneously a success and a failure, depending on which patient is assessed. The overall outcome is statistical insignificance because success is lost in the noise of failure.

Treating the individual. To individualize your treatment approach, it may be useful to recast the case and treatment strategy into Shneidman’s cubic model.⁶ Identifying the uniquely personal drivers behind a patient’s thoughts and actions helps point toward the most effective management approach. Tailored pharmacologic treatments and psychotherapy can be used to help guide the patient away from maximum suicide risk.

Table 2

Symptom-targeted pharmacologic treatment of suicidal patients

Outcomes of self-harm

When considering outcomes of SA, it is important to separate the short-term outcome of a single SA from the long-term outcome of suicidality. Short-term outcome depends on the characteristics and management of the acute episode, whereas long-term encompasses ongoing management of suicidality as a trait.

In the short term, surviving a SA depends heavily on the lethality of method and access to acute treatment. It also depends on medical fitness to withstand injury, which may help account for the higher death rate among elderly suicide attempters. A frail or medically ill person is less likely to survive the bodily insult of a SA.

Long-term outcomes are harder to predict. Some patients’ index attempts result from a transient state—an isolated incident that never will be repeated. In others, suicidality is a trait—a chronic maladaptive pattern that is potentially lethal. After an index attempt, the most reliable predictors for eventual death by suicide are:

• diagnosed mental illness
  
• high-lethality method on the index SA
  
• number of reattempts.⁴
  

Mood disorders impact long-term outcome, yet only a limited number of studies have found a reduction in suicide rates in response to mood disorder treatment. In a 44-year follow-up study, long-term treatment of depression and bipolar disorder with lithium significantly reduced the suicide rate.³⁰ A meta-analysis of recurrent major affective disorder studies found that subjects on lithium maintenance treatment were 15 times less likely to commit suicidal acts, compared with those not on lithium.³¹

An important confounding factor in these findings is that effective lithium treatment requires long-term adherence, which implies a long-term doctor-patient relationship. As Cipriani et al³² noted, patients who can maintain an ongoing therapeutic relationship may be “less disturbed” than those who cannot, making them less likely to kill themselves regardless of pharmacologic treatment. Furthermore, patient interviews reveal that the therapeutic alliance created by a continuous relationship can be a protective support against further SA.³³

Clinical implications

Suicide survivors often continue to struggle with suicidality well beyond the index attempt. This suicidality is a maladaptive problem-solving method that functions as a chronic morbid illness. As such, it is not enough to analyze the phenomenon of surviving an SA; one must examine the ongoing process of surviving suicidality.

Consider 3 factors. Consider all 3 factors— motive, method, and management—when addressing suicide survivorship.

Method lethality significantly influences survival likelihood. In clinical practice, we have observed that the index attempt is a learning experience for some patients that will inform their choice of method on the next attempt. When interacting with a suicide survivor, carefully assess the reasoning behind their initial choice of method and whether it has evolved toward higher lethality since the index attempt.

Management recommendations after SA continue to evolve. Risk factor management—such as treating underlying mood disorders, home visits to reduce social isolation, and prioritized “green card” contact with psychiatrists—has been shown to decrease reattempt rates, but many other interventions have not shown the expected benefit. Increased intervention rates have not yielded proportional decreases in suicidal ideation, attempts, or completion.

Box 2

• American Association of Suicidology. www.suicidology.org.
  
• American Foundation for Suicide Prevention. www.afsp.org.
  
• Mayo Clinic Patient/Family Education. Suicide: What to do when someone is suicidal. www.mayoclinic.com/health/suicide/MH00058.
  

• Carbamazepine • Carbatrol
  
• Lithium • Eskalith, Lithobid
  
• Valproic acid • Depakene, Depakote
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Comment on this article

Completed suicide provokes a multitude of questions: What motivated it? What interventions could have diverted it? Could anyone or anything have prevented it? The question of who dies by suicide often overshadows the question of what lessons suicide attempt (SA) survivors can teach us. Their story does not end with the attempt episode. For these patients, we have ongoing opportunities for interventions to make a difference.

A history of SA strongly predicts eventual completion, so we must try to identify which survivors will reattempt and complete suicide. This article addresses what is known about the psychiatry of suicide survivors—suicide motives and methods, clinical management, and short- and long-term outcomes—from the perspective that suicidality in this population may be a trait, with SA or deliberate self-harm (DSH) as its state-driven manifestations. When viewed in this manner, it is not just a question of who survives a suicide attempt, but who survives suicidality.

CASE REPORT: End of the game

Ms. T, age 39, was admitted to the intensive care unit after an aspirin overdose. She had been living with a man in a southern state for 8 years since the demise of her first marriage, but kept deferring remarriage. She returned to Minnesota with her teenage daughter to visit her family and stayed 6 months. Her partner phoned Ms. T every day, telling her he wanted her to come back. One day he tired of the game and said, “Fine, don’t come back.” She immediately overdosed, then called him to tell him what she’d done. He called her daughter, telling her to go check on her mother and to call 911. When later asked why she did it, Ms. T said, “So he would know how much he loved me.”

Motive for self-harm

Ms. T’s suicide attempt was nonlethal, and she reported it immediately—characteristics of parasuicidal gesturing as a motive. A useful categorization of suicidal behavior divides it into discrete categories or narratives. Gardner and Cowdry describe 4: true suicidal acts, parasuicidal gesturing, self-mutilation, and retributive rage.¹ We modify this schema with 4 additional categories: altruism, acute shame, command hallucinations, and panic ( Table 1 ).^1-3 Categories are differentiated by affective state, motivation, and goal of behavior, but all involve situations in which the individual feels a lack of other options and resorts to maladaptive strategies.

Although this classification scheme helps clinicians understand a patient’s mindset, the specific motive underpinning DSH or SA is not consistently linked to its lethality. True suicidal acts frequently are marked by careful planning and high-lethality methods that increase the risk of completed suicide, but any motive can lead to a lethal act, whether or not death was intended.^2,3

Factors that increase the risk of SA and completed suicide include male gender, age (adolescent or age >60), low socioeconomic status, and alcohol or drug abuse.⁴ An underlying mood disorder accounts for 73% of attributable risk of suicide or medically serious SA in older adults.⁵ This connection between mood and suicidality highlights the concept that emotional pain can cause so much suffering that patients seek release from distress by ending their lives.

A useful model by Shneidman⁶ casts psychological pain as 1 dimension in a 3-dimensional system that includes press and perturbation. In this model:

• Pain refers to psychological pain (from little or no pain to intolerable agony).
  
• Press means actual or imagined events in the inner or outer world that cause a person to react. It ranges from positive press (good fortune, happy events, protective factors) to negative press (stressors, failures, losses, persecution), which in turn decrease or increase the likelihood of suicide.
  
• Perturbation refers to the state of being disturbed or upset.
  

Table 1

8 categories or narratives of suicidal behavior

CASE REPORT: Caught in the act

Mrs. L, age 35, works at a nail salon and took $12 from the cash register to buy gas so she could visit her husband in the next town. She’d never done anything like that before. She planned to return the money the next day, but her act was captured by a security camera and reported before she had a chance. Her boss said she had to go to the police.

Mrs. L was so ashamed that she decided she wanted to die. She drove her car to a remote hunting area where she tried to shoot herself in the head. The gun bucked, however, and shot her in the shoulder instead. She climbed into the front seat and drove herself to the hospital.

Method of self-harm

Survival of a suicide attempt depends in part on the lethality of the suicide method. Although she survived, Mrs. L’s attempt was intended to be quite lethal and illustrates shame as a motive.

The method’s lethality does not always correlate with the intent to die.⁹ Attempters with the highest suicidal intent do not reliably choose the most lethal method, either because they overestimate the lethality of methods such as cutting or overdose or because less lethal methods were most accessible.

Firearms, which are both accessible and lethal, remain the most common and deadly method in the United States, with more suicides from gunshot than all other methods combined.¹³ Cultural factors also are involved, such as in India where poisoning (especially with readily available organophosphates) is more common than gunshot.¹⁴ Suicidality screening in psychiatric practice and in the emergency department should always include questioning about convenient access to lethal means, especially those commonly used among the local population.

Clinical management

Treatment goals for patients who have demonstrated suicidal behavior may include decreasing the occurrence of suicidal thoughts, plans, gestures, or attempts. At a population level, accepted management strategies include:

• psychotherapy (cognitive-behavioral therapy [CBT], dialectical behavioral therapy)
  
• contracts for safety (widely employed but lacking evidence of efficacy)
  
• medications that target underlying disorders (antidepressants, mood stabilizers, antipsychotics).
  

Ineffective interventions? A study examining suicide trends since 1990 in the United States¹⁸ found disheartening evidence that although treatment dramatically increased, the incidence of suicidal thoughts, plans, gestures, or attempts did not significantly decrease ( Box 1 ).^18–26 Based on a systematic review of 15 randomized controlled trials, Arensman et al¹⁹ offered 2 explanations for why studies of various psychosocial and pharmacologic interventions showed no significant effect on suicidality compared with usual care:

• the intervention had a negligible effect on patient outcomes
  
• the sample size was too small to detect clinically important differences in reattempt rates.
  

Suicide research deploys a single intervention for a diverse group of subjects rather than tailoring the approach to each particular case. A certain intervention may be highly effective for 1 patient because it is well matched to the specific blend of issues driving that patient’s suicidality, yet ineffective for another because it fails to address that individual’s underlying issues. Thus, a single treatment program standardized for research can be simultaneously a success and a failure, depending on which patient is assessed. The overall outcome is statistical insignificance because success is lost in the noise of failure.

Treating the individual. To individualize your treatment approach, it may be useful to recast the case and treatment strategy into Shneidman’s cubic model.⁶ Identifying the uniquely personal drivers behind a patient’s thoughts and actions helps point toward the most effective management approach. Tailored pharmacologic treatments and psychotherapy can be used to help guide the patient away from maximum suicide risk.

Table 2

Symptom-targeted pharmacologic treatment of suicidal patients

Outcomes of self-harm

When considering outcomes of SA, it is important to separate the short-term outcome of a single SA from the long-term outcome of suicidality. Short-term outcome depends on the characteristics and management of the acute episode, whereas long-term encompasses ongoing management of suicidality as a trait.

In the short term, surviving a SA depends heavily on the lethality of method and access to acute treatment. It also depends on medical fitness to withstand injury, which may help account for the higher death rate among elderly suicide attempters. A frail or medically ill person is less likely to survive the bodily insult of a SA.

Long-term outcomes are harder to predict. Some patients’ index attempts result from a transient state—an isolated incident that never will be repeated. In others, suicidality is a trait—a chronic maladaptive pattern that is potentially lethal. After an index attempt, the most reliable predictors for eventual death by suicide are:

• diagnosed mental illness
  
• high-lethality method on the index SA
  
• number of reattempts.⁴
  

Mood disorders impact long-term outcome, yet only a limited number of studies have found a reduction in suicide rates in response to mood disorder treatment. In a 44-year follow-up study, long-term treatment of depression and bipolar disorder with lithium significantly reduced the suicide rate.³⁰ A meta-analysis of recurrent major affective disorder studies found that subjects on lithium maintenance treatment were 15 times less likely to commit suicidal acts, compared with those not on lithium.³¹

An important confounding factor in these findings is that effective lithium treatment requires long-term adherence, which implies a long-term doctor-patient relationship. As Cipriani et al³² noted, patients who can maintain an ongoing therapeutic relationship may be “less disturbed” than those who cannot, making them less likely to kill themselves regardless of pharmacologic treatment. Furthermore, patient interviews reveal that the therapeutic alliance created by a continuous relationship can be a protective support against further SA.³³

Clinical implications

Suicide survivors often continue to struggle with suicidality well beyond the index attempt. This suicidality is a maladaptive problem-solving method that functions as a chronic morbid illness. As such, it is not enough to analyze the phenomenon of surviving an SA; one must examine the ongoing process of surviving suicidality.

Consider 3 factors. Consider all 3 factors— motive, method, and management—when addressing suicide survivorship.

Method lethality significantly influences survival likelihood. In clinical practice, we have observed that the index attempt is a learning experience for some patients that will inform their choice of method on the next attempt. When interacting with a suicide survivor, carefully assess the reasoning behind their initial choice of method and whether it has evolved toward higher lethality since the index attempt.

Management recommendations after SA continue to evolve. Risk factor management—such as treating underlying mood disorders, home visits to reduce social isolation, and prioritized “green card” contact with psychiatrists—has been shown to decrease reattempt rates, but many other interventions have not shown the expected benefit. Increased intervention rates have not yielded proportional decreases in suicidal ideation, attempts, or completion.

Box 2

• American Association of Suicidology. www.suicidology.org.
  
• American Foundation for Suicide Prevention. www.afsp.org.
  
• Mayo Clinic Patient/Family Education. Suicide: What to do when someone is suicidal. www.mayoclinic.com/health/suicide/MH00058.
  

• Carbamazepine • Carbatrol
  
• Lithium • Eskalith, Lithobid
  
• Valproic acid • Depakene, Depakote
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Comment on this article

Completed suicide provokes a multitude of questions: What motivated it? What interventions could have diverted it? Could anyone or anything have prevented it? The question of who dies by suicide often overshadows the question of what lessons suicide attempt (SA) survivors can teach us. Their story does not end with the attempt episode. For these patients, we have ongoing opportunities for interventions to make a difference.

A history of SA strongly predicts eventual completion, so we must try to identify which survivors will reattempt and complete suicide. This article addresses what is known about the psychiatry of suicide survivors—suicide motives and methods, clinical management, and short- and long-term outcomes—from the perspective that suicidality in this population may be a trait, with SA or deliberate self-harm (DSH) as its state-driven manifestations. When viewed in this manner, it is not just a question of who survives a suicide attempt, but who survives suicidality.

CASE REPORT: End of the game

Ms. T, age 39, was admitted to the intensive care unit after an aspirin overdose. She had been living with a man in a southern state for 8 years since the demise of her first marriage, but kept deferring remarriage. She returned to Minnesota with her teenage daughter to visit her family and stayed 6 months. Her partner phoned Ms. T every day, telling her he wanted her to come back. One day he tired of the game and said, “Fine, don’t come back.” She immediately overdosed, then called him to tell him what she’d done. He called her daughter, telling her to go check on her mother and to call 911. When later asked why she did it, Ms. T said, “So he would know how much he loved me.”

Motive for self-harm

Ms. T’s suicide attempt was nonlethal, and she reported it immediately—characteristics of parasuicidal gesturing as a motive. A useful categorization of suicidal behavior divides it into discrete categories or narratives. Gardner and Cowdry describe 4: true suicidal acts, parasuicidal gesturing, self-mutilation, and retributive rage.¹ We modify this schema with 4 additional categories: altruism, acute shame, command hallucinations, and panic ( Table 1 ).^1-3 Categories are differentiated by affective state, motivation, and goal of behavior, but all involve situations in which the individual feels a lack of other options and resorts to maladaptive strategies.

Although this classification scheme helps clinicians understand a patient’s mindset, the specific motive underpinning DSH or SA is not consistently linked to its lethality. True suicidal acts frequently are marked by careful planning and high-lethality methods that increase the risk of completed suicide, but any motive can lead to a lethal act, whether or not death was intended.^2,3

Factors that increase the risk of SA and completed suicide include male gender, age (adolescent or age >60), low socioeconomic status, and alcohol or drug abuse.⁴ An underlying mood disorder accounts for 73% of attributable risk of suicide or medically serious SA in older adults.⁵ This connection between mood and suicidality highlights the concept that emotional pain can cause so much suffering that patients seek release from distress by ending their lives.

A useful model by Shneidman⁶ casts psychological pain as 1 dimension in a 3-dimensional system that includes press and perturbation. In this model:

• Pain refers to psychological pain (from little or no pain to intolerable agony).
  
• Press means actual or imagined events in the inner or outer world that cause a person to react. It ranges from positive press (good fortune, happy events, protective factors) to negative press (stressors, failures, losses, persecution), which in turn decrease or increase the likelihood of suicide.
  
• Perturbation refers to the state of being disturbed or upset.
  

Table 1

8 categories or narratives of suicidal behavior

CASE REPORT: Caught in the act

Mrs. L, age 35, works at a nail salon and took $12 from the cash register to buy gas so she could visit her husband in the next town. She’d never done anything like that before. She planned to return the money the next day, but her act was captured by a security camera and reported before she had a chance. Her boss said she had to go to the police.

Mrs. L was so ashamed that she decided she wanted to die. She drove her car to a remote hunting area where she tried to shoot herself in the head. The gun bucked, however, and shot her in the shoulder instead. She climbed into the front seat and drove herself to the hospital.

Method of self-harm

Survival of a suicide attempt depends in part on the lethality of the suicide method. Although she survived, Mrs. L’s attempt was intended to be quite lethal and illustrates shame as a motive.

The method’s lethality does not always correlate with the intent to die.⁹ Attempters with the highest suicidal intent do not reliably choose the most lethal method, either because they overestimate the lethality of methods such as cutting or overdose or because less lethal methods were most accessible.

Firearms, which are both accessible and lethal, remain the most common and deadly method in the United States, with more suicides from gunshot than all other methods combined.¹³ Cultural factors also are involved, such as in India where poisoning (especially with readily available organophosphates) is more common than gunshot.¹⁴ Suicidality screening in psychiatric practice and in the emergency department should always include questioning about convenient access to lethal means, especially those commonly used among the local population.

Clinical management

Treatment goals for patients who have demonstrated suicidal behavior may include decreasing the occurrence of suicidal thoughts, plans, gestures, or attempts. At a population level, accepted management strategies include:

• psychotherapy (cognitive-behavioral therapy [CBT], dialectical behavioral therapy)
  
• contracts for safety (widely employed but lacking evidence of efficacy)
  
• medications that target underlying disorders (antidepressants, mood stabilizers, antipsychotics).
  

Ineffective interventions? A study examining suicide trends since 1990 in the United States¹⁸ found disheartening evidence that although treatment dramatically increased, the incidence of suicidal thoughts, plans, gestures, or attempts did not significantly decrease ( Box 1 ).^18–26 Based on a systematic review of 15 randomized controlled trials, Arensman et al¹⁹ offered 2 explanations for why studies of various psychosocial and pharmacologic interventions showed no significant effect on suicidality compared with usual care:

• the intervention had a negligible effect on patient outcomes
  
• the sample size was too small to detect clinically important differences in reattempt rates.
  

Suicide research deploys a single intervention for a diverse group of subjects rather than tailoring the approach to each particular case. A certain intervention may be highly effective for 1 patient because it is well matched to the specific blend of issues driving that patient’s suicidality, yet ineffective for another because it fails to address that individual’s underlying issues. Thus, a single treatment program standardized for research can be simultaneously a success and a failure, depending on which patient is assessed. The overall outcome is statistical insignificance because success is lost in the noise of failure.

Treating the individual. To individualize your treatment approach, it may be useful to recast the case and treatment strategy into Shneidman’s cubic model.⁶ Identifying the uniquely personal drivers behind a patient’s thoughts and actions helps point toward the most effective management approach. Tailored pharmacologic treatments and psychotherapy can be used to help guide the patient away from maximum suicide risk.

Table 2

Symptom-targeted pharmacologic treatment of suicidal patients

Outcomes of self-harm

When considering outcomes of SA, it is important to separate the short-term outcome of a single SA from the long-term outcome of suicidality. Short-term outcome depends on the characteristics and management of the acute episode, whereas long-term encompasses ongoing management of suicidality as a trait.

In the short term, surviving a SA depends heavily on the lethality of method and access to acute treatment. It also depends on medical fitness to withstand injury, which may help account for the higher death rate among elderly suicide attempters. A frail or medically ill person is less likely to survive the bodily insult of a SA.

Long-term outcomes are harder to predict. Some patients’ index attempts result from a transient state—an isolated incident that never will be repeated. In others, suicidality is a trait—a chronic maladaptive pattern that is potentially lethal. After an index attempt, the most reliable predictors for eventual death by suicide are:

• diagnosed mental illness
  
• high-lethality method on the index SA
  
• number of reattempts.⁴
  

Mood disorders impact long-term outcome, yet only a limited number of studies have found a reduction in suicide rates in response to mood disorder treatment. In a 44-year follow-up study, long-term treatment of depression and bipolar disorder with lithium significantly reduced the suicide rate.³⁰ A meta-analysis of recurrent major affective disorder studies found that subjects on lithium maintenance treatment were 15 times less likely to commit suicidal acts, compared with those not on lithium.³¹

An important confounding factor in these findings is that effective lithium treatment requires long-term adherence, which implies a long-term doctor-patient relationship. As Cipriani et al³² noted, patients who can maintain an ongoing therapeutic relationship may be “less disturbed” than those who cannot, making them less likely to kill themselves regardless of pharmacologic treatment. Furthermore, patient interviews reveal that the therapeutic alliance created by a continuous relationship can be a protective support against further SA.³³

Clinical implications

Suicide survivors often continue to struggle with suicidality well beyond the index attempt. This suicidality is a maladaptive problem-solving method that functions as a chronic morbid illness. As such, it is not enough to analyze the phenomenon of surviving an SA; one must examine the ongoing process of surviving suicidality.

Consider 3 factors. Consider all 3 factors— motive, method, and management—when addressing suicide survivorship.

Method lethality significantly influences survival likelihood. In clinical practice, we have observed that the index attempt is a learning experience for some patients that will inform their choice of method on the next attempt. When interacting with a suicide survivor, carefully assess the reasoning behind their initial choice of method and whether it has evolved toward higher lethality since the index attempt.

Management recommendations after SA continue to evolve. Risk factor management—such as treating underlying mood disorders, home visits to reduce social isolation, and prioritized “green card” contact with psychiatrists—has been shown to decrease reattempt rates, but many other interventions have not shown the expected benefit. Increased intervention rates have not yielded proportional decreases in suicidal ideation, attempts, or completion.

Box 2

• American Association of Suicidology. www.suicidology.org.
  
• American Foundation for Suicide Prevention. www.afsp.org.
  
• Mayo Clinic Patient/Family Education. Suicide: What to do when someone is suicidal. www.mayoclinic.com/health/suicide/MH00058.
  

• Carbamazepine • Carbatrol
  
• Lithium • Eskalith, Lithobid
  
• Valproic acid • Depakene, Depakote
  

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Comment on this article

Exposure and response (or ritual) prevention has been shown to be effective in improving the therapeutic outlook for patients with obsessive-compulsive disorder (OCD). Yet barriers—including patient unwillingness to enter into the intensive therapy—prevent more persons with OCD from achieving an improved quality of life.

This article focuses on the clinical picture of OCD and the multifaceted cognitive-behavioral therapy (CBT) that has received the most empirical support. We also describe initiatives to make CBT more accessible to OCD patients, such as providing twice-weekly instead of daily treatment sessions.

OCD definition: Anxiety/distress

OCD is a relatively common, debilitating condition that often develops early in life (Box 1).^1,2 The obsessions of this disorder are not simply excessive worries about real-life problems. The compulsions are excessive or unreasonable and serve to reduce the discomfort associated with the obsessions. The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is the gold standard tool for quantifying OCD (Box 2).^3,4

Obsessions vs compulsions. When diagnosing and treating OCD, it is important to ascertain the functional relationship between a patient’s obsessions and compulsions and anxiety/distress:

• Obsessions give rise to anxiety/distress.
  
• Compulsions aim to reduce this anxiety/distress.
  

Box 2

OCD’s clinical picture

Classic vs nonclassic obsessions. Frequently reported obsessions in OCD include fears related to:

• contamination (dirt, germs, bodily waste, chemicals)
  
• making mistakes (locks, appliances, paperwork, decisions)
  
• having unwanted impulses (violent, sexual, religious, embarrassing)
  
• orderliness (neatness, symmetry, numbers).
  

• intrusive, irrational, or excessive worries about loss of identity, essence, or intelligence, mostly seen in teenagers or young adults
  
• contamination by “evil” or fear of becoming a “bad person”
  
• fear of harm to a newborn child by new parents
  
• fear of unintentionally performing socially inappropriate behaviors, such as shoplifting, molesting, or insulting someone.
  

A common theme among OCD patients is overwhelming distress associated with uncertainty. Patients with OCD often appraise low-probability events as extremely high-probability events, and as a result require reassurance and guarantees that dreaded outcomes will not occur. That reassurance can come in many forms:

• searching the Internet for answers
  
• asking family members, friends, or experts for confirmation or disconfirmation
  
• mentally checking and reevaluating whether they had opportunity or propensity to perform any of those acts.
  

A recent model of OCD may further advance our understanding of how obsessions and compulsions frequently appear together because of their functional link. This model clusters OCD symptoms into “symptom dimensions” that include:

• symmetry/ordering
  
• contamination/cleaning
  
• sexual/religious/aggressive/checking
  
• hoarding.^5–7
  

Multifaceted CBT

OCD is conceptualized by both behavioral and cognitive theory (Box 3). Cognitive-behavioral treatment for OCD includes:

• exposure in vivo—repeated, prolonged confrontation with anxiety-evoking stimuli
  
• repeated, prolonged imaginal confrontation with feared disasters
  
• ritual prevention—blocking or preventing compulsions
  
• cognitive interventions—correcting erroneous cognitions about potential consequences if confrontation with feared situations is not followed by “ritualizing” (engaging in compulsive behavior).
  

Imaginal exposure involves repeated confrontation (in imagination) with the disastrous consequences the patient anticipates if the rituals are not performed (eg, a parent’s children will contract a disease many years from now because of failure to protect them from harmful toxins).

Cognitive interventions involve discussing the changes that take place during in vivo and imaginal exposure, such as:

• the patient’s anxiety decreases with repeated exposure even without ritualistic behavior
  
• the feared consequences often do not materialize
  
• in some cases tolerance of uncertainty is what is being practiced.
  

Evidence supports EX/RP

Several randomized controlled trials (RCTs) have demonstrated the efficacy of EX/RP for reducing OCD symptoms.^8–10 To address the potential generalizability of these results to typical clinical practice, Franklin et al¹¹ compared findings from 4 RCTs of EX/RP with treatment outcome data from 110 outpatients receiving EX/RP. The outpatients had varying OCD severity, treatment histories, concomitant pharmacotherapy regimens, psychiatric comorbidity profiles, and ages. Following EX/RP, they achieved substantial and clinically meaningful reductions in their OCD and depressive symptoms that were comparable with those reported in the RCTs, which suggests the benefits of EX/RP are not limited to select patient samples.

Foa et al¹² compared the relative and combined efficacy of clomipramine (maximum dosage 250 mg/d) and EX/RP for treating OCD in adults. At week 12, all active treatments were more effective than placebo. EX/RP and EX/RP plus clomipramine were comparable, and both were more effective than clomipramine alone. The study also suggested that with regular supervision, treatment modalities could be successfully implemented in clinics with differing expertise.

Most OCD patients who receive an adequate selective serotonin reuptake inhibitor (SSRI) trial (Table) continue to have clinically significant OCD symptoms. Simpson et al¹³ studied 108 outpatients with OCD and found that augmenting SSRIs with EX/RP further reduces OCD symptoms and is more effective than stress management training. However, the now-standard 17 sessions of EX/RP were not sufficient to help most patients achieve minimal symptoms, defined as a Y-BOCS score ≤12. Ongoing augmentation studies are examining ways to increase OCD remission rates and achieve greater palatability, accessibility, and duration of effects.

Table

SSRIs for OCD: Recommended dosages

Using EX/RP in practice

When EX/RP was developed and studied in the 1960s and ‘70s, it was conducted daily. However, intensive OCD treatments are not always practical or readily available. This consideration prompted us to examine—in a nonrandomized study—the efficacy of a twice-weekly EX/RP program that is otherwise identical to the intensive treatment program at 3-month follow-up. Results indicated that this less intensive program was as effective as the intensive treatment.¹⁴

Less-intensive, once- or twice-weekly programs may be suitable for most OCD patients. Consider intensive EX/RP for:

• patients who wish to complete their treatment in a short period at expert centers
  
• patients for whom less intensive treatment fails to produce the desired outcome.
  

In addition to lack of adherence, other predictors of poorer outcome include:

• poor insight by the patient that the feared consequences were unrealistic¹⁶
  
• comorbid severe depression that interferes with utilization of EX/RP¹⁷
  
• family members’ expressed emotion (mainly hostility).¹⁸
  

Despite major improvements in OCD identification, treatment, and dissemination of knowledge to clinicians, the situation is far from ideal. Future research will help uncover additional factors for improving treatment outcome and portability.

Related resources

• Foa EB, Wilson R. Stop obsessing! New York, NY: Bantam Books; 2001.
  
• Abramowitz JS, Houts AC, eds. Concepts and controversies in obsessive-compulsive disorder. New York, NY: Springer; 2005.
  
• The Obsessive-Compulsive Foundation. www.ocfoundation.org
  

• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Yadin reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Foa receives research support from the American Psychiatric Association, BASF (formerly Ciba Geigy), Bristol-Myers Squibb, Cephalon, Eli Lilly and Company, Forest Pharmaceuticals, GlaxoSmithKline, Kali-Duphar, Pfizer Inc., and Solvay. She has been a speaker for the American Psychiatric Association, Forest Pharmaceuticals, GlaxoSmithKline, Jazz Pharmaceuticals, and Pfizer Inc. and a consultant to Actelion Pharmaceuticals.

Comment on this article

Exposure and response (or ritual) prevention has been shown to be effective in improving the therapeutic outlook for patients with obsessive-compulsive disorder (OCD). Yet barriers—including patient unwillingness to enter into the intensive therapy—prevent more persons with OCD from achieving an improved quality of life.

This article focuses on the clinical picture of OCD and the multifaceted cognitive-behavioral therapy (CBT) that has received the most empirical support. We also describe initiatives to make CBT more accessible to OCD patients, such as providing twice-weekly instead of daily treatment sessions.

OCD definition: Anxiety/distress

OCD is a relatively common, debilitating condition that often develops early in life (Box 1).^1,2 The obsessions of this disorder are not simply excessive worries about real-life problems. The compulsions are excessive or unreasonable and serve to reduce the discomfort associated with the obsessions. The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is the gold standard tool for quantifying OCD (Box 2).^3,4

Obsessions vs compulsions. When diagnosing and treating OCD, it is important to ascertain the functional relationship between a patient’s obsessions and compulsions and anxiety/distress:

• Obsessions give rise to anxiety/distress.
  
• Compulsions aim to reduce this anxiety/distress.
  

Box 2

OCD’s clinical picture

Classic vs nonclassic obsessions. Frequently reported obsessions in OCD include fears related to:

• contamination (dirt, germs, bodily waste, chemicals)
  
• making mistakes (locks, appliances, paperwork, decisions)
  
• having unwanted impulses (violent, sexual, religious, embarrassing)
  
• orderliness (neatness, symmetry, numbers).
  

• intrusive, irrational, or excessive worries about loss of identity, essence, or intelligence, mostly seen in teenagers or young adults
  
• contamination by “evil” or fear of becoming a “bad person”
  
• fear of harm to a newborn child by new parents
  
• fear of unintentionally performing socially inappropriate behaviors, such as shoplifting, molesting, or insulting someone.
  

A common theme among OCD patients is overwhelming distress associated with uncertainty. Patients with OCD often appraise low-probability events as extremely high-probability events, and as a result require reassurance and guarantees that dreaded outcomes will not occur. That reassurance can come in many forms:

• searching the Internet for answers
  
• asking family members, friends, or experts for confirmation or disconfirmation
  
• mentally checking and reevaluating whether they had opportunity or propensity to perform any of those acts.
  

A recent model of OCD may further advance our understanding of how obsessions and compulsions frequently appear together because of their functional link. This model clusters OCD symptoms into “symptom dimensions” that include:

• symmetry/ordering
  
• contamination/cleaning
  
• sexual/religious/aggressive/checking
  
• hoarding.^5–7
  

Multifaceted CBT

OCD is conceptualized by both behavioral and cognitive theory (Box 3). Cognitive-behavioral treatment for OCD includes:

• exposure in vivo—repeated, prolonged confrontation with anxiety-evoking stimuli
  
• repeated, prolonged imaginal confrontation with feared disasters
  
• ritual prevention—blocking or preventing compulsions
  
• cognitive interventions—correcting erroneous cognitions about potential consequences if confrontation with feared situations is not followed by “ritualizing” (engaging in compulsive behavior).
  

Imaginal exposure involves repeated confrontation (in imagination) with the disastrous consequences the patient anticipates if the rituals are not performed (eg, a parent’s children will contract a disease many years from now because of failure to protect them from harmful toxins).

Cognitive interventions involve discussing the changes that take place during in vivo and imaginal exposure, such as:

• the patient’s anxiety decreases with repeated exposure even without ritualistic behavior
  
• the feared consequences often do not materialize
  
• in some cases tolerance of uncertainty is what is being practiced.
  

Evidence supports EX/RP

Several randomized controlled trials (RCTs) have demonstrated the efficacy of EX/RP for reducing OCD symptoms.^8–10 To address the potential generalizability of these results to typical clinical practice, Franklin et al¹¹ compared findings from 4 RCTs of EX/RP with treatment outcome data from 110 outpatients receiving EX/RP. The outpatients had varying OCD severity, treatment histories, concomitant pharmacotherapy regimens, psychiatric comorbidity profiles, and ages. Following EX/RP, they achieved substantial and clinically meaningful reductions in their OCD and depressive symptoms that were comparable with those reported in the RCTs, which suggests the benefits of EX/RP are not limited to select patient samples.

Foa et al¹² compared the relative and combined efficacy of clomipramine (maximum dosage 250 mg/d) and EX/RP for treating OCD in adults. At week 12, all active treatments were more effective than placebo. EX/RP and EX/RP plus clomipramine were comparable, and both were more effective than clomipramine alone. The study also suggested that with regular supervision, treatment modalities could be successfully implemented in clinics with differing expertise.

Most OCD patients who receive an adequate selective serotonin reuptake inhibitor (SSRI) trial (Table) continue to have clinically significant OCD symptoms. Simpson et al¹³ studied 108 outpatients with OCD and found that augmenting SSRIs with EX/RP further reduces OCD symptoms and is more effective than stress management training. However, the now-standard 17 sessions of EX/RP were not sufficient to help most patients achieve minimal symptoms, defined as a Y-BOCS score ≤12. Ongoing augmentation studies are examining ways to increase OCD remission rates and achieve greater palatability, accessibility, and duration of effects.

Table

SSRIs for OCD: Recommended dosages

Using EX/RP in practice

When EX/RP was developed and studied in the 1960s and ‘70s, it was conducted daily. However, intensive OCD treatments are not always practical or readily available. This consideration prompted us to examine—in a nonrandomized study—the efficacy of a twice-weekly EX/RP program that is otherwise identical to the intensive treatment program at 3-month follow-up. Results indicated that this less intensive program was as effective as the intensive treatment.¹⁴

Less-intensive, once- or twice-weekly programs may be suitable for most OCD patients. Consider intensive EX/RP for:

• patients who wish to complete their treatment in a short period at expert centers
  
• patients for whom less intensive treatment fails to produce the desired outcome.
  

In addition to lack of adherence, other predictors of poorer outcome include:

• poor insight by the patient that the feared consequences were unrealistic¹⁶
  
• comorbid severe depression that interferes with utilization of EX/RP¹⁷
  
• family members’ expressed emotion (mainly hostility).¹⁸
  

Despite major improvements in OCD identification, treatment, and dissemination of knowledge to clinicians, the situation is far from ideal. Future research will help uncover additional factors for improving treatment outcome and portability.

Related resources

• Foa EB, Wilson R. Stop obsessing! New York, NY: Bantam Books; 2001.
  
• Abramowitz JS, Houts AC, eds. Concepts and controversies in obsessive-compulsive disorder. New York, NY: Springer; 2005.
  
• The Obsessive-Compulsive Foundation. www.ocfoundation.org
  

• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Yadin reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Foa receives research support from the American Psychiatric Association, BASF (formerly Ciba Geigy), Bristol-Myers Squibb, Cephalon, Eli Lilly and Company, Forest Pharmaceuticals, GlaxoSmithKline, Kali-Duphar, Pfizer Inc., and Solvay. She has been a speaker for the American Psychiatric Association, Forest Pharmaceuticals, GlaxoSmithKline, Jazz Pharmaceuticals, and Pfizer Inc. and a consultant to Actelion Pharmaceuticals.

Comment on this article

Exposure and response (or ritual) prevention has been shown to be effective in improving the therapeutic outlook for patients with obsessive-compulsive disorder (OCD). Yet barriers—including patient unwillingness to enter into the intensive therapy—prevent more persons with OCD from achieving an improved quality of life.

This article focuses on the clinical picture of OCD and the multifaceted cognitive-behavioral therapy (CBT) that has received the most empirical support. We also describe initiatives to make CBT more accessible to OCD patients, such as providing twice-weekly instead of daily treatment sessions.

OCD definition: Anxiety/distress

OCD is a relatively common, debilitating condition that often develops early in life (Box 1).^1,2 The obsessions of this disorder are not simply excessive worries about real-life problems. The compulsions are excessive or unreasonable and serve to reduce the discomfort associated with the obsessions. The Yale-Brown Obsessive Compulsive Scale (Y-BOCS) is the gold standard tool for quantifying OCD (Box 2).^3,4

Obsessions vs compulsions. When diagnosing and treating OCD, it is important to ascertain the functional relationship between a patient’s obsessions and compulsions and anxiety/distress:

• Obsessions give rise to anxiety/distress.
  
• Compulsions aim to reduce this anxiety/distress.
  

Box 2

OCD’s clinical picture

Classic vs nonclassic obsessions. Frequently reported obsessions in OCD include fears related to:

• contamination (dirt, germs, bodily waste, chemicals)
  
• making mistakes (locks, appliances, paperwork, decisions)
  
• having unwanted impulses (violent, sexual, religious, embarrassing)
  
• orderliness (neatness, symmetry, numbers).
  

• intrusive, irrational, or excessive worries about loss of identity, essence, or intelligence, mostly seen in teenagers or young adults
  
• contamination by “evil” or fear of becoming a “bad person”
  
• fear of harm to a newborn child by new parents
  
• fear of unintentionally performing socially inappropriate behaviors, such as shoplifting, molesting, or insulting someone.
  

A common theme among OCD patients is overwhelming distress associated with uncertainty. Patients with OCD often appraise low-probability events as extremely high-probability events, and as a result require reassurance and guarantees that dreaded outcomes will not occur. That reassurance can come in many forms:

• searching the Internet for answers
  
• asking family members, friends, or experts for confirmation or disconfirmation
  
• mentally checking and reevaluating whether they had opportunity or propensity to perform any of those acts.
  

A recent model of OCD may further advance our understanding of how obsessions and compulsions frequently appear together because of their functional link. This model clusters OCD symptoms into “symptom dimensions” that include:

• symmetry/ordering
  
• contamination/cleaning
  
• sexual/religious/aggressive/checking
  
• hoarding.^5–7
  

Multifaceted CBT

OCD is conceptualized by both behavioral and cognitive theory (Box 3). Cognitive-behavioral treatment for OCD includes:

• exposure in vivo—repeated, prolonged confrontation with anxiety-evoking stimuli
  
• repeated, prolonged imaginal confrontation with feared disasters
  
• ritual prevention—blocking or preventing compulsions
  
• cognitive interventions—correcting erroneous cognitions about potential consequences if confrontation with feared situations is not followed by “ritualizing” (engaging in compulsive behavior).
  

Imaginal exposure involves repeated confrontation (in imagination) with the disastrous consequences the patient anticipates if the rituals are not performed (eg, a parent’s children will contract a disease many years from now because of failure to protect them from harmful toxins).

Cognitive interventions involve discussing the changes that take place during in vivo and imaginal exposure, such as:

• the patient’s anxiety decreases with repeated exposure even without ritualistic behavior
  
• the feared consequences often do not materialize
  
• in some cases tolerance of uncertainty is what is being practiced.
  

Evidence supports EX/RP

Several randomized controlled trials (RCTs) have demonstrated the efficacy of EX/RP for reducing OCD symptoms.^8–10 To address the potential generalizability of these results to typical clinical practice, Franklin et al¹¹ compared findings from 4 RCTs of EX/RP with treatment outcome data from 110 outpatients receiving EX/RP. The outpatients had varying OCD severity, treatment histories, concomitant pharmacotherapy regimens, psychiatric comorbidity profiles, and ages. Following EX/RP, they achieved substantial and clinically meaningful reductions in their OCD and depressive symptoms that were comparable with those reported in the RCTs, which suggests the benefits of EX/RP are not limited to select patient samples.

Foa et al¹² compared the relative and combined efficacy of clomipramine (maximum dosage 250 mg/d) and EX/RP for treating OCD in adults. At week 12, all active treatments were more effective than placebo. EX/RP and EX/RP plus clomipramine were comparable, and both were more effective than clomipramine alone. The study also suggested that with regular supervision, treatment modalities could be successfully implemented in clinics with differing expertise.

Most OCD patients who receive an adequate selective serotonin reuptake inhibitor (SSRI) trial (Table) continue to have clinically significant OCD symptoms. Simpson et al¹³ studied 108 outpatients with OCD and found that augmenting SSRIs with EX/RP further reduces OCD symptoms and is more effective than stress management training. However, the now-standard 17 sessions of EX/RP were not sufficient to help most patients achieve minimal symptoms, defined as a Y-BOCS score ≤12. Ongoing augmentation studies are examining ways to increase OCD remission rates and achieve greater palatability, accessibility, and duration of effects.

Table

SSRIs for OCD: Recommended dosages

Using EX/RP in practice

When EX/RP was developed and studied in the 1960s and ‘70s, it was conducted daily. However, intensive OCD treatments are not always practical or readily available. This consideration prompted us to examine—in a nonrandomized study—the efficacy of a twice-weekly EX/RP program that is otherwise identical to the intensive treatment program at 3-month follow-up. Results indicated that this less intensive program was as effective as the intensive treatment.¹⁴

Less-intensive, once- or twice-weekly programs may be suitable for most OCD patients. Consider intensive EX/RP for:

• patients who wish to complete their treatment in a short period at expert centers
  
• patients for whom less intensive treatment fails to produce the desired outcome.
  

In addition to lack of adherence, other predictors of poorer outcome include:

• poor insight by the patient that the feared consequences were unrealistic¹⁶
  
• comorbid severe depression that interferes with utilization of EX/RP¹⁷
  
• family members’ expressed emotion (mainly hostility).¹⁸
  

Despite major improvements in OCD identification, treatment, and dissemination of knowledge to clinicians, the situation is far from ideal. Future research will help uncover additional factors for improving treatment outcome and portability.

Related resources

• Foa EB, Wilson R. Stop obsessing! New York, NY: Bantam Books; 2001.
  
• Abramowitz JS, Houts AC, eds. Concepts and controversies in obsessive-compulsive disorder. New York, NY: Springer; 2005.
  
• The Obsessive-Compulsive Foundation. www.ocfoundation.org
  

• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  

Dr. Yadin reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Foa receives research support from the American Psychiatric Association, BASF (formerly Ciba Geigy), Bristol-Myers Squibb, Cephalon, Eli Lilly and Company, Forest Pharmaceuticals, GlaxoSmithKline, Kali-Duphar, Pfizer Inc., and Solvay. She has been a speaker for the American Psychiatric Association, Forest Pharmaceuticals, GlaxoSmithKline, Jazz Pharmaceuticals, and Pfizer Inc. and a consultant to Actelion Pharmaceuticals.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.

Psychogenic polydipsia (PPD) is a chronic, relapsing, and potentially life-threatening disorder characterized by compulsive consumption of large quantities of water resulting in “delutional hyponatremia.” PPD occurs in 6% to 20% of psychiatric patients, most often with schizophrenia.¹

In most patients with PPD, an electrolyte disturbance remains asymptomatic. However, superimposed and sudden ingestion of 3 to 4 liters of water can rapidly further dilute plasma and overwhelm the body’s compensatory reserves, leading to brain edema, seizures, coma, and even death.

The following prevention and treatment strategies might reduce morbidity and mortality in hospitalized patients diagnosed with PPD and lessen the cost of treating this serious illness.

Develop rapport. Understand that your patient has little control over his or her compulsive water intake. Remain nonjudgmental to help gain your patient’s trust.

Inquire about underlying psychiatric symptoms that might contribute to PPD. Does your patient have an overwhelming anxiety, delusional belief, or both? Effectively targeting specific symptoms will improve your chances of success.

Encourage communication among treatment team members. PPD patients are notoriously creative in sneaking water from unexpected places such as toilets and shower rooms. Staff vigilance is required to detect and prevent such clandestine behaviors.

Consult with an internist when necessary, especially if your patient has a comorbid cardiac condition that requires a low-sodium diet and/or diuretics.

Review psychotropic medications. In case reports of schizophrenia patients with PPD, switching from a typical to an atypical antipsychotic has shown efficacy in treating PPD.²

Restricting fluids to 2 to 3 liters a day combined with “a token economy”—a method of positive reinforcement to increase desired behavior—has been used to successfully treat the disorder.²

Monitor adherence by weighing patients twice a day and checking serum sodium levels frequently. Normal water retention is cyclic and peaks in the early afternoon; therefore, early-morning screening for hyponatremia may not accurately reflect the severity of water abuse. A diurnal weight gain of ≥0.6% is unusual and might point to PPD.²

Consider administering an angiotensin-converting enzyme (ACE) inhibitor. In clinical trials 60% of patients taking ACE inhibitors show decreased water consumption.²

Order 24-hour, 1-to-1 observation if you suspect continuous water abuse.

Think about placing a patient with severe PPD in a locked unit in a long-term psychiatric institution, away from all water sources.

As Internet use grows, so has patient demand for e-mail access to their physicians. Using e-mail in psychiatric practice has many advantages but also some unique drawbacks.

Advantages

For you, e-mail’s advantages include:

• decreased “phone tag” with patients
  
• ability to respond to requests at your convenience
  
• an automatically generated medical record¹
  
• easy distribution of handouts and references to patients, eliminating the need to store paper copies.
  

E-mail’s advantages for patients include:

• increased satisfaction and participation in care
  
• convenience
  
• better understanding of instructions that can be reread vs verbal information that might not be recalled.
  

For example, a patient of mine with a history of trauma dropped out of treatment after revealing aspects of the trauma early in therapy. He did not respond to my phone calls, but after several weeks he unexpectedly e-mailed me. After an e-mail exchange about what happened, he returned to therapy and came weekly for several years. I feel this positive outcome occurred because he could contact me in a way that provided him a sense of distance, control, and safety.

E-mail guidelines

Potential risk of malpractice is a drawback of using e-mail in clinical practice. Malpractice by definition requires 2 elements:

• a patient-physician relationship—which unsolicited e-mail likely can establish if a physician gives advice that the patient takes²
  
• a breach of duty that results in harm to the patient.
  

Don’t diagnose or treat by e-mail

Diagnosis and treatment via e-mail could be considered substandard care. Patients might not be forthcoming about symptoms in an e-mail, either because of concerns about how symptoms might be perceived or poor insight. The lack of auditory and visual cues makes proper assessment difficult and can increase the risk of misdiagnosis and inappropriate treatment.² This is especially true in psychiatry, where diagnosis can rely heavily on analyzing a patient’s physical presentation, including psychomotor behavior, affect, and speech patterns.

For example, if a patient you are treating with a selective serotonin reuptake inhibitor for a depressive episode e-mails you about feeling anxiety in the presence of others, it may be tempting to diagnose a comorbid anxiety disorder. However, anxious feelings also can be caused by paranoia related to an evolving first lifetime episode of mania with psychotic features. Clues to this diagnosis—such as expansive affect, pressured speech, and psychomotor agitation—might be detected during an in-person assessment but missed in an e-mail.

For this reason, avoid making new diagnostic assessments or changing a treatment plan based on an e-mail exchange. If you are tempted to do so, call the patient to discuss the issue or ask him or her to come in for an office visit.

Set e-mail boundaries

Using e-mail in clinical practice could be time-consuming, adding extra work to already packed days. A subset of patients—such as those with personality disorders—might e-mail excessively, bring up subjects that are inappropriate for e-mail, or try to build permeable boundaries into the patient-physician relationship. Minimize these concerns by clearly outlining which topics are and are not appropriate for e-mail.³

Table

6 strategies to minimize liability when using e-mail

Inappropriate use of e-mail can be addressed during a session as you would any other transference-countertransference or boundary issue, potentially yielding important therapeutic gains.

As Internet use grows, so has patient demand for e-mail access to their physicians. Using e-mail in psychiatric practice has many advantages but also some unique drawbacks.

Advantages

For you, e-mail’s advantages include:

• decreased “phone tag” with patients
  
• ability to respond to requests at your convenience
  
• an automatically generated medical record¹
  
• easy distribution of handouts and references to patients, eliminating the need to store paper copies.
  

E-mail’s advantages for patients include:

• increased satisfaction and participation in care
  
• convenience
  
• better understanding of instructions that can be reread vs verbal information that might not be recalled.
  

For example, a patient of mine with a history of trauma dropped out of treatment after revealing aspects of the trauma early in therapy. He did not respond to my phone calls, but after several weeks he unexpectedly e-mailed me. After an e-mail exchange about what happened, he returned to therapy and came weekly for several years. I feel this positive outcome occurred because he could contact me in a way that provided him a sense of distance, control, and safety.

E-mail guidelines

Potential risk of malpractice is a drawback of using e-mail in clinical practice. Malpractice by definition requires 2 elements:

• a patient-physician relationship—which unsolicited e-mail likely can establish if a physician gives advice that the patient takes²
  
• a breach of duty that results in harm to the patient.
  

Don’t diagnose or treat by e-mail

Diagnosis and treatment via e-mail could be considered substandard care. Patients might not be forthcoming about symptoms in an e-mail, either because of concerns about how symptoms might be perceived or poor insight. The lack of auditory and visual cues makes proper assessment difficult and can increase the risk of misdiagnosis and inappropriate treatment.² This is especially true in psychiatry, where diagnosis can rely heavily on analyzing a patient’s physical presentation, including psychomotor behavior, affect, and speech patterns.

For example, if a patient you are treating with a selective serotonin reuptake inhibitor for a depressive episode e-mails you about feeling anxiety in the presence of others, it may be tempting to diagnose a comorbid anxiety disorder. However, anxious feelings also can be caused by paranoia related to an evolving first lifetime episode of mania with psychotic features. Clues to this diagnosis—such as expansive affect, pressured speech, and psychomotor agitation—might be detected during an in-person assessment but missed in an e-mail.

For this reason, avoid making new diagnostic assessments or changing a treatment plan based on an e-mail exchange. If you are tempted to do so, call the patient to discuss the issue or ask him or her to come in for an office visit.

Set e-mail boundaries

Using e-mail in clinical practice could be time-consuming, adding extra work to already packed days. A subset of patients—such as those with personality disorders—might e-mail excessively, bring up subjects that are inappropriate for e-mail, or try to build permeable boundaries into the patient-physician relationship. Minimize these concerns by clearly outlining which topics are and are not appropriate for e-mail.³

Table

6 strategies to minimize liability when using e-mail

Inappropriate use of e-mail can be addressed during a session as you would any other transference-countertransference or boundary issue, potentially yielding important therapeutic gains.

As Internet use grows, so has patient demand for e-mail access to their physicians. Using e-mail in psychiatric practice has many advantages but also some unique drawbacks.

Advantages

For you, e-mail’s advantages include:

• decreased “phone tag” with patients
  
• ability to respond to requests at your convenience
  
• an automatically generated medical record¹
  
• easy distribution of handouts and references to patients, eliminating the need to store paper copies.
  

E-mail’s advantages for patients include:

• increased satisfaction and participation in care
  
• convenience
  
• better understanding of instructions that can be reread vs verbal information that might not be recalled.
  

For example, a patient of mine with a history of trauma dropped out of treatment after revealing aspects of the trauma early in therapy. He did not respond to my phone calls, but after several weeks he unexpectedly e-mailed me. After an e-mail exchange about what happened, he returned to therapy and came weekly for several years. I feel this positive outcome occurred because he could contact me in a way that provided him a sense of distance, control, and safety.

E-mail guidelines

Potential risk of malpractice is a drawback of using e-mail in clinical practice. Malpractice by definition requires 2 elements:

• a patient-physician relationship—which unsolicited e-mail likely can establish if a physician gives advice that the patient takes²
  
• a breach of duty that results in harm to the patient.
  

Don’t diagnose or treat by e-mail

Diagnosis and treatment via e-mail could be considered substandard care. Patients might not be forthcoming about symptoms in an e-mail, either because of concerns about how symptoms might be perceived or poor insight. The lack of auditory and visual cues makes proper assessment difficult and can increase the risk of misdiagnosis and inappropriate treatment.² This is especially true in psychiatry, where diagnosis can rely heavily on analyzing a patient’s physical presentation, including psychomotor behavior, affect, and speech patterns.

For example, if a patient you are treating with a selective serotonin reuptake inhibitor for a depressive episode e-mails you about feeling anxiety in the presence of others, it may be tempting to diagnose a comorbid anxiety disorder. However, anxious feelings also can be caused by paranoia related to an evolving first lifetime episode of mania with psychotic features. Clues to this diagnosis—such as expansive affect, pressured speech, and psychomotor agitation—might be detected during an in-person assessment but missed in an e-mail.

For this reason, avoid making new diagnostic assessments or changing a treatment plan based on an e-mail exchange. If you are tempted to do so, call the patient to discuss the issue or ask him or her to come in for an office visit.

Set e-mail boundaries

Using e-mail in clinical practice could be time-consuming, adding extra work to already packed days. A subset of patients—such as those with personality disorders—might e-mail excessively, bring up subjects that are inappropriate for e-mail, or try to build permeable boundaries into the patient-physician relationship. Minimize these concerns by clearly outlining which topics are and are not appropriate for e-mail.³

Table

6 strategies to minimize liability when using e-mail

Inappropriate use of e-mail can be addressed during a session as you would any other transference-countertransference or boundary issue, potentially yielding important therapeutic gains.

Dr. Gagliardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Principal Source: Johnson L, Sabel A, Burman WJ, et al. Emergence of fluoroquinolone resistance in outpatient urinary Escherichia coli isolates. Am J Med. 2008;121:876-884.

More than 8 million urinary tract infections (UTIs) are diagnosed annually in the United States¹ and UTI is thought to be the most common bacterial infection.² Half of all women report having a UTI at some time in their lives.^2,3 UTI is rare in men, occurring in an estimated 5 to 8 of every 10,000 young to middle-aged men,⁴ but increases with age such that UTI rates in men age >70 are approximately one-third the rates in women.²

Up to 85% percent of UTIs are attributed to Escherichia coli.³ The hallmark symptoms of bacterial cystitis are dysuria and urinary frequency; additional symptoms include urgency, suprapubic pain, and hematuria.⁵

Being familiar with UTI symptoms can help expedite diagnosis and treatment because you might be a psychiatric patient’s primary contact with the healthcare system. Also, psychiatric inpatients could test positive for UTIs during routine medical screening. A 1-day urinalysis study of psychiatric inpatients without urinary catheters detected UTIs in approximately 5% of patients.⁶ In addition, UTI is a common cause of delirium.

Screening

The utility of routine screening urinalysis is under debate, and testing is best used in cases of suspected UTI. However, medical disorders frequently are not recognized in psychiatric patients, especially in older patients⁷ or those with risk factors for UTI. Sexually transmitted diseases (STDs) are not major contributors to UTI risk; however, they may share common symptoms and urinalysis findings. If patients report symptoms of UTI (urgency, dysuria, frequency), urinalysis is indicated. In a urinalysis, >2 to 5 leukocytes per high-powered field in an uncontaminated centrifuged urine specimen without a high number of squamous epithelial cells suggest UTI.

In patients with abnormal urinalysis, ask about dysuria, urinary frequency, history of UTIs, and use of antibiotics. Antibiotic use in the preceding 12 months is associated with increased risk of bacterial resistance.¹ Assess for symptoms of complicated UTI such as fever, flank pain, nausea, and vomiting. Urine culture is not recommended for uncomplicated UTI but may be necessary when symptoms do not resolve or signs of complicated UTI emerge. Consider possible STDs in patients with sterile pyuria.⁵

Treatment and antibiotic resistance

For patients with uncomplicated UTI, a short course of empiric antibiotics is appropriate even in the absence of confirmatory culture data. Fluoroquinolones (FQs), such as ciprofloxacin and levofloxacin, have been used as a first-line treatment. However, FQs are associated with:

• QTc-prolongation, a concern when co-administered with antipsychotics⁸
• delirium
• increased risk of tendinitis and tendon rupture⁹
• antibiotic resistance.

A study of a comprehensive urban public health system in Denver, CO, showed that rates of FQ-resistant E coli increased after levofloxacin was established as first-line therapy for UTIs. This occurred after E coli strains developed high resistance to an earlier first-line therapy, trimethoprim/sulfamethoxazole (TMP/SMZ).¹ Using pharmacy and laboratory databases, investigators found that as levofloxacin prescriptions increased, rates of FQ-resistant E coli rose almost 10-fold, from 1% in 1999 to 9.4% in 2005. A detailed analysis of 2005 E coli isolates showed that previous levofloxacin prescription was strongly associated with FQ resistance (odds ratio 5.6, 95% confidence interval: 2.1 to 27.5). Levofloxacin-resistant strains of E coli also were more likely than levofloxacin-sensitive strains to be resistant to other antibiotics—90% compared with 43% for control specimens (Table).

Table

Antibiotic resistance among levofloxacin-resistant and levofloxacin-susceptible strains of E coli*

The use of FQs as first-line treatment of UTIs also is leading to resistant strains of Streptococcus pneumoniae,¹⁰ Salmonella,^11,12 Neisseria meningitides,¹³ and other bacteria. From an individual and public health perspective, it is important that psychiatrists monitor local resistance patterns and treatment recommendations.

In areas without widespread bacterial resistance to TMP/SMZ, a 3-day course of TMP/SMZ could be considered first-line treatment for uncomplicated UTI in patients without allergies or contraindications. However, in areas where resistance to TMP/SMZ is high, a 7-day course of nitrofurantoin is recommended for uncomplicated cystitis. Resistance patterns can vary from hospital to hospital and even among units in the same hospital;¹⁴ therefore, refer to local microbiology labs for “antibiograms” or information regarding resistance patterns.

Related resource

• National Guideline Clearinghouse. Urinary tract infection. www.guidelines.gov/summary/summary.aspx?doc_id=7407.

Drug brand names

• Ampicillin • Principen
• Cefazolin • Ancef
• Ceftriaxone • Rocephin
• Ciprofloxacin • Ciloxan, Cipro, Cipro XR, ProQuin XR
• Gentamicin • Garamycin
• Levofloxacin • Levaquin
• Nitrofurantoin • Furadantin, Macrodantin, Macrobid, Urotoin
• Trimethoprim/Sulfamethoxazole • Bacter-Aid DS, Bactrim, Septra, Sulfatrim, Sultrex
• Tobramycin • Nebcin

Disclosure

Dr. Gagliardi reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Gagliardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Principal Source: Johnson L, Sabel A, Burman WJ, et al. Emergence of fluoroquinolone resistance in outpatient urinary Escherichia coli isolates. Am J Med. 2008;121:876-884.

More than 8 million urinary tract infections (UTIs) are diagnosed annually in the United States¹ and UTI is thought to be the most common bacterial infection.² Half of all women report having a UTI at some time in their lives.^2,3 UTI is rare in men, occurring in an estimated 5 to 8 of every 10,000 young to middle-aged men,⁴ but increases with age such that UTI rates in men age >70 are approximately one-third the rates in women.²

Up to 85% percent of UTIs are attributed to Escherichia coli.³ The hallmark symptoms of bacterial cystitis are dysuria and urinary frequency; additional symptoms include urgency, suprapubic pain, and hematuria.⁵

Being familiar with UTI symptoms can help expedite diagnosis and treatment because you might be a psychiatric patient’s primary contact with the healthcare system. Also, psychiatric inpatients could test positive for UTIs during routine medical screening. A 1-day urinalysis study of psychiatric inpatients without urinary catheters detected UTIs in approximately 5% of patients.⁶ In addition, UTI is a common cause of delirium.

Screening

The utility of routine screening urinalysis is under debate, and testing is best used in cases of suspected UTI. However, medical disorders frequently are not recognized in psychiatric patients, especially in older patients⁷ or those with risk factors for UTI. Sexually transmitted diseases (STDs) are not major contributors to UTI risk; however, they may share common symptoms and urinalysis findings. If patients report symptoms of UTI (urgency, dysuria, frequency), urinalysis is indicated. In a urinalysis, >2 to 5 leukocytes per high-powered field in an uncontaminated centrifuged urine specimen without a high number of squamous epithelial cells suggest UTI.

In patients with abnormal urinalysis, ask about dysuria, urinary frequency, history of UTIs, and use of antibiotics. Antibiotic use in the preceding 12 months is associated with increased risk of bacterial resistance.¹ Assess for symptoms of complicated UTI such as fever, flank pain, nausea, and vomiting. Urine culture is not recommended for uncomplicated UTI but may be necessary when symptoms do not resolve or signs of complicated UTI emerge. Consider possible STDs in patients with sterile pyuria.⁵

Treatment and antibiotic resistance

For patients with uncomplicated UTI, a short course of empiric antibiotics is appropriate even in the absence of confirmatory culture data. Fluoroquinolones (FQs), such as ciprofloxacin and levofloxacin, have been used as a first-line treatment. However, FQs are associated with:

• QTc-prolongation, a concern when co-administered with antipsychotics⁸
• delirium
• increased risk of tendinitis and tendon rupture⁹
• antibiotic resistance.

A study of a comprehensive urban public health system in Denver, CO, showed that rates of FQ-resistant E coli increased after levofloxacin was established as first-line therapy for UTIs. This occurred after E coli strains developed high resistance to an earlier first-line therapy, trimethoprim/sulfamethoxazole (TMP/SMZ).¹ Using pharmacy and laboratory databases, investigators found that as levofloxacin prescriptions increased, rates of FQ-resistant E coli rose almost 10-fold, from 1% in 1999 to 9.4% in 2005. A detailed analysis of 2005 E coli isolates showed that previous levofloxacin prescription was strongly associated with FQ resistance (odds ratio 5.6, 95% confidence interval: 2.1 to 27.5). Levofloxacin-resistant strains of E coli also were more likely than levofloxacin-sensitive strains to be resistant to other antibiotics—90% compared with 43% for control specimens (Table).

Table

Antibiotic resistance among levofloxacin-resistant and levofloxacin-susceptible strains of E coli*

The use of FQs as first-line treatment of UTIs also is leading to resistant strains of Streptococcus pneumoniae,¹⁰ Salmonella,^11,12 Neisseria meningitides,¹³ and other bacteria. From an individual and public health perspective, it is important that psychiatrists monitor local resistance patterns and treatment recommendations.

In areas without widespread bacterial resistance to TMP/SMZ, a 3-day course of TMP/SMZ could be considered first-line treatment for uncomplicated UTI in patients without allergies or contraindications. However, in areas where resistance to TMP/SMZ is high, a 7-day course of nitrofurantoin is recommended for uncomplicated cystitis. Resistance patterns can vary from hospital to hospital and even among units in the same hospital;¹⁴ therefore, refer to local microbiology labs for “antibiograms” or information regarding resistance patterns.

Related resource

• National Guideline Clearinghouse. Urinary tract infection. www.guidelines.gov/summary/summary.aspx?doc_id=7407.

Drug brand names

• Ampicillin • Principen
• Cefazolin • Ancef
• Ceftriaxone • Rocephin
• Ciprofloxacin • Ciloxan, Cipro, Cipro XR, ProQuin XR
• Gentamicin • Garamycin
• Levofloxacin • Levaquin
• Nitrofurantoin • Furadantin, Macrodantin, Macrobid, Urotoin
• Trimethoprim/Sulfamethoxazole • Bacter-Aid DS, Bactrim, Septra, Sulfatrim, Sultrex
• Tobramycin • Nebcin

Disclosure

Dr. Gagliardi reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Gagliardi is assistant professor of psychiatry and behavioral sciences and assistant clinical professor of medicine, Duke University School of Medicine, Durham, NC.

Principal Source: Johnson L, Sabel A, Burman WJ, et al. Emergence of fluoroquinolone resistance in outpatient urinary Escherichia coli isolates. Am J Med. 2008;121:876-884.

More than 8 million urinary tract infections (UTIs) are diagnosed annually in the United States¹ and UTI is thought to be the most common bacterial infection.² Half of all women report having a UTI at some time in their lives.^2,3 UTI is rare in men, occurring in an estimated 5 to 8 of every 10,000 young to middle-aged men,⁴ but increases with age such that UTI rates in men age >70 are approximately one-third the rates in women.²

Up to 85% percent of UTIs are attributed to Escherichia coli.³ The hallmark symptoms of bacterial cystitis are dysuria and urinary frequency; additional symptoms include urgency, suprapubic pain, and hematuria.⁵

Being familiar with UTI symptoms can help expedite diagnosis and treatment because you might be a psychiatric patient’s primary contact with the healthcare system. Also, psychiatric inpatients could test positive for UTIs during routine medical screening. A 1-day urinalysis study of psychiatric inpatients without urinary catheters detected UTIs in approximately 5% of patients.⁶ In addition, UTI is a common cause of delirium.

Screening

The utility of routine screening urinalysis is under debate, and testing is best used in cases of suspected UTI. However, medical disorders frequently are not recognized in psychiatric patients, especially in older patients⁷ or those with risk factors for UTI. Sexually transmitted diseases (STDs) are not major contributors to UTI risk; however, they may share common symptoms and urinalysis findings. If patients report symptoms of UTI (urgency, dysuria, frequency), urinalysis is indicated. In a urinalysis, >2 to 5 leukocytes per high-powered field in an uncontaminated centrifuged urine specimen without a high number of squamous epithelial cells suggest UTI.

In patients with abnormal urinalysis, ask about dysuria, urinary frequency, history of UTIs, and use of antibiotics. Antibiotic use in the preceding 12 months is associated with increased risk of bacterial resistance.¹ Assess for symptoms of complicated UTI such as fever, flank pain, nausea, and vomiting. Urine culture is not recommended for uncomplicated UTI but may be necessary when symptoms do not resolve or signs of complicated UTI emerge. Consider possible STDs in patients with sterile pyuria.⁵

Treatment and antibiotic resistance

For patients with uncomplicated UTI, a short course of empiric antibiotics is appropriate even in the absence of confirmatory culture data. Fluoroquinolones (FQs), such as ciprofloxacin and levofloxacin, have been used as a first-line treatment. However, FQs are associated with:

• QTc-prolongation, a concern when co-administered with antipsychotics⁸
• delirium
• increased risk of tendinitis and tendon rupture⁹
• antibiotic resistance.

A study of a comprehensive urban public health system in Denver, CO, showed that rates of FQ-resistant E coli increased after levofloxacin was established as first-line therapy for UTIs. This occurred after E coli strains developed high resistance to an earlier first-line therapy, trimethoprim/sulfamethoxazole (TMP/SMZ).¹ Using pharmacy and laboratory databases, investigators found that as levofloxacin prescriptions increased, rates of FQ-resistant E coli rose almost 10-fold, from 1% in 1999 to 9.4% in 2005. A detailed analysis of 2005 E coli isolates showed that previous levofloxacin prescription was strongly associated with FQ resistance (odds ratio 5.6, 95% confidence interval: 2.1 to 27.5). Levofloxacin-resistant strains of E coli also were more likely than levofloxacin-sensitive strains to be resistant to other antibiotics—90% compared with 43% for control specimens (Table).

Table

Antibiotic resistance among levofloxacin-resistant and levofloxacin-susceptible strains of E coli*

The use of FQs as first-line treatment of UTIs also is leading to resistant strains of Streptococcus pneumoniae,¹⁰ Salmonella,^11,12 Neisseria meningitides,¹³ and other bacteria. From an individual and public health perspective, it is important that psychiatrists monitor local resistance patterns and treatment recommendations.

In areas without widespread bacterial resistance to TMP/SMZ, a 3-day course of TMP/SMZ could be considered first-line treatment for uncomplicated UTI in patients without allergies or contraindications. However, in areas where resistance to TMP/SMZ is high, a 7-day course of nitrofurantoin is recommended for uncomplicated cystitis. Resistance patterns can vary from hospital to hospital and even among units in the same hospital;¹⁴ therefore, refer to local microbiology labs for “antibiograms” or information regarding resistance patterns.

Related resource

• National Guideline Clearinghouse. Urinary tract infection. www.guidelines.gov/summary/summary.aspx?doc_id=7407.

Drug brand names

• Ampicillin • Principen
• Cefazolin • Ancef
• Ceftriaxone • Rocephin
• Ciprofloxacin • Ciloxan, Cipro, Cipro XR, ProQuin XR
• Gentamicin • Garamycin
• Levofloxacin • Levaquin
• Nitrofurantoin • Furadantin, Macrodantin, Macrobid, Urotoin
• Trimethoprim/Sulfamethoxazole • Bacter-Aid DS, Bactrim, Septra, Sulfatrim, Sultrex
• Tobramycin • Nebcin

Disclosure

Dr. Gagliardi reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Thank you for bringing the issue of measurement-based psychiatric practice to light (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). As nurse practitioners, we were strictly taught to elaborate on psychiatric symptoms and progress, which is why the notes are called “progress notes” and not “shorthand notes.” I use blank forms of various modified scales—such as the Hamilton Rating Scale for Depression and Positive and Negative Syndrome Scale—and I checkmark and write all 4 axis and global assessment of functioning scores. These objective findings include a short version of the mental status exam. On the top of the chart, I note subjective symptoms. I never use general syntax such as “Pt. is improving, doing well.” Also, I utilize a 0-to-10 scale for overall improvement, with 0 being the worst and 10 being no symptoms.

In my treatment plan, I state which symptoms have resolved and which have not. My psychiatrist friends object to that because it is time-consuming. The fact is it takes only approximately 5 minutes.

Khalid Hussain
Board-certified psychiatric nurse practitioner
Kingman, AZ

Thank you for bringing the issue of measurement-based psychiatric practice to light (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). As nurse practitioners, we were strictly taught to elaborate on psychiatric symptoms and progress, which is why the notes are called “progress notes” and not “shorthand notes.” I use blank forms of various modified scales—such as the Hamilton Rating Scale for Depression and Positive and Negative Syndrome Scale—and I checkmark and write all 4 axis and global assessment of functioning scores. These objective findings include a short version of the mental status exam. On the top of the chart, I note subjective symptoms. I never use general syntax such as “Pt. is improving, doing well.” Also, I utilize a 0-to-10 scale for overall improvement, with 0 being the worst and 10 being no symptoms.

In my treatment plan, I state which symptoms have resolved and which have not. My psychiatrist friends object to that because it is time-consuming. The fact is it takes only approximately 5 minutes.

Khalid Hussain
Board-certified psychiatric nurse practitioner
Kingman, AZ

Thank you for bringing the issue of measurement-based psychiatric practice to light (“Long overdue: Measurement-based psychiatric practice,” From the Editor, Current Psychiatry, April 2009). As nurse practitioners, we were strictly taught to elaborate on psychiatric symptoms and progress, which is why the notes are called “progress notes” and not “shorthand notes.” I use blank forms of various modified scales—such as the Hamilton Rating Scale for Depression and Positive and Negative Syndrome Scale—and I checkmark and write all 4 axis and global assessment of functioning scores. These objective findings include a short version of the mental status exam. On the top of the chart, I note subjective symptoms. I never use general syntax such as “Pt. is improving, doing well.” Also, I utilize a 0-to-10 scale for overall improvement, with 0 being the worst and 10 being no symptoms.

In my treatment plan, I state which symptoms have resolved and which have not. My psychiatrist friends object to that because it is time-consuming. The fact is it takes only approximately 5 minutes.

Khalid Hussain
Board-certified psychiatric nurse practitioner
Kingman, AZ