Current Psychiatry

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CASE: Depressed and delusional

Mrs. P, age 58, is a retired art teacher who presents for inpatient psychiatric admission after an 8-month depressive and psychotic illness. She reports profound feelings of worthlessness, anhedonia, psychomotor retardation, daily spontaneous crying spells, and worsening suicidal ideation. She is unkempt, disheveled, and makes limited eye contact. She is floridly psychotic, exhibits hebephrenia at times, and appears to be having conversations with people who are not there. Mrs. P reports derogatory intracranial auditory hallucinations of her brother’s and father’s voices. She also describes a complex delusional system relating to sexual trauma she experienced as a child perpetrated by her brother. Her family corroborates some details of the trauma; however, she says her father, neighbors, pastor, and outpatient psychiatrist are involved. Mrs. P believes these individuals are members of a cult, she has been the victim of a satanic sexual rite, and a television news personality knows about this conspiracy and has been attempting to contact her.

Mrs. P suffers from severe, debilitating chronic pain experienced as shock-like pain lasting for several minutes that starts in her throat and radiates to her left ear. Her pain began several years ago and prompted a neurologic workup, including MRI of the head and somatosensory evoked potentials of the glossopharyngeal nerve. She was diagnosed with “probable” glossopharyngeal neuralgia and failed multiple medication trials, including carbamazepine, phenytoin, gabapentin, and amitriptyline. She underwent microvascular decompression surgery 3 years ago. The operation, which has an 80% to 90% success rate for neuralgias,^1,2 offered only brief symptomatic relief. She was maintained on immediate-release opiates until the pain became “unbearable” 8 months ago. This prompted a second neurologic workup, which was unremarkable. Mrs. P was diagnosed with pain disorder associated with psychological factors and a general medical condition.

Ten years ago she had 2 major depressive episodes with inpatient hospitalization and 2 suicide attempts within 1 year, but no history of psychosis before 8 months ago. Mrs. P’s husband says his wife has no history of manic or hypomanic episodes. Her medications are ziprasidone, 20 mg/d, thiothixene, 10 mg/d, benztropine, 3 mg/d, and escitalopram, 30 mg/d. She also receives oxycodone/acetaminophen, 5 mg/325 mg as needed for facial pain and headaches, and clonazepam, 1 mg as needed for panic attacks.

The authors’ observations

Psychosis can be a feature of any of the disorders listed in Table 1³; however, several features of Mrs. P’s illness led us to diagnose MDD, recurrent, severe with psychotic features.⁴ Mrs. P and her husband described several discreet episodes of major debilitating depression without alternating periods of hypomanic or manic symptoms (Table 2).⁴ Comorbid depressive symptoms and a timeline indicating persistence of psychotic symptoms make a brief psychotic episode less likely. Although uncommon, patients can develop psychotic or mood disorders as a result of opiate abuse or dependence. However, Mrs. P was taking opiates as prescribed and not asking for early refills, which makes substance abuse an unlikely cause of her psychosis. In addition, because Mrs. P had 2 major depressive episodes in the absence of opiate use, a primary mood disorder seemed the more appropriate diagnosis. Schizophrenia is ruled out based on history. Although Mrs. P was suffering from complex delusional constructs, auditory hallucinations, and grossly disorganized behavior, these symptoms occurred only within the context of her depressive episode. New-onset delusional guilt relating to her childhood sexual trauma and hypochondriacal preoccupations within the context of pain complaints make psychotic depression more likely.⁵

Table 1

Psychiatric diseases in which patients may present with psychotic symptoms

Table 2

DSM-IV-TR criteria for major depressive episode

Depression, psychosis, and pain

From the beginning of Mrs. P’s treatment, we considered psychotic depression worsened—if not completely explained—her pain. Her somatic complaints appeared to be subtly woven into her delusional constructs. For instance, she complained that a device had been implanted in her head and she had the scar to prove it, pointing to the scar from her microvascular decompression surgery. Research indicates that depressive illness and chronic pain syndromes are highly comorbid and depressive illness can worsen pain syndromes.^6,7 In addition, Mrs. P failed several medical and 1 surgical interventions for her pain condition that had high success rates. Her husband notes that when her outpatient psychiatrist started olanzapine 3 months ago for emerging psychotic symptoms, her pain complaints initially decreased with her psychotic symptoms, and she used less opiate medication during that time. Several months later Mrs. P’s pain complaints increased as her psychotic symptoms worsened. Second-generation antipsychotics have been evaluated as treatment for chronic pain syndromes, and may exert a primary analgesic effect.^8,9 However, because of the correlation between her fluctuating psychotic symptoms and pain complaints, the more plausible explanation for olanzapine’s initial efficacy in treating Mrs. P’s pain is a secondary analgesic effect from decreased psychotic somatic preoccupation.

TREATMENT: ECT

Mrs. P is admitted to the inpatient psychiatric unit and placed on suicide precautions. Oxycodone/acetaminophen and clonazepam are tapered and limited to twice daily as needed. Escitalopram is tapered and discontinued. Thiothixene is tapered and replaced by olanzapine, 5 mg/d. Mrs. P receives 3 bifrontal, brief pulse-width ECT treatments. These result in marked improvement in her depressive and psychotic symptoms. In addition, her pain complaints become minimal. She becomes less preoccupied with her sexual trauma and grows to trust many staff members whom she previously believed were part of her traumatic childhood events. Mrs. P is no longer suicidal and asks to continue ECT treatments as an outpatient. She is discharged on olanzapine, 5 mg/d, trazodone, 100 mg/d for insomnia, benztropine, 2 mg/d, clonazepam 0.5 mg twice daily as needed for panic attacks, and oxycodone/acetaminophen, 5 mg/325 mg twice daily as needed for pain.

The authors’ observations

According to the Harvard South Shore Algorithm, treatment strategies for psychotic depression include antidepressant and antipsychotic combinations, lithium augmentation, clozapine, and ECT.¹⁰ Several factors made ECT the best option for Mrs. P. She had failed multiple treatment strategies and was suicidal. ECT is an effective treatment for MDD with psychotic features, single or recurrent episode.¹¹ ECT can be used as a primary treatment before psychotropic medications or secondarily when there has been lack of clinical response to medications, intolerable side effects, deterioration in psychiatric condition, or suicidality.^11,12 In addition, when treated with ECT, psychotic depression has a significantly higher remission rate than major depression without psychosis.¹² Delusional guilt, psychomotor retardation, hypochondriacal preoccupations, loss of insight, paranoia, and obsessive-compulsive symptoms predict a favorable response.¹² ECT also has demonstrated efficacy for treating pain secondary to psychotic depression or melancholic depression.¹³ In addition, ECT has been shown to have analgesic properties beyond treating underlying depression.¹⁴ Our primary focus was not to treat Mrs. P’s pain syndrome with ECT; however, in treating her psychotic depression we had hoped that her pain tolerance would improve and she would rely less on opiates.

OUTCOME: Pain relief

As an outpatient, Mrs. P receives 11 bifrontal ECT treatments in her initial series, followed by 7 bifrontal maintenance treatments. Her speech is more spontaneous, her grooming and hygiene improve, and she exhibits a brighter and more reactive affect. Suicidal ideation has resolved. Pain improves from a “10 out of 10” to a “2 out of 10.” Mrs. P consistently requires less oxycodone/acetaminophen. She relates better to her family and begins exploring new hobbies such as pottery. In addition to monthly maintenance bifrontal ECT treatments, she is stable on citalopram, 60 mg/d, and trazodone, 50 mg/d as needed for insomnia.

The authors’ observations

The relationship between depressive illness and chronic pain is complex. Treating a primary depressive illness can lead to improved functional outcomes and decreased disability from chronic pain complaints.¹⁵ Patients with comorbid chronic pain and depressive illness are more likely to suffer from unremitting pain despite compliance with evidence-based treatment strategies.¹⁶ Mrs. P had 2 co-occurring disorders: psychotic depression and chronic pain disorder secondary to glossopharyngeal neuralgia. Our opinion is that Mrs. P’s psychotic depression worsened her experience of pain.

Treatment strategies that address both depressive symptoms and chronic pain are ideal.¹⁷ These treatment modalities include psychotherapeutic techniques such as cognitive-behavioral therapy, medications, and somatic treatments such as ECT.¹⁸ In Mrs. P’s case, ECT was an effective treatment that caused remission of psychotic depressive symptoms, which lead to improved pain control and restored social and occupational functioning.

Related Resources

• Schreiber S, Shmueli D, Grunhaus L, et al. The influence of electroconvulsive therapy on pain threshold and pain tolerance in major depression patients before, during and after treatment. Eur J Pain. 2003;7(5):419-424.
• Suzuki K, Ebina Y, Shindo T, et al. Repeated electroconvulsive therapy courses improved chronic regional pain with depression caused by failed back syndrome. Med Sci Monit. 2009;15(4):CS77-CS79.
• Giesecke T, Gracely RH, Williams DA, et al. The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort. Arthritis Rheum. 2005;52(5):1577-1584.

Drug Brand Names

• Amitriptyline • Elavil
• Benztropine • Cogentin
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clozapine • Clozaril
• Escitalopram • Lexapro
• Gabapentin • Neurontin
• Lithium • Eskalith, Lithobid
• Olanzapine • Zyprexa
• Oxycodone/ acetaminophen • Vicodin
• Phenytoin • Dilantin
• Thiothixene • Navane
• Trazodone • Desyrel, Oleptro
• Ziprasidone • Geodon

Disclosures

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

Dr. Magid receives NARSAD grant support.

Discuss this article at www.facebook.com/CurrentPsychiatry

CASE: Depressed and delusional

Mrs. P, age 58, is a retired art teacher who presents for inpatient psychiatric admission after an 8-month depressive and psychotic illness. She reports profound feelings of worthlessness, anhedonia, psychomotor retardation, daily spontaneous crying spells, and worsening suicidal ideation. She is unkempt, disheveled, and makes limited eye contact. She is floridly psychotic, exhibits hebephrenia at times, and appears to be having conversations with people who are not there. Mrs. P reports derogatory intracranial auditory hallucinations of her brother’s and father’s voices. She also describes a complex delusional system relating to sexual trauma she experienced as a child perpetrated by her brother. Her family corroborates some details of the trauma; however, she says her father, neighbors, pastor, and outpatient psychiatrist are involved. Mrs. P believes these individuals are members of a cult, she has been the victim of a satanic sexual rite, and a television news personality knows about this conspiracy and has been attempting to contact her.

Mrs. P suffers from severe, debilitating chronic pain experienced as shock-like pain lasting for several minutes that starts in her throat and radiates to her left ear. Her pain began several years ago and prompted a neurologic workup, including MRI of the head and somatosensory evoked potentials of the glossopharyngeal nerve. She was diagnosed with “probable” glossopharyngeal neuralgia and failed multiple medication trials, including carbamazepine, phenytoin, gabapentin, and amitriptyline. She underwent microvascular decompression surgery 3 years ago. The operation, which has an 80% to 90% success rate for neuralgias,^1,2 offered only brief symptomatic relief. She was maintained on immediate-release opiates until the pain became “unbearable” 8 months ago. This prompted a second neurologic workup, which was unremarkable. Mrs. P was diagnosed with pain disorder associated with psychological factors and a general medical condition.

Ten years ago she had 2 major depressive episodes with inpatient hospitalization and 2 suicide attempts within 1 year, but no history of psychosis before 8 months ago. Mrs. P’s husband says his wife has no history of manic or hypomanic episodes. Her medications are ziprasidone, 20 mg/d, thiothixene, 10 mg/d, benztropine, 3 mg/d, and escitalopram, 30 mg/d. She also receives oxycodone/acetaminophen, 5 mg/325 mg as needed for facial pain and headaches, and clonazepam, 1 mg as needed for panic attacks.

The authors’ observations

Psychosis can be a feature of any of the disorders listed in Table 1³; however, several features of Mrs. P’s illness led us to diagnose MDD, recurrent, severe with psychotic features.⁴ Mrs. P and her husband described several discreet episodes of major debilitating depression without alternating periods of hypomanic or manic symptoms (Table 2).⁴ Comorbid depressive symptoms and a timeline indicating persistence of psychotic symptoms make a brief psychotic episode less likely. Although uncommon, patients can develop psychotic or mood disorders as a result of opiate abuse or dependence. However, Mrs. P was taking opiates as prescribed and not asking for early refills, which makes substance abuse an unlikely cause of her psychosis. In addition, because Mrs. P had 2 major depressive episodes in the absence of opiate use, a primary mood disorder seemed the more appropriate diagnosis. Schizophrenia is ruled out based on history. Although Mrs. P was suffering from complex delusional constructs, auditory hallucinations, and grossly disorganized behavior, these symptoms occurred only within the context of her depressive episode. New-onset delusional guilt relating to her childhood sexual trauma and hypochondriacal preoccupations within the context of pain complaints make psychotic depression more likely.⁵

Table 1

Psychiatric diseases in which patients may present with psychotic symptoms

Table 2

DSM-IV-TR criteria for major depressive episode

Depression, psychosis, and pain

From the beginning of Mrs. P’s treatment, we considered psychotic depression worsened—if not completely explained—her pain. Her somatic complaints appeared to be subtly woven into her delusional constructs. For instance, she complained that a device had been implanted in her head and she had the scar to prove it, pointing to the scar from her microvascular decompression surgery. Research indicates that depressive illness and chronic pain syndromes are highly comorbid and depressive illness can worsen pain syndromes.^6,7 In addition, Mrs. P failed several medical and 1 surgical interventions for her pain condition that had high success rates. Her husband notes that when her outpatient psychiatrist started olanzapine 3 months ago for emerging psychotic symptoms, her pain complaints initially decreased with her psychotic symptoms, and she used less opiate medication during that time. Several months later Mrs. P’s pain complaints increased as her psychotic symptoms worsened. Second-generation antipsychotics have been evaluated as treatment for chronic pain syndromes, and may exert a primary analgesic effect.^8,9 However, because of the correlation between her fluctuating psychotic symptoms and pain complaints, the more plausible explanation for olanzapine’s initial efficacy in treating Mrs. P’s pain is a secondary analgesic effect from decreased psychotic somatic preoccupation.

TREATMENT: ECT

Mrs. P is admitted to the inpatient psychiatric unit and placed on suicide precautions. Oxycodone/acetaminophen and clonazepam are tapered and limited to twice daily as needed. Escitalopram is tapered and discontinued. Thiothixene is tapered and replaced by olanzapine, 5 mg/d. Mrs. P receives 3 bifrontal, brief pulse-width ECT treatments. These result in marked improvement in her depressive and psychotic symptoms. In addition, her pain complaints become minimal. She becomes less preoccupied with her sexual trauma and grows to trust many staff members whom she previously believed were part of her traumatic childhood events. Mrs. P is no longer suicidal and asks to continue ECT treatments as an outpatient. She is discharged on olanzapine, 5 mg/d, trazodone, 100 mg/d for insomnia, benztropine, 2 mg/d, clonazepam 0.5 mg twice daily as needed for panic attacks, and oxycodone/acetaminophen, 5 mg/325 mg twice daily as needed for pain.

The authors’ observations

According to the Harvard South Shore Algorithm, treatment strategies for psychotic depression include antidepressant and antipsychotic combinations, lithium augmentation, clozapine, and ECT.¹⁰ Several factors made ECT the best option for Mrs. P. She had failed multiple treatment strategies and was suicidal. ECT is an effective treatment for MDD with psychotic features, single or recurrent episode.¹¹ ECT can be used as a primary treatment before psychotropic medications or secondarily when there has been lack of clinical response to medications, intolerable side effects, deterioration in psychiatric condition, or suicidality.^11,12 In addition, when treated with ECT, psychotic depression has a significantly higher remission rate than major depression without psychosis.¹² Delusional guilt, psychomotor retardation, hypochondriacal preoccupations, loss of insight, paranoia, and obsessive-compulsive symptoms predict a favorable response.¹² ECT also has demonstrated efficacy for treating pain secondary to psychotic depression or melancholic depression.¹³ In addition, ECT has been shown to have analgesic properties beyond treating underlying depression.¹⁴ Our primary focus was not to treat Mrs. P’s pain syndrome with ECT; however, in treating her psychotic depression we had hoped that her pain tolerance would improve and she would rely less on opiates.

OUTCOME: Pain relief

As an outpatient, Mrs. P receives 11 bifrontal ECT treatments in her initial series, followed by 7 bifrontal maintenance treatments. Her speech is more spontaneous, her grooming and hygiene improve, and she exhibits a brighter and more reactive affect. Suicidal ideation has resolved. Pain improves from a “10 out of 10” to a “2 out of 10.” Mrs. P consistently requires less oxycodone/acetaminophen. She relates better to her family and begins exploring new hobbies such as pottery. In addition to monthly maintenance bifrontal ECT treatments, she is stable on citalopram, 60 mg/d, and trazodone, 50 mg/d as needed for insomnia.

The authors’ observations

The relationship between depressive illness and chronic pain is complex. Treating a primary depressive illness can lead to improved functional outcomes and decreased disability from chronic pain complaints.¹⁵ Patients with comorbid chronic pain and depressive illness are more likely to suffer from unremitting pain despite compliance with evidence-based treatment strategies.¹⁶ Mrs. P had 2 co-occurring disorders: psychotic depression and chronic pain disorder secondary to glossopharyngeal neuralgia. Our opinion is that Mrs. P’s psychotic depression worsened her experience of pain.

Treatment strategies that address both depressive symptoms and chronic pain are ideal.¹⁷ These treatment modalities include psychotherapeutic techniques such as cognitive-behavioral therapy, medications, and somatic treatments such as ECT.¹⁸ In Mrs. P’s case, ECT was an effective treatment that caused remission of psychotic depressive symptoms, which lead to improved pain control and restored social and occupational functioning.

Related Resources

• Schreiber S, Shmueli D, Grunhaus L, et al. The influence of electroconvulsive therapy on pain threshold and pain tolerance in major depression patients before, during and after treatment. Eur J Pain. 2003;7(5):419-424.
• Suzuki K, Ebina Y, Shindo T, et al. Repeated electroconvulsive therapy courses improved chronic regional pain with depression caused by failed back syndrome. Med Sci Monit. 2009;15(4):CS77-CS79.
• Giesecke T, Gracely RH, Williams DA, et al. The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort. Arthritis Rheum. 2005;52(5):1577-1584.

Drug Brand Names

• Amitriptyline • Elavil
• Benztropine • Cogentin
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clozapine • Clozaril
• Escitalopram • Lexapro
• Gabapentin • Neurontin
• Lithium • Eskalith, Lithobid
• Olanzapine • Zyprexa
• Oxycodone/ acetaminophen • Vicodin
• Phenytoin • Dilantin
• Thiothixene • Navane
• Trazodone • Desyrel, Oleptro
• Ziprasidone • Geodon

Disclosures

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

Dr. Magid receives NARSAD grant support.

Discuss this article at www.facebook.com/CurrentPsychiatry

CASE: Depressed and delusional

Mrs. P, age 58, is a retired art teacher who presents for inpatient psychiatric admission after an 8-month depressive and psychotic illness. She reports profound feelings of worthlessness, anhedonia, psychomotor retardation, daily spontaneous crying spells, and worsening suicidal ideation. She is unkempt, disheveled, and makes limited eye contact. She is floridly psychotic, exhibits hebephrenia at times, and appears to be having conversations with people who are not there. Mrs. P reports derogatory intracranial auditory hallucinations of her brother’s and father’s voices. She also describes a complex delusional system relating to sexual trauma she experienced as a child perpetrated by her brother. Her family corroborates some details of the trauma; however, she says her father, neighbors, pastor, and outpatient psychiatrist are involved. Mrs. P believes these individuals are members of a cult, she has been the victim of a satanic sexual rite, and a television news personality knows about this conspiracy and has been attempting to contact her.

Mrs. P suffers from severe, debilitating chronic pain experienced as shock-like pain lasting for several minutes that starts in her throat and radiates to her left ear. Her pain began several years ago and prompted a neurologic workup, including MRI of the head and somatosensory evoked potentials of the glossopharyngeal nerve. She was diagnosed with “probable” glossopharyngeal neuralgia and failed multiple medication trials, including carbamazepine, phenytoin, gabapentin, and amitriptyline. She underwent microvascular decompression surgery 3 years ago. The operation, which has an 80% to 90% success rate for neuralgias,^1,2 offered only brief symptomatic relief. She was maintained on immediate-release opiates until the pain became “unbearable” 8 months ago. This prompted a second neurologic workup, which was unremarkable. Mrs. P was diagnosed with pain disorder associated with psychological factors and a general medical condition.

Ten years ago she had 2 major depressive episodes with inpatient hospitalization and 2 suicide attempts within 1 year, but no history of psychosis before 8 months ago. Mrs. P’s husband says his wife has no history of manic or hypomanic episodes. Her medications are ziprasidone, 20 mg/d, thiothixene, 10 mg/d, benztropine, 3 mg/d, and escitalopram, 30 mg/d. She also receives oxycodone/acetaminophen, 5 mg/325 mg as needed for facial pain and headaches, and clonazepam, 1 mg as needed for panic attacks.

The authors’ observations

Psychosis can be a feature of any of the disorders listed in Table 1³; however, several features of Mrs. P’s illness led us to diagnose MDD, recurrent, severe with psychotic features.⁴ Mrs. P and her husband described several discreet episodes of major debilitating depression without alternating periods of hypomanic or manic symptoms (Table 2).⁴ Comorbid depressive symptoms and a timeline indicating persistence of psychotic symptoms make a brief psychotic episode less likely. Although uncommon, patients can develop psychotic or mood disorders as a result of opiate abuse or dependence. However, Mrs. P was taking opiates as prescribed and not asking for early refills, which makes substance abuse an unlikely cause of her psychosis. In addition, because Mrs. P had 2 major depressive episodes in the absence of opiate use, a primary mood disorder seemed the more appropriate diagnosis. Schizophrenia is ruled out based on history. Although Mrs. P was suffering from complex delusional constructs, auditory hallucinations, and grossly disorganized behavior, these symptoms occurred only within the context of her depressive episode. New-onset delusional guilt relating to her childhood sexual trauma and hypochondriacal preoccupations within the context of pain complaints make psychotic depression more likely.⁵

Table 1

Psychiatric diseases in which patients may present with psychotic symptoms

Table 2

DSM-IV-TR criteria for major depressive episode

Depression, psychosis, and pain

From the beginning of Mrs. P’s treatment, we considered psychotic depression worsened—if not completely explained—her pain. Her somatic complaints appeared to be subtly woven into her delusional constructs. For instance, she complained that a device had been implanted in her head and she had the scar to prove it, pointing to the scar from her microvascular decompression surgery. Research indicates that depressive illness and chronic pain syndromes are highly comorbid and depressive illness can worsen pain syndromes.^6,7 In addition, Mrs. P failed several medical and 1 surgical interventions for her pain condition that had high success rates. Her husband notes that when her outpatient psychiatrist started olanzapine 3 months ago for emerging psychotic symptoms, her pain complaints initially decreased with her psychotic symptoms, and she used less opiate medication during that time. Several months later Mrs. P’s pain complaints increased as her psychotic symptoms worsened. Second-generation antipsychotics have been evaluated as treatment for chronic pain syndromes, and may exert a primary analgesic effect.^8,9 However, because of the correlation between her fluctuating psychotic symptoms and pain complaints, the more plausible explanation for olanzapine’s initial efficacy in treating Mrs. P’s pain is a secondary analgesic effect from decreased psychotic somatic preoccupation.

TREATMENT: ECT

Mrs. P is admitted to the inpatient psychiatric unit and placed on suicide precautions. Oxycodone/acetaminophen and clonazepam are tapered and limited to twice daily as needed. Escitalopram is tapered and discontinued. Thiothixene is tapered and replaced by olanzapine, 5 mg/d. Mrs. P receives 3 bifrontal, brief pulse-width ECT treatments. These result in marked improvement in her depressive and psychotic symptoms. In addition, her pain complaints become minimal. She becomes less preoccupied with her sexual trauma and grows to trust many staff members whom she previously believed were part of her traumatic childhood events. Mrs. P is no longer suicidal and asks to continue ECT treatments as an outpatient. She is discharged on olanzapine, 5 mg/d, trazodone, 100 mg/d for insomnia, benztropine, 2 mg/d, clonazepam 0.5 mg twice daily as needed for panic attacks, and oxycodone/acetaminophen, 5 mg/325 mg twice daily as needed for pain.

The authors’ observations

According to the Harvard South Shore Algorithm, treatment strategies for psychotic depression include antidepressant and antipsychotic combinations, lithium augmentation, clozapine, and ECT.¹⁰ Several factors made ECT the best option for Mrs. P. She had failed multiple treatment strategies and was suicidal. ECT is an effective treatment for MDD with psychotic features, single or recurrent episode.¹¹ ECT can be used as a primary treatment before psychotropic medications or secondarily when there has been lack of clinical response to medications, intolerable side effects, deterioration in psychiatric condition, or suicidality.^11,12 In addition, when treated with ECT, psychotic depression has a significantly higher remission rate than major depression without psychosis.¹² Delusional guilt, psychomotor retardation, hypochondriacal preoccupations, loss of insight, paranoia, and obsessive-compulsive symptoms predict a favorable response.¹² ECT also has demonstrated efficacy for treating pain secondary to psychotic depression or melancholic depression.¹³ In addition, ECT has been shown to have analgesic properties beyond treating underlying depression.¹⁴ Our primary focus was not to treat Mrs. P’s pain syndrome with ECT; however, in treating her psychotic depression we had hoped that her pain tolerance would improve and she would rely less on opiates.

OUTCOME: Pain relief

As an outpatient, Mrs. P receives 11 bifrontal ECT treatments in her initial series, followed by 7 bifrontal maintenance treatments. Her speech is more spontaneous, her grooming and hygiene improve, and she exhibits a brighter and more reactive affect. Suicidal ideation has resolved. Pain improves from a “10 out of 10” to a “2 out of 10.” Mrs. P consistently requires less oxycodone/acetaminophen. She relates better to her family and begins exploring new hobbies such as pottery. In addition to monthly maintenance bifrontal ECT treatments, she is stable on citalopram, 60 mg/d, and trazodone, 50 mg/d as needed for insomnia.

The authors’ observations

The relationship between depressive illness and chronic pain is complex. Treating a primary depressive illness can lead to improved functional outcomes and decreased disability from chronic pain complaints.¹⁵ Patients with comorbid chronic pain and depressive illness are more likely to suffer from unremitting pain despite compliance with evidence-based treatment strategies.¹⁶ Mrs. P had 2 co-occurring disorders: psychotic depression and chronic pain disorder secondary to glossopharyngeal neuralgia. Our opinion is that Mrs. P’s psychotic depression worsened her experience of pain.

Treatment strategies that address both depressive symptoms and chronic pain are ideal.¹⁷ These treatment modalities include psychotherapeutic techniques such as cognitive-behavioral therapy, medications, and somatic treatments such as ECT.¹⁸ In Mrs. P’s case, ECT was an effective treatment that caused remission of psychotic depressive symptoms, which lead to improved pain control and restored social and occupational functioning.

Related Resources

• Schreiber S, Shmueli D, Grunhaus L, et al. The influence of electroconvulsive therapy on pain threshold and pain tolerance in major depression patients before, during and after treatment. Eur J Pain. 2003;7(5):419-424.
• Suzuki K, Ebina Y, Shindo T, et al. Repeated electroconvulsive therapy courses improved chronic regional pain with depression caused by failed back syndrome. Med Sci Monit. 2009;15(4):CS77-CS79.
• Giesecke T, Gracely RH, Williams DA, et al. The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort. Arthritis Rheum. 2005;52(5):1577-1584.

Drug Brand Names

• Amitriptyline • Elavil
• Benztropine • Cogentin
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Clonazepam • Klonopin
• Clozapine • Clozaril
• Escitalopram • Lexapro
• Gabapentin • Neurontin
• Lithium • Eskalith, Lithobid
• Olanzapine • Zyprexa
• Oxycodone/ acetaminophen • Vicodin
• Phenytoin • Dilantin
• Thiothixene • Navane
• Trazodone • Desyrel, Oleptro
• Ziprasidone • Geodon

Disclosures

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

Dr. Magid receives NARSAD grant support.

Discuss this article at www.facebook.com/CurrentPsychiatry

Although forensic psychiatrists typically are consulted in complex legal matters, geriatric, consultation-liaison, and general psychiatrists are on the front lines of assessing capacity to give informed consent and need for guardianship. Psychiatrists often find such consultations daunting because residency training usually includes little to no formal training in performing psycho-legal assessments. Evaluating issues such as decision-making capacity, guardianship, and capacity to give informed consent requires a delicate balance between autonomy and beneficence. This article reviews 4 common legal issues in geriatric consultation—capacity evaluations, informed consent, guardianship, and elder abuse—and suggests a systematic approach to psycho-legal consultations in older adults.

Confidentiality and dual agency

Every psychiatrist should be familiar with basic principles of medical ethics as well as key aspects of local mental health law. Relevant ethical principles include autonomy, beneficence, confidentiality, and dual agency. A review of all these ethical issues is beyond the scope of this article, so here I highlight confidentiality and dual agency.

Confidentiality—the clinician’s obligation not to disclose private medical information—is a legal as well as an ethical requirement. A psychiatrist who performs a psycho-legal evaluation must disclose to the patient the purpose of the evaluation, that a report will be prepared, and to whom it will be submitted. Exceptions to confidentiality include medical emergencies, mandatory reporting of abuse and infectious diseases, and the duty to protect (warning police and the intended victim when a patient makes a threat).

Dual agency or dual role refers to serving as both a treating physician and a forensic evaluator. Although it is ideal to avoid serving in a dual role, sometimes it is impractical or impossible to avoid doing so, such as in guardianship or civil commitment evaluations, or in state forensic hospitals. In such cases, the psychiatrist must be aware of potential conflicts between clinical and forensic evaluations. A treating psychiatrist primarily serves his or her patient’s best interest, whereas a forensic psychiatrist primarily seeks truth.¹ A treating psychiatrist is at risk of consciously or unconsciously biasing his or her psycho-legal evaluation in favor of or against the patient/litigant, depending upon the psychiatrist’s countertransference. Further, performing a psycho-legal evaluation can cause problems in ongoing treatment. A psychiatrist who testifies that his or her fiercely independent patient needs a guardian or nursing home placement will experience significant challenges in continuing to work with that patient.

4 common issues for older adults

Decision-making capacity. Although “capacity” and “competence” often are used interchangeably, “capacity” broadly refers to the ability to perform a specific task, whereas “competence” refers to the legally defined standard for performing a specific task such as making a will. “Competence” is legally determined, whereas “capacity” may be determined clinically.

Capacity usually is task-specific rather than a general construct. The existence of physical or mental illness per se does not mean that a patient lacks capacity. Rather, capacity is determined by whether an individual has specific abilities, regardless of diagnosis. Specific capacities include the ability to give informed consent, manage finances, make a will, or enter into contracts (Table 1).^2-4 Appelbaum and Gutheil describe 4 components for assessing specific capacity:

• communication of a choice
• factual understanding of the issues
• appreciation of the situation and its consequences
• rational manipulation of information.^5,6

Table 1

Criteria of 3 specific capacities

Ability to communicate a choice refers to a patient’s ability to express his or her wishes in a reasonably stable manner. Factual understanding of the issues refers to an individual’s ability to understand the relevant facts before making a decision. Appreciation of the situation and its consequences refers to a person’s ability to rationally understand the effect of decisions. Appreciation is a higher level of understanding than mere factual understanding—eg, a delusional patient who believes himself immortal may intellectually understand that a surgical procedure carries a 50% mortality risk, but may be unable to appreciate the information as it relates to him because he believes he is immortal. Rational manipulation of information refers to a patient’s reasoning process and how the patient integrates data into his or her decision-making process.⁵

Informed consent. In my experience, capacity to give informed consent is the most commonly requested specific capacity assessment in general medical settings. Informed consent must be knowing, voluntary, and competent. All material information—information that would cause a reasonable person to accept or reject a proposed treatment—should be communicated to the patient. Informed consent requires an understanding of the patient’s condition and indication for treatment, risks and benefits of and alternatives to treatment, and risks of declining treatment.^2,3 Exceptions to informed consent include incompetence, medical emergencies, patient waiver of informed consent, and a limited therapeutic privilege (when a physician determines that the information would harm the patient).³

Several instruments can help clinicians assess patients’ capacity to give informed consent. The benefits of using a structured instrument include:

• ensuring that specific information is covered during each evaluation
• systematically recording a patient’s response.⁵

Disadvantages of using instruments include the fact that no instrument can take into account all aspects of a particular case, and some instruments are time-consuming and require training. Structured instruments can be a useful adjunct to the clinical interview in some cases, but should not substitute for it. In a review of 23 instruments for assessing decisional capacity to consent to treatment or clinical research, the MacArthur Competence Assessment Tool for Clinical Research and the MacArthur Competence Assessment Tool for Treatment had the most empirical support, although the authors noted that other instruments might be better suited to specific situations.⁷

Psychiatrists may be consulted when a patient refuses treatment or decides to leave the hospital against medical advice. The key issue in both situations is whether the patient has capacity to refuse treatment.⁸ If there is evidence that the patient is mentally ill and poses an imminent risk of suicide or violence or is unable to provide for his or her basic needs, the psychiatrist should assess whether the patient meets criteria for civil commitment.

Many clinicians employ a “sliding scale” approach to competence, requiring a lower degree of competence for consenting to low-risk, high-benefit interventions and a greater degree of competence for higher-risk procedures.^5,9 Family members often serve as informal surrogate decision makers for incapacitated patients, except when there is significant family discord or no family members are available.⁵

Guardianship. Guardians are appointed by courts to make decisions for individuals who have been found incompetent (wards). Although its purposes are beneficent, the guardianship system could do significant harm.¹⁰ Determining that an individual is incompetent is tantamount to depriving him or her of basic personhood. In many cases, the ward loses the ability to consent to or refuse medical care, manage his or her finances, enter into contracts, marry, and determine where he or she will live. On the other hand, failing to recognize incompetence can leave a vulnerable person in danger of physical deterioration, abuse, neglect, or exploitation.

It is critical that guardianship evaluations be conducted carefully. In a review of 298 guardianship cases from 3 states, Moye and colleagues¹¹ found that the quality of the reports was significantly better in Colorado, a state with guardianship reforms, but documentation of functional strengths and weaknesses was “particularly rare” in guardianship evaluations and prognosis often was not included. This information is relevant to judges, who need to determine which areas of function are impaired and how long the impairment is likely to last.

Guardianship evaluations often focus on general rather than specific capacity. In other words, often there is not a specific task such as consenting to surgery that the alleged incompetent person needs to perform. Rather, the question is whether an individual can manage his or her finances or make treatment decisions in general. Appelbaum and Gutheil suggest considering 6 factors when assessing general capacity:

• awareness of the situation
• factual understanding of the issues
• appreciation of the likely consequences
• rational manipulation of information
• functioning in one’s environment
• extent of demands on patient.⁵

The first 4 are closely related to the elements of specific capacity described above. Functioning in one’s environment and extent of demands on the patient attempt to anticipate the tasks that an individual will need to perform. A patient with mild dementia may be unable to manage a complex estate but can handle a bank account and a fixed income. Similarly, it is important to consider the patient’s support system. An impaired patient may function adequately with his wife’s help but may lose the capacity to live independently if his wife dies or becomes impaired.

Traditionally, guardianship has resulted in a complete loss of decision-making ability. Several state legislatures have passed laws allowing for limited guardianship, although orders for limited guardianship remain underutilized.¹⁰ Limited guardianship delineates specific areas of incompetence and limits the guardian’s decision-making authority to those areas while leaving intact the ward’s ability to make all other decisions for himself or herself.

The use of less-restrictive alternatives to guardianship—such as powers of attorney, durable powers of attorney, living wills, payees, and trusts—is increasing. A power of attorney allows a patient to authorize a specific individual to act on his or her behalf. The scope of the power of attorney can be limited, such as to manage finances or even to a specific transaction, such as selling a home or car. A durable power of attorney also allows an agent to make decisions on the patient’s behalf but becomes active only when the patient becomes incompetent. It often is used to appoint an individual to make medical decisions on behalf of an incompetent patient. Living wills allow patients to determine what treatment they would like in the event they become incompetent.

Elder abuse. An estimated 1 to 2 million adults age >65 have been abused, exploited, or neglected.¹² Elder abuse includes physical abuse, neglect, emotional abuse, sexual abuse, and financial exploitation (including undue influence). Most states have mandatory reporting of elder abuse, although they vary regarding who must report and what the report must entail. Psychiatrists should be vigilant in looking for signs of elder abuse (Table 2),¹³ regardless of the reason for the consult.

Table 2

Signs of elder abuse: What to wlook for

10 tips for thorough evaluations

1. Consider the context of the consultation. This includes medical factors (such as the patient’s condition, prognosis, relationship with the treatment team, and recommended course of treatment), legal factors (eg, pending litigation and relevant legal standards for issues such as guardianship), and psychosocial issues (eg, the patient’s current support structure and family conflicts).

2. Identify the legal issue and any relevant legal standards. The legal standard will inform you of the issues you need to address in the evaluation. If an attorney has consulted you, ask him or her to provide the legal standard.

3. Gather relevant collateral information, which may include interviews with family members or a review of financial or medical records.

4. Explain the purpose of the examination and the limits of confidentiality.

5. Perform a focused psychiatric evaluation, paying special attention to cognitive functioning, reasoning, and unusual thought content such as delusional beliefs.

6. Perform an interview specific to the referral issue.

7. Consider using a relevant assessment instrument.

8. Consider psychological testing, laboratory testing, imaging, or further medical evaluation. These assessments can help determine the diagnosis, the cause of any deficits in capacity, and whether any deficits are reversible.

9. Determine what opinions you are able to render. Limit opinions and remember that it may be appropriate to decline to address certain issues if there is insufficient information or if the issue is outside your area of expertise.

10. Prepare a written report. Consider the audience. Minimize the use of medical jargon and define all medical terms. State your opinions clearly and with reasonable medical certainty (in most jurisdictions, this means more likely than not). State the basis for all opinions.

For a case study that provides an example of a psycho-legal evaluation of a geriatric patient, see the Box.

Box

Related Resources

• American Academy of Psychiatry and the Law. www.aapl.org.
• American Bar Association Commission on Law and Aging. www.americanbar.org/groups/law_aging.html.
• National Center on Elder Abuse. www.ncea.aoa.gov.

Disclosure

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

Acknowledgement

The author thanks forensic psychiatry fellow Abhishek Jain, MD for reviewing the article and offering editorial suggestions.

Discuss this article at www.facebook.com/CurrentPsychiatry

Although forensic psychiatrists typically are consulted in complex legal matters, geriatric, consultation-liaison, and general psychiatrists are on the front lines of assessing capacity to give informed consent and need for guardianship. Psychiatrists often find such consultations daunting because residency training usually includes little to no formal training in performing psycho-legal assessments. Evaluating issues such as decision-making capacity, guardianship, and capacity to give informed consent requires a delicate balance between autonomy and beneficence. This article reviews 4 common legal issues in geriatric consultation—capacity evaluations, informed consent, guardianship, and elder abuse—and suggests a systematic approach to psycho-legal consultations in older adults.

Confidentiality and dual agency

Every psychiatrist should be familiar with basic principles of medical ethics as well as key aspects of local mental health law. Relevant ethical principles include autonomy, beneficence, confidentiality, and dual agency. A review of all these ethical issues is beyond the scope of this article, so here I highlight confidentiality and dual agency.

Confidentiality—the clinician’s obligation not to disclose private medical information—is a legal as well as an ethical requirement. A psychiatrist who performs a psycho-legal evaluation must disclose to the patient the purpose of the evaluation, that a report will be prepared, and to whom it will be submitted. Exceptions to confidentiality include medical emergencies, mandatory reporting of abuse and infectious diseases, and the duty to protect (warning police and the intended victim when a patient makes a threat).

Dual agency or dual role refers to serving as both a treating physician and a forensic evaluator. Although it is ideal to avoid serving in a dual role, sometimes it is impractical or impossible to avoid doing so, such as in guardianship or civil commitment evaluations, or in state forensic hospitals. In such cases, the psychiatrist must be aware of potential conflicts between clinical and forensic evaluations. A treating psychiatrist primarily serves his or her patient’s best interest, whereas a forensic psychiatrist primarily seeks truth.¹ A treating psychiatrist is at risk of consciously or unconsciously biasing his or her psycho-legal evaluation in favor of or against the patient/litigant, depending upon the psychiatrist’s countertransference. Further, performing a psycho-legal evaluation can cause problems in ongoing treatment. A psychiatrist who testifies that his or her fiercely independent patient needs a guardian or nursing home placement will experience significant challenges in continuing to work with that patient.

4 common issues for older adults

Decision-making capacity. Although “capacity” and “competence” often are used interchangeably, “capacity” broadly refers to the ability to perform a specific task, whereas “competence” refers to the legally defined standard for performing a specific task such as making a will. “Competence” is legally determined, whereas “capacity” may be determined clinically.

Capacity usually is task-specific rather than a general construct. The existence of physical or mental illness per se does not mean that a patient lacks capacity. Rather, capacity is determined by whether an individual has specific abilities, regardless of diagnosis. Specific capacities include the ability to give informed consent, manage finances, make a will, or enter into contracts (Table 1).^2-4 Appelbaum and Gutheil describe 4 components for assessing specific capacity:

• communication of a choice
• factual understanding of the issues
• appreciation of the situation and its consequences
• rational manipulation of information.^5,6

Table 1

Criteria of 3 specific capacities

Ability to communicate a choice refers to a patient’s ability to express his or her wishes in a reasonably stable manner. Factual understanding of the issues refers to an individual’s ability to understand the relevant facts before making a decision. Appreciation of the situation and its consequences refers to a person’s ability to rationally understand the effect of decisions. Appreciation is a higher level of understanding than mere factual understanding—eg, a delusional patient who believes himself immortal may intellectually understand that a surgical procedure carries a 50% mortality risk, but may be unable to appreciate the information as it relates to him because he believes he is immortal. Rational manipulation of information refers to a patient’s reasoning process and how the patient integrates data into his or her decision-making process.⁵

Informed consent. In my experience, capacity to give informed consent is the most commonly requested specific capacity assessment in general medical settings. Informed consent must be knowing, voluntary, and competent. All material information—information that would cause a reasonable person to accept or reject a proposed treatment—should be communicated to the patient. Informed consent requires an understanding of the patient’s condition and indication for treatment, risks and benefits of and alternatives to treatment, and risks of declining treatment.^2,3 Exceptions to informed consent include incompetence, medical emergencies, patient waiver of informed consent, and a limited therapeutic privilege (when a physician determines that the information would harm the patient).³

Several instruments can help clinicians assess patients’ capacity to give informed consent. The benefits of using a structured instrument include:

• ensuring that specific information is covered during each evaluation
• systematically recording a patient’s response.⁵

Disadvantages of using instruments include the fact that no instrument can take into account all aspects of a particular case, and some instruments are time-consuming and require training. Structured instruments can be a useful adjunct to the clinical interview in some cases, but should not substitute for it. In a review of 23 instruments for assessing decisional capacity to consent to treatment or clinical research, the MacArthur Competence Assessment Tool for Clinical Research and the MacArthur Competence Assessment Tool for Treatment had the most empirical support, although the authors noted that other instruments might be better suited to specific situations.⁷

Psychiatrists may be consulted when a patient refuses treatment or decides to leave the hospital against medical advice. The key issue in both situations is whether the patient has capacity to refuse treatment.⁸ If there is evidence that the patient is mentally ill and poses an imminent risk of suicide or violence or is unable to provide for his or her basic needs, the psychiatrist should assess whether the patient meets criteria for civil commitment.

Many clinicians employ a “sliding scale” approach to competence, requiring a lower degree of competence for consenting to low-risk, high-benefit interventions and a greater degree of competence for higher-risk procedures.^5,9 Family members often serve as informal surrogate decision makers for incapacitated patients, except when there is significant family discord or no family members are available.⁵

Guardianship. Guardians are appointed by courts to make decisions for individuals who have been found incompetent (wards). Although its purposes are beneficent, the guardianship system could do significant harm.¹⁰ Determining that an individual is incompetent is tantamount to depriving him or her of basic personhood. In many cases, the ward loses the ability to consent to or refuse medical care, manage his or her finances, enter into contracts, marry, and determine where he or she will live. On the other hand, failing to recognize incompetence can leave a vulnerable person in danger of physical deterioration, abuse, neglect, or exploitation.

It is critical that guardianship evaluations be conducted carefully. In a review of 298 guardianship cases from 3 states, Moye and colleagues¹¹ found that the quality of the reports was significantly better in Colorado, a state with guardianship reforms, but documentation of functional strengths and weaknesses was “particularly rare” in guardianship evaluations and prognosis often was not included. This information is relevant to judges, who need to determine which areas of function are impaired and how long the impairment is likely to last.

Guardianship evaluations often focus on general rather than specific capacity. In other words, often there is not a specific task such as consenting to surgery that the alleged incompetent person needs to perform. Rather, the question is whether an individual can manage his or her finances or make treatment decisions in general. Appelbaum and Gutheil suggest considering 6 factors when assessing general capacity:

• awareness of the situation
• factual understanding of the issues
• appreciation of the likely consequences
• rational manipulation of information
• functioning in one’s environment
• extent of demands on patient.⁵

The first 4 are closely related to the elements of specific capacity described above. Functioning in one’s environment and extent of demands on the patient attempt to anticipate the tasks that an individual will need to perform. A patient with mild dementia may be unable to manage a complex estate but can handle a bank account and a fixed income. Similarly, it is important to consider the patient’s support system. An impaired patient may function adequately with his wife’s help but may lose the capacity to live independently if his wife dies or becomes impaired.

Traditionally, guardianship has resulted in a complete loss of decision-making ability. Several state legislatures have passed laws allowing for limited guardianship, although orders for limited guardianship remain underutilized.¹⁰ Limited guardianship delineates specific areas of incompetence and limits the guardian’s decision-making authority to those areas while leaving intact the ward’s ability to make all other decisions for himself or herself.

The use of less-restrictive alternatives to guardianship—such as powers of attorney, durable powers of attorney, living wills, payees, and trusts—is increasing. A power of attorney allows a patient to authorize a specific individual to act on his or her behalf. The scope of the power of attorney can be limited, such as to manage finances or even to a specific transaction, such as selling a home or car. A durable power of attorney also allows an agent to make decisions on the patient’s behalf but becomes active only when the patient becomes incompetent. It often is used to appoint an individual to make medical decisions on behalf of an incompetent patient. Living wills allow patients to determine what treatment they would like in the event they become incompetent.

Elder abuse. An estimated 1 to 2 million adults age >65 have been abused, exploited, or neglected.¹² Elder abuse includes physical abuse, neglect, emotional abuse, sexual abuse, and financial exploitation (including undue influence). Most states have mandatory reporting of elder abuse, although they vary regarding who must report and what the report must entail. Psychiatrists should be vigilant in looking for signs of elder abuse (Table 2),¹³ regardless of the reason for the consult.

Table 2

Signs of elder abuse: What to wlook for

10 tips for thorough evaluations

1. Consider the context of the consultation. This includes medical factors (such as the patient’s condition, prognosis, relationship with the treatment team, and recommended course of treatment), legal factors (eg, pending litigation and relevant legal standards for issues such as guardianship), and psychosocial issues (eg, the patient’s current support structure and family conflicts).

2. Identify the legal issue and any relevant legal standards. The legal standard will inform you of the issues you need to address in the evaluation. If an attorney has consulted you, ask him or her to provide the legal standard.

3. Gather relevant collateral information, which may include interviews with family members or a review of financial or medical records.

4. Explain the purpose of the examination and the limits of confidentiality.

5. Perform a focused psychiatric evaluation, paying special attention to cognitive functioning, reasoning, and unusual thought content such as delusional beliefs.

6. Perform an interview specific to the referral issue.

7. Consider using a relevant assessment instrument.

8. Consider psychological testing, laboratory testing, imaging, or further medical evaluation. These assessments can help determine the diagnosis, the cause of any deficits in capacity, and whether any deficits are reversible.

9. Determine what opinions you are able to render. Limit opinions and remember that it may be appropriate to decline to address certain issues if there is insufficient information or if the issue is outside your area of expertise.

10. Prepare a written report. Consider the audience. Minimize the use of medical jargon and define all medical terms. State your opinions clearly and with reasonable medical certainty (in most jurisdictions, this means more likely than not). State the basis for all opinions.

For a case study that provides an example of a psycho-legal evaluation of a geriatric patient, see the Box.

Box

Related Resources

• American Academy of Psychiatry and the Law. www.aapl.org.
• American Bar Association Commission on Law and Aging. www.americanbar.org/groups/law_aging.html.
• National Center on Elder Abuse. www.ncea.aoa.gov.

Disclosure

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

Acknowledgement

The author thanks forensic psychiatry fellow Abhishek Jain, MD for reviewing the article and offering editorial suggestions.

Discuss this article at www.facebook.com/CurrentPsychiatry

Although forensic psychiatrists typically are consulted in complex legal matters, geriatric, consultation-liaison, and general psychiatrists are on the front lines of assessing capacity to give informed consent and need for guardianship. Psychiatrists often find such consultations daunting because residency training usually includes little to no formal training in performing psycho-legal assessments. Evaluating issues such as decision-making capacity, guardianship, and capacity to give informed consent requires a delicate balance between autonomy and beneficence. This article reviews 4 common legal issues in geriatric consultation—capacity evaluations, informed consent, guardianship, and elder abuse—and suggests a systematic approach to psycho-legal consultations in older adults.

Confidentiality and dual agency

Every psychiatrist should be familiar with basic principles of medical ethics as well as key aspects of local mental health law. Relevant ethical principles include autonomy, beneficence, confidentiality, and dual agency. A review of all these ethical issues is beyond the scope of this article, so here I highlight confidentiality and dual agency.

Confidentiality—the clinician’s obligation not to disclose private medical information—is a legal as well as an ethical requirement. A psychiatrist who performs a psycho-legal evaluation must disclose to the patient the purpose of the evaluation, that a report will be prepared, and to whom it will be submitted. Exceptions to confidentiality include medical emergencies, mandatory reporting of abuse and infectious diseases, and the duty to protect (warning police and the intended victim when a patient makes a threat).

Dual agency or dual role refers to serving as both a treating physician and a forensic evaluator. Although it is ideal to avoid serving in a dual role, sometimes it is impractical or impossible to avoid doing so, such as in guardianship or civil commitment evaluations, or in state forensic hospitals. In such cases, the psychiatrist must be aware of potential conflicts between clinical and forensic evaluations. A treating psychiatrist primarily serves his or her patient’s best interest, whereas a forensic psychiatrist primarily seeks truth.¹ A treating psychiatrist is at risk of consciously or unconsciously biasing his or her psycho-legal evaluation in favor of or against the patient/litigant, depending upon the psychiatrist’s countertransference. Further, performing a psycho-legal evaluation can cause problems in ongoing treatment. A psychiatrist who testifies that his or her fiercely independent patient needs a guardian or nursing home placement will experience significant challenges in continuing to work with that patient.

4 common issues for older adults

Decision-making capacity. Although “capacity” and “competence” often are used interchangeably, “capacity” broadly refers to the ability to perform a specific task, whereas “competence” refers to the legally defined standard for performing a specific task such as making a will. “Competence” is legally determined, whereas “capacity” may be determined clinically.

Capacity usually is task-specific rather than a general construct. The existence of physical or mental illness per se does not mean that a patient lacks capacity. Rather, capacity is determined by whether an individual has specific abilities, regardless of diagnosis. Specific capacities include the ability to give informed consent, manage finances, make a will, or enter into contracts (Table 1).^2-4 Appelbaum and Gutheil describe 4 components for assessing specific capacity:

• communication of a choice
• factual understanding of the issues
• appreciation of the situation and its consequences
• rational manipulation of information.^5,6

Table 1

Criteria of 3 specific capacities

Ability to communicate a choice refers to a patient’s ability to express his or her wishes in a reasonably stable manner. Factual understanding of the issues refers to an individual’s ability to understand the relevant facts before making a decision. Appreciation of the situation and its consequences refers to a person’s ability to rationally understand the effect of decisions. Appreciation is a higher level of understanding than mere factual understanding—eg, a delusional patient who believes himself immortal may intellectually understand that a surgical procedure carries a 50% mortality risk, but may be unable to appreciate the information as it relates to him because he believes he is immortal. Rational manipulation of information refers to a patient’s reasoning process and how the patient integrates data into his or her decision-making process.⁵

Informed consent. In my experience, capacity to give informed consent is the most commonly requested specific capacity assessment in general medical settings. Informed consent must be knowing, voluntary, and competent. All material information—information that would cause a reasonable person to accept or reject a proposed treatment—should be communicated to the patient. Informed consent requires an understanding of the patient’s condition and indication for treatment, risks and benefits of and alternatives to treatment, and risks of declining treatment.^2,3 Exceptions to informed consent include incompetence, medical emergencies, patient waiver of informed consent, and a limited therapeutic privilege (when a physician determines that the information would harm the patient).³

Several instruments can help clinicians assess patients’ capacity to give informed consent. The benefits of using a structured instrument include:

• ensuring that specific information is covered during each evaluation
• systematically recording a patient’s response.⁵

Disadvantages of using instruments include the fact that no instrument can take into account all aspects of a particular case, and some instruments are time-consuming and require training. Structured instruments can be a useful adjunct to the clinical interview in some cases, but should not substitute for it. In a review of 23 instruments for assessing decisional capacity to consent to treatment or clinical research, the MacArthur Competence Assessment Tool for Clinical Research and the MacArthur Competence Assessment Tool for Treatment had the most empirical support, although the authors noted that other instruments might be better suited to specific situations.⁷

Psychiatrists may be consulted when a patient refuses treatment or decides to leave the hospital against medical advice. The key issue in both situations is whether the patient has capacity to refuse treatment.⁸ If there is evidence that the patient is mentally ill and poses an imminent risk of suicide or violence or is unable to provide for his or her basic needs, the psychiatrist should assess whether the patient meets criteria for civil commitment.

Many clinicians employ a “sliding scale” approach to competence, requiring a lower degree of competence for consenting to low-risk, high-benefit interventions and a greater degree of competence for higher-risk procedures.^5,9 Family members often serve as informal surrogate decision makers for incapacitated patients, except when there is significant family discord or no family members are available.⁵

Guardianship. Guardians are appointed by courts to make decisions for individuals who have been found incompetent (wards). Although its purposes are beneficent, the guardianship system could do significant harm.¹⁰ Determining that an individual is incompetent is tantamount to depriving him or her of basic personhood. In many cases, the ward loses the ability to consent to or refuse medical care, manage his or her finances, enter into contracts, marry, and determine where he or she will live. On the other hand, failing to recognize incompetence can leave a vulnerable person in danger of physical deterioration, abuse, neglect, or exploitation.

It is critical that guardianship evaluations be conducted carefully. In a review of 298 guardianship cases from 3 states, Moye and colleagues¹¹ found that the quality of the reports was significantly better in Colorado, a state with guardianship reforms, but documentation of functional strengths and weaknesses was “particularly rare” in guardianship evaluations and prognosis often was not included. This information is relevant to judges, who need to determine which areas of function are impaired and how long the impairment is likely to last.

Guardianship evaluations often focus on general rather than specific capacity. In other words, often there is not a specific task such as consenting to surgery that the alleged incompetent person needs to perform. Rather, the question is whether an individual can manage his or her finances or make treatment decisions in general. Appelbaum and Gutheil suggest considering 6 factors when assessing general capacity:

• awareness of the situation
• factual understanding of the issues
• appreciation of the likely consequences
• rational manipulation of information
• functioning in one’s environment
• extent of demands on patient.⁵

The first 4 are closely related to the elements of specific capacity described above. Functioning in one’s environment and extent of demands on the patient attempt to anticipate the tasks that an individual will need to perform. A patient with mild dementia may be unable to manage a complex estate but can handle a bank account and a fixed income. Similarly, it is important to consider the patient’s support system. An impaired patient may function adequately with his wife’s help but may lose the capacity to live independently if his wife dies or becomes impaired.

Traditionally, guardianship has resulted in a complete loss of decision-making ability. Several state legislatures have passed laws allowing for limited guardianship, although orders for limited guardianship remain underutilized.¹⁰ Limited guardianship delineates specific areas of incompetence and limits the guardian’s decision-making authority to those areas while leaving intact the ward’s ability to make all other decisions for himself or herself.

The use of less-restrictive alternatives to guardianship—such as powers of attorney, durable powers of attorney, living wills, payees, and trusts—is increasing. A power of attorney allows a patient to authorize a specific individual to act on his or her behalf. The scope of the power of attorney can be limited, such as to manage finances or even to a specific transaction, such as selling a home or car. A durable power of attorney also allows an agent to make decisions on the patient’s behalf but becomes active only when the patient becomes incompetent. It often is used to appoint an individual to make medical decisions on behalf of an incompetent patient. Living wills allow patients to determine what treatment they would like in the event they become incompetent.

Elder abuse. An estimated 1 to 2 million adults age >65 have been abused, exploited, or neglected.¹² Elder abuse includes physical abuse, neglect, emotional abuse, sexual abuse, and financial exploitation (including undue influence). Most states have mandatory reporting of elder abuse, although they vary regarding who must report and what the report must entail. Psychiatrists should be vigilant in looking for signs of elder abuse (Table 2),¹³ regardless of the reason for the consult.

Table 2

Signs of elder abuse: What to wlook for

10 tips for thorough evaluations

1. Consider the context of the consultation. This includes medical factors (such as the patient’s condition, prognosis, relationship with the treatment team, and recommended course of treatment), legal factors (eg, pending litigation and relevant legal standards for issues such as guardianship), and psychosocial issues (eg, the patient’s current support structure and family conflicts).

2. Identify the legal issue and any relevant legal standards. The legal standard will inform you of the issues you need to address in the evaluation. If an attorney has consulted you, ask him or her to provide the legal standard.

3. Gather relevant collateral information, which may include interviews with family members or a review of financial or medical records.

4. Explain the purpose of the examination and the limits of confidentiality.

5. Perform a focused psychiatric evaluation, paying special attention to cognitive functioning, reasoning, and unusual thought content such as delusional beliefs.

6. Perform an interview specific to the referral issue.

7. Consider using a relevant assessment instrument.

8. Consider psychological testing, laboratory testing, imaging, or further medical evaluation. These assessments can help determine the diagnosis, the cause of any deficits in capacity, and whether any deficits are reversible.

9. Determine what opinions you are able to render. Limit opinions and remember that it may be appropriate to decline to address certain issues if there is insufficient information or if the issue is outside your area of expertise.

10. Prepare a written report. Consider the audience. Minimize the use of medical jargon and define all medical terms. State your opinions clearly and with reasonable medical certainty (in most jurisdictions, this means more likely than not). State the basis for all opinions.

For a case study that provides an example of a psycho-legal evaluation of a geriatric patient, see the Box.

Box

Related Resources

• American Academy of Psychiatry and the Law. www.aapl.org.
• American Bar Association Commission on Law and Aging. www.americanbar.org/groups/law_aging.html.
• National Center on Elder Abuse. www.ncea.aoa.gov.

Disclosure

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

Acknowledgement

The author thanks forensic psychiatry fellow Abhishek Jain, MD for reviewing the article and offering editorial suggestions.

Discuss this article at www.facebook.com/CurrentPsychiatry

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

The Centers for Disease Control and Prevention recommends that all health care professionals use an ethanol-based hand sanitizer to decontaminate their hands before and after direct contact with patients to prevent infection.^1,2 As a result, many psychiatric hospitals use alcohol-based hand sanitizers as a primary infection control measure.

Patient misuse of these products as intoxicants has been reported in prisons, emergency rooms, and medical units.^3-7 We report 2 cases of psychiatric inpatients who intentionally ingested alcohol-based hand sanitizers to become intoxicated; there were no permanent toxic effects in either case.

Case 1

Mr. F, age 52, is diagnosed with polysubstance dependence and bipolar disorder and hospitalized for acute exacerbation of mania characterized by unrestrained buying sprees, racing thoughts, grandiosity, and a persistently irritable mood. On day 3 of admission, he presents as stuporous and disorganized, with a strong odor of alcohol on his breath. He admits drinking an alcohol-based hand sanitizer foaming solution, an empty bottle of which is found in his room. His serum alcohol level is 176 mg/dL; the threshold concentration above which a person is considered legally drunk when operating a motor vehicle is 100 mg/dL. Other laboratory values, including urine toxicology, were negative.

Case 2

Mr. V, age 47, has schizophrenia, cocaine dependence, and antisocial personality disorder. He is admitted for command auditory hallucinations and a suicide attempt by overdose. On day 6 of hospitalization, staff members find him delirious and confused. Mr. V confesses to drinking an alcohol-based hand sanitizer solution for the past 3 days. His vital signs are stable, and his serum alcohol level is 142 mg/dL.

Limiting access

Hand sanitizer has a much higher alcohol concentration than several common alcoholic drinks Table^8,9 Ethyl alcohol, the active ingredient in hand sanitizers, is responsible for the adverse effects seen in our patients; the inactive ingredients—glycerin, propylene glycol, tocopherol acetate, isopropyl myristate, and aminomethyl propanol—generally are recognized as safe by the FDA and the Cosmetic Ingredient Review Expert Panel.^10,11 Although hospitals routinely restrict patients’ access to traditional forms of alcohol, hand sanitizer is easily accessible in many facilities. In our cases, having the alcohol-based sanitizer placed throughout the unit and readily available to patients made it easy for at-risk patients to become intoxicated. As suggested by Weiner,⁷ replacing bottles of hand sanitizer with self-contained, wall-mounted dispensers that are difficult for patients to remove might decrease the likelihood of ingestion.

Table

Alcohol content of hand sanitizers and beverages

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Over the past 20 years, the recovery movement in mental health care has transformed the way in which clinicians and behavioral health agencies view and treat persons with serious mental illnesses. The New Freedom Commission on Mental Health defined recovery as “the process in which people are able to live, work, learn, and participate in their communities.” This process supports a clinical approach to psychiatric care that promotes opportunity, hope, and social inclusion.¹ As professionals, “our primary interest should be to take the principles and concepts of [r]ecovery and to look at ways in which our practices and services could be orientated to facilitate [r]ecovery in the people who use them.”²

Drawing upon the Substance Abuse and Mental Health Services Administration’s core principles of a recovery-oriented approach,³ the mnemonic PARTNERS may help you recall key concepts to delivering and assessing recovery-oriented care.

Person-centered approaches recognize the patient’s unique gifts, strengths, needs, and cultural perspectives. Treatment is based upon the patient’s resiliencies, deficits, and personal goals, not just algorithms.

Autonomy emphasizes the patient’s right to determine his or her own destiny. It serves as the justification for the recovery maxim of “no decision about me, without me.”

Responsibility recognizes that the choices, decisions, and consequences about the type, amount, and frequency of care are a shared responsibility between physician and patient.

Transformational interactions and attitudes occur between the physician, the patient, and the system in a recovery-oriented model of care. The physician, patient, and agency are transformed into partners in the healing process.

Nonlinear concepts highlight the expectation that a patient’s pathway to recovery inevitably will be punctuated by personal gains, uneventful plateaus, and the occasional setback.

Empowerment is patients’ growing sense that they can speak openly and freely about their needs, hopes, and life goals, individually or through support and advocacy groups.

Respect is the bedrock value that defines the physician/patient relationship and ensures the absence of discrimination and stigmatization within behavioral health systems.

Strength-based approaches remind the physician that valuing and building upon the patient’s core strengths, talents, and positive attributes, rather than narrowly focusing on personal deficits, fuels the recovery process.

Disclosure

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

Approximately 75% of women experience a premenstrual change in emotional or physical symptoms commonly referred to as premenstrual syndrome (PMS). These symptoms—including increased irritability, tension, depressed mood, and somatic complaints such as breast tenderness and bloating—often are mild to moderate and cause minimal distress.¹ However, approximately 3% to 9% of women experience moderate to severe premenstrual mood symptoms that meet criteria for premenstrual dysphoric disorder (PMDD).²

PMDD includes depressed or labile mood, anxiety, irritability, anger, insomnia, difficulty concentrating, and other symptoms that occur exclusively during the 2 weeks before menses and cause significant deterioration in daily functioning. Women with PMDD use general and mental health services more often than women without the condition.³ They may experience impairment in marital and parental relationships as severe as that experienced by women with recurrent or chronic major depression.²

PMDD often responds to treatment. Unfortunately, many women with PMDD do not seek treatment, and up to 90% may go undiagnosed.⁴ In this article, we review the prevalence, etiology, diagnosis, and treatment of PMDD.

A complex disorder

A distinguishing characteristic of PMDD is the timing of symptom onset. In women with PMDD, mood symptoms occur only during the luteal phase of the menstrual cycle (ovulation until onset of menses) and resolve after menstruation onset. Women with PMDD report normal mood and functioning during the follicular phase of the menstrual cycle (first day of the menstrual cycle until ovulation).

Although PMS and PMDD criteria share affective and somatic symptoms, more symptoms are required for a PMDD diagnosis, and symptoms often are more severe.⁵ As defined in DSM-IV-TR (Table),⁶ PMDD has a broader range of symptoms than PMS and includes symptoms not included in the American College of Obstetrics and Gynecology criteria for PMS,⁷ such as impaired concentration, appetite, and sleep (hypersomnia or insomnia); and mood lability. PMDD symptoms must occur only during the 2 weeks preceding menses, although on average symptoms last 6 days and severity usually peaks in the 2 days before menses.¹ The prevalence of subthreshold PMDD is fairly common; approximately 19% of women will meet some—but not all—DSM-IV-TR criteria for PMDD.³

In a revision proposed for DSM-5, PMDD would be included as a mood disorder, which represents a significant change from DSM-IV-TR, where it is listed in the appendix as “research criteria.”⁸ In addition, in oral contraceptive users, a PMDD diagnosis should not be made unless the premenstrual symptoms are reported to be present and as severe when the woman is not taking the oral contraceptive.⁸

Comorbidity with other axis I disorders such as major depressive disorder (MDD), bipolar disorder (BD), and anxiety disorders is high.^9-11 Women with an MDD history have the highest correlation with PMDD,⁹ and worsening premenstrual mood symptoms are more common in women with BD.¹² Payne et al¹¹ found that premenstrual symptoms were reported by twice as many women diagnosed with mood disorders (68%) than women without a psychiatric diagnosis (34%). Moreover, 38% to 46% of women with PMDD have comorbid seasonal affective disorder, and 11% to 38% report a comorbid anxiety disorder.¹² Women with PMDD and a history of MDD have lower cortisol concentrations than non-PMDD women.¹⁰ Although interventions for PMDD and a comorbid axis I disorder may be similar, it is important to consider both when planning treatment.

Abuse, trauma, and PMDD. An association between PMS/PMDD and a history of sexual and physical abuse is well-documented.¹³ Studies have reported abuse histories among almost 60% of women with PMDD,¹⁴ although studies comparing abuse and trauma in PMDD vs non-PMDD women have been small. A recent study found that trauma and posttraumatic stress disorder are independently associated with PMDD and premenstrual symptoms.¹⁵

Evidence suggests that a history of abuse is associated with specific biological sequelae in PMDD women, particularly with respect to hypothalamic-pituitary-thyroid axis measures and noradrenergic activity.^16-18 Women with PMDD and a history of sexual abuse show:

• markedly elevated triiodothyronine (T3) concentrations (the more biologically potent thyroid hormone) that appear to result from increased conversion of thyroxine (T4) to T3¹⁶
• lower circulating plasma norepinephrine concentrations¹⁷
• greater resting and stress-induced heart rates and systolic blood pressure compared with non-abused PMDD women, an effect that is eliminated by clonidine (an α-2 adrenergic receptor agonist).¹⁸

One study showed that PMDD women with abuse histories had higher blood pressure measurements at rest and during stress and exhibited greater vascular tone than non-abused women; these effects were not seen in non-PMDD women with similar abuse histories.¹⁴ This body of evidence is consistent with the concept that PMDD is a stress-related disorder,¹⁹ and that a history of abuse is prevalent and may identify a clinically distinct subgroup of PMDD women with respect to thyroid axis and adrenergic physiology. Screening PMDD patients for abuse histories may help manage the disorder.

For a discussion of the etiology of PMDD, see Box 1.

Table

DSM-IV-TR research criteria for PMDD

Box 1

Mood charting aids diagnosis

A PMDD diagnosis requires prospective daily monitoring of symptoms for ≥2 consecutive months. Because only 25% to 35% of women who present with PMDD meet diagnostic criteria when prospective daily monitoring is used,²⁰ it is important for patients to keep a daily diary of PMDD symptoms to distinguish the disorder from PMS (Box 2). The Prospective Record of the Impact and Severity of Premenstrual Symptoms calendar and the Daily Record of Severity of Problems (DRSPP)²¹ may help make the diagnosis.

The widely used DRSPP allows clinicians to quantify the severity of physical, emotional, and behavioral symptoms and may be the easiest to use in clinical practice because it creates a graphic representation of cyclical symptom changes. The DRSPP includes all PMDD symptoms and severity ratings²¹ and is recognized as a valid instrument for diagnosing PMDD. Another option is a revised visual analogue scale. Lastly, a new revised Premenstrual Tension Syndrome (PMTS) rating scale, which combines the PMTS Observer rating scale plus multiple visual analogue scales, shows promise as a tool to assess PMDD symptoms.

Box 2

Treatment options

Hormonal interventions. Attempts to treat PMS with progesterone during the luteal phase have been largely unsuccessful, although progesterone is approved to treat PMS in the United Kingdom. Long-acting gonadotropin-releasing hormone (GnRH) agonists are effective but result in medical menopause with its accompanying symptoms, which puts women at risk for osteoporosis.²² Approximately 60% to 70% of women with PMDD respond to leuprolide (a GnRH agonist), but it is difficult to predict who will respond; daily mood self-ratings of sadness, anxiety, and irritability predict a positive response to leuprolide with high probability.²³ Side effects of GnRH agonists (hot flashes, night sweats, vaginal dryness, etc.) can be tempered by “adding back” some estrogen with a hormonal agent with progestational activity to reduce the risks of unopposed estrogen (ie, endometrial hyperplasia).²⁴

Surgical bilateral oophorectomy is effective but extremely invasive, especially in younger women in whom removal of ovaries generally is inadvisable. Patients should receive a trial of a GnRH agonist before a surgical intervention, because oophorectomy may not reduce symptoms and is irreversible. Oophorectomy also would require hormone replacement therapy.

High-dose estrogen as transdermal patches or subcutaneous implants to inhibit ovulation is effective, but because of the risks of unopposed estrogen, a progestin would be needed. Risks of estrogen therapy (alone and in combination with progestins) include increased risk of endometrial cancer, coronary heart disease, breast cancer, stroke, and pulmonary embolism.²⁵ Danazol, a synthetic androgen and gonadotropin inhibitor, effectively blocks ovulation, but side effects include hirsutism and possible teratogenicity.²⁶ Although these hormonal manipulations may effectively treat PMDD, none are considered practical.

The use of combined oral contraceptives (estrogen and progestin) is common. Although continuous cycle oral contraceptives often are recommended for PMDD, limited evidence supports their use; studies have been mostly negative.^27,28 A recent review of 4 studies of a continuous oral contraceptive (levonorgestrel 90 mcg/ethinyl estradiol 20 mcg) for PMDD and PMS had more promising results, although the results were highly variable among studies and a large placebo effect was observed.²⁹

A combination oral contraceptive, drospirenone/ethinyl estradiol, is FDA-approved for treating PMDD in women seeking hormonal contraception because it has shown efficacy compared with placebo, with reported improvements in perceived productivity, social activities, and interpersonal relationships.³⁰ The nature of hormone delivery (ie, a reduction in the pill-free interval from 7 to 4 days) in drospirenone/ethinyl estradiol may contribute to its efficacy because a reduced pill-free interval minimizes the degree of follicular recruitment and subsequent estrogen production and cyclicity seen with standard oral contraceptive.³¹

Antidepressants have been shown to effectively ameliorate affective and physical symptoms and improve quality of life and psychosocial function in patients with PMS and PMDD. The response rates for selective serotonin reuptake inhibitors (SSRIs) in PMDD treatment vary from 60% to 90%, vs 30% to 40% for placebo.³² A 2009 Cochrane review found SSRIs reduced premenstrual symptoms compared with placebo.³³ However, a literature review suggested that the percentage of women with PMDD who respond to SSRIs or continuous oral contraceptives is lower than the percentage of women who do not respond at all, once the placebo effect is taken into account, and that approximately 40% of women with PMDD do not respond to SSRIs.³⁴ A small study found that citalopram may be effective for women with PMDD who did not respond to a prior SSRI.³⁵

However, only antidepressants that affect serotonergic—not noradrenergic—transmission are effective in PMDD.²² These include:

• the tricyclic antidepressant clomipramine
• the SSRIs citalopram, escitalopram, fluoxetine, paroxetine, and sertraline
• the serotonin-noradrenergic reuptake inhibitor venlafaxine.

It appears that in PMDD, serotonergic agents play a role other than their antidepressant effect.³⁶ The effect of these agents is rapid in PMS/PMDD; women with PMDD who take antidepressants often experience reduced symptoms within the first menstrual cycle, whereas in MDD the onset of action can take weeks or months.³⁷

Although why onset of antidepressant action is quick in PMDD is unclear, rapid onset allows for several dosing options. Some women prefer continuous dosing throughout the month because they do not have to keep track of ovulation. Dosing antidepressants only in the luteal phase (taking the antidepressant from ovulation onset to the start of menses) is an effective treatment strategy.³⁸ Many women prefer to take medication for only 2 weeks per month, which can decrease side effects and lower treatment costs. Alternatively, symptom-onset dosing—initiating the antidepressant when PMDD symptoms begin and stopping at menses onset or within 3 days thereafter—has shown promising results.^39,40 Paroxetine, sertraline, and fluoxetine are FDA-approved for PMDD as continuous or intermittent regimens, although using fluoxetine intermittently may not make sense because its biologically active metabolite has an extended half-life.³⁷

Other treatments. Dietary interventions, psychotherapy, vitamins, bright light treatment, and spironolactone have been assessed for PMS/PMDD, although for many evidence-based findings are lacking (Box 3).

See the Bibliography below for studies that support using antidepressants to treat PMDD

Box 3

Bibliography

Treatment selection

To enhance compliance and improve the likelihood of successful treatment, tailor treatment decisions to your patient’s needs. Carefully discuss with your patient the evidence-based literature to select the best option for her. Factors to consider when counseling patients include:

• the patient’s age, cigarette smoking habits, and body mass index, which may contraindicate oral contraceptives
• does the patient have regular cycle lengths?
• can she adhere to an on-off schedule? If so, intermittent SSRI dosing may be a good treatment option
• does the patient have irregular cycles?
• is there evidence that symptoms persist into the follicular phase, albeit at a lower level? If so, continuous SSRI dosing may be the best option.

Related Resources

• American Psychiatric Association. DSM-5 development: D 04 Premenstrual dysphoric disorder. www.dsm5.org/proposedrevision/pages/proposedrevision.aspx?rid=484.

Drug Brand Names

• Citalopram • Celexa
• Clomipramine • Anafranil
• Clonidine • Catapres, others
• Danazol • Danocrine
• Drospirenone/ethinyl estradiol • Yaz
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Leuprolide • Lupron
• Levonorgestrel/ethinyl estradiol • Seasonale, others
• Paroxetine • Paxil
• Progesterone • Prometrium
• Sertraline • Zoloft
• Spironolactone • Aldactone
• Venlafaxine • Effexor

Disclosures

Drs. Wakil and Girdler report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, The Foundation of Hope, and the National Institutes of Health.

Approximately 75% of women experience a premenstrual change in emotional or physical symptoms commonly referred to as premenstrual syndrome (PMS). These symptoms—including increased irritability, tension, depressed mood, and somatic complaints such as breast tenderness and bloating—often are mild to moderate and cause minimal distress.¹ However, approximately 3% to 9% of women experience moderate to severe premenstrual mood symptoms that meet criteria for premenstrual dysphoric disorder (PMDD).²

PMDD includes depressed or labile mood, anxiety, irritability, anger, insomnia, difficulty concentrating, and other symptoms that occur exclusively during the 2 weeks before menses and cause significant deterioration in daily functioning. Women with PMDD use general and mental health services more often than women without the condition.³ They may experience impairment in marital and parental relationships as severe as that experienced by women with recurrent or chronic major depression.²

PMDD often responds to treatment. Unfortunately, many women with PMDD do not seek treatment, and up to 90% may go undiagnosed.⁴ In this article, we review the prevalence, etiology, diagnosis, and treatment of PMDD.

A complex disorder

A distinguishing characteristic of PMDD is the timing of symptom onset. In women with PMDD, mood symptoms occur only during the luteal phase of the menstrual cycle (ovulation until onset of menses) and resolve after menstruation onset. Women with PMDD report normal mood and functioning during the follicular phase of the menstrual cycle (first day of the menstrual cycle until ovulation).

Although PMS and PMDD criteria share affective and somatic symptoms, more symptoms are required for a PMDD diagnosis, and symptoms often are more severe.⁵ As defined in DSM-IV-TR (Table),⁶ PMDD has a broader range of symptoms than PMS and includes symptoms not included in the American College of Obstetrics and Gynecology criteria for PMS,⁷ such as impaired concentration, appetite, and sleep (hypersomnia or insomnia); and mood lability. PMDD symptoms must occur only during the 2 weeks preceding menses, although on average symptoms last 6 days and severity usually peaks in the 2 days before menses.¹ The prevalence of subthreshold PMDD is fairly common; approximately 19% of women will meet some—but not all—DSM-IV-TR criteria for PMDD.³

In a revision proposed for DSM-5, PMDD would be included as a mood disorder, which represents a significant change from DSM-IV-TR, where it is listed in the appendix as “research criteria.”⁸ In addition, in oral contraceptive users, a PMDD diagnosis should not be made unless the premenstrual symptoms are reported to be present and as severe when the woman is not taking the oral contraceptive.⁸

Comorbidity with other axis I disorders such as major depressive disorder (MDD), bipolar disorder (BD), and anxiety disorders is high.^9-11 Women with an MDD history have the highest correlation with PMDD,⁹ and worsening premenstrual mood symptoms are more common in women with BD.¹² Payne et al¹¹ found that premenstrual symptoms were reported by twice as many women diagnosed with mood disorders (68%) than women without a psychiatric diagnosis (34%). Moreover, 38% to 46% of women with PMDD have comorbid seasonal affective disorder, and 11% to 38% report a comorbid anxiety disorder.¹² Women with PMDD and a history of MDD have lower cortisol concentrations than non-PMDD women.¹⁰ Although interventions for PMDD and a comorbid axis I disorder may be similar, it is important to consider both when planning treatment.

Abuse, trauma, and PMDD. An association between PMS/PMDD and a history of sexual and physical abuse is well-documented.¹³ Studies have reported abuse histories among almost 60% of women with PMDD,¹⁴ although studies comparing abuse and trauma in PMDD vs non-PMDD women have been small. A recent study found that trauma and posttraumatic stress disorder are independently associated with PMDD and premenstrual symptoms.¹⁵

Evidence suggests that a history of abuse is associated with specific biological sequelae in PMDD women, particularly with respect to hypothalamic-pituitary-thyroid axis measures and noradrenergic activity.^16-18 Women with PMDD and a history of sexual abuse show:

• markedly elevated triiodothyronine (T3) concentrations (the more biologically potent thyroid hormone) that appear to result from increased conversion of thyroxine (T4) to T3¹⁶
• lower circulating plasma norepinephrine concentrations¹⁷
• greater resting and stress-induced heart rates and systolic blood pressure compared with non-abused PMDD women, an effect that is eliminated by clonidine (an α-2 adrenergic receptor agonist).¹⁸

One study showed that PMDD women with abuse histories had higher blood pressure measurements at rest and during stress and exhibited greater vascular tone than non-abused women; these effects were not seen in non-PMDD women with similar abuse histories.¹⁴ This body of evidence is consistent with the concept that PMDD is a stress-related disorder,¹⁹ and that a history of abuse is prevalent and may identify a clinically distinct subgroup of PMDD women with respect to thyroid axis and adrenergic physiology. Screening PMDD patients for abuse histories may help manage the disorder.

For a discussion of the etiology of PMDD, see Box 1.

Table

DSM-IV-TR research criteria for PMDD

Box 1

Mood charting aids diagnosis

A PMDD diagnosis requires prospective daily monitoring of symptoms for ≥2 consecutive months. Because only 25% to 35% of women who present with PMDD meet diagnostic criteria when prospective daily monitoring is used,²⁰ it is important for patients to keep a daily diary of PMDD symptoms to distinguish the disorder from PMS (Box 2). The Prospective Record of the Impact and Severity of Premenstrual Symptoms calendar and the Daily Record of Severity of Problems (DRSPP)²¹ may help make the diagnosis.

The widely used DRSPP allows clinicians to quantify the severity of physical, emotional, and behavioral symptoms and may be the easiest to use in clinical practice because it creates a graphic representation of cyclical symptom changes. The DRSPP includes all PMDD symptoms and severity ratings²¹ and is recognized as a valid instrument for diagnosing PMDD. Another option is a revised visual analogue scale. Lastly, a new revised Premenstrual Tension Syndrome (PMTS) rating scale, which combines the PMTS Observer rating scale plus multiple visual analogue scales, shows promise as a tool to assess PMDD symptoms.

Box 2

Treatment options

Hormonal interventions. Attempts to treat PMS with progesterone during the luteal phase have been largely unsuccessful, although progesterone is approved to treat PMS in the United Kingdom. Long-acting gonadotropin-releasing hormone (GnRH) agonists are effective but result in medical menopause with its accompanying symptoms, which puts women at risk for osteoporosis.²² Approximately 60% to 70% of women with PMDD respond to leuprolide (a GnRH agonist), but it is difficult to predict who will respond; daily mood self-ratings of sadness, anxiety, and irritability predict a positive response to leuprolide with high probability.²³ Side effects of GnRH agonists (hot flashes, night sweats, vaginal dryness, etc.) can be tempered by “adding back” some estrogen with a hormonal agent with progestational activity to reduce the risks of unopposed estrogen (ie, endometrial hyperplasia).²⁴

Surgical bilateral oophorectomy is effective but extremely invasive, especially in younger women in whom removal of ovaries generally is inadvisable. Patients should receive a trial of a GnRH agonist before a surgical intervention, because oophorectomy may not reduce symptoms and is irreversible. Oophorectomy also would require hormone replacement therapy.

High-dose estrogen as transdermal patches or subcutaneous implants to inhibit ovulation is effective, but because of the risks of unopposed estrogen, a progestin would be needed. Risks of estrogen therapy (alone and in combination with progestins) include increased risk of endometrial cancer, coronary heart disease, breast cancer, stroke, and pulmonary embolism.²⁵ Danazol, a synthetic androgen and gonadotropin inhibitor, effectively blocks ovulation, but side effects include hirsutism and possible teratogenicity.²⁶ Although these hormonal manipulations may effectively treat PMDD, none are considered practical.

The use of combined oral contraceptives (estrogen and progestin) is common. Although continuous cycle oral contraceptives often are recommended for PMDD, limited evidence supports their use; studies have been mostly negative.^27,28 A recent review of 4 studies of a continuous oral contraceptive (levonorgestrel 90 mcg/ethinyl estradiol 20 mcg) for PMDD and PMS had more promising results, although the results were highly variable among studies and a large placebo effect was observed.²⁹

A combination oral contraceptive, drospirenone/ethinyl estradiol, is FDA-approved for treating PMDD in women seeking hormonal contraception because it has shown efficacy compared with placebo, with reported improvements in perceived productivity, social activities, and interpersonal relationships.³⁰ The nature of hormone delivery (ie, a reduction in the pill-free interval from 7 to 4 days) in drospirenone/ethinyl estradiol may contribute to its efficacy because a reduced pill-free interval minimizes the degree of follicular recruitment and subsequent estrogen production and cyclicity seen with standard oral contraceptive.³¹

Antidepressants have been shown to effectively ameliorate affective and physical symptoms and improve quality of life and psychosocial function in patients with PMS and PMDD. The response rates for selective serotonin reuptake inhibitors (SSRIs) in PMDD treatment vary from 60% to 90%, vs 30% to 40% for placebo.³² A 2009 Cochrane review found SSRIs reduced premenstrual symptoms compared with placebo.³³ However, a literature review suggested that the percentage of women with PMDD who respond to SSRIs or continuous oral contraceptives is lower than the percentage of women who do not respond at all, once the placebo effect is taken into account, and that approximately 40% of women with PMDD do not respond to SSRIs.³⁴ A small study found that citalopram may be effective for women with PMDD who did not respond to a prior SSRI.³⁵

However, only antidepressants that affect serotonergic—not noradrenergic—transmission are effective in PMDD.²² These include:

• the tricyclic antidepressant clomipramine
• the SSRIs citalopram, escitalopram, fluoxetine, paroxetine, and sertraline
• the serotonin-noradrenergic reuptake inhibitor venlafaxine.

It appears that in PMDD, serotonergic agents play a role other than their antidepressant effect.³⁶ The effect of these agents is rapid in PMS/PMDD; women with PMDD who take antidepressants often experience reduced symptoms within the first menstrual cycle, whereas in MDD the onset of action can take weeks or months.³⁷

Although why onset of antidepressant action is quick in PMDD is unclear, rapid onset allows for several dosing options. Some women prefer continuous dosing throughout the month because they do not have to keep track of ovulation. Dosing antidepressants only in the luteal phase (taking the antidepressant from ovulation onset to the start of menses) is an effective treatment strategy.³⁸ Many women prefer to take medication for only 2 weeks per month, which can decrease side effects and lower treatment costs. Alternatively, symptom-onset dosing—initiating the antidepressant when PMDD symptoms begin and stopping at menses onset or within 3 days thereafter—has shown promising results.^39,40 Paroxetine, sertraline, and fluoxetine are FDA-approved for PMDD as continuous or intermittent regimens, although using fluoxetine intermittently may not make sense because its biologically active metabolite has an extended half-life.³⁷

Other treatments. Dietary interventions, psychotherapy, vitamins, bright light treatment, and spironolactone have been assessed for PMS/PMDD, although for many evidence-based findings are lacking (Box 3).

See the Bibliography below for studies that support using antidepressants to treat PMDD

Box 3

Bibliography

Treatment selection

To enhance compliance and improve the likelihood of successful treatment, tailor treatment decisions to your patient’s needs. Carefully discuss with your patient the evidence-based literature to select the best option for her. Factors to consider when counseling patients include:

• the patient’s age, cigarette smoking habits, and body mass index, which may contraindicate oral contraceptives
• does the patient have regular cycle lengths?
• can she adhere to an on-off schedule? If so, intermittent SSRI dosing may be a good treatment option
• does the patient have irregular cycles?
• is there evidence that symptoms persist into the follicular phase, albeit at a lower level? If so, continuous SSRI dosing may be the best option.

Related Resources

• American Psychiatric Association. DSM-5 development: D 04 Premenstrual dysphoric disorder. www.dsm5.org/proposedrevision/pages/proposedrevision.aspx?rid=484.

Drug Brand Names

• Citalopram • Celexa
• Clomipramine • Anafranil
• Clonidine • Catapres, others
• Danazol • Danocrine
• Drospirenone/ethinyl estradiol • Yaz
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Leuprolide • Lupron
• Levonorgestrel/ethinyl estradiol • Seasonale, others
• Paroxetine • Paxil
• Progesterone • Prometrium
• Sertraline • Zoloft
• Spironolactone • Aldactone
• Venlafaxine • Effexor

Disclosures

Drs. Wakil and Girdler report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, The Foundation of Hope, and the National Institutes of Health.

Approximately 75% of women experience a premenstrual change in emotional or physical symptoms commonly referred to as premenstrual syndrome (PMS). These symptoms—including increased irritability, tension, depressed mood, and somatic complaints such as breast tenderness and bloating—often are mild to moderate and cause minimal distress.¹ However, approximately 3% to 9% of women experience moderate to severe premenstrual mood symptoms that meet criteria for premenstrual dysphoric disorder (PMDD).²

PMDD includes depressed or labile mood, anxiety, irritability, anger, insomnia, difficulty concentrating, and other symptoms that occur exclusively during the 2 weeks before menses and cause significant deterioration in daily functioning. Women with PMDD use general and mental health services more often than women without the condition.³ They may experience impairment in marital and parental relationships as severe as that experienced by women with recurrent or chronic major depression.²

PMDD often responds to treatment. Unfortunately, many women with PMDD do not seek treatment, and up to 90% may go undiagnosed.⁴ In this article, we review the prevalence, etiology, diagnosis, and treatment of PMDD.

A complex disorder

A distinguishing characteristic of PMDD is the timing of symptom onset. In women with PMDD, mood symptoms occur only during the luteal phase of the menstrual cycle (ovulation until onset of menses) and resolve after menstruation onset. Women with PMDD report normal mood and functioning during the follicular phase of the menstrual cycle (first day of the menstrual cycle until ovulation).

Although PMS and PMDD criteria share affective and somatic symptoms, more symptoms are required for a PMDD diagnosis, and symptoms often are more severe.⁵ As defined in DSM-IV-TR (Table),⁶ PMDD has a broader range of symptoms than PMS and includes symptoms not included in the American College of Obstetrics and Gynecology criteria for PMS,⁷ such as impaired concentration, appetite, and sleep (hypersomnia or insomnia); and mood lability. PMDD symptoms must occur only during the 2 weeks preceding menses, although on average symptoms last 6 days and severity usually peaks in the 2 days before menses.¹ The prevalence of subthreshold PMDD is fairly common; approximately 19% of women will meet some—but not all—DSM-IV-TR criteria for PMDD.³

In a revision proposed for DSM-5, PMDD would be included as a mood disorder, which represents a significant change from DSM-IV-TR, where it is listed in the appendix as “research criteria.”⁸ In addition, in oral contraceptive users, a PMDD diagnosis should not be made unless the premenstrual symptoms are reported to be present and as severe when the woman is not taking the oral contraceptive.⁸

Comorbidity with other axis I disorders such as major depressive disorder (MDD), bipolar disorder (BD), and anxiety disorders is high.^9-11 Women with an MDD history have the highest correlation with PMDD,⁹ and worsening premenstrual mood symptoms are more common in women with BD.¹² Payne et al¹¹ found that premenstrual symptoms were reported by twice as many women diagnosed with mood disorders (68%) than women without a psychiatric diagnosis (34%). Moreover, 38% to 46% of women with PMDD have comorbid seasonal affective disorder, and 11% to 38% report a comorbid anxiety disorder.¹² Women with PMDD and a history of MDD have lower cortisol concentrations than non-PMDD women.¹⁰ Although interventions for PMDD and a comorbid axis I disorder may be similar, it is important to consider both when planning treatment.

Abuse, trauma, and PMDD. An association between PMS/PMDD and a history of sexual and physical abuse is well-documented.¹³ Studies have reported abuse histories among almost 60% of women with PMDD,¹⁴ although studies comparing abuse and trauma in PMDD vs non-PMDD women have been small. A recent study found that trauma and posttraumatic stress disorder are independently associated with PMDD and premenstrual symptoms.¹⁵

Evidence suggests that a history of abuse is associated with specific biological sequelae in PMDD women, particularly with respect to hypothalamic-pituitary-thyroid axis measures and noradrenergic activity.^16-18 Women with PMDD and a history of sexual abuse show:

• markedly elevated triiodothyronine (T3) concentrations (the more biologically potent thyroid hormone) that appear to result from increased conversion of thyroxine (T4) to T3¹⁶
• lower circulating plasma norepinephrine concentrations¹⁷
• greater resting and stress-induced heart rates and systolic blood pressure compared with non-abused PMDD women, an effect that is eliminated by clonidine (an α-2 adrenergic receptor agonist).¹⁸

One study showed that PMDD women with abuse histories had higher blood pressure measurements at rest and during stress and exhibited greater vascular tone than non-abused women; these effects were not seen in non-PMDD women with similar abuse histories.¹⁴ This body of evidence is consistent with the concept that PMDD is a stress-related disorder,¹⁹ and that a history of abuse is prevalent and may identify a clinically distinct subgroup of PMDD women with respect to thyroid axis and adrenergic physiology. Screening PMDD patients for abuse histories may help manage the disorder.

For a discussion of the etiology of PMDD, see Box 1.

Table

DSM-IV-TR research criteria for PMDD

Box 1

Mood charting aids diagnosis

A PMDD diagnosis requires prospective daily monitoring of symptoms for ≥2 consecutive months. Because only 25% to 35% of women who present with PMDD meet diagnostic criteria when prospective daily monitoring is used,²⁰ it is important for patients to keep a daily diary of PMDD symptoms to distinguish the disorder from PMS (Box 2). The Prospective Record of the Impact and Severity of Premenstrual Symptoms calendar and the Daily Record of Severity of Problems (DRSPP)²¹ may help make the diagnosis.

The widely used DRSPP allows clinicians to quantify the severity of physical, emotional, and behavioral symptoms and may be the easiest to use in clinical practice because it creates a graphic representation of cyclical symptom changes. The DRSPP includes all PMDD symptoms and severity ratings²¹ and is recognized as a valid instrument for diagnosing PMDD. Another option is a revised visual analogue scale. Lastly, a new revised Premenstrual Tension Syndrome (PMTS) rating scale, which combines the PMTS Observer rating scale plus multiple visual analogue scales, shows promise as a tool to assess PMDD symptoms.

Box 2

Treatment options

Hormonal interventions. Attempts to treat PMS with progesterone during the luteal phase have been largely unsuccessful, although progesterone is approved to treat PMS in the United Kingdom. Long-acting gonadotropin-releasing hormone (GnRH) agonists are effective but result in medical menopause with its accompanying symptoms, which puts women at risk for osteoporosis.²² Approximately 60% to 70% of women with PMDD respond to leuprolide (a GnRH agonist), but it is difficult to predict who will respond; daily mood self-ratings of sadness, anxiety, and irritability predict a positive response to leuprolide with high probability.²³ Side effects of GnRH agonists (hot flashes, night sweats, vaginal dryness, etc.) can be tempered by “adding back” some estrogen with a hormonal agent with progestational activity to reduce the risks of unopposed estrogen (ie, endometrial hyperplasia).²⁴

Surgical bilateral oophorectomy is effective but extremely invasive, especially in younger women in whom removal of ovaries generally is inadvisable. Patients should receive a trial of a GnRH agonist before a surgical intervention, because oophorectomy may not reduce symptoms and is irreversible. Oophorectomy also would require hormone replacement therapy.

High-dose estrogen as transdermal patches or subcutaneous implants to inhibit ovulation is effective, but because of the risks of unopposed estrogen, a progestin would be needed. Risks of estrogen therapy (alone and in combination with progestins) include increased risk of endometrial cancer, coronary heart disease, breast cancer, stroke, and pulmonary embolism.²⁵ Danazol, a synthetic androgen and gonadotropin inhibitor, effectively blocks ovulation, but side effects include hirsutism and possible teratogenicity.²⁶ Although these hormonal manipulations may effectively treat PMDD, none are considered practical.

The use of combined oral contraceptives (estrogen and progestin) is common. Although continuous cycle oral contraceptives often are recommended for PMDD, limited evidence supports their use; studies have been mostly negative.^27,28 A recent review of 4 studies of a continuous oral contraceptive (levonorgestrel 90 mcg/ethinyl estradiol 20 mcg) for PMDD and PMS had more promising results, although the results were highly variable among studies and a large placebo effect was observed.²⁹

A combination oral contraceptive, drospirenone/ethinyl estradiol, is FDA-approved for treating PMDD in women seeking hormonal contraception because it has shown efficacy compared with placebo, with reported improvements in perceived productivity, social activities, and interpersonal relationships.³⁰ The nature of hormone delivery (ie, a reduction in the pill-free interval from 7 to 4 days) in drospirenone/ethinyl estradiol may contribute to its efficacy because a reduced pill-free interval minimizes the degree of follicular recruitment and subsequent estrogen production and cyclicity seen with standard oral contraceptive.³¹

Antidepressants have been shown to effectively ameliorate affective and physical symptoms and improve quality of life and psychosocial function in patients with PMS and PMDD. The response rates for selective serotonin reuptake inhibitors (SSRIs) in PMDD treatment vary from 60% to 90%, vs 30% to 40% for placebo.³² A 2009 Cochrane review found SSRIs reduced premenstrual symptoms compared with placebo.³³ However, a literature review suggested that the percentage of women with PMDD who respond to SSRIs or continuous oral contraceptives is lower than the percentage of women who do not respond at all, once the placebo effect is taken into account, and that approximately 40% of women with PMDD do not respond to SSRIs.³⁴ A small study found that citalopram may be effective for women with PMDD who did not respond to a prior SSRI.³⁵

However, only antidepressants that affect serotonergic—not noradrenergic—transmission are effective in PMDD.²² These include:

• the tricyclic antidepressant clomipramine
• the SSRIs citalopram, escitalopram, fluoxetine, paroxetine, and sertraline
• the serotonin-noradrenergic reuptake inhibitor venlafaxine.

It appears that in PMDD, serotonergic agents play a role other than their antidepressant effect.³⁶ The effect of these agents is rapid in PMS/PMDD; women with PMDD who take antidepressants often experience reduced symptoms within the first menstrual cycle, whereas in MDD the onset of action can take weeks or months.³⁷

Although why onset of antidepressant action is quick in PMDD is unclear, rapid onset allows for several dosing options. Some women prefer continuous dosing throughout the month because they do not have to keep track of ovulation. Dosing antidepressants only in the luteal phase (taking the antidepressant from ovulation onset to the start of menses) is an effective treatment strategy.³⁸ Many women prefer to take medication for only 2 weeks per month, which can decrease side effects and lower treatment costs. Alternatively, symptom-onset dosing—initiating the antidepressant when PMDD symptoms begin and stopping at menses onset or within 3 days thereafter—has shown promising results.^39,40 Paroxetine, sertraline, and fluoxetine are FDA-approved for PMDD as continuous or intermittent regimens, although using fluoxetine intermittently may not make sense because its biologically active metabolite has an extended half-life.³⁷

Other treatments. Dietary interventions, psychotherapy, vitamins, bright light treatment, and spironolactone have been assessed for PMS/PMDD, although for many evidence-based findings are lacking (Box 3).

See the Bibliography below for studies that support using antidepressants to treat PMDD

Box 3

Bibliography

Treatment selection

To enhance compliance and improve the likelihood of successful treatment, tailor treatment decisions to your patient’s needs. Carefully discuss with your patient the evidence-based literature to select the best option for her. Factors to consider when counseling patients include:

• the patient’s age, cigarette smoking habits, and body mass index, which may contraindicate oral contraceptives
• does the patient have regular cycle lengths?
• can she adhere to an on-off schedule? If so, intermittent SSRI dosing may be a good treatment option
• does the patient have irregular cycles?
• is there evidence that symptoms persist into the follicular phase, albeit at a lower level? If so, continuous SSRI dosing may be the best option.

Related Resources

• American Psychiatric Association. DSM-5 development: D 04 Premenstrual dysphoric disorder. www.dsm5.org/proposedrevision/pages/proposedrevision.aspx?rid=484.

Drug Brand Names

• Citalopram • Celexa
• Clomipramine • Anafranil
• Clonidine • Catapres, others
• Danazol • Danocrine
• Drospirenone/ethinyl estradiol • Yaz
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Leuprolide • Lupron
• Levonorgestrel/ethinyl estradiol • Seasonale, others
• Paroxetine • Paxil
• Progesterone • Prometrium
• Sertraline • Zoloft
• Spironolactone • Aldactone
• Venlafaxine • Effexor

Disclosures

Drs. Wakil and Girdler report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, The Foundation of Hope, and the National Institutes of Health.

Psychiatry has many strengths, some weaknesses, and quite a few threats. Therefore, it is vital that psychiatry aggressively focuses on emerging opportunities and exploits them to reinvent its future.

To do that effectively, psychiatry must undergo a process of “creative destruction”¹ to shed its old baggage and tenets, and reinvent itself as a premier medical specialty anchored in evidence-based behavioral neuroscience.

For quite some time, psychiatrists have been patiently waiting for disruptive discoveries catalyzed by ongoing momentous advances and innovative technologies generated by discoveries in molecular genetics and neurobiology. However, psychiatry needs to embrace not only disruptive technologies but also “disruptive thinking” to help reengineer its structure and function and lead to a quantum leap toward a brilliant future anchored in cutting-edge neuroscience.

What facets of psychiatry could undergo creative destruction? What sacred cows should be sacrificed on the altar of necessary, creative change? Imagine the following scenarios:

Create a new name. The term “psychiatry” is based on the archaic concept of “the psyche” from an era of ignorance about the brain generating the mind. Psyche has outlived its usefulness and needs to be shed. A new name incorporating neural structures and functions must reflect the brain mechanisms that generate abnormal thought, mood, or cognition. In addition, the labels currently attached to psychiatric disorders also could also be changed, including stigmatizing diagnoses such as schizophrenia, mania, or borderline personality disorder. New names for such disorders can be linked to brain lesions, pathways, or circuits underlying them. Several years ago Japan replaced the term “schizophrenia” with “integration disorder,” which was met with a positive response from patients and practitioners.²

Destroy false mythology. Misconception and lore of what psychiatry is or is not continues to mislead and distort its scientific principles, goals, and procedures. Creative destruction will give rise to a scientific identity, transcending the absurd fables that shrouded psychiatry since its formative years.

Revolutionize diagnostic models. Current diagnostic schemes are obsolete and must be deconstructed and creatively reinvented based on scientific findings, not just a set of clinical signs and symptoms. The creative destruction process will draw upon scientific breakthroughs and pathophysiological findings psychiatric neuroscientists are discovering (almost daily!). Numerous lab data have been developed for psychiatric disorders, but extensive heterogeneity has prevented diagnostic or commercial use of those tests because of sensitivity/specificity variability.

Design novel treatment approaches. Innovations are desperately needed to create new therapeutics for psychiatric brain disorders. Several dogmas must be slain (such as “chemical imbalance”) and replaced with modern “brain repair” processes, including neuroplasticity and neuroprotection. This would accelerate novel brain interventions such as neuromodulation (eg, repetitive transcranial magnetic simulation, vagus nerve stimulation, and deep brain stimulation) and may set the stage for gene-based therapies, including epigenetic silencing of genes associated with specific disorders. Psychotherapy must be reframed as “verbal neurotherapy” because it certainly leads to salutary neuroplastic changes. As for pharmacologic agents, a new paradigm translating neurobiologic discoveries into effective “neurobiotherapies” must become the pharmaceutical industry’s new focus; a paradigm shift to different delivery systems (intravenous, intranasal, intrathecal, etc.) that can rapidly switch off hallucinations, anxiety attacks, depression, or suicidal urges. Examples of this already exist.³

Transform the delivery system setting. The disastrously dysfunctional public mental health bureaucracy must be abandoned and transformed into “brain institutes,” in all states, similar to cancer centers or cardiovascular institutes, where state-of-the-art clinical care, training, and research are integrated.

New specialization and training model. The psychiatrist of the future ideally will be double boarded in neurology and psychiatry, function more like behavioral neurologists, and provide psychotherapy as needed. A full, accurate assessment of the “mind” cannot be accomplished without a complete assessment of the brain because the mind essentially is the virtual brain. Assessment and management of schizophrenia, depression, or obsessive-compulsive disorder should be no less rigorous neurologically than that of stroke, multiple sclerosis, or Parkinson’s disease.

New image. Psychiatry’s new identity must project a distinctly scientific new image as a superb and highly regarded medical discipline. Creative destruction would involve a difficult transition for “grandfathered” psychiatrists, who will have to abandon old habits and attitudes and retool to adopt new skills. Embracing radical change can be challenging, but we can count on psychiatrists’ abilities and their resilience in adapting to change to when it occurs.

A new destiny. Just as the stunning metamorphosis from embryo to larva, pupa, and imago precedes the emergence of a magnificent butterfly, psychiatry must shatter its cocoon and emerge into a new reality and destiny. Creative destruction is the means for renewal. It is scary to some and exciting to others, but imperative for all.

Psychiatry has many strengths, some weaknesses, and quite a few threats. Therefore, it is vital that psychiatry aggressively focuses on emerging opportunities and exploits them to reinvent its future.

To do that effectively, psychiatry must undergo a process of “creative destruction”¹ to shed its old baggage and tenets, and reinvent itself as a premier medical specialty anchored in evidence-based behavioral neuroscience.

For quite some time, psychiatrists have been patiently waiting for disruptive discoveries catalyzed by ongoing momentous advances and innovative technologies generated by discoveries in molecular genetics and neurobiology. However, psychiatry needs to embrace not only disruptive technologies but also “disruptive thinking” to help reengineer its structure and function and lead to a quantum leap toward a brilliant future anchored in cutting-edge neuroscience.

What facets of psychiatry could undergo creative destruction? What sacred cows should be sacrificed on the altar of necessary, creative change? Imagine the following scenarios:

Create a new name. The term “psychiatry” is based on the archaic concept of “the psyche” from an era of ignorance about the brain generating the mind. Psyche has outlived its usefulness and needs to be shed. A new name incorporating neural structures and functions must reflect the brain mechanisms that generate abnormal thought, mood, or cognition. In addition, the labels currently attached to psychiatric disorders also could also be changed, including stigmatizing diagnoses such as schizophrenia, mania, or borderline personality disorder. New names for such disorders can be linked to brain lesions, pathways, or circuits underlying them. Several years ago Japan replaced the term “schizophrenia” with “integration disorder,” which was met with a positive response from patients and practitioners.²

Destroy false mythology. Misconception and lore of what psychiatry is or is not continues to mislead and distort its scientific principles, goals, and procedures. Creative destruction will give rise to a scientific identity, transcending the absurd fables that shrouded psychiatry since its formative years.

Revolutionize diagnostic models. Current diagnostic schemes are obsolete and must be deconstructed and creatively reinvented based on scientific findings, not just a set of clinical signs and symptoms. The creative destruction process will draw upon scientific breakthroughs and pathophysiological findings psychiatric neuroscientists are discovering (almost daily!). Numerous lab data have been developed for psychiatric disorders, but extensive heterogeneity has prevented diagnostic or commercial use of those tests because of sensitivity/specificity variability.

Design novel treatment approaches. Innovations are desperately needed to create new therapeutics for psychiatric brain disorders. Several dogmas must be slain (such as “chemical imbalance”) and replaced with modern “brain repair” processes, including neuroplasticity and neuroprotection. This would accelerate novel brain interventions such as neuromodulation (eg, repetitive transcranial magnetic simulation, vagus nerve stimulation, and deep brain stimulation) and may set the stage for gene-based therapies, including epigenetic silencing of genes associated with specific disorders. Psychotherapy must be reframed as “verbal neurotherapy” because it certainly leads to salutary neuroplastic changes. As for pharmacologic agents, a new paradigm translating neurobiologic discoveries into effective “neurobiotherapies” must become the pharmaceutical industry’s new focus; a paradigm shift to different delivery systems (intravenous, intranasal, intrathecal, etc.) that can rapidly switch off hallucinations, anxiety attacks, depression, or suicidal urges. Examples of this already exist.³

Transform the delivery system setting. The disastrously dysfunctional public mental health bureaucracy must be abandoned and transformed into “brain institutes,” in all states, similar to cancer centers or cardiovascular institutes, where state-of-the-art clinical care, training, and research are integrated.

New specialization and training model. The psychiatrist of the future ideally will be double boarded in neurology and psychiatry, function more like behavioral neurologists, and provide psychotherapy as needed. A full, accurate assessment of the “mind” cannot be accomplished without a complete assessment of the brain because the mind essentially is the virtual brain. Assessment and management of schizophrenia, depression, or obsessive-compulsive disorder should be no less rigorous neurologically than that of stroke, multiple sclerosis, or Parkinson’s disease.

New image. Psychiatry’s new identity must project a distinctly scientific new image as a superb and highly regarded medical discipline. Creative destruction would involve a difficult transition for “grandfathered” psychiatrists, who will have to abandon old habits and attitudes and retool to adopt new skills. Embracing radical change can be challenging, but we can count on psychiatrists’ abilities and their resilience in adapting to change to when it occurs.

A new destiny. Just as the stunning metamorphosis from embryo to larva, pupa, and imago precedes the emergence of a magnificent butterfly, psychiatry must shatter its cocoon and emerge into a new reality and destiny. Creative destruction is the means for renewal. It is scary to some and exciting to others, but imperative for all.

Psychiatry has many strengths, some weaknesses, and quite a few threats. Therefore, it is vital that psychiatry aggressively focuses on emerging opportunities and exploits them to reinvent its future.

To do that effectively, psychiatry must undergo a process of “creative destruction”¹ to shed its old baggage and tenets, and reinvent itself as a premier medical specialty anchored in evidence-based behavioral neuroscience.

For quite some time, psychiatrists have been patiently waiting for disruptive discoveries catalyzed by ongoing momentous advances and innovative technologies generated by discoveries in molecular genetics and neurobiology. However, psychiatry needs to embrace not only disruptive technologies but also “disruptive thinking” to help reengineer its structure and function and lead to a quantum leap toward a brilliant future anchored in cutting-edge neuroscience.

What facets of psychiatry could undergo creative destruction? What sacred cows should be sacrificed on the altar of necessary, creative change? Imagine the following scenarios:

Create a new name. The term “psychiatry” is based on the archaic concept of “the psyche” from an era of ignorance about the brain generating the mind. Psyche has outlived its usefulness and needs to be shed. A new name incorporating neural structures and functions must reflect the brain mechanisms that generate abnormal thought, mood, or cognition. In addition, the labels currently attached to psychiatric disorders also could also be changed, including stigmatizing diagnoses such as schizophrenia, mania, or borderline personality disorder. New names for such disorders can be linked to brain lesions, pathways, or circuits underlying them. Several years ago Japan replaced the term “schizophrenia” with “integration disorder,” which was met with a positive response from patients and practitioners.²

Destroy false mythology. Misconception and lore of what psychiatry is or is not continues to mislead and distort its scientific principles, goals, and procedures. Creative destruction will give rise to a scientific identity, transcending the absurd fables that shrouded psychiatry since its formative years.

Revolutionize diagnostic models. Current diagnostic schemes are obsolete and must be deconstructed and creatively reinvented based on scientific findings, not just a set of clinical signs and symptoms. The creative destruction process will draw upon scientific breakthroughs and pathophysiological findings psychiatric neuroscientists are discovering (almost daily!). Numerous lab data have been developed for psychiatric disorders, but extensive heterogeneity has prevented diagnostic or commercial use of those tests because of sensitivity/specificity variability.

Design novel treatment approaches. Innovations are desperately needed to create new therapeutics for psychiatric brain disorders. Several dogmas must be slain (such as “chemical imbalance”) and replaced with modern “brain repair” processes, including neuroplasticity and neuroprotection. This would accelerate novel brain interventions such as neuromodulation (eg, repetitive transcranial magnetic simulation, vagus nerve stimulation, and deep brain stimulation) and may set the stage for gene-based therapies, including epigenetic silencing of genes associated with specific disorders. Psychotherapy must be reframed as “verbal neurotherapy” because it certainly leads to salutary neuroplastic changes. As for pharmacologic agents, a new paradigm translating neurobiologic discoveries into effective “neurobiotherapies” must become the pharmaceutical industry’s new focus; a paradigm shift to different delivery systems (intravenous, intranasal, intrathecal, etc.) that can rapidly switch off hallucinations, anxiety attacks, depression, or suicidal urges. Examples of this already exist.³

Transform the delivery system setting. The disastrously dysfunctional public mental health bureaucracy must be abandoned and transformed into “brain institutes,” in all states, similar to cancer centers or cardiovascular institutes, where state-of-the-art clinical care, training, and research are integrated.

New specialization and training model. The psychiatrist of the future ideally will be double boarded in neurology and psychiatry, function more like behavioral neurologists, and provide psychotherapy as needed. A full, accurate assessment of the “mind” cannot be accomplished without a complete assessment of the brain because the mind essentially is the virtual brain. Assessment and management of schizophrenia, depression, or obsessive-compulsive disorder should be no less rigorous neurologically than that of stroke, multiple sclerosis, or Parkinson’s disease.

New image. Psychiatry’s new identity must project a distinctly scientific new image as a superb and highly regarded medical discipline. Creative destruction would involve a difficult transition for “grandfathered” psychiatrists, who will have to abandon old habits and attitudes and retool to adopt new skills. Embracing radical change can be challenging, but we can count on psychiatrists’ abilities and their resilience in adapting to change to when it occurs.

A new destiny. Just as the stunning metamorphosis from embryo to larva, pupa, and imago precedes the emergence of a magnificent butterfly, psychiatry must shatter its cocoon and emerge into a new reality and destiny. Creative destruction is the means for renewal. It is scary to some and exciting to others, but imperative for all.

Discuss this article at www.facebook.com/CurrentPsychiatry

In DSM-IV,¹ the section on schizophrenia and other psychotic disorders includes schizophrenia (with 5 subtypes), schizophreniform disorder, schizoaffective disorder, delusional disorder, shared psychotic disorder, brief psychotic disorder, substance-induced psychotic disorder, psychotic disorder due to a general medical condition, and psychotic disorder not otherwise specified. As we consider proposed changes to DSM-5 (Table 1),² it is useful to consider limitations in our current construct of schizophrenia.

Table 1

Psychotic disorders in DSM-5: Summary of proposed changes

First, many etiological factors and pathophysiological processes appear relevant to what we consider schizophrenia and it is almost certain that our construct of schizophrenia encompasses not one but numerous diseases with a shared phenotype.^3-5

Second, the boundary between schizophrenia and schizoaffective disorder is imprecisely defined, and a proportion of patients with schizophrenia with some mood symptoms may inappropriately receive a schizoaffective disorder diagnosis. This is compounded by the poor reliability and low diagnostic stability of a schizoaffective disorder diagnosis.^6-8

Third, the current classic schizophrenia subtypes provide an inadequate description of the enormous heterogeneity of this condition. Additionally, subtype stability is low, and only the paranoid and undifferentiated subtypes are used frequently in clinical practice.

Fourth, the prominence given to Schneiderian first-rank symptoms (“bizarre” delusions or “special” hallucinations) appears misplaced.

Fifth, the current construct of schizophrenia inadequately describes the major psychopathological dimensions of the condition and stages of its evolution.^8,9

Finally, the current clinical construct of schizophrenia does not match neurobiological markers and genetic findings or specific pharmacological treatment provided.^5,10 Proposed DSM-5 revisions² to the definition of schizophrenia to address these limitations are summarized below.

Schizophrenia syndrome

Proposed changes to the diagnostic criteria for schizophrenia are modest and continuity with DSM-IV is broadly maintained. Two modest changes to criterion A (active phase symptoms) are proposed:

• Eliminate special treatment of bizarre delusions and other Schneiderian first-rank symptoms. In DSM-IV, only 1 criterion A is required if it is a bizarre delusion or hallucination. Because Schneiderian first-rank symptoms do not have diagnostic specificity and diagnosing “bizarreness” of delusions and hallucinations has low reliability, it is proposed that these positive symptoms be treated like any other with regard to their diagnostic implications.
• Require that at least 1 of the 2 symptoms required to meet criterion A be delusions, hallucinations, or disorganized thinking. These are core positive symptoms diagnosed with high reliability and might reasonably be considered necessary for a reliable schizophrenia diagnosis.

Subtypes

The DSM-5 proposal for describing schizophrenia advocates eliminating DSM-IV schizophrenia subtypes. These subtypes have limited diagnostic stability, low reliability, and poor validity. Furthermore, except for the paranoid and undifferentiated subtypes, other subtypes rarely are used in most mental health care systems.

Schizoaffective disorder

Characterizing patients with both psychotic and mood symptoms either concurrently or at different points during their illness always has been controversial. In DSM-I and DSM-II, a diagnosis of schizophrenia, schizoaffective subtype, generally was recommended for such patients. DSM-III reversed this recommendation and specified that schizophrenia was to be diagnosed only in the absence of prominent mood symptoms. Furthermore, in DSM-III, diagnosing schizoaffective disorder was strongly discouraged, and it was the only condition in DSM-III without operational criteria. Schizoaffective disorder saw a revival in DSM-III-R that has continued through DSM-IV. In fact, in many mental health care systems, almost one-third of patients with psychotic symptoms receive a schizoaffective disorder diagnosis. One of the insidious changes to the definition of schizoaffective disorder from DSM-III to DSM-IV is that it moved from being a lifetime diagnosis to a cross-sectional diagnosis—ie, in DSM-IV, only mood/psychotic symptoms in the current episode are considered, and the longitudinal course of these symptoms in the patient’s life are ignored. The current DSM-5 proposal attempts to improve reliability of this diagnosis by providing more specific criteria and is reconceptualizing schizoaffective disorder as a longitudinal diagnosis. To this end, the most significant proposed change is to criterion C of schizoaffective disorder, which attempts to demarcate schizoaffective disorder from schizophrenia with prominent mood symptoms. Criterion C will be revised to state “symptoms that meet criteria for a mood episode are present for a majority (>50%) of the total duration of the active and residual periods of the illness.”²

Psychopathological dimensions

Schizophrenic illness is characterized by several psychopathological domains, with a distinctive course, patterns of treatment-response, and prognostic implications. The relative severity of symptom dimensions—positive, negative, mood, disorganization, motor, and cognitive—vary among patients and also within patients at different stages of their illness. Measuring the relative severity of these symptom dimensions throughout the illness course can provide clinicians with useful information about the nature of a patient’s schizophrenic illness and the specific impact of treatment on different aspects of his or her illness (Table 2). In addition to being clinically useful, dimensional measurement also should improve schizophrenia research because having dimensional information will permit studies on etiology and pathogenesis that cut across current diagnostic categories. Although field trials are evaluating 9 dimensions—delusions, hallucinations, disorganization, depression, mania, cognitive impairment, restricted emotional expression, avolition, and psychomotor—it is likely that fewer dimensions will be recommended for DSM-5, based on reliability results of these trials, clinical utility, and logistic feasibility in routine clinical settings.

Table 2

Goals of a dimensional approach to schizophrenia

Attenuated psychosis syndrome

Some clinicians and researchers believe that many patients with schizophrenia experience unsatisfactory outcomes because we identify the illness and initiate treatment after substantial brain tissue damage has occurred. Introducing attenuated psychosis syndrome will support clinicians’ efforts to recognize mild psychotic symptoms early in their evolution and to monitor—and if necessary, intervene—during these crucial early stages. Risks include possible stigma and inappropriate use of medications and other treatments. This controversial proposal is being field tested. It is unclear if this category will be included in DSM-5 and if it does, whether it will be in the main text or the appendix.

Catatonia

Catatonia will be used as a specifier for various psychotic disorders, major mood disorders, and associated with a general medical condition. Additionally, the same criteria will be used to diagnose catatonia across DSM-5. Catatonia Not Elsewhere Classified might be added as a residual category for other conditions in which a clear catatonic syndrome is present and the parent disorder has not yet been identified.²

Other psychotic disorders

Relatively minor changes are proposed in criteria for other disorders in this section. There are likely to be changes in the text, however, that incorporate new information about these conditions generated since publication of DSM-IV-TR in 2000. Some proposed changes include:

• deleting shared delusional disorder (folie à deux) as a separate diagnosis and instead characterizing it as a specifier for delusional disorder
• clarifying the distinction between substance-induced psychotic disorder and other psychotic disorders accompanied by comorbid substance use.

Current status of DSM-5

Field trials are being completed and their results remain to be analyzed. Major changes being evaluated in the field trials include:

• the impact of the change in concept and criteria for schizoaffective disorder
• the addition of a series of psychopathology dimensions
• the impact of adding attenuated psychosis syndrome as a new class.

Changes proposed by the Psychosis Disorders Work Group are intended to increase clinical utility (fewer diagnoses, better demarcation between disorders, greater treatment relevance [dimensions]) and modestly improve validity (more consistent with current information about the nature of various psychotic disorders), while retaining reliability in diagnosing various psychotic disorders (and improving it for schizoaffective disorder). Proposed changes are modest by and large but hope to set a better stage for a future etiopathophysiological classification.

The Psychosis Disorders Work Group’s recommendations are posted on the DSM-5 Web site² at www.dsm5.org and are being reviewed by 2 expert committees established by the American Psychiatric Association Board of Trustees: a Scientific Review Committee and a Clinical and Public Health Implications Committee. Based on the results of the field trials, ongoing reviews, and other emerging data and discussions, additional changes to the current DSM-5 proposals may occur. DSM-5 is likely to be finalized in early 2013 and the published manual will be released in May 2013.

Related Resources

• American Psychiatric Association. DSM-5 Development. www.dsm5.org.
• Woods SW, McGlashan TH. The risk-benefit ratio of the proposed DSM-5 attenuated psychosis syndrome. Am J Psychiatry. 2011;168(12):1338.

Disclosure

Dr. Tandon is a member of the DSM-5 Psychotic Disorders Work Group. He is solely responsible for the content of this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

In DSM-IV,¹ the section on schizophrenia and other psychotic disorders includes schizophrenia (with 5 subtypes), schizophreniform disorder, schizoaffective disorder, delusional disorder, shared psychotic disorder, brief psychotic disorder, substance-induced psychotic disorder, psychotic disorder due to a general medical condition, and psychotic disorder not otherwise specified. As we consider proposed changes to DSM-5 (Table 1),² it is useful to consider limitations in our current construct of schizophrenia.

Table 1

Psychotic disorders in DSM-5: Summary of proposed changes

First, many etiological factors and pathophysiological processes appear relevant to what we consider schizophrenia and it is almost certain that our construct of schizophrenia encompasses not one but numerous diseases with a shared phenotype.^3-5

Second, the boundary between schizophrenia and schizoaffective disorder is imprecisely defined, and a proportion of patients with schizophrenia with some mood symptoms may inappropriately receive a schizoaffective disorder diagnosis. This is compounded by the poor reliability and low diagnostic stability of a schizoaffective disorder diagnosis.^6-8

Third, the current classic schizophrenia subtypes provide an inadequate description of the enormous heterogeneity of this condition. Additionally, subtype stability is low, and only the paranoid and undifferentiated subtypes are used frequently in clinical practice.

Fourth, the prominence given to Schneiderian first-rank symptoms (“bizarre” delusions or “special” hallucinations) appears misplaced.

Fifth, the current construct of schizophrenia inadequately describes the major psychopathological dimensions of the condition and stages of its evolution.^8,9

Finally, the current clinical construct of schizophrenia does not match neurobiological markers and genetic findings or specific pharmacological treatment provided.^5,10 Proposed DSM-5 revisions² to the definition of schizophrenia to address these limitations are summarized below.

Schizophrenia syndrome

Proposed changes to the diagnostic criteria for schizophrenia are modest and continuity with DSM-IV is broadly maintained. Two modest changes to criterion A (active phase symptoms) are proposed:

• Eliminate special treatment of bizarre delusions and other Schneiderian first-rank symptoms. In DSM-IV, only 1 criterion A is required if it is a bizarre delusion or hallucination. Because Schneiderian first-rank symptoms do not have diagnostic specificity and diagnosing “bizarreness” of delusions and hallucinations has low reliability, it is proposed that these positive symptoms be treated like any other with regard to their diagnostic implications.
• Require that at least 1 of the 2 symptoms required to meet criterion A be delusions, hallucinations, or disorganized thinking. These are core positive symptoms diagnosed with high reliability and might reasonably be considered necessary for a reliable schizophrenia diagnosis.

Subtypes

The DSM-5 proposal for describing schizophrenia advocates eliminating DSM-IV schizophrenia subtypes. These subtypes have limited diagnostic stability, low reliability, and poor validity. Furthermore, except for the paranoid and undifferentiated subtypes, other subtypes rarely are used in most mental health care systems.

Schizoaffective disorder

Characterizing patients with both psychotic and mood symptoms either concurrently or at different points during their illness always has been controversial. In DSM-I and DSM-II, a diagnosis of schizophrenia, schizoaffective subtype, generally was recommended for such patients. DSM-III reversed this recommendation and specified that schizophrenia was to be diagnosed only in the absence of prominent mood symptoms. Furthermore, in DSM-III, diagnosing schizoaffective disorder was strongly discouraged, and it was the only condition in DSM-III without operational criteria. Schizoaffective disorder saw a revival in DSM-III-R that has continued through DSM-IV. In fact, in many mental health care systems, almost one-third of patients with psychotic symptoms receive a schizoaffective disorder diagnosis. One of the insidious changes to the definition of schizoaffective disorder from DSM-III to DSM-IV is that it moved from being a lifetime diagnosis to a cross-sectional diagnosis—ie, in DSM-IV, only mood/psychotic symptoms in the current episode are considered, and the longitudinal course of these symptoms in the patient’s life are ignored. The current DSM-5 proposal attempts to improve reliability of this diagnosis by providing more specific criteria and is reconceptualizing schizoaffective disorder as a longitudinal diagnosis. To this end, the most significant proposed change is to criterion C of schizoaffective disorder, which attempts to demarcate schizoaffective disorder from schizophrenia with prominent mood symptoms. Criterion C will be revised to state “symptoms that meet criteria for a mood episode are present for a majority (>50%) of the total duration of the active and residual periods of the illness.”²

Psychopathological dimensions

Schizophrenic illness is characterized by several psychopathological domains, with a distinctive course, patterns of treatment-response, and prognostic implications. The relative severity of symptom dimensions—positive, negative, mood, disorganization, motor, and cognitive—vary among patients and also within patients at different stages of their illness. Measuring the relative severity of these symptom dimensions throughout the illness course can provide clinicians with useful information about the nature of a patient’s schizophrenic illness and the specific impact of treatment on different aspects of his or her illness (Table 2). In addition to being clinically useful, dimensional measurement also should improve schizophrenia research because having dimensional information will permit studies on etiology and pathogenesis that cut across current diagnostic categories. Although field trials are evaluating 9 dimensions—delusions, hallucinations, disorganization, depression, mania, cognitive impairment, restricted emotional expression, avolition, and psychomotor—it is likely that fewer dimensions will be recommended for DSM-5, based on reliability results of these trials, clinical utility, and logistic feasibility in routine clinical settings.

Table 2

Goals of a dimensional approach to schizophrenia

Attenuated psychosis syndrome

Some clinicians and researchers believe that many patients with schizophrenia experience unsatisfactory outcomes because we identify the illness and initiate treatment after substantial brain tissue damage has occurred. Introducing attenuated psychosis syndrome will support clinicians’ efforts to recognize mild psychotic symptoms early in their evolution and to monitor—and if necessary, intervene—during these crucial early stages. Risks include possible stigma and inappropriate use of medications and other treatments. This controversial proposal is being field tested. It is unclear if this category will be included in DSM-5 and if it does, whether it will be in the main text or the appendix.

Catatonia

Catatonia will be used as a specifier for various psychotic disorders, major mood disorders, and associated with a general medical condition. Additionally, the same criteria will be used to diagnose catatonia across DSM-5. Catatonia Not Elsewhere Classified might be added as a residual category for other conditions in which a clear catatonic syndrome is present and the parent disorder has not yet been identified.²

Other psychotic disorders

Relatively minor changes are proposed in criteria for other disorders in this section. There are likely to be changes in the text, however, that incorporate new information about these conditions generated since publication of DSM-IV-TR in 2000. Some proposed changes include:

• deleting shared delusional disorder (folie à deux) as a separate diagnosis and instead characterizing it as a specifier for delusional disorder
• clarifying the distinction between substance-induced psychotic disorder and other psychotic disorders accompanied by comorbid substance use.

Current status of DSM-5

Field trials are being completed and their results remain to be analyzed. Major changes being evaluated in the field trials include:

• the impact of the change in concept and criteria for schizoaffective disorder
• the addition of a series of psychopathology dimensions
• the impact of adding attenuated psychosis syndrome as a new class.

Changes proposed by the Psychosis Disorders Work Group are intended to increase clinical utility (fewer diagnoses, better demarcation between disorders, greater treatment relevance [dimensions]) and modestly improve validity (more consistent with current information about the nature of various psychotic disorders), while retaining reliability in diagnosing various psychotic disorders (and improving it for schizoaffective disorder). Proposed changes are modest by and large but hope to set a better stage for a future etiopathophysiological classification.

The Psychosis Disorders Work Group’s recommendations are posted on the DSM-5 Web site² at www.dsm5.org and are being reviewed by 2 expert committees established by the American Psychiatric Association Board of Trustees: a Scientific Review Committee and a Clinical and Public Health Implications Committee. Based on the results of the field trials, ongoing reviews, and other emerging data and discussions, additional changes to the current DSM-5 proposals may occur. DSM-5 is likely to be finalized in early 2013 and the published manual will be released in May 2013.

Related Resources

• American Psychiatric Association. DSM-5 Development. www.dsm5.org.
• Woods SW, McGlashan TH. The risk-benefit ratio of the proposed DSM-5 attenuated psychosis syndrome. Am J Psychiatry. 2011;168(12):1338.

Disclosure

Dr. Tandon is a member of the DSM-5 Psychotic Disorders Work Group. He is solely responsible for the content of this article.

Discuss this article at www.facebook.com/CurrentPsychiatry

In DSM-IV,¹ the section on schizophrenia and other psychotic disorders includes schizophrenia (with 5 subtypes), schizophreniform disorder, schizoaffective disorder, delusional disorder, shared psychotic disorder, brief psychotic disorder, substance-induced psychotic disorder, psychotic disorder due to a general medical condition, and psychotic disorder not otherwise specified. As we consider proposed changes to DSM-5 (Table 1),² it is useful to consider limitations in our current construct of schizophrenia.

Table 1

Psychotic disorders in DSM-5: Summary of proposed changes

First, many etiological factors and pathophysiological processes appear relevant to what we consider schizophrenia and it is almost certain that our construct of schizophrenia encompasses not one but numerous diseases with a shared phenotype.^3-5

Second, the boundary between schizophrenia and schizoaffective disorder is imprecisely defined, and a proportion of patients with schizophrenia with some mood symptoms may inappropriately receive a schizoaffective disorder diagnosis. This is compounded by the poor reliability and low diagnostic stability of a schizoaffective disorder diagnosis.^6-8

Third, the current classic schizophrenia subtypes provide an inadequate description of the enormous heterogeneity of this condition. Additionally, subtype stability is low, and only the paranoid and undifferentiated subtypes are used frequently in clinical practice.

Fourth, the prominence given to Schneiderian first-rank symptoms (“bizarre” delusions or “special” hallucinations) appears misplaced.

Fifth, the current construct of schizophrenia inadequately describes the major psychopathological dimensions of the condition and stages of its evolution.^8,9

Finally, the current clinical construct of schizophrenia does not match neurobiological markers and genetic findings or specific pharmacological treatment provided.^5,10 Proposed DSM-5 revisions² to the definition of schizophrenia to address these limitations are summarized below.

Schizophrenia syndrome

Proposed changes to the diagnostic criteria for schizophrenia are modest and continuity with DSM-IV is broadly maintained. Two modest changes to criterion A (active phase symptoms) are proposed:

• Eliminate special treatment of bizarre delusions and other Schneiderian first-rank symptoms. In DSM-IV, only 1 criterion A is required if it is a bizarre delusion or hallucination. Because Schneiderian first-rank symptoms do not have diagnostic specificity and diagnosing “bizarreness” of delusions and hallucinations has low reliability, it is proposed that these positive symptoms be treated like any other with regard to their diagnostic implications.
• Require that at least 1 of the 2 symptoms required to meet criterion A be delusions, hallucinations, or disorganized thinking. These are core positive symptoms diagnosed with high reliability and might reasonably be considered necessary for a reliable schizophrenia diagnosis.

Subtypes

The DSM-5 proposal for describing schizophrenia advocates eliminating DSM-IV schizophrenia subtypes. These subtypes have limited diagnostic stability, low reliability, and poor validity. Furthermore, except for the paranoid and undifferentiated subtypes, other subtypes rarely are used in most mental health care systems.

Schizoaffective disorder

Characterizing patients with both psychotic and mood symptoms either concurrently or at different points during their illness always has been controversial. In DSM-I and DSM-II, a diagnosis of schizophrenia, schizoaffective subtype, generally was recommended for such patients. DSM-III reversed this recommendation and specified that schizophrenia was to be diagnosed only in the absence of prominent mood symptoms. Furthermore, in DSM-III, diagnosing schizoaffective disorder was strongly discouraged, and it was the only condition in DSM-III without operational criteria. Schizoaffective disorder saw a revival in DSM-III-R that has continued through DSM-IV. In fact, in many mental health care systems, almost one-third of patients with psychotic symptoms receive a schizoaffective disorder diagnosis. One of the insidious changes to the definition of schizoaffective disorder from DSM-III to DSM-IV is that it moved from being a lifetime diagnosis to a cross-sectional diagnosis—ie, in DSM-IV, only mood/psychotic symptoms in the current episode are considered, and the longitudinal course of these symptoms in the patient’s life are ignored. The current DSM-5 proposal attempts to improve reliability of this diagnosis by providing more specific criteria and is reconceptualizing schizoaffective disorder as a longitudinal diagnosis. To this end, the most significant proposed change is to criterion C of schizoaffective disorder, which attempts to demarcate schizoaffective disorder from schizophrenia with prominent mood symptoms. Criterion C will be revised to state “symptoms that meet criteria for a mood episode are present for a majority (>50%) of the total duration of the active and residual periods of the illness.”²

Psychopathological dimensions

Schizophrenic illness is characterized by several psychopathological domains, with a distinctive course, patterns of treatment-response, and prognostic implications. The relative severity of symptom dimensions—positive, negative, mood, disorganization, motor, and cognitive—vary among patients and also within patients at different stages of their illness. Measuring the relative severity of these symptom dimensions throughout the illness course can provide clinicians with useful information about the nature of a patient’s schizophrenic illness and the specific impact of treatment on different aspects of his or her illness (Table 2). In addition to being clinically useful, dimensional measurement also should improve schizophrenia research because having dimensional information will permit studies on etiology and pathogenesis that cut across current diagnostic categories. Although field trials are evaluating 9 dimensions—delusions, hallucinations, disorganization, depression, mania, cognitive impairment, restricted emotional expression, avolition, and psychomotor—it is likely that fewer dimensions will be recommended for DSM-5, based on reliability results of these trials, clinical utility, and logistic feasibility in routine clinical settings.

Table 2

Goals of a dimensional approach to schizophrenia

Attenuated psychosis syndrome

Some clinicians and researchers believe that many patients with schizophrenia experience unsatisfactory outcomes because we identify the illness and initiate treatment after substantial brain tissue damage has occurred. Introducing attenuated psychosis syndrome will support clinicians’ efforts to recognize mild psychotic symptoms early in their evolution and to monitor—and if necessary, intervene—during these crucial early stages. Risks include possible stigma and inappropriate use of medications and other treatments. This controversial proposal is being field tested. It is unclear if this category will be included in DSM-5 and if it does, whether it will be in the main text or the appendix.

Catatonia

Catatonia will be used as a specifier for various psychotic disorders, major mood disorders, and associated with a general medical condition. Additionally, the same criteria will be used to diagnose catatonia across DSM-5. Catatonia Not Elsewhere Classified might be added as a residual category for other conditions in which a clear catatonic syndrome is present and the parent disorder has not yet been identified.²

Other psychotic disorders

Relatively minor changes are proposed in criteria for other disorders in this section. There are likely to be changes in the text, however, that incorporate new information about these conditions generated since publication of DSM-IV-TR in 2000. Some proposed changes include:

• deleting shared delusional disorder (folie à deux) as a separate diagnosis and instead characterizing it as a specifier for delusional disorder
• clarifying the distinction between substance-induced psychotic disorder and other psychotic disorders accompanied by comorbid substance use.

Current status of DSM-5

Field trials are being completed and their results remain to be analyzed. Major changes being evaluated in the field trials include:

• the impact of the change in concept and criteria for schizoaffective disorder
• the addition of a series of psychopathology dimensions
• the impact of adding attenuated psychosis syndrome as a new class.

Changes proposed by the Psychosis Disorders Work Group are intended to increase clinical utility (fewer diagnoses, better demarcation between disorders, greater treatment relevance [dimensions]) and modestly improve validity (more consistent with current information about the nature of various psychotic disorders), while retaining reliability in diagnosing various psychotic disorders (and improving it for schizoaffective disorder). Proposed changes are modest by and large but hope to set a better stage for a future etiopathophysiological classification.

The Psychosis Disorders Work Group’s recommendations are posted on the DSM-5 Web site² at www.dsm5.org and are being reviewed by 2 expert committees established by the American Psychiatric Association Board of Trustees: a Scientific Review Committee and a Clinical and Public Health Implications Committee. Based on the results of the field trials, ongoing reviews, and other emerging data and discussions, additional changes to the current DSM-5 proposals may occur. DSM-5 is likely to be finalized in early 2013 and the published manual will be released in May 2013.

Related Resources

• American Psychiatric Association. DSM-5 Development. www.dsm5.org.
• Woods SW, McGlashan TH. The risk-benefit ratio of the proposed DSM-5 attenuated psychosis syndrome. Am J Psychiatry. 2011;168(12):1338.

Disclosure

Dr. Tandon is a member of the DSM-5 Psychotic Disorders Work Group. He is solely responsible for the content of this article.