Current Psychiatry

Cannabis is the most commonly abused drug in the United States. Since 2008, Cannabis use has significantly increased,¹ in part because of legalization for medicinal and recreational use. Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily Cannabis use, recurrent nausea, vomiting and abdominal pain, compulsive bathing for symptom relief, and symptom resolution with cessation of use.

Prompt recognition of CHS can reduce costs associated with unnecessary workups, emergency department (ED) and urgent care visits, and hospital admissions.^2,3 This article provides a review of CHS with discussion of diagnostic and management considerations.

CASE REPORT Nauseated and vomiting—and stoned

Mr. M, age 24, self-presents to the ED complaining of two days of severe nausea, colicky abdominal pain, and nonbloody, nonbilious vomiting, as often as 20 times a day. His symptoms become worse with food, and he has difficulty eating and drinking because of his vomiting. Mr. M reports transient symptom relief when he takes hot showers, and has been taking more than 14 showers a day. He reports similar episodes, occurring every two or three months over the last two years, resulting in several ED visits and three hospital admissions.

Mr. M has smoked two to three joints a day for seven years; he has increased his Cannabis use in an attempt to alleviate his symptoms, but isn’t sure if doing so was helpful. He denies use of tobacco and other illicit drugs, and reports drinking one to three drinks no more than twice a month. He reports dizziness when standing, but no other symptoms. He does not take any medications, and medical and psychiatric histories are unremarkable.

Physical exam reveals a thin, uncomfortable, young man. Vital signs were significant for tachycardia and mild orthostatic hypotension. His abdomen was diffusely tender, soft, and nondistended. Urine toxicology is positive for delta-9-tetrahydrocannabinol (THC) only. Labs, including a complete blood count (CBC), basic metabolic panel, liver function tests, and lipase, are within normal limits. Prior workup included abdominal radiographs, abdominal ultrasonography, abdominal CT, and gastric biopsy; all are normal. He has mild gastritis and esophagitis on esophagogastroduodenoscopy and mildly delayed gastric emptying. HIV and hepatitis screenings are negative. Six months ago he received antibiotic therapy for Helicobacter pylori infection. 

Mr. M is admitted to the hospital and seen by the psychiatric consultation service. He is treated with IV ondansetron and prochlorperazine, with little effect. He showers frequently until his symptoms begin to abate within 36 hours of stopping Cannabis use, and is discharged soon after. Psychiatric clinicians provide brief motivational interviewing while Mr. M is in the hospital, and refer him to outpatient psychiatric care and Narcotics Anonymous. Mr. M is then lost to follow up.

In 2011, 18.1 million people reported Cannabis use in the previous month; 39% reported use in 20 of the last 30 days.¹ A high rate of use and a relatively low number of cases suggests that CHS is rare. However, it is likely that CHS is under-recognized and under-reported.^2,4,5 CHS symptoms may be misattributed to cyclic vomiting syndrome,³ because 50% of patients diagnosed with cyclic vomiting syndrome report daily Cannabis use.⁶ There is no epidemiological data on the incidence or prevalence of CHS among regular Cannabis users.⁷

Allen and colleagues first described this syndrome in 2004.⁴ Since then, CHS has been documented in a growing number of case reports and reviews,^2,3,5,7-13 yet it continues to be under-recognized. Many CHS patients experience delays in diagnosis—often years—resulting in prolonged suffering, and costs incurred by frequent ED and urgent care visits, hospital admissions, and unnecessary workups.^2,3,7

Clinical characteristics

CHS is characterized by recurrent, hyperemetic episodes in the context of chronic, daily Cannabis use.⁴ The average age of onset is 25.6 years (range: 16 to 51 years).³ Ninety-five percent of CHS patients used Cannabis daily, for, on average, 9.8 years before symptom onset.³ The amount of Cannabis used, although generally high, is difficult to quantify, and has been described as heavy and hourly in units of blunts, cones, joints, bongs, etc. Patients are most likely to present during acute hyperemetic episodes, which occur in a cyclic pattern, every four to eight weeks,³ interspersed with symptom-free periods. Three phases have been described:

• prodromal or pre-emetic phase
• hyperemetic phase
• recovery phase.^4,10

Many patients report a prodromal phase, with one or two weeks of morning nausea, food aversion, preserved eating patterns, possible weight loss, and occasional vomiting. The acute, hyperemetic phase is characterized by severe nausea, frequent vomiting, abdominal pain, and compulsive bathing for temporary symptom relief. In the recovery phase, symptom improvement and resolution occur with cessation of Cannabis use.^4,10 Symptom improvement can occur within 12 hours of Cannabis cessation, but can take as long as three weeks.³ Patients remain symptom-free while abstinent, but symptoms rapidly recur when they resume use.^3,4

Cannabis is used as an antiemetic and appetite stimulant for chemotherapy-associated nausea and for anorexia in HIV infection. The pathogenesis of paradoxical hyperemetic symptoms of CHS remain unclear, but several mechanisms have been proposed. The principle active cannabinoid in Cannabis is the highly lipophilic compound THC, which binds to cannabinoid type 1 (CB1) and type 2 (CB2) receptors in the CNS and other tissues. It is thought that the antiemetic and appetite-stimulating effects of Cannabis are mediated by CB1 receptor activation in the hypothalamus. Nausea and vomiting are thought to be mediated by CB1 receptor activation in the enteric nervous system, which causes slowed peristalsis, delayed gastric emptying, and splanchnic vasodilation.^4,14

In sensitive persons, chronic heavy Cannabis use can cause THC to accumulate to a toxic level in fatty tissues, causing enteric receptor binding effects to override the CNS receptor-binding effects.⁴ This is supported by case studies describing severe vomiting with IV injection of crude marijuana extract.¹⁵ Nearly 100 different THC metabolites have been identified. The Cannabis plant contains more than 400 chemicals, with 60 cannabinoid structures, any of which could cause CHS in toxic concentrations.^4,7 Among them, cannabidiol, a 5-HT1A partial agonist, was shown to cause vomiting at higher doses in animal studies.^4,7

Mechanisms of action

Cannabis has been used for centuries, so it is unclear why CHS is only recently being recognized. It may be because of higher THC content through selective breeding of plants and a more selective use of female buds that contain more concentrated THC levels than leaves and stems.³ Alternately, CHS may be caused by exogenous substances, such as pesticides, additives, preservatives, or other chemicals used in marijuana preparation, although there is little evidence to support this.³

The mechanism of symptom relief with hot bathing also is unclear. Patients report consistent, global symptom improvement with hot bathing.³ Relief is rapid, transient, and temperature dependent.⁴ CB1 receptors are located near the thermoregulatory center of the hypothalamus. Increased body temperature with hot bathing may counteract the thermoregulatory dysregulation associated with Cannabis use.^4,9 It has been proposed that splanchnic vasodilation might contribute to CHS symptoms. Thus, redistribution of blood from the gut to the skin with warm bathing causes a “cutaneous steal syndrome,” resulting in symptom relief.¹¹

Diagnostic approach

Four key features should be present when making a diagnosis of CHS:

• heavy marijuana use
• recurrent episodes of severe nausea, vomiting, and abdominal cramping       
• compulsive bathing for transient symptom relief
• resolution of symptoms with cessation of Cannabis use.^2,4,8

Compulsive, hot bathing for symptom relief was described in 98% of all reported cases,³ and should be considered pathognomonic.² CHS patients can present with other symptoms, including polydipsia, mild fever, weight loss, and orthostasis.³ Although lab studies usually are normal, mild leukocytosis, hypokalemia, hypochloremia, elevated salivary amylase, mild gastritis on esophagogastroduodenoscopy, and delayed gastric emptying have been described during acute episodes (Table 1).^2-4,7,8

Diagnosis starts with a history and physical exam, followed by a basic workup geared towards ruling out other causes of acute nausea and vomiting.^2,7 Establish temporal relationships between symptoms, Cannabis use (onset, frequency, amount, duration), and bathing behaviors. A positive urine toxicology screen supports a CHS diagnosis and can facilitate discussion of Cannabis use.² If you suspect CHS, rule out potentially life-threatening causes of acute nausea, vomiting, and abdominal pain, such as intestinal obstruction or perforation, pancreaticobiliary disease, and pregnancy. The initial workup should include a CBC, basic metabolic panel, liver function tests, amylase, lipase, pregnancy test, urinalysis, urine toxicology screen, and abdominal radiographs (Table 2).^2,4,7 The differential diagnosis of recurrent vomiting is broad and should be considered (Table 3).^2,4,7,16 Further workup can proceed non-emergently, and should be prompted by clinical suspicion.^2,7

Supportive treatment, education

Treatment of acute hyperemetic episodes in CHS primarily is supportive; address dehydration with IV fluids and electrolyte replenishment as needed.^2,4,7 Standard antiemetics, including 5-HT3 receptor antagonists, D2 receptor antagonists, and H1 receptor antagonists, are largely ineffective.^5,9 Although narcotics have been used to treat abdominal pain, use caution when prescribing because they can exacerbate nausea and vomiting.⁷ Case reports have described symptom relief with inpatient treatment with lorazepam¹² and self-medication with alprazolam,⁴ but more evidence is needed. A recent case report described prompt resolution of symptoms with IV haloperidol.¹³ Treating gastritis symptoms with acid suppression therapy, such as a proton pump inhibitor, has been suggested.⁷ Symptoms abate during hospitalization regardless of treatment, marking the progression into the recovery phase with abstinence. There are no proven treatments for CHS, aside from cessation of Cannabis use. Treatment should focus on motivating your patient to stop using Cannabis.

Acute, hyperemetic episodes are ideal teachable moments because of the acuity of symptoms and clear association with Cannabis use. However, some patients may be skeptical about CHS because of the better-known antiemetic effects of Cannabis. For such patients, provide informational materials describing CHS and take time to address their concerns or doubts.

Motivational interviewing can help provoke behavior change by exploring patient ambivalence in a directive, patient-focused manner. Randomized controlled trials have documented significant reductions in Cannabis use with single-session motivational interviewing, with greater effect among heavy users.¹⁷ Single-session motivational interviewing showed results comparable to providing drug information and advice, suggesting that education and information are useful interventions.¹⁸ Although these single-session studies appear promising, they focus on younger users who have not been using Cannabis as long as typical CHS patients. Multi-session interventions may be needed to address longstanding, heavy Cannabis use in adult CHS patients.

Cognitive-behavioral therapy. In a series of randomized controlled trials,
motivational enhancement training and cognitive-behavioral therapy (CBT) were effective for Cannabis use cessation and maintenance of abstinence.¹⁹

Although these interventions take more time—six to 14 sessions for CBT and one to four sessions for motivational enhancement training—they should be considered for CHS patients with persistent use.

Bottom Line

Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily, heavy Cannabis use, cyclic nausea and vomiting, and compulsive bathing. Symptoms resolve with Cannabis cessation. Workup of suspected CHS should rule out life- threatening causes of nausea and vomiting. Acute hyperemetic episodes should be managed supportively. Motivational enhancement therapy or cognitive-behavioral therapy should be considered for persistent Cannibis use.

Related Resources

• Motivational interviewing for substance use disorders. www.motivationalinterview.org.
• Danovitch I, Gorelick DA. State of the art treatments for cannabis dependence. Psychiatr Clin North Am. 2012;35(2):309-326.

Drug Brand Names

Alprazolam • Xanax        Haloperidol • Haldol         Lorazepam • Ativan

Ondansetron • Zofran     Prochlorperazine • Compazine

Disclosure

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

Cannabis is the most commonly abused drug in the United States. Since 2008, Cannabis use has significantly increased,¹ in part because of legalization for medicinal and recreational use. Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily Cannabis use, recurrent nausea, vomiting and abdominal pain, compulsive bathing for symptom relief, and symptom resolution with cessation of use.

Prompt recognition of CHS can reduce costs associated with unnecessary workups, emergency department (ED) and urgent care visits, and hospital admissions.^2,3 This article provides a review of CHS with discussion of diagnostic and management considerations.

CASE REPORT Nauseated and vomiting—and stoned

Mr. M, age 24, self-presents to the ED complaining of two days of severe nausea, colicky abdominal pain, and nonbloody, nonbilious vomiting, as often as 20 times a day. His symptoms become worse with food, and he has difficulty eating and drinking because of his vomiting. Mr. M reports transient symptom relief when he takes hot showers, and has been taking more than 14 showers a day. He reports similar episodes, occurring every two or three months over the last two years, resulting in several ED visits and three hospital admissions.

Mr. M has smoked two to three joints a day for seven years; he has increased his Cannabis use in an attempt to alleviate his symptoms, but isn’t sure if doing so was helpful. He denies use of tobacco and other illicit drugs, and reports drinking one to three drinks no more than twice a month. He reports dizziness when standing, but no other symptoms. He does not take any medications, and medical and psychiatric histories are unremarkable.

Physical exam reveals a thin, uncomfortable, young man. Vital signs were significant for tachycardia and mild orthostatic hypotension. His abdomen was diffusely tender, soft, and nondistended. Urine toxicology is positive for delta-9-tetrahydrocannabinol (THC) only. Labs, including a complete blood count (CBC), basic metabolic panel, liver function tests, and lipase, are within normal limits. Prior workup included abdominal radiographs, abdominal ultrasonography, abdominal CT, and gastric biopsy; all are normal. He has mild gastritis and esophagitis on esophagogastroduodenoscopy and mildly delayed gastric emptying. HIV and hepatitis screenings are negative. Six months ago he received antibiotic therapy for Helicobacter pylori infection. 

Mr. M is admitted to the hospital and seen by the psychiatric consultation service. He is treated with IV ondansetron and prochlorperazine, with little effect. He showers frequently until his symptoms begin to abate within 36 hours of stopping Cannabis use, and is discharged soon after. Psychiatric clinicians provide brief motivational interviewing while Mr. M is in the hospital, and refer him to outpatient psychiatric care and Narcotics Anonymous. Mr. M is then lost to follow up.

In 2011, 18.1 million people reported Cannabis use in the previous month; 39% reported use in 20 of the last 30 days.¹ A high rate of use and a relatively low number of cases suggests that CHS is rare. However, it is likely that CHS is under-recognized and under-reported.^2,4,5 CHS symptoms may be misattributed to cyclic vomiting syndrome,³ because 50% of patients diagnosed with cyclic vomiting syndrome report daily Cannabis use.⁶ There is no epidemiological data on the incidence or prevalence of CHS among regular Cannabis users.⁷

Allen and colleagues first described this syndrome in 2004.⁴ Since then, CHS has been documented in a growing number of case reports and reviews,^2,3,5,7-13 yet it continues to be under-recognized. Many CHS patients experience delays in diagnosis—often years—resulting in prolonged suffering, and costs incurred by frequent ED and urgent care visits, hospital admissions, and unnecessary workups.^2,3,7

Clinical characteristics

CHS is characterized by recurrent, hyperemetic episodes in the context of chronic, daily Cannabis use.⁴ The average age of onset is 25.6 years (range: 16 to 51 years).³ Ninety-five percent of CHS patients used Cannabis daily, for, on average, 9.8 years before symptom onset.³ The amount of Cannabis used, although generally high, is difficult to quantify, and has been described as heavy and hourly in units of blunts, cones, joints, bongs, etc. Patients are most likely to present during acute hyperemetic episodes, which occur in a cyclic pattern, every four to eight weeks,³ interspersed with symptom-free periods. Three phases have been described:

• prodromal or pre-emetic phase
• hyperemetic phase
• recovery phase.^4,10

Many patients report a prodromal phase, with one or two weeks of morning nausea, food aversion, preserved eating patterns, possible weight loss, and occasional vomiting. The acute, hyperemetic phase is characterized by severe nausea, frequent vomiting, abdominal pain, and compulsive bathing for temporary symptom relief. In the recovery phase, symptom improvement and resolution occur with cessation of Cannabis use.^4,10 Symptom improvement can occur within 12 hours of Cannabis cessation, but can take as long as three weeks.³ Patients remain symptom-free while abstinent, but symptoms rapidly recur when they resume use.^3,4

Cannabis is used as an antiemetic and appetite stimulant for chemotherapy-associated nausea and for anorexia in HIV infection. The pathogenesis of paradoxical hyperemetic symptoms of CHS remain unclear, but several mechanisms have been proposed. The principle active cannabinoid in Cannabis is the highly lipophilic compound THC, which binds to cannabinoid type 1 (CB1) and type 2 (CB2) receptors in the CNS and other tissues. It is thought that the antiemetic and appetite-stimulating effects of Cannabis are mediated by CB1 receptor activation in the hypothalamus. Nausea and vomiting are thought to be mediated by CB1 receptor activation in the enteric nervous system, which causes slowed peristalsis, delayed gastric emptying, and splanchnic vasodilation.^4,14

In sensitive persons, chronic heavy Cannabis use can cause THC to accumulate to a toxic level in fatty tissues, causing enteric receptor binding effects to override the CNS receptor-binding effects.⁴ This is supported by case studies describing severe vomiting with IV injection of crude marijuana extract.¹⁵ Nearly 100 different THC metabolites have been identified. The Cannabis plant contains more than 400 chemicals, with 60 cannabinoid structures, any of which could cause CHS in toxic concentrations.^4,7 Among them, cannabidiol, a 5-HT1A partial agonist, was shown to cause vomiting at higher doses in animal studies.^4,7

Mechanisms of action

Cannabis has been used for centuries, so it is unclear why CHS is only recently being recognized. It may be because of higher THC content through selective breeding of plants and a more selective use of female buds that contain more concentrated THC levels than leaves and stems.³ Alternately, CHS may be caused by exogenous substances, such as pesticides, additives, preservatives, or other chemicals used in marijuana preparation, although there is little evidence to support this.³

The mechanism of symptom relief with hot bathing also is unclear. Patients report consistent, global symptom improvement with hot bathing.³ Relief is rapid, transient, and temperature dependent.⁴ CB1 receptors are located near the thermoregulatory center of the hypothalamus. Increased body temperature with hot bathing may counteract the thermoregulatory dysregulation associated with Cannabis use.^4,9 It has been proposed that splanchnic vasodilation might contribute to CHS symptoms. Thus, redistribution of blood from the gut to the skin with warm bathing causes a “cutaneous steal syndrome,” resulting in symptom relief.¹¹

Diagnostic approach

Four key features should be present when making a diagnosis of CHS:

• heavy marijuana use
• recurrent episodes of severe nausea, vomiting, and abdominal cramping       
• compulsive bathing for transient symptom relief
• resolution of symptoms with cessation of Cannabis use.^2,4,8

Compulsive, hot bathing for symptom relief was described in 98% of all reported cases,³ and should be considered pathognomonic.² CHS patients can present with other symptoms, including polydipsia, mild fever, weight loss, and orthostasis.³ Although lab studies usually are normal, mild leukocytosis, hypokalemia, hypochloremia, elevated salivary amylase, mild gastritis on esophagogastroduodenoscopy, and delayed gastric emptying have been described during acute episodes (Table 1).^2-4,7,8

Diagnosis starts with a history and physical exam, followed by a basic workup geared towards ruling out other causes of acute nausea and vomiting.^2,7 Establish temporal relationships between symptoms, Cannabis use (onset, frequency, amount, duration), and bathing behaviors. A positive urine toxicology screen supports a CHS diagnosis and can facilitate discussion of Cannabis use.² If you suspect CHS, rule out potentially life-threatening causes of acute nausea, vomiting, and abdominal pain, such as intestinal obstruction or perforation, pancreaticobiliary disease, and pregnancy. The initial workup should include a CBC, basic metabolic panel, liver function tests, amylase, lipase, pregnancy test, urinalysis, urine toxicology screen, and abdominal radiographs (Table 2).^2,4,7 The differential diagnosis of recurrent vomiting is broad and should be considered (Table 3).^2,4,7,16 Further workup can proceed non-emergently, and should be prompted by clinical suspicion.^2,7

Supportive treatment, education

Treatment of acute hyperemetic episodes in CHS primarily is supportive; address dehydration with IV fluids and electrolyte replenishment as needed.^2,4,7 Standard antiemetics, including 5-HT3 receptor antagonists, D2 receptor antagonists, and H1 receptor antagonists, are largely ineffective.^5,9 Although narcotics have been used to treat abdominal pain, use caution when prescribing because they can exacerbate nausea and vomiting.⁷ Case reports have described symptom relief with inpatient treatment with lorazepam¹² and self-medication with alprazolam,⁴ but more evidence is needed. A recent case report described prompt resolution of symptoms with IV haloperidol.¹³ Treating gastritis symptoms with acid suppression therapy, such as a proton pump inhibitor, has been suggested.⁷ Symptoms abate during hospitalization regardless of treatment, marking the progression into the recovery phase with abstinence. There are no proven treatments for CHS, aside from cessation of Cannabis use. Treatment should focus on motivating your patient to stop using Cannabis.

Acute, hyperemetic episodes are ideal teachable moments because of the acuity of symptoms and clear association with Cannabis use. However, some patients may be skeptical about CHS because of the better-known antiemetic effects of Cannabis. For such patients, provide informational materials describing CHS and take time to address their concerns or doubts.

Motivational interviewing can help provoke behavior change by exploring patient ambivalence in a directive, patient-focused manner. Randomized controlled trials have documented significant reductions in Cannabis use with single-session motivational interviewing, with greater effect among heavy users.¹⁷ Single-session motivational interviewing showed results comparable to providing drug information and advice, suggesting that education and information are useful interventions.¹⁸ Although these single-session studies appear promising, they focus on younger users who have not been using Cannabis as long as typical CHS patients. Multi-session interventions may be needed to address longstanding, heavy Cannabis use in adult CHS patients.

Cognitive-behavioral therapy. In a series of randomized controlled trials,
motivational enhancement training and cognitive-behavioral therapy (CBT) were effective for Cannabis use cessation and maintenance of abstinence.¹⁹

Although these interventions take more time—six to 14 sessions for CBT and one to four sessions for motivational enhancement training—they should be considered for CHS patients with persistent use.

Bottom Line

Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily, heavy Cannabis use, cyclic nausea and vomiting, and compulsive bathing. Symptoms resolve with Cannabis cessation. Workup of suspected CHS should rule out life- threatening causes of nausea and vomiting. Acute hyperemetic episodes should be managed supportively. Motivational enhancement therapy or cognitive-behavioral therapy should be considered for persistent Cannibis use.

Related Resources

• Motivational interviewing for substance use disorders. www.motivationalinterview.org.
• Danovitch I, Gorelick DA. State of the art treatments for cannabis dependence. Psychiatr Clin North Am. 2012;35(2):309-326.

Drug Brand Names

Alprazolam • Xanax        Haloperidol • Haldol         Lorazepam • Ativan

Ondansetron • Zofran     Prochlorperazine • Compazine

Disclosure

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

Cannabis is the most commonly abused drug in the United States. Since 2008, Cannabis use has significantly increased,¹ in part because of legalization for medicinal and recreational use. Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily Cannabis use, recurrent nausea, vomiting and abdominal pain, compulsive bathing for symptom relief, and symptom resolution with cessation of use.

Prompt recognition of CHS can reduce costs associated with unnecessary workups, emergency department (ED) and urgent care visits, and hospital admissions.^2,3 This article provides a review of CHS with discussion of diagnostic and management considerations.

CASE REPORT Nauseated and vomiting—and stoned

Mr. M, age 24, self-presents to the ED complaining of two days of severe nausea, colicky abdominal pain, and nonbloody, nonbilious vomiting, as often as 20 times a day. His symptoms become worse with food, and he has difficulty eating and drinking because of his vomiting. Mr. M reports transient symptom relief when he takes hot showers, and has been taking more than 14 showers a day. He reports similar episodes, occurring every two or three months over the last two years, resulting in several ED visits and three hospital admissions.

Mr. M has smoked two to three joints a day for seven years; he has increased his Cannabis use in an attempt to alleviate his symptoms, but isn’t sure if doing so was helpful. He denies use of tobacco and other illicit drugs, and reports drinking one to three drinks no more than twice a month. He reports dizziness when standing, but no other symptoms. He does not take any medications, and medical and psychiatric histories are unremarkable.

Physical exam reveals a thin, uncomfortable, young man. Vital signs were significant for tachycardia and mild orthostatic hypotension. His abdomen was diffusely tender, soft, and nondistended. Urine toxicology is positive for delta-9-tetrahydrocannabinol (THC) only. Labs, including a complete blood count (CBC), basic metabolic panel, liver function tests, and lipase, are within normal limits. Prior workup included abdominal radiographs, abdominal ultrasonography, abdominal CT, and gastric biopsy; all are normal. He has mild gastritis and esophagitis on esophagogastroduodenoscopy and mildly delayed gastric emptying. HIV and hepatitis screenings are negative. Six months ago he received antibiotic therapy for Helicobacter pylori infection. 

Mr. M is admitted to the hospital and seen by the psychiatric consultation service. He is treated with IV ondansetron and prochlorperazine, with little effect. He showers frequently until his symptoms begin to abate within 36 hours of stopping Cannabis use, and is discharged soon after. Psychiatric clinicians provide brief motivational interviewing while Mr. M is in the hospital, and refer him to outpatient psychiatric care and Narcotics Anonymous. Mr. M is then lost to follow up.

In 2011, 18.1 million people reported Cannabis use in the previous month; 39% reported use in 20 of the last 30 days.¹ A high rate of use and a relatively low number of cases suggests that CHS is rare. However, it is likely that CHS is under-recognized and under-reported.^2,4,5 CHS symptoms may be misattributed to cyclic vomiting syndrome,³ because 50% of patients diagnosed with cyclic vomiting syndrome report daily Cannabis use.⁶ There is no epidemiological data on the incidence or prevalence of CHS among regular Cannabis users.⁷

Allen and colleagues first described this syndrome in 2004.⁴ Since then, CHS has been documented in a growing number of case reports and reviews,^2,3,5,7-13 yet it continues to be under-recognized. Many CHS patients experience delays in diagnosis—often years—resulting in prolonged suffering, and costs incurred by frequent ED and urgent care visits, hospital admissions, and unnecessary workups.^2,3,7

Clinical characteristics

CHS is characterized by recurrent, hyperemetic episodes in the context of chronic, daily Cannabis use.⁴ The average age of onset is 25.6 years (range: 16 to 51 years).³ Ninety-five percent of CHS patients used Cannabis daily, for, on average, 9.8 years before symptom onset.³ The amount of Cannabis used, although generally high, is difficult to quantify, and has been described as heavy and hourly in units of blunts, cones, joints, bongs, etc. Patients are most likely to present during acute hyperemetic episodes, which occur in a cyclic pattern, every four to eight weeks,³ interspersed with symptom-free periods. Three phases have been described:

• prodromal or pre-emetic phase
• hyperemetic phase
• recovery phase.^4,10

Many patients report a prodromal phase, with one or two weeks of morning nausea, food aversion, preserved eating patterns, possible weight loss, and occasional vomiting. The acute, hyperemetic phase is characterized by severe nausea, frequent vomiting, abdominal pain, and compulsive bathing for temporary symptom relief. In the recovery phase, symptom improvement and resolution occur with cessation of Cannabis use.^4,10 Symptom improvement can occur within 12 hours of Cannabis cessation, but can take as long as three weeks.³ Patients remain symptom-free while abstinent, but symptoms rapidly recur when they resume use.^3,4

Cannabis is used as an antiemetic and appetite stimulant for chemotherapy-associated nausea and for anorexia in HIV infection. The pathogenesis of paradoxical hyperemetic symptoms of CHS remain unclear, but several mechanisms have been proposed. The principle active cannabinoid in Cannabis is the highly lipophilic compound THC, which binds to cannabinoid type 1 (CB1) and type 2 (CB2) receptors in the CNS and other tissues. It is thought that the antiemetic and appetite-stimulating effects of Cannabis are mediated by CB1 receptor activation in the hypothalamus. Nausea and vomiting are thought to be mediated by CB1 receptor activation in the enteric nervous system, which causes slowed peristalsis, delayed gastric emptying, and splanchnic vasodilation.^4,14

In sensitive persons, chronic heavy Cannabis use can cause THC to accumulate to a toxic level in fatty tissues, causing enteric receptor binding effects to override the CNS receptor-binding effects.⁴ This is supported by case studies describing severe vomiting with IV injection of crude marijuana extract.¹⁵ Nearly 100 different THC metabolites have been identified. The Cannabis plant contains more than 400 chemicals, with 60 cannabinoid structures, any of which could cause CHS in toxic concentrations.^4,7 Among them, cannabidiol, a 5-HT1A partial agonist, was shown to cause vomiting at higher doses in animal studies.^4,7

Mechanisms of action

Cannabis has been used for centuries, so it is unclear why CHS is only recently being recognized. It may be because of higher THC content through selective breeding of plants and a more selective use of female buds that contain more concentrated THC levels than leaves and stems.³ Alternately, CHS may be caused by exogenous substances, such as pesticides, additives, preservatives, or other chemicals used in marijuana preparation, although there is little evidence to support this.³

The mechanism of symptom relief with hot bathing also is unclear. Patients report consistent, global symptom improvement with hot bathing.³ Relief is rapid, transient, and temperature dependent.⁴ CB1 receptors are located near the thermoregulatory center of the hypothalamus. Increased body temperature with hot bathing may counteract the thermoregulatory dysregulation associated with Cannabis use.^4,9 It has been proposed that splanchnic vasodilation might contribute to CHS symptoms. Thus, redistribution of blood from the gut to the skin with warm bathing causes a “cutaneous steal syndrome,” resulting in symptom relief.¹¹

Diagnostic approach

Four key features should be present when making a diagnosis of CHS:

• heavy marijuana use
• recurrent episodes of severe nausea, vomiting, and abdominal cramping       
• compulsive bathing for transient symptom relief
• resolution of symptoms with cessation of Cannabis use.^2,4,8

Compulsive, hot bathing for symptom relief was described in 98% of all reported cases,³ and should be considered pathognomonic.² CHS patients can present with other symptoms, including polydipsia, mild fever, weight loss, and orthostasis.³ Although lab studies usually are normal, mild leukocytosis, hypokalemia, hypochloremia, elevated salivary amylase, mild gastritis on esophagogastroduodenoscopy, and delayed gastric emptying have been described during acute episodes (Table 1).^2-4,7,8

Diagnosis starts with a history and physical exam, followed by a basic workup geared towards ruling out other causes of acute nausea and vomiting.^2,7 Establish temporal relationships between symptoms, Cannabis use (onset, frequency, amount, duration), and bathing behaviors. A positive urine toxicology screen supports a CHS diagnosis and can facilitate discussion of Cannabis use.² If you suspect CHS, rule out potentially life-threatening causes of acute nausea, vomiting, and abdominal pain, such as intestinal obstruction or perforation, pancreaticobiliary disease, and pregnancy. The initial workup should include a CBC, basic metabolic panel, liver function tests, amylase, lipase, pregnancy test, urinalysis, urine toxicology screen, and abdominal radiographs (Table 2).^2,4,7 The differential diagnosis of recurrent vomiting is broad and should be considered (Table 3).^2,4,7,16 Further workup can proceed non-emergently, and should be prompted by clinical suspicion.^2,7

Supportive treatment, education

Treatment of acute hyperemetic episodes in CHS primarily is supportive; address dehydration with IV fluids and electrolyte replenishment as needed.^2,4,7 Standard antiemetics, including 5-HT3 receptor antagonists, D2 receptor antagonists, and H1 receptor antagonists, are largely ineffective.^5,9 Although narcotics have been used to treat abdominal pain, use caution when prescribing because they can exacerbate nausea and vomiting.⁷ Case reports have described symptom relief with inpatient treatment with lorazepam¹² and self-medication with alprazolam,⁴ but more evidence is needed. A recent case report described prompt resolution of symptoms with IV haloperidol.¹³ Treating gastritis symptoms with acid suppression therapy, such as a proton pump inhibitor, has been suggested.⁷ Symptoms abate during hospitalization regardless of treatment, marking the progression into the recovery phase with abstinence. There are no proven treatments for CHS, aside from cessation of Cannabis use. Treatment should focus on motivating your patient to stop using Cannabis.

Acute, hyperemetic episodes are ideal teachable moments because of the acuity of symptoms and clear association with Cannabis use. However, some patients may be skeptical about CHS because of the better-known antiemetic effects of Cannabis. For such patients, provide informational materials describing CHS and take time to address their concerns or doubts.

Motivational interviewing can help provoke behavior change by exploring patient ambivalence in a directive, patient-focused manner. Randomized controlled trials have documented significant reductions in Cannabis use with single-session motivational interviewing, with greater effect among heavy users.¹⁷ Single-session motivational interviewing showed results comparable to providing drug information and advice, suggesting that education and information are useful interventions.¹⁸ Although these single-session studies appear promising, they focus on younger users who have not been using Cannabis as long as typical CHS patients. Multi-session interventions may be needed to address longstanding, heavy Cannabis use in adult CHS patients.

Cognitive-behavioral therapy. In a series of randomized controlled trials,
motivational enhancement training and cognitive-behavioral therapy (CBT) were effective for Cannabis use cessation and maintenance of abstinence.¹⁹

Although these interventions take more time—six to 14 sessions for CBT and one to four sessions for motivational enhancement training—they should be considered for CHS patients with persistent use.

Bottom Line

Cannabinoid hyperemesis syndrome (CHS) is characterized by years of daily, heavy Cannabis use, cyclic nausea and vomiting, and compulsive bathing. Symptoms resolve with Cannabis cessation. Workup of suspected CHS should rule out life- threatening causes of nausea and vomiting. Acute hyperemetic episodes should be managed supportively. Motivational enhancement therapy or cognitive-behavioral therapy should be considered for persistent Cannibis use.

Related Resources

• Motivational interviewing for substance use disorders. www.motivationalinterview.org.
• Danovitch I, Gorelick DA. State of the art treatments for cannabis dependence. Psychiatr Clin North Am. 2012;35(2):309-326.

Drug Brand Names

Alprazolam • Xanax        Haloperidol • Haldol         Lorazepam • Ativan

Ondansetron • Zofran     Prochlorperazine • Compazine

Disclosure

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

When Kanner first described autism,¹ the disorder was believed to be an uncommon condition, occurring in 4 of every 10,000 children. Over the past few years, however, the rate of autism has increased substantially. Autism is now regarded as a childhood-onset spectrum disorder^a characterized by persistent deficits in social communication, with a restricted pattern of interests and activities, occurring in approximately 1% of children.³

In DSM-IV-TR, Asperger’s disorder (AD), first described as “autistic psychopathy,”⁴ is categorized as a subtype of ASD in which the patient, without a history of language delay or mental retardation, has autistic social deficits that do not meet full criteria for autism.

DSM-5 eliminated AD as an independent category, including it instead as part of ASD.⁵ The label “high-functioning autism” is sometimes used to refer to persons with autism who have normal intelligence (usually defined as full-scale IQ >70), whereas those who have severe intellectual and communication disability are referred to as “low-functioning.” I use “high-functioning autism” and “Asperger’s disorder” interchangeably.

Violent crime and ASD/AD

Reports in the past 2 decades have described violent behavior in persons with ASD/AD. Because of the sensational and unusual nature of these criminal incidents, there is a perception by the public that persons with these disorders, especially those with AD, are predisposed to violent behavior. (Incidents allegedly committed by persons with ASD include the 2007 Virginia Tech campus shooting and the 2012 Newtown, Connecticut, school massacre.⁶)

Yet neither the original descriptions by Kanner (of autism) and Asperger, nor follow-up studies based on the initial samples studied, showed an increased prevalence of violent crime among persons with ASD/AD.⁷

In this article, I examine the evidence behind the claim that people who have ASD/AD are predisposed to criminal violence. At the conclusion, you should, as a physician without special training in autism, have a better understanding of when to suspect ASD/AD in an adult who is involved in criminal behavior.

When should you suspect ASD/AD in an adult?

Although autism is a childhood-onset disorder, its symptoms persist across the life
span. If the diagnosis is missed in childhood, which is likely to happen if the person has normal intelligence and relatively good verbal skills, he (she) might come to medical attention for the first time as an adult.

Because most psychiatrists who treat adults do not receive adequate training in the assessment of childhood psychiatric disorders, ASD/AD might be misdiagnosed as schizophrenia or another psychotic disorder. What clues help identify underlying ASD/AD when a patient is referred to you for psychiatric evaluation after allegedly committing a violent crime?

Clue #1. He makes no attempt to deny or conceal the act. The behavior appears to be part of ritualistic behavior or excessive interest (Table).

Often, the alleged crime occurs when the patient’s excessive interests “get out of control,” perhaps because of an external event. For example, a teenager with AD who is fixated on video games might stumble upon pornographic web sites and begin making obscene telephone calls. Particular attention should be paid to a history of rigid, restricted interests beginning in early childhood.

These restricted interests change over time and correlate with intelligence level: The higher the level of intelligence, the more sophisticated the level of fixation.  Examples of fixations include computers, technology, and scientific experiments and pursuits. Repeated acts of arson have been reported to be part of an autistic person’s fixation with starting fires.⁸

Clue #2. He appears to lack sound and prudent judgment despite normal intelligence.

Although most patients with ASD score in the intellectually disabled or mentally retarded range, at least one-third have an IQ in the normal range.⁹ Examine school records and reports from other agencies when evaluating a patient. Pay attention to a history of difficulty relating to peers at an early age, combined with evidence of rigid, restricted fixations and interests.

It is important to obtain a reliable history going back to early childhood, and not rely just on the patient’s mental status; presenting symptoms might mask underlying traits of ASD, especially in higher-functioning adults. (I once cared for a young man with ASD who had been fired a few days after landing his first job selling used cars because he was “sexually harassing” his colleagues. When questioned, he said that he was only trying to be “friendly” and “practicing his social skills.”)

Clue #3. He has been given a diagnosis of schizophrenia without a clear history of hallucinations or delusions.

Differentiating chronic schizophrenia and autism in adults is not always easy, especially in those who have an intellectual disability. In patients whose cognitive and verbal skills are relatively well preserved (such as AD), the presence of intense, focused interests, a pedantic manner of speaking, and abnormalities of nonverbal communication can help clarify the diagnosis. In particular, a recorded history of “childhood schizophrenia” or “obsessive-compulsive behavior” going back to preschool years should alert you to possible ASD.

Scales and screens. Apart from obtaining an accurate developmental history from a variety of sources, you can use rating scales and screening instruments, such as the Social and Communication Questionnaire¹⁰—although their utility is limited in adults. It is important not to risk overdiagnosis on the basis of these instruments alone: The gold standard of diagnosis remains clinical. The critical point is that the combination of core symptoms of social communication deficits and restricted interests is more important than the presence of a single symptom. A touch of oddity does not mean that one has ASD/AD.

Is the prevalence of violent crime increased in ASD/AD?

It is important to distinguish violent crime from aggressive behavior. The latter, which can be verbal or nonverbal, is not always intentional or malevolent. In some persons who have an intellectual disability, a desire to communicate might lead to inappropriate touching or pushing. This distinction is particularly relevant to psychiatrists because many people who have ASD have an intellectual disability.

Violent crime is more deliberate, serious, and planned. It involves force or threat of force. According to the Federal Bureau of Investigation Uniform Crime Reporting Program, violent crime comprises four offenses: murder and non-negligent manslaughter, forcible rape, robbery, and aggravated assault.¹¹

Earlier descriptions of ASD/AD did not mention criminal violence as an important feature of these disorders. However, reports began to emerge about two decades ago suggesting that people who have ASD—particularly AD—are prone to violent crime. Some of the patients described in Wing’s original series¹² of AD showed violent tendencies, ranging from sudden outbursts of violence to injury to others because of fixation on hobbies such as chemistry experimentation.

Reports such as these were based on isolated case reports or select samples, such as residents of maximum-security hospitals. Scragg and Shah, for example, surveyed the male population of Broadmoor Hospital, a high-security facility in the United Kingdom, and found that the prevalence of AD was higher than expected in the general population.¹³

Recent reports have not been able to confirm that violent crime is increased in persons with ASD, however:

• In a clinical sample of 313 Danish adults with ASD (age 25 to 59) drawn from the Danish Register of Criminality, Mouridsen and colleagues found that persons with ASD had a lower rate of criminal conviction than matched controls (9%, compared with 18%).¹⁴
• In a small community study, Woodbury-Smith and colleagues examined the prevalence rates and types of offending behavior in persons with ASD. Based on official records, only two (18%) had a history of criminal conviction.¹⁵

The role of psychiatric comorbidity

Psychiatric disorders are common in persons who have ASD. In one study, 70% of a sample of 114 children with ASD (age 10 to 14) had a psychiatric disorder, based on a parent interview.¹⁶ Although people with mental illness are not inherently criminal or violent, having an additional psychiatric disorder independently increases the risk of offending behavior.¹⁷ For example, the association of attention-deficit/hyperactivity disorder with criminality is well established.¹⁶ Some patients with severe depression and psychotic disorders, including schizophrenia, also are at increased risk of committing a violent act.

To examine the contribution of mental health factors to the commission of crime by persons with ASD, Newman and Ghaziuddin¹⁸ used online databases to identify relevant articles, which were then cross-referenced with keyword searches for “violence,” “crime,” “murder,” “assault,” “rape,” and “sex offenses.” Thirty-seven cases were identified in the 17 publications that met inclusion criteria. Out of these, 30% had a definite psychiatric disorder and 54% had a probable psychiatric disorder at the time they committed the crime.¹⁸

Any patient with ASD/AD who is evaluated for criminal behavior should be screened for a comorbid psychiatric disorder. In adolescents, stressors such as bullying in school and problems surrounding dating might contribute to offending behavior.

What are management options in the face of violence?

Managing ASD/AD when an offending behavior has occurred first requires a correct diagnosis.¹⁹ Professionals working in the criminal justice system have little awareness of the variants of ASD; a defendant with an intellectual disability and a characteristic facial appearance (for example, someone with Down syndrome) can be easily identified, but a high-functioning person who has mild autistic features often is missed. This is more likely to occur in adults because the symptoms of ASD, including the type and severity of isolated interests, change over time.

Here is how I recommend that you proceed:

Step #1. Confirm the ASD diagnosis based on developmental history and the presence of persistent social and communication deficits plus restricted interests.

Step #2. Screen for comorbid psychiatric and medical disorders, including depression, psychosis, and seizure disorder.

Step #3. Treat any disorders you identify with a combination of medication and behavioral intervention.

Step #4. Carefully examine the circumstances surrounding the offending behavior. Involve forensic services on a case-by-case basis, depending on the type and seriousness of the offending behavior (see Related Resources for information on the role of forensic services). When the crime does not involve serious violence, lengthy incarceration might be unnecessary. Because psychopathy and ASD/AD are not mutually exclusive, persons who commit a heinous crime, such as rape or murder, should be dealt with in accordance with the law.

Need for greater awareness of the complexion of ASD

Patients who have ASD/AD form a heterogeneous group in which the levels of cognitive and communication skills are variable. Those who are low-functioning and who have severe behavioral and adaptive deficits occasionally commit aggressive acts against their caregivers.

Most patients with ASD/AD are neither violent nor criminal. Those who are at the higher end of the spectrum, with relatively preserved communication and intellectual skills, occasionally indulge in criminal behavior—behavior that is nonviolent and results from their inability to read social cues or excessive preoccupations.

Most reports that link criminal violence with ASD are based on isolated case reports or on biased samples that use unreliable diagnostic criteria. In higher-functioning persons with ASD, violent crime is almost always precipitated by a comorbid psychiatric disorder, such as severe depression and psychosis.

In short: There is a need to increase our awareness of the special challenges faced by persons with ASD/AD in the criminal justice system.

aGiven the term pervasive developmental disorders (PDD) in the DSM-IV-TR, the spectrum includes autistic disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified.2

Bottom Line

Most people who have an autism spectrum disorder (ASD) do not commit violent crime. When violent crime occurs at the hands of a person with ASD, it is almost always precipitated by a comorbid psychiatric disorder, such as severe depression or psychosis. Treating a person with ASD who has committed a violent crime is multimodal, including forensic services when necessary.

Related Resources

• Autism Speaks. No link between autism and violence. www.autismspeaks.org/science/science-news/no-link-between-autism-and-violence.
• Haskins BG, Silva JA. Asperger’s disorder and criminal behavior: Forensic-psychiatric considerations. J Am Acad Psychiatry Law. 2006;34(3):374-384.
• Newman SS, Ghaziuddin M. Violent crime and Asperger syndrome: the role of psychiatric comorbidity. J Autism Dev Disord. 2008;38:1848-1852.
• Wing L. Asperger’s syndrome: a clinical account. Psychol Med. 1981;11(1):115-129.

Disclosure

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

When Kanner first described autism,¹ the disorder was believed to be an uncommon condition, occurring in 4 of every 10,000 children. Over the past few years, however, the rate of autism has increased substantially. Autism is now regarded as a childhood-onset spectrum disorder^a characterized by persistent deficits in social communication, with a restricted pattern of interests and activities, occurring in approximately 1% of children.³

In DSM-IV-TR, Asperger’s disorder (AD), first described as “autistic psychopathy,”⁴ is categorized as a subtype of ASD in which the patient, without a history of language delay or mental retardation, has autistic social deficits that do not meet full criteria for autism.

DSM-5 eliminated AD as an independent category, including it instead as part of ASD.⁵ The label “high-functioning autism” is sometimes used to refer to persons with autism who have normal intelligence (usually defined as full-scale IQ >70), whereas those who have severe intellectual and communication disability are referred to as “low-functioning.” I use “high-functioning autism” and “Asperger’s disorder” interchangeably.

Violent crime and ASD/AD

Reports in the past 2 decades have described violent behavior in persons with ASD/AD. Because of the sensational and unusual nature of these criminal incidents, there is a perception by the public that persons with these disorders, especially those with AD, are predisposed to violent behavior. (Incidents allegedly committed by persons with ASD include the 2007 Virginia Tech campus shooting and the 2012 Newtown, Connecticut, school massacre.⁶)

Yet neither the original descriptions by Kanner (of autism) and Asperger, nor follow-up studies based on the initial samples studied, showed an increased prevalence of violent crime among persons with ASD/AD.⁷

In this article, I examine the evidence behind the claim that people who have ASD/AD are predisposed to criminal violence. At the conclusion, you should, as a physician without special training in autism, have a better understanding of when to suspect ASD/AD in an adult who is involved in criminal behavior.

When should you suspect ASD/AD in an adult?

Although autism is a childhood-onset disorder, its symptoms persist across the life
span. If the diagnosis is missed in childhood, which is likely to happen if the person has normal intelligence and relatively good verbal skills, he (she) might come to medical attention for the first time as an adult.

Because most psychiatrists who treat adults do not receive adequate training in the assessment of childhood psychiatric disorders, ASD/AD might be misdiagnosed as schizophrenia or another psychotic disorder. What clues help identify underlying ASD/AD when a patient is referred to you for psychiatric evaluation after allegedly committing a violent crime?

Clue #1. He makes no attempt to deny or conceal the act. The behavior appears to be part of ritualistic behavior or excessive interest (Table).

Often, the alleged crime occurs when the patient’s excessive interests “get out of control,” perhaps because of an external event. For example, a teenager with AD who is fixated on video games might stumble upon pornographic web sites and begin making obscene telephone calls. Particular attention should be paid to a history of rigid, restricted interests beginning in early childhood.

These restricted interests change over time and correlate with intelligence level: The higher the level of intelligence, the more sophisticated the level of fixation.  Examples of fixations include computers, technology, and scientific experiments and pursuits. Repeated acts of arson have been reported to be part of an autistic person’s fixation with starting fires.⁸

Clue #2. He appears to lack sound and prudent judgment despite normal intelligence.

Although most patients with ASD score in the intellectually disabled or mentally retarded range, at least one-third have an IQ in the normal range.⁹ Examine school records and reports from other agencies when evaluating a patient. Pay attention to a history of difficulty relating to peers at an early age, combined with evidence of rigid, restricted fixations and interests.

It is important to obtain a reliable history going back to early childhood, and not rely just on the patient’s mental status; presenting symptoms might mask underlying traits of ASD, especially in higher-functioning adults. (I once cared for a young man with ASD who had been fired a few days after landing his first job selling used cars because he was “sexually harassing” his colleagues. When questioned, he said that he was only trying to be “friendly” and “practicing his social skills.”)

Clue #3. He has been given a diagnosis of schizophrenia without a clear history of hallucinations or delusions.

Differentiating chronic schizophrenia and autism in adults is not always easy, especially in those who have an intellectual disability. In patients whose cognitive and verbal skills are relatively well preserved (such as AD), the presence of intense, focused interests, a pedantic manner of speaking, and abnormalities of nonverbal communication can help clarify the diagnosis. In particular, a recorded history of “childhood schizophrenia” or “obsessive-compulsive behavior” going back to preschool years should alert you to possible ASD.

Scales and screens. Apart from obtaining an accurate developmental history from a variety of sources, you can use rating scales and screening instruments, such as the Social and Communication Questionnaire¹⁰—although their utility is limited in adults. It is important not to risk overdiagnosis on the basis of these instruments alone: The gold standard of diagnosis remains clinical. The critical point is that the combination of core symptoms of social communication deficits and restricted interests is more important than the presence of a single symptom. A touch of oddity does not mean that one has ASD/AD.

Is the prevalence of violent crime increased in ASD/AD?

It is important to distinguish violent crime from aggressive behavior. The latter, which can be verbal or nonverbal, is not always intentional or malevolent. In some persons who have an intellectual disability, a desire to communicate might lead to inappropriate touching or pushing. This distinction is particularly relevant to psychiatrists because many people who have ASD have an intellectual disability.

Violent crime is more deliberate, serious, and planned. It involves force or threat of force. According to the Federal Bureau of Investigation Uniform Crime Reporting Program, violent crime comprises four offenses: murder and non-negligent manslaughter, forcible rape, robbery, and aggravated assault.¹¹

Earlier descriptions of ASD/AD did not mention criminal violence as an important feature of these disorders. However, reports began to emerge about two decades ago suggesting that people who have ASD—particularly AD—are prone to violent crime. Some of the patients described in Wing’s original series¹² of AD showed violent tendencies, ranging from sudden outbursts of violence to injury to others because of fixation on hobbies such as chemistry experimentation.

Reports such as these were based on isolated case reports or select samples, such as residents of maximum-security hospitals. Scragg and Shah, for example, surveyed the male population of Broadmoor Hospital, a high-security facility in the United Kingdom, and found that the prevalence of AD was higher than expected in the general population.¹³

Recent reports have not been able to confirm that violent crime is increased in persons with ASD, however:

• In a clinical sample of 313 Danish adults with ASD (age 25 to 59) drawn from the Danish Register of Criminality, Mouridsen and colleagues found that persons with ASD had a lower rate of criminal conviction than matched controls (9%, compared with 18%).¹⁴
• In a small community study, Woodbury-Smith and colleagues examined the prevalence rates and types of offending behavior in persons with ASD. Based on official records, only two (18%) had a history of criminal conviction.¹⁵

The role of psychiatric comorbidity

Psychiatric disorders are common in persons who have ASD. In one study, 70% of a sample of 114 children with ASD (age 10 to 14) had a psychiatric disorder, based on a parent interview.¹⁶ Although people with mental illness are not inherently criminal or violent, having an additional psychiatric disorder independently increases the risk of offending behavior.¹⁷ For example, the association of attention-deficit/hyperactivity disorder with criminality is well established.¹⁶ Some patients with severe depression and psychotic disorders, including schizophrenia, also are at increased risk of committing a violent act.

To examine the contribution of mental health factors to the commission of crime by persons with ASD, Newman and Ghaziuddin¹⁸ used online databases to identify relevant articles, which were then cross-referenced with keyword searches for “violence,” “crime,” “murder,” “assault,” “rape,” and “sex offenses.” Thirty-seven cases were identified in the 17 publications that met inclusion criteria. Out of these, 30% had a definite psychiatric disorder and 54% had a probable psychiatric disorder at the time they committed the crime.¹⁸

Any patient with ASD/AD who is evaluated for criminal behavior should be screened for a comorbid psychiatric disorder. In adolescents, stressors such as bullying in school and problems surrounding dating might contribute to offending behavior.

What are management options in the face of violence?

Managing ASD/AD when an offending behavior has occurred first requires a correct diagnosis.¹⁹ Professionals working in the criminal justice system have little awareness of the variants of ASD; a defendant with an intellectual disability and a characteristic facial appearance (for example, someone with Down syndrome) can be easily identified, but a high-functioning person who has mild autistic features often is missed. This is more likely to occur in adults because the symptoms of ASD, including the type and severity of isolated interests, change over time.

Here is how I recommend that you proceed:

Step #1. Confirm the ASD diagnosis based on developmental history and the presence of persistent social and communication deficits plus restricted interests.

Step #2. Screen for comorbid psychiatric and medical disorders, including depression, psychosis, and seizure disorder.

Step #3. Treat any disorders you identify with a combination of medication and behavioral intervention.

Step #4. Carefully examine the circumstances surrounding the offending behavior. Involve forensic services on a case-by-case basis, depending on the type and seriousness of the offending behavior (see Related Resources for information on the role of forensic services). When the crime does not involve serious violence, lengthy incarceration might be unnecessary. Because psychopathy and ASD/AD are not mutually exclusive, persons who commit a heinous crime, such as rape or murder, should be dealt with in accordance with the law.

Need for greater awareness of the complexion of ASD

Patients who have ASD/AD form a heterogeneous group in which the levels of cognitive and communication skills are variable. Those who are low-functioning and who have severe behavioral and adaptive deficits occasionally commit aggressive acts against their caregivers.

Most patients with ASD/AD are neither violent nor criminal. Those who are at the higher end of the spectrum, with relatively preserved communication and intellectual skills, occasionally indulge in criminal behavior—behavior that is nonviolent and results from their inability to read social cues or excessive preoccupations.

Most reports that link criminal violence with ASD are based on isolated case reports or on biased samples that use unreliable diagnostic criteria. In higher-functioning persons with ASD, violent crime is almost always precipitated by a comorbid psychiatric disorder, such as severe depression and psychosis.

In short: There is a need to increase our awareness of the special challenges faced by persons with ASD/AD in the criminal justice system.

aGiven the term pervasive developmental disorders (PDD) in the DSM-IV-TR, the spectrum includes autistic disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified.2

Bottom Line

Most people who have an autism spectrum disorder (ASD) do not commit violent crime. When violent crime occurs at the hands of a person with ASD, it is almost always precipitated by a comorbid psychiatric disorder, such as severe depression or psychosis. Treating a person with ASD who has committed a violent crime is multimodal, including forensic services when necessary.

Related Resources

• Autism Speaks. No link between autism and violence. www.autismspeaks.org/science/science-news/no-link-between-autism-and-violence.
• Haskins BG, Silva JA. Asperger’s disorder and criminal behavior: Forensic-psychiatric considerations. J Am Acad Psychiatry Law. 2006;34(3):374-384.
• Newman SS, Ghaziuddin M. Violent crime and Asperger syndrome: the role of psychiatric comorbidity. J Autism Dev Disord. 2008;38:1848-1852.
• Wing L. Asperger’s syndrome: a clinical account. Psychol Med. 1981;11(1):115-129.

Disclosure

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

When Kanner first described autism,¹ the disorder was believed to be an uncommon condition, occurring in 4 of every 10,000 children. Over the past few years, however, the rate of autism has increased substantially. Autism is now regarded as a childhood-onset spectrum disorder^a characterized by persistent deficits in social communication, with a restricted pattern of interests and activities, occurring in approximately 1% of children.³

In DSM-IV-TR, Asperger’s disorder (AD), first described as “autistic psychopathy,”⁴ is categorized as a subtype of ASD in which the patient, without a history of language delay or mental retardation, has autistic social deficits that do not meet full criteria for autism.

DSM-5 eliminated AD as an independent category, including it instead as part of ASD.⁵ The label “high-functioning autism” is sometimes used to refer to persons with autism who have normal intelligence (usually defined as full-scale IQ >70), whereas those who have severe intellectual and communication disability are referred to as “low-functioning.” I use “high-functioning autism” and “Asperger’s disorder” interchangeably.

Violent crime and ASD/AD

Reports in the past 2 decades have described violent behavior in persons with ASD/AD. Because of the sensational and unusual nature of these criminal incidents, there is a perception by the public that persons with these disorders, especially those with AD, are predisposed to violent behavior. (Incidents allegedly committed by persons with ASD include the 2007 Virginia Tech campus shooting and the 2012 Newtown, Connecticut, school massacre.⁶)

Yet neither the original descriptions by Kanner (of autism) and Asperger, nor follow-up studies based on the initial samples studied, showed an increased prevalence of violent crime among persons with ASD/AD.⁷

In this article, I examine the evidence behind the claim that people who have ASD/AD are predisposed to criminal violence. At the conclusion, you should, as a physician without special training in autism, have a better understanding of when to suspect ASD/AD in an adult who is involved in criminal behavior.

When should you suspect ASD/AD in an adult?

Although autism is a childhood-onset disorder, its symptoms persist across the life
span. If the diagnosis is missed in childhood, which is likely to happen if the person has normal intelligence and relatively good verbal skills, he (she) might come to medical attention for the first time as an adult.

Because most psychiatrists who treat adults do not receive adequate training in the assessment of childhood psychiatric disorders, ASD/AD might be misdiagnosed as schizophrenia or another psychotic disorder. What clues help identify underlying ASD/AD when a patient is referred to you for psychiatric evaluation after allegedly committing a violent crime?

Clue #1. He makes no attempt to deny or conceal the act. The behavior appears to be part of ritualistic behavior or excessive interest (Table).

Often, the alleged crime occurs when the patient’s excessive interests “get out of control,” perhaps because of an external event. For example, a teenager with AD who is fixated on video games might stumble upon pornographic web sites and begin making obscene telephone calls. Particular attention should be paid to a history of rigid, restricted interests beginning in early childhood.

These restricted interests change over time and correlate with intelligence level: The higher the level of intelligence, the more sophisticated the level of fixation.  Examples of fixations include computers, technology, and scientific experiments and pursuits. Repeated acts of arson have been reported to be part of an autistic person’s fixation with starting fires.⁸

Clue #2. He appears to lack sound and prudent judgment despite normal intelligence.

Although most patients with ASD score in the intellectually disabled or mentally retarded range, at least one-third have an IQ in the normal range.⁹ Examine school records and reports from other agencies when evaluating a patient. Pay attention to a history of difficulty relating to peers at an early age, combined with evidence of rigid, restricted fixations and interests.

It is important to obtain a reliable history going back to early childhood, and not rely just on the patient’s mental status; presenting symptoms might mask underlying traits of ASD, especially in higher-functioning adults. (I once cared for a young man with ASD who had been fired a few days after landing his first job selling used cars because he was “sexually harassing” his colleagues. When questioned, he said that he was only trying to be “friendly” and “practicing his social skills.”)

Clue #3. He has been given a diagnosis of schizophrenia without a clear history of hallucinations or delusions.

Differentiating chronic schizophrenia and autism in adults is not always easy, especially in those who have an intellectual disability. In patients whose cognitive and verbal skills are relatively well preserved (such as AD), the presence of intense, focused interests, a pedantic manner of speaking, and abnormalities of nonverbal communication can help clarify the diagnosis. In particular, a recorded history of “childhood schizophrenia” or “obsessive-compulsive behavior” going back to preschool years should alert you to possible ASD.

Scales and screens. Apart from obtaining an accurate developmental history from a variety of sources, you can use rating scales and screening instruments, such as the Social and Communication Questionnaire¹⁰—although their utility is limited in adults. It is important not to risk overdiagnosis on the basis of these instruments alone: The gold standard of diagnosis remains clinical. The critical point is that the combination of core symptoms of social communication deficits and restricted interests is more important than the presence of a single symptom. A touch of oddity does not mean that one has ASD/AD.

Is the prevalence of violent crime increased in ASD/AD?

It is important to distinguish violent crime from aggressive behavior. The latter, which can be verbal or nonverbal, is not always intentional or malevolent. In some persons who have an intellectual disability, a desire to communicate might lead to inappropriate touching or pushing. This distinction is particularly relevant to psychiatrists because many people who have ASD have an intellectual disability.

Violent crime is more deliberate, serious, and planned. It involves force or threat of force. According to the Federal Bureau of Investigation Uniform Crime Reporting Program, violent crime comprises four offenses: murder and non-negligent manslaughter, forcible rape, robbery, and aggravated assault.¹¹

Earlier descriptions of ASD/AD did not mention criminal violence as an important feature of these disorders. However, reports began to emerge about two decades ago suggesting that people who have ASD—particularly AD—are prone to violent crime. Some of the patients described in Wing’s original series¹² of AD showed violent tendencies, ranging from sudden outbursts of violence to injury to others because of fixation on hobbies such as chemistry experimentation.

Reports such as these were based on isolated case reports or select samples, such as residents of maximum-security hospitals. Scragg and Shah, for example, surveyed the male population of Broadmoor Hospital, a high-security facility in the United Kingdom, and found that the prevalence of AD was higher than expected in the general population.¹³

Recent reports have not been able to confirm that violent crime is increased in persons with ASD, however:

• In a clinical sample of 313 Danish adults with ASD (age 25 to 59) drawn from the Danish Register of Criminality, Mouridsen and colleagues found that persons with ASD had a lower rate of criminal conviction than matched controls (9%, compared with 18%).¹⁴
• In a small community study, Woodbury-Smith and colleagues examined the prevalence rates and types of offending behavior in persons with ASD. Based on official records, only two (18%) had a history of criminal conviction.¹⁵

The role of psychiatric comorbidity

Psychiatric disorders are common in persons who have ASD. In one study, 70% of a sample of 114 children with ASD (age 10 to 14) had a psychiatric disorder, based on a parent interview.¹⁶ Although people with mental illness are not inherently criminal or violent, having an additional psychiatric disorder independently increases the risk of offending behavior.¹⁷ For example, the association of attention-deficit/hyperactivity disorder with criminality is well established.¹⁶ Some patients with severe depression and psychotic disorders, including schizophrenia, also are at increased risk of committing a violent act.

To examine the contribution of mental health factors to the commission of crime by persons with ASD, Newman and Ghaziuddin¹⁸ used online databases to identify relevant articles, which were then cross-referenced with keyword searches for “violence,” “crime,” “murder,” “assault,” “rape,” and “sex offenses.” Thirty-seven cases were identified in the 17 publications that met inclusion criteria. Out of these, 30% had a definite psychiatric disorder and 54% had a probable psychiatric disorder at the time they committed the crime.¹⁸

Any patient with ASD/AD who is evaluated for criminal behavior should be screened for a comorbid psychiatric disorder. In adolescents, stressors such as bullying in school and problems surrounding dating might contribute to offending behavior.

What are management options in the face of violence?

Managing ASD/AD when an offending behavior has occurred first requires a correct diagnosis.¹⁹ Professionals working in the criminal justice system have little awareness of the variants of ASD; a defendant with an intellectual disability and a characteristic facial appearance (for example, someone with Down syndrome) can be easily identified, but a high-functioning person who has mild autistic features often is missed. This is more likely to occur in adults because the symptoms of ASD, including the type and severity of isolated interests, change over time.

Here is how I recommend that you proceed:

Step #1. Confirm the ASD diagnosis based on developmental history and the presence of persistent social and communication deficits plus restricted interests.

Step #2. Screen for comorbid psychiatric and medical disorders, including depression, psychosis, and seizure disorder.

Step #3. Treat any disorders you identify with a combination of medication and behavioral intervention.

Step #4. Carefully examine the circumstances surrounding the offending behavior. Involve forensic services on a case-by-case basis, depending on the type and seriousness of the offending behavior (see Related Resources for information on the role of forensic services). When the crime does not involve serious violence, lengthy incarceration might be unnecessary. Because psychopathy and ASD/AD are not mutually exclusive, persons who commit a heinous crime, such as rape or murder, should be dealt with in accordance with the law.

Need for greater awareness of the complexion of ASD

Patients who have ASD/AD form a heterogeneous group in which the levels of cognitive and communication skills are variable. Those who are low-functioning and who have severe behavioral and adaptive deficits occasionally commit aggressive acts against their caregivers.

Most patients with ASD/AD are neither violent nor criminal. Those who are at the higher end of the spectrum, with relatively preserved communication and intellectual skills, occasionally indulge in criminal behavior—behavior that is nonviolent and results from their inability to read social cues or excessive preoccupations.

Most reports that link criminal violence with ASD are based on isolated case reports or on biased samples that use unreliable diagnostic criteria. In higher-functioning persons with ASD, violent crime is almost always precipitated by a comorbid psychiatric disorder, such as severe depression and psychosis.

In short: There is a need to increase our awareness of the special challenges faced by persons with ASD/AD in the criminal justice system.

aGiven the term pervasive developmental disorders (PDD) in the DSM-IV-TR, the spectrum includes autistic disorder, Asperger’s disorder, and pervasive developmental disorder not otherwise specified.2

Bottom Line

Most people who have an autism spectrum disorder (ASD) do not commit violent crime. When violent crime occurs at the hands of a person with ASD, it is almost always precipitated by a comorbid psychiatric disorder, such as severe depression or psychosis. Treating a person with ASD who has committed a violent crime is multimodal, including forensic services when necessary.

Related Resources

• Autism Speaks. No link between autism and violence. www.autismspeaks.org/science/science-news/no-link-between-autism-and-violence.
• Haskins BG, Silva JA. Asperger’s disorder and criminal behavior: Forensic-psychiatric considerations. J Am Acad Psychiatry Law. 2006;34(3):374-384.
• Newman SS, Ghaziuddin M. Violent crime and Asperger syndrome: the role of psychiatric comorbidity. J Autism Dev Disord. 2008;38:1848-1852.
• Wing L. Asperger’s syndrome: a clinical account. Psychol Med. 1981;11(1):115-129.

Disclosure

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

The economic downturn in the United States has prompted numerous state and county budget cuts, in turn forcing many patients to receive their mental health care in the emergency room (ER). Most patients evaluated in the ER for mental health-related reasons have a legitimate psychiatric crisis—but that isn’t always the case. And as the number of people seeking care in the ER has increased, it appears that so too has the number of those who feign symptoms for secondary gain—that is, who are malingering.

This article highlights several red flags for malingered behavior; emphasizes typical (compared with atypical) symptoms of psychosis; and provides an overview of four instruments that you can use to help assess for malingering in the ED.

A difficult diagnosis

No single factor is indicative of malingering, and no objective tests exist to diagnose malingering definitively. Rather, the tests we discuss provide additional information that can help formulate a clinical impression. 

According to DSM-5, malingering is “…the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives…”¹ Despite a relatively straightforward definition, the diagnosis is difficult to make because it is a diagnosis of exclusion.

Even with sufficient evidence, many clinicians are reluctant to diagnose malingering because they fear retaliation and diagnostic uncertainty. Psychiatrists also might be reluctant to diagnose malingering because the negative connotation that the label carries risks stigmatizing a patient who might, in fact, be suffering. This is true especially when there is suspicion of partial malingering, the conscious exaggeration of existing symptoms.

Despite physicians’ reluctance to diagnose malingering, it is a real problem, especially in the ER. Research suggests that as many as 13% of patients in the ER feign illness, and that their secondary gain most often includes food, shelter, prescription drugs, financial gain, and avoidance of jail, work, or family responsibilities.²

CASE REPORT ‘The voices are telling me to kill myself’

Mr. K, a 36-year-old white man, walks into the ER on a late December day. He tells the triage nurse that he suicidal; she escorts him to the psychiatric pod of the ER. Nursing staff provide line-of-sight care, monitor his vital signs, and draw blood for testing.

Within hours, Mr. K is deemed “medically cleared” and ready for assessment by the psychiatric social worker.

Interview and assessment. During the interview with the social worker, Mr. K reports that he has been depressed, adamantly maintaining that he is suicidal, with a plan to “walk in traffic” or “eat the end of a gun.” The social worker places him on a 72-hour involuntary psychiatric hold. ER physicians order psychiatric consultation.

Mr. K is well-known to the psychiatrist on call, from prior ER visits and psychiatric hospital admissions. In fact, two days earlier, he put a psychiatric nurse in a headlock while being escorted from the psychiatric inpatient unit under protest.

On assessment by the psychiatrist, Mr. K continues to endorse feeling suicidal; he adds: “If I don’t get some help, I’m gonna kill somebody else!”

Without prompting, the patient states that “the voices are telling me to kill myself.” He says that those voices have been relentless since he left the hospital two days earlier. According to Mr. K, nothing he did helped quiet the voices, although previous prescriptions for quetiapine have been helpful.

Mr. K says that he is unable to recall the clinic or name of his prior psychiatrist. He claims that he was hospitalized four months ago, (despite the psychiatrist’s knowledge that he had been discharged two days ago) and estimates that his psychotic symptoms began one year ago. He explains that he is homeless and does not have social support. He is unable to provide a telephone number or a name to contact family for collateral information.

Mental status exam. The mental status examination reveals a tall, thin, disheveled man who has poor dentition. He is now calm and cooperative despite his reported level of distress. His speech is unremarkable and his eye contact is appropriate. His thought process is linear, organized, and coherent.

Mr. K does not endorse additional symptoms, but is quick to agree with the psychiatrist’s follow-up questions about hallucinations: “Yeah! I’ve been seeing all kinds of crazy stuff.” When prompted for details, he says, “I just saw Big Bird… He was 100 feet tall!”

Lab testing. Mr. K’s blood work is remarkable for positive urine toxicology for amphetamines.

Nursing notes indicate that Mr. K slept overnight and ate 100% of the food on his dinner and breakfast trays.

Red flags flying

Mr. K’s case highlights several red flags that should raise suspicion of malingering (Table 1)^3,4:

• A conditional statement by which a patient threatens to harm himself or others, contingent upon a demand—for example, “If I don’t get A, I’ll do B.”
• An overly dramatic presentation, in which the patient is quick to endorse
  distressing symptoms. Consider Mr. K: He was quick to report that he saw Big Bird, and that this Sesame Street character “was 100 feet tall.” Patients who have been experiencing true psychotic symptoms might be reluctant to speak of their distressing symptoms, especially if they have not experienced such symptoms in the past (the first psychotic break). Mr. K, however, volunteered and called attention to particularly dramatic psychotic symptoms.
• A subjective report of distress that is inconsistent with the objective presentation. Mr. K’s report of depression—a diagnosis that typically includes insomnia and poor appetite—was inconsistent with his behavior: He slept and he ate all of his meals.

Atypical (vs typical) psychosis

Malingering can occur in various arenas and take many different forms. In forensic settings, such as prison, malingered conditions more often present as posttraumatic stress disorder or cognitive impairment.⁵ In non-forensic settings, such as the ER, the most commonly malingered conditions include suicidality and psychosis.

To detect malingered psychosis, one must first understand how true psychotic symptoms manifest. The following discussion describes and compares typical and atypical symptoms of psychosis; examples are given in Table 2.^6,7No single atypical psychotic symptom is indicative of malingering. Rather, a collection of atypical symptoms, when considered in clinical context, should raise suspicion of malingering and prompt you to seek additional collateral information or perform appropriate testing for malingering.

Hallucinations

Typically, hallucinations take three forms: auditory, visual, and tactile. In primary psychiatric conditions, auditory hallucinations are the most common of those three.

Tactile hallucinations can be present during episodes of substance intoxication or withdrawal (eg, so-called coke bugs). 

Auditory hallucinations. Patients who malinger psychosis are often unaware of the nuances of hallucinations. For example, they might report the atypical symptom of continuous voices; in fact, most patients who have schizophrenia hear voices intermittently. Keep in mind, too, that 75% of patients who have schizophrenia hear male and female voices, and that 70% have some type of coping strategy to minimize their internal stimuli (eg, listening to music).^6,7

Visual hallucinations are most often associated with neurologic disease, but also occur often in primary psychotic disorders, such as schizophrenia.

Patients who malinger psychotic symptoms often are open to suggestion, and are quick to endorse visual hallucinations. When asked to describe their hallucinations, however, they often respond without details (“I don’t know”). Other times, they overcompensate with wild exaggeration of atypical visions—recall Mr. K’s description of a towering Big Bird. Asked if the visions are in black and white, they might eagerly agree. Research suggests, however, that patients who have schizophrenia more often experience life-sized hallucinations of vivid scenes with family members, religious figures, or animals.⁸ Furthermore, genuine visual hallucinations typically are in color.

Putting malingering in the differential

Regardless of the number of atypical symptoms a patient exhibits, malingering will be missed if you do not include it in the differential diagnosis. This fact was made evident in a 1973 study.⁹

In that study, Rosenhan and seven of his colleagues—a psychology graduate student, three psychologists, a pediatrician, a psychiatrist, a painter, and a housewife—presented to various ERs and intake units, and, as they had been instructed, endorsed vague auditory hallucinations of “empty,” “hollow,” or “thud” sounds—but nothing more. All were admitted to psychiatric hospitals. Once admitted, they refrained (again, as instructed) from endorsing or exhibiting any psychotic symptoms.

Despite the vague nature of the reported auditory hallucinations and how rapidly symptoms resolved on admission, seven of these pseudo-patients were given a diagnosis of schizophrenia, and one was given a diagnosis of manic-depressive psychosis. Duration of admission ranged from 7 to 52 days (average, 19 days). None of the study participants were suspected of feigning symptoms.

It’s fortunate that, since then, mental health professionals have developed more structured techniques of assessment to detect malingering in inpatient and triage settings.

Testing to identify and assess malingering

The ER is a fast-paced environment, in which treatment teams are challenged to make rapid clinical assessments. With the overwhelming number of patients seeking mental health care in the ER, however, overall wait times are increasing; in some regions, it is common to write, then to rewrite, involuntary psychiatric holds for patients awaiting transfer to a psychiatric hospital. This extended duration presents an opportunity to serially evaluate patients suspected of malingering.

Even in environments that allow for a more comprehensive evaluation (eg, jail or inpatient psychiatric wards), few psychometric tests have been validated to detect malingering. The most validated tests include the Structured Interview of Reported Symptoms (SIRS), distributed now as the Structured Interview of Reported Symptoms, 2nd edition (SIRS-2), and the Minnesota Multiphasic Personality Inventory Revised (MMPI-2). These tests typically require ≥30 minutes to administer and generally are not feasible in the fast-paced ER.

Despite the high prevalence of malingered behaviors in the ER, no single test has been validated in such a setting. Furthermore, there is no test designed to specifically assess for malingered suicidality or homicidality. The results of one test do not, in isolation, represent a comprehensive neuropsychological examination; rather, those results provide additional data to formulate a clinical impression. The instruments discussed below are administered and scored in a defined, objective manner.

When evaluating a patient whom you suspect of malingering, gathering collateral information—from family members, friends, nurses, social workers, emergency medicine physicians, and others—becomes important. You might discover pertinent information in ambulance and police reports and a review of the patient’s prior ER visits.

During the initial interview, ask open-ended questions; do not lead the patient by listing clusters of symptoms associated with a particular diagnosis. Because it is often difficult for a patient to malinger symptoms for a prolonged period, serial observations of a patient’s behavior and interview responses over time can provide additional information to make a clinical diagnosis of malingering.⁴

What testing is feasible in the ER?

Miller Forensic Assessment of Symptoms Test. The M-FAST measures rare symptom combinations, excessive reporting, and atypical symptoms of psychosis, using the same principles as the SIRS-2.

The 25-item screen begins by advising the examinee that he (she) will be asked questions about his psychological symptoms and that the questions that follow might or might not apply to his specific symptoms.

After that brief introduction, the examinee is asked if he hears ringing in his ears. Based on his response, the examiner reads one of two responses—both of which suggest the false notion that patients with true mental illness will suffer from ringing in their ears.

The examinee is then asked a series of Yes or No questions. Some pertain to legitimate symptoms a person with a psychotic illness might suffer (such as, “Do voices tell you to do things? Yes or No?”). Conversely, other questions screen for improbable symptoms that are atypical of patients who have a true psychotic disorder (such as “On many days I feel so bad that I can’t even remember my full name: Yes or No?”).

The exam concludes with a question about a ringing in the examinee’s ear. Affirmative responses are tallied; a score of ≥6 in a clinical setting is 83% specific and 93% sensitive for malingering.¹⁰

Visual Memory Test. Rey’s 15-Item Visual Memory Test capitalizes on the false belief that intellectual deficits, in addition to psychotic symptoms, make a claim of mental illness more believable.

In this simple test, the provider tells the examinee, “I am going to show you a card with 15 things on it that I want you to remember. When I take the card away, I want you to write down as many of the 15 things as you can remember.”³ The examinee is shown 15 common symbols (eg, 1, 2, 3; A, B, C; I, II, III, a, b, c; and the geometrics ●, ■, ▲).

At 5 seconds, the examinee is prompted, “Be sure to remember all of them.” After 10 seconds, the stimulus is removed, and the examinee is asked to recreate the figure.

Normative data indicate that even a patient who has a severe traumatic brain injury is able to recreate at least eight of the symbols. Although controversial, research indicates that a score of <9 symbols is predictive of malingering with 40% sensitivity and 100% specificity.¹¹

Critics argued that confounding variables (IQ, memory disorder, age) might skew the quantitative score. For that reason, the same group developed the Rey’s II Test, which includes a supplementary qualitative scoring system that emphasizes embellishment errors (eg, the wrong symbol) and ordering errors (eg, wrong row). The Rey’s II Test proved to be more sensitive (accurate classification of malingers): A cut-off score of ≥2 qualitative errors is predictive of malingering with 86% sensitivity and 100% specificity.¹²

Coin-in-the-Hand Test. Perhaps the simplest test to administer is the Coin-in-the-Hand, designed to seem—superficially—to be a challenging memory test.

The patient must guess in which hand the examiner is holding a coin. The patient is shown the coin for two seconds, and then asked to close his eyes and count back from 10. The patient then points to one of the two clenched hands.

This task is repeated 10 times; each time, the provider gives verbal feedback about the accuracy or inaccuracy of that attempt. Studies indicate that a patient who has a severe traumatic brain injury is able to score 85% correct. A score <85%, however, suggests feigning of symptoms (sensitivity, 92.5%; specificity 87.5%).¹³ Hanley and co-workers demonstrated that people who are simulating cognitive impairment had a mean accurate response of 4.1, whereas people who had true amnesia had a mean accurate response of 9.65.¹⁴

Persons who feign psychosis or mood symptoms often inaccurately believe that people with mental illness also have cognitive impairment. Both Rey’s test and the Coin-in-the-Hand Test capitalize on this misconception.

Mini-Mental State Examination. Research also has shown that the Folstein Mini-Mental State Examination (MMSE) can screen for malingered cognitive impairment. Powell compared 40 mental health clinicians who were instructed to feign psychosis and 40 patients with schizophrenia. Using the MMSE, the researchers found that the malingers more often gave approximate answers.¹⁵ Moreover, Myers argued that, when compared with Rey’s Test, the MMSE is superior for assessing malingered cognitive impairment because it has a higher positive predictive value (67%, compared with 43% for Rey’s Test) and a higher negative predictive value (93% and 89%).¹⁶

What can you do for these patients after diagnosis?

Malingering is not considered a psychiatric diagnosis; there are no indicated therapies with which to manage it—only guidelines. When you suspect a patient of malingering, you should avoid accusing him (her) of faking symptoms. Rather, when feasible, gently confront the person and provide the opportunity for him to explain his current behaviors. For example, you might say: “I’ve treated many patients with the symptoms that you’re reporting, but the details you provide are different, and don’t ring completely true. Is there anything else that could explain this?”¹⁷

Regardless of a patient’s challenging behaviors, it is important to remember that people who feign illness—whether partial malingering or pure malingering—often do need help. The assistance they require, however, might be best obtained from a housing agency, a chemical dependency program, or another social service—not from the ER. Identifying malingered behaviors saves time and money and shifts limited resources to people who have a legitimate mental health condition.

Last, despite an empathetic approach, some malingering patients continue to feign symptoms—as Mr. K did.

CASE CONTINUED

Although the psychiatrist on call considered forsaking the police to escort Mr. K out of the ER, he eventually agreed to leave the hospital on his own, stating, “My death is going to be on your hands.”

Eight days later, Mr. K visited the ER at a different hospital, endorsing chronic pain and demanding narcotics.

Bottom Line

As the number of people seeking care in the emergency room (ER) has increased, so has the number of those who feign symptoms for secondary gain. No single factor is indicative of malingering, and no objective tests exist to diagnose it definitively. Furthermore, there are no indicated therapies with which to manage malingering—only guidelines. Keep in mind that people who feign illness, whether partial or pure malingering, often do need help—although not the services of an ER.

Related Resources

• Miller Forensic Assessment of Symptoms Test (M-FAST). Psychological Assessment Resources, Inc. www4.parinc.com (enter “M-FAST” in search field).
• Duffy S. Malingering psychological symptoms: An empirical review. Illinois State University, Department of Psychology. http://psychology.illinoisstate.edu/cc/Comps/Duffy%20-%20Malingering.pdf. Accessed September 10, 2013.

Drug Brand Names

Quetiapine • Seroquel

Disclosure

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

Featured Audio
M. Cait Brady, MD, shares strategies for assessing malingering. Dr. Brady is a Third-Year Resident in General Psychiatry, University of California, Davis Medical Center - Sacramento, Sacramento, California.

The economic downturn in the United States has prompted numerous state and county budget cuts, in turn forcing many patients to receive their mental health care in the emergency room (ER). Most patients evaluated in the ER for mental health-related reasons have a legitimate psychiatric crisis—but that isn’t always the case. And as the number of people seeking care in the ER has increased, it appears that so too has the number of those who feign symptoms for secondary gain—that is, who are malingering.

This article highlights several red flags for malingered behavior; emphasizes typical (compared with atypical) symptoms of psychosis; and provides an overview of four instruments that you can use to help assess for malingering in the ED.

A difficult diagnosis

No single factor is indicative of malingering, and no objective tests exist to diagnose malingering definitively. Rather, the tests we discuss provide additional information that can help formulate a clinical impression. 

According to DSM-5, malingering is “…the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives…”¹ Despite a relatively straightforward definition, the diagnosis is difficult to make because it is a diagnosis of exclusion.

Even with sufficient evidence, many clinicians are reluctant to diagnose malingering because they fear retaliation and diagnostic uncertainty. Psychiatrists also might be reluctant to diagnose malingering because the negative connotation that the label carries risks stigmatizing a patient who might, in fact, be suffering. This is true especially when there is suspicion of partial malingering, the conscious exaggeration of existing symptoms.

Despite physicians’ reluctance to diagnose malingering, it is a real problem, especially in the ER. Research suggests that as many as 13% of patients in the ER feign illness, and that their secondary gain most often includes food, shelter, prescription drugs, financial gain, and avoidance of jail, work, or family responsibilities.²

CASE REPORT ‘The voices are telling me to kill myself’

Mr. K, a 36-year-old white man, walks into the ER on a late December day. He tells the triage nurse that he suicidal; she escorts him to the psychiatric pod of the ER. Nursing staff provide line-of-sight care, monitor his vital signs, and draw blood for testing.

Within hours, Mr. K is deemed “medically cleared” and ready for assessment by the psychiatric social worker.

Interview and assessment. During the interview with the social worker, Mr. K reports that he has been depressed, adamantly maintaining that he is suicidal, with a plan to “walk in traffic” or “eat the end of a gun.” The social worker places him on a 72-hour involuntary psychiatric hold. ER physicians order psychiatric consultation.

Mr. K is well-known to the psychiatrist on call, from prior ER visits and psychiatric hospital admissions. In fact, two days earlier, he put a psychiatric nurse in a headlock while being escorted from the psychiatric inpatient unit under protest.

On assessment by the psychiatrist, Mr. K continues to endorse feeling suicidal; he adds: “If I don’t get some help, I’m gonna kill somebody else!”

Without prompting, the patient states that “the voices are telling me to kill myself.” He says that those voices have been relentless since he left the hospital two days earlier. According to Mr. K, nothing he did helped quiet the voices, although previous prescriptions for quetiapine have been helpful.

Mr. K says that he is unable to recall the clinic or name of his prior psychiatrist. He claims that he was hospitalized four months ago, (despite the psychiatrist’s knowledge that he had been discharged two days ago) and estimates that his psychotic symptoms began one year ago. He explains that he is homeless and does not have social support. He is unable to provide a telephone number or a name to contact family for collateral information.

Mental status exam. The mental status examination reveals a tall, thin, disheveled man who has poor dentition. He is now calm and cooperative despite his reported level of distress. His speech is unremarkable and his eye contact is appropriate. His thought process is linear, organized, and coherent.

Mr. K does not endorse additional symptoms, but is quick to agree with the psychiatrist’s follow-up questions about hallucinations: “Yeah! I’ve been seeing all kinds of crazy stuff.” When prompted for details, he says, “I just saw Big Bird… He was 100 feet tall!”

Lab testing. Mr. K’s blood work is remarkable for positive urine toxicology for amphetamines.

Nursing notes indicate that Mr. K slept overnight and ate 100% of the food on his dinner and breakfast trays.

Red flags flying

Mr. K’s case highlights several red flags that should raise suspicion of malingering (Table 1)^3,4:

• A conditional statement by which a patient threatens to harm himself or others, contingent upon a demand—for example, “If I don’t get A, I’ll do B.”
• An overly dramatic presentation, in which the patient is quick to endorse
  distressing symptoms. Consider Mr. K: He was quick to report that he saw Big Bird, and that this Sesame Street character “was 100 feet tall.” Patients who have been experiencing true psychotic symptoms might be reluctant to speak of their distressing symptoms, especially if they have not experienced such symptoms in the past (the first psychotic break). Mr. K, however, volunteered and called attention to particularly dramatic psychotic symptoms.
• A subjective report of distress that is inconsistent with the objective presentation. Mr. K’s report of depression—a diagnosis that typically includes insomnia and poor appetite—was inconsistent with his behavior: He slept and he ate all of his meals.

Atypical (vs typical) psychosis

Malingering can occur in various arenas and take many different forms. In forensic settings, such as prison, malingered conditions more often present as posttraumatic stress disorder or cognitive impairment.⁵ In non-forensic settings, such as the ER, the most commonly malingered conditions include suicidality and psychosis.

To detect malingered psychosis, one must first understand how true psychotic symptoms manifest. The following discussion describes and compares typical and atypical symptoms of psychosis; examples are given in Table 2.^6,7No single atypical psychotic symptom is indicative of malingering. Rather, a collection of atypical symptoms, when considered in clinical context, should raise suspicion of malingering and prompt you to seek additional collateral information or perform appropriate testing for malingering.

Hallucinations

Typically, hallucinations take three forms: auditory, visual, and tactile. In primary psychiatric conditions, auditory hallucinations are the most common of those three.

Tactile hallucinations can be present during episodes of substance intoxication or withdrawal (eg, so-called coke bugs). 

Auditory hallucinations. Patients who malinger psychosis are often unaware of the nuances of hallucinations. For example, they might report the atypical symptom of continuous voices; in fact, most patients who have schizophrenia hear voices intermittently. Keep in mind, too, that 75% of patients who have schizophrenia hear male and female voices, and that 70% have some type of coping strategy to minimize their internal stimuli (eg, listening to music).^6,7

Visual hallucinations are most often associated with neurologic disease, but also occur often in primary psychotic disorders, such as schizophrenia.

Patients who malinger psychotic symptoms often are open to suggestion, and are quick to endorse visual hallucinations. When asked to describe their hallucinations, however, they often respond without details (“I don’t know”). Other times, they overcompensate with wild exaggeration of atypical visions—recall Mr. K’s description of a towering Big Bird. Asked if the visions are in black and white, they might eagerly agree. Research suggests, however, that patients who have schizophrenia more often experience life-sized hallucinations of vivid scenes with family members, religious figures, or animals.⁸ Furthermore, genuine visual hallucinations typically are in color.

Putting malingering in the differential

Regardless of the number of atypical symptoms a patient exhibits, malingering will be missed if you do not include it in the differential diagnosis. This fact was made evident in a 1973 study.⁹

In that study, Rosenhan and seven of his colleagues—a psychology graduate student, three psychologists, a pediatrician, a psychiatrist, a painter, and a housewife—presented to various ERs and intake units, and, as they had been instructed, endorsed vague auditory hallucinations of “empty,” “hollow,” or “thud” sounds—but nothing more. All were admitted to psychiatric hospitals. Once admitted, they refrained (again, as instructed) from endorsing or exhibiting any psychotic symptoms.

Despite the vague nature of the reported auditory hallucinations and how rapidly symptoms resolved on admission, seven of these pseudo-patients were given a diagnosis of schizophrenia, and one was given a diagnosis of manic-depressive psychosis. Duration of admission ranged from 7 to 52 days (average, 19 days). None of the study participants were suspected of feigning symptoms.

It’s fortunate that, since then, mental health professionals have developed more structured techniques of assessment to detect malingering in inpatient and triage settings.

Testing to identify and assess malingering

The ER is a fast-paced environment, in which treatment teams are challenged to make rapid clinical assessments. With the overwhelming number of patients seeking mental health care in the ER, however, overall wait times are increasing; in some regions, it is common to write, then to rewrite, involuntary psychiatric holds for patients awaiting transfer to a psychiatric hospital. This extended duration presents an opportunity to serially evaluate patients suspected of malingering.

Even in environments that allow for a more comprehensive evaluation (eg, jail or inpatient psychiatric wards), few psychometric tests have been validated to detect malingering. The most validated tests include the Structured Interview of Reported Symptoms (SIRS), distributed now as the Structured Interview of Reported Symptoms, 2nd edition (SIRS-2), and the Minnesota Multiphasic Personality Inventory Revised (MMPI-2). These tests typically require ≥30 minutes to administer and generally are not feasible in the fast-paced ER.

Despite the high prevalence of malingered behaviors in the ER, no single test has been validated in such a setting. Furthermore, there is no test designed to specifically assess for malingered suicidality or homicidality. The results of one test do not, in isolation, represent a comprehensive neuropsychological examination; rather, those results provide additional data to formulate a clinical impression. The instruments discussed below are administered and scored in a defined, objective manner.

When evaluating a patient whom you suspect of malingering, gathering collateral information—from family members, friends, nurses, social workers, emergency medicine physicians, and others—becomes important. You might discover pertinent information in ambulance and police reports and a review of the patient’s prior ER visits.

During the initial interview, ask open-ended questions; do not lead the patient by listing clusters of symptoms associated with a particular diagnosis. Because it is often difficult for a patient to malinger symptoms for a prolonged period, serial observations of a patient’s behavior and interview responses over time can provide additional information to make a clinical diagnosis of malingering.⁴

What testing is feasible in the ER?

Miller Forensic Assessment of Symptoms Test. The M-FAST measures rare symptom combinations, excessive reporting, and atypical symptoms of psychosis, using the same principles as the SIRS-2.

The 25-item screen begins by advising the examinee that he (she) will be asked questions about his psychological symptoms and that the questions that follow might or might not apply to his specific symptoms.

After that brief introduction, the examinee is asked if he hears ringing in his ears. Based on his response, the examiner reads one of two responses—both of which suggest the false notion that patients with true mental illness will suffer from ringing in their ears.

The examinee is then asked a series of Yes or No questions. Some pertain to legitimate symptoms a person with a psychotic illness might suffer (such as, “Do voices tell you to do things? Yes or No?”). Conversely, other questions screen for improbable symptoms that are atypical of patients who have a true psychotic disorder (such as “On many days I feel so bad that I can’t even remember my full name: Yes or No?”).

The exam concludes with a question about a ringing in the examinee’s ear. Affirmative responses are tallied; a score of ≥6 in a clinical setting is 83% specific and 93% sensitive for malingering.¹⁰

Visual Memory Test. Rey’s 15-Item Visual Memory Test capitalizes on the false belief that intellectual deficits, in addition to psychotic symptoms, make a claim of mental illness more believable.

In this simple test, the provider tells the examinee, “I am going to show you a card with 15 things on it that I want you to remember. When I take the card away, I want you to write down as many of the 15 things as you can remember.”³ The examinee is shown 15 common symbols (eg, 1, 2, 3; A, B, C; I, II, III, a, b, c; and the geometrics ●, ■, ▲).

At 5 seconds, the examinee is prompted, “Be sure to remember all of them.” After 10 seconds, the stimulus is removed, and the examinee is asked to recreate the figure.

Normative data indicate that even a patient who has a severe traumatic brain injury is able to recreate at least eight of the symbols. Although controversial, research indicates that a score of <9 symbols is predictive of malingering with 40% sensitivity and 100% specificity.¹¹

Critics argued that confounding variables (IQ, memory disorder, age) might skew the quantitative score. For that reason, the same group developed the Rey’s II Test, which includes a supplementary qualitative scoring system that emphasizes embellishment errors (eg, the wrong symbol) and ordering errors (eg, wrong row). The Rey’s II Test proved to be more sensitive (accurate classification of malingers): A cut-off score of ≥2 qualitative errors is predictive of malingering with 86% sensitivity and 100% specificity.¹²

Coin-in-the-Hand Test. Perhaps the simplest test to administer is the Coin-in-the-Hand, designed to seem—superficially—to be a challenging memory test.

The patient must guess in which hand the examiner is holding a coin. The patient is shown the coin for two seconds, and then asked to close his eyes and count back from 10. The patient then points to one of the two clenched hands.

This task is repeated 10 times; each time, the provider gives verbal feedback about the accuracy or inaccuracy of that attempt. Studies indicate that a patient who has a severe traumatic brain injury is able to score 85% correct. A score <85%, however, suggests feigning of symptoms (sensitivity, 92.5%; specificity 87.5%).¹³ Hanley and co-workers demonstrated that people who are simulating cognitive impairment had a mean accurate response of 4.1, whereas people who had true amnesia had a mean accurate response of 9.65.¹⁴

Persons who feign psychosis or mood symptoms often inaccurately believe that people with mental illness also have cognitive impairment. Both Rey’s test and the Coin-in-the-Hand Test capitalize on this misconception.

Mini-Mental State Examination. Research also has shown that the Folstein Mini-Mental State Examination (MMSE) can screen for malingered cognitive impairment. Powell compared 40 mental health clinicians who were instructed to feign psychosis and 40 patients with schizophrenia. Using the MMSE, the researchers found that the malingers more often gave approximate answers.¹⁵ Moreover, Myers argued that, when compared with Rey’s Test, the MMSE is superior for assessing malingered cognitive impairment because it has a higher positive predictive value (67%, compared with 43% for Rey’s Test) and a higher negative predictive value (93% and 89%).¹⁶

What can you do for these patients after diagnosis?

Malingering is not considered a psychiatric diagnosis; there are no indicated therapies with which to manage it—only guidelines. When you suspect a patient of malingering, you should avoid accusing him (her) of faking symptoms. Rather, when feasible, gently confront the person and provide the opportunity for him to explain his current behaviors. For example, you might say: “I’ve treated many patients with the symptoms that you’re reporting, but the details you provide are different, and don’t ring completely true. Is there anything else that could explain this?”¹⁷

Regardless of a patient’s challenging behaviors, it is important to remember that people who feign illness—whether partial malingering or pure malingering—often do need help. The assistance they require, however, might be best obtained from a housing agency, a chemical dependency program, or another social service—not from the ER. Identifying malingered behaviors saves time and money and shifts limited resources to people who have a legitimate mental health condition.

Last, despite an empathetic approach, some malingering patients continue to feign symptoms—as Mr. K did.

CASE CONTINUED

Although the psychiatrist on call considered forsaking the police to escort Mr. K out of the ER, he eventually agreed to leave the hospital on his own, stating, “My death is going to be on your hands.”

Eight days later, Mr. K visited the ER at a different hospital, endorsing chronic pain and demanding narcotics.

Bottom Line

As the number of people seeking care in the emergency room (ER) has increased, so has the number of those who feign symptoms for secondary gain. No single factor is indicative of malingering, and no objective tests exist to diagnose it definitively. Furthermore, there are no indicated therapies with which to manage malingering—only guidelines. Keep in mind that people who feign illness, whether partial or pure malingering, often do need help—although not the services of an ER.

Related Resources

• Miller Forensic Assessment of Symptoms Test (M-FAST). Psychological Assessment Resources, Inc. www4.parinc.com (enter “M-FAST” in search field).
• Duffy S. Malingering psychological symptoms: An empirical review. Illinois State University, Department of Psychology. http://psychology.illinoisstate.edu/cc/Comps/Duffy%20-%20Malingering.pdf. Accessed September 10, 2013.

Drug Brand Names

Quetiapine • Seroquel

Disclosure

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

Featured Audio
M. Cait Brady, MD, shares strategies for assessing malingering. Dr. Brady is a Third-Year Resident in General Psychiatry, University of California, Davis Medical Center - Sacramento, Sacramento, California.

The economic downturn in the United States has prompted numerous state and county budget cuts, in turn forcing many patients to receive their mental health care in the emergency room (ER). Most patients evaluated in the ER for mental health-related reasons have a legitimate psychiatric crisis—but that isn’t always the case. And as the number of people seeking care in the ER has increased, it appears that so too has the number of those who feign symptoms for secondary gain—that is, who are malingering.

This article highlights several red flags for malingered behavior; emphasizes typical (compared with atypical) symptoms of psychosis; and provides an overview of four instruments that you can use to help assess for malingering in the ED.

A difficult diagnosis

No single factor is indicative of malingering, and no objective tests exist to diagnose malingering definitively. Rather, the tests we discuss provide additional information that can help formulate a clinical impression. 

According to DSM-5, malingering is “…the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives…”¹ Despite a relatively straightforward definition, the diagnosis is difficult to make because it is a diagnosis of exclusion.

Even with sufficient evidence, many clinicians are reluctant to diagnose malingering because they fear retaliation and diagnostic uncertainty. Psychiatrists also might be reluctant to diagnose malingering because the negative connotation that the label carries risks stigmatizing a patient who might, in fact, be suffering. This is true especially when there is suspicion of partial malingering, the conscious exaggeration of existing symptoms.

Despite physicians’ reluctance to diagnose malingering, it is a real problem, especially in the ER. Research suggests that as many as 13% of patients in the ER feign illness, and that their secondary gain most often includes food, shelter, prescription drugs, financial gain, and avoidance of jail, work, or family responsibilities.²

CASE REPORT ‘The voices are telling me to kill myself’

Mr. K, a 36-year-old white man, walks into the ER on a late December day. He tells the triage nurse that he suicidal; she escorts him to the psychiatric pod of the ER. Nursing staff provide line-of-sight care, monitor his vital signs, and draw blood for testing.

Within hours, Mr. K is deemed “medically cleared” and ready for assessment by the psychiatric social worker.

Interview and assessment. During the interview with the social worker, Mr. K reports that he has been depressed, adamantly maintaining that he is suicidal, with a plan to “walk in traffic” or “eat the end of a gun.” The social worker places him on a 72-hour involuntary psychiatric hold. ER physicians order psychiatric consultation.

Mr. K is well-known to the psychiatrist on call, from prior ER visits and psychiatric hospital admissions. In fact, two days earlier, he put a psychiatric nurse in a headlock while being escorted from the psychiatric inpatient unit under protest.

On assessment by the psychiatrist, Mr. K continues to endorse feeling suicidal; he adds: “If I don’t get some help, I’m gonna kill somebody else!”

Without prompting, the patient states that “the voices are telling me to kill myself.” He says that those voices have been relentless since he left the hospital two days earlier. According to Mr. K, nothing he did helped quiet the voices, although previous prescriptions for quetiapine have been helpful.

Mr. K says that he is unable to recall the clinic or name of his prior psychiatrist. He claims that he was hospitalized four months ago, (despite the psychiatrist’s knowledge that he had been discharged two days ago) and estimates that his psychotic symptoms began one year ago. He explains that he is homeless and does not have social support. He is unable to provide a telephone number or a name to contact family for collateral information.

Mental status exam. The mental status examination reveals a tall, thin, disheveled man who has poor dentition. He is now calm and cooperative despite his reported level of distress. His speech is unremarkable and his eye contact is appropriate. His thought process is linear, organized, and coherent.

Mr. K does not endorse additional symptoms, but is quick to agree with the psychiatrist’s follow-up questions about hallucinations: “Yeah! I’ve been seeing all kinds of crazy stuff.” When prompted for details, he says, “I just saw Big Bird… He was 100 feet tall!”

Lab testing. Mr. K’s blood work is remarkable for positive urine toxicology for amphetamines.

Nursing notes indicate that Mr. K slept overnight and ate 100% of the food on his dinner and breakfast trays.

Red flags flying

Mr. K’s case highlights several red flags that should raise suspicion of malingering (Table 1)^3,4:

• A conditional statement by which a patient threatens to harm himself or others, contingent upon a demand—for example, “If I don’t get A, I’ll do B.”
• An overly dramatic presentation, in which the patient is quick to endorse
  distressing symptoms. Consider Mr. K: He was quick to report that he saw Big Bird, and that this Sesame Street character “was 100 feet tall.” Patients who have been experiencing true psychotic symptoms might be reluctant to speak of their distressing symptoms, especially if they have not experienced such symptoms in the past (the first psychotic break). Mr. K, however, volunteered and called attention to particularly dramatic psychotic symptoms.
• A subjective report of distress that is inconsistent with the objective presentation. Mr. K’s report of depression—a diagnosis that typically includes insomnia and poor appetite—was inconsistent with his behavior: He slept and he ate all of his meals.

Atypical (vs typical) psychosis

Malingering can occur in various arenas and take many different forms. In forensic settings, such as prison, malingered conditions more often present as posttraumatic stress disorder or cognitive impairment.⁵ In non-forensic settings, such as the ER, the most commonly malingered conditions include suicidality and psychosis.

To detect malingered psychosis, one must first understand how true psychotic symptoms manifest. The following discussion describes and compares typical and atypical symptoms of psychosis; examples are given in Table 2.^6,7No single atypical psychotic symptom is indicative of malingering. Rather, a collection of atypical symptoms, when considered in clinical context, should raise suspicion of malingering and prompt you to seek additional collateral information or perform appropriate testing for malingering.

Hallucinations

Typically, hallucinations take three forms: auditory, visual, and tactile. In primary psychiatric conditions, auditory hallucinations are the most common of those three.

Tactile hallucinations can be present during episodes of substance intoxication or withdrawal (eg, so-called coke bugs). 

Auditory hallucinations. Patients who malinger psychosis are often unaware of the nuances of hallucinations. For example, they might report the atypical symptom of continuous voices; in fact, most patients who have schizophrenia hear voices intermittently. Keep in mind, too, that 75% of patients who have schizophrenia hear male and female voices, and that 70% have some type of coping strategy to minimize their internal stimuli (eg, listening to music).^6,7

Visual hallucinations are most often associated with neurologic disease, but also occur often in primary psychotic disorders, such as schizophrenia.

Patients who malinger psychotic symptoms often are open to suggestion, and are quick to endorse visual hallucinations. When asked to describe their hallucinations, however, they often respond without details (“I don’t know”). Other times, they overcompensate with wild exaggeration of atypical visions—recall Mr. K’s description of a towering Big Bird. Asked if the visions are in black and white, they might eagerly agree. Research suggests, however, that patients who have schizophrenia more often experience life-sized hallucinations of vivid scenes with family members, religious figures, or animals.⁸ Furthermore, genuine visual hallucinations typically are in color.

Putting malingering in the differential

Regardless of the number of atypical symptoms a patient exhibits, malingering will be missed if you do not include it in the differential diagnosis. This fact was made evident in a 1973 study.⁹

In that study, Rosenhan and seven of his colleagues—a psychology graduate student, three psychologists, a pediatrician, a psychiatrist, a painter, and a housewife—presented to various ERs and intake units, and, as they had been instructed, endorsed vague auditory hallucinations of “empty,” “hollow,” or “thud” sounds—but nothing more. All were admitted to psychiatric hospitals. Once admitted, they refrained (again, as instructed) from endorsing or exhibiting any psychotic symptoms.

Despite the vague nature of the reported auditory hallucinations and how rapidly symptoms resolved on admission, seven of these pseudo-patients were given a diagnosis of schizophrenia, and one was given a diagnosis of manic-depressive psychosis. Duration of admission ranged from 7 to 52 days (average, 19 days). None of the study participants were suspected of feigning symptoms.

It’s fortunate that, since then, mental health professionals have developed more structured techniques of assessment to detect malingering in inpatient and triage settings.

Testing to identify and assess malingering

The ER is a fast-paced environment, in which treatment teams are challenged to make rapid clinical assessments. With the overwhelming number of patients seeking mental health care in the ER, however, overall wait times are increasing; in some regions, it is common to write, then to rewrite, involuntary psychiatric holds for patients awaiting transfer to a psychiatric hospital. This extended duration presents an opportunity to serially evaluate patients suspected of malingering.

Even in environments that allow for a more comprehensive evaluation (eg, jail or inpatient psychiatric wards), few psychometric tests have been validated to detect malingering. The most validated tests include the Structured Interview of Reported Symptoms (SIRS), distributed now as the Structured Interview of Reported Symptoms, 2nd edition (SIRS-2), and the Minnesota Multiphasic Personality Inventory Revised (MMPI-2). These tests typically require ≥30 minutes to administer and generally are not feasible in the fast-paced ER.

Despite the high prevalence of malingered behaviors in the ER, no single test has been validated in such a setting. Furthermore, there is no test designed to specifically assess for malingered suicidality or homicidality. The results of one test do not, in isolation, represent a comprehensive neuropsychological examination; rather, those results provide additional data to formulate a clinical impression. The instruments discussed below are administered and scored in a defined, objective manner.

When evaluating a patient whom you suspect of malingering, gathering collateral information—from family members, friends, nurses, social workers, emergency medicine physicians, and others—becomes important. You might discover pertinent information in ambulance and police reports and a review of the patient’s prior ER visits.

During the initial interview, ask open-ended questions; do not lead the patient by listing clusters of symptoms associated with a particular diagnosis. Because it is often difficult for a patient to malinger symptoms for a prolonged period, serial observations of a patient’s behavior and interview responses over time can provide additional information to make a clinical diagnosis of malingering.⁴

What testing is feasible in the ER?

Miller Forensic Assessment of Symptoms Test. The M-FAST measures rare symptom combinations, excessive reporting, and atypical symptoms of psychosis, using the same principles as the SIRS-2.

The 25-item screen begins by advising the examinee that he (she) will be asked questions about his psychological symptoms and that the questions that follow might or might not apply to his specific symptoms.

After that brief introduction, the examinee is asked if he hears ringing in his ears. Based on his response, the examiner reads one of two responses—both of which suggest the false notion that patients with true mental illness will suffer from ringing in their ears.

The examinee is then asked a series of Yes or No questions. Some pertain to legitimate symptoms a person with a psychotic illness might suffer (such as, “Do voices tell you to do things? Yes or No?”). Conversely, other questions screen for improbable symptoms that are atypical of patients who have a true psychotic disorder (such as “On many days I feel so bad that I can’t even remember my full name: Yes or No?”).

The exam concludes with a question about a ringing in the examinee’s ear. Affirmative responses are tallied; a score of ≥6 in a clinical setting is 83% specific and 93% sensitive for malingering.¹⁰

Visual Memory Test. Rey’s 15-Item Visual Memory Test capitalizes on the false belief that intellectual deficits, in addition to psychotic symptoms, make a claim of mental illness more believable.

In this simple test, the provider tells the examinee, “I am going to show you a card with 15 things on it that I want you to remember. When I take the card away, I want you to write down as many of the 15 things as you can remember.”³ The examinee is shown 15 common symbols (eg, 1, 2, 3; A, B, C; I, II, III, a, b, c; and the geometrics ●, ■, ▲).

At 5 seconds, the examinee is prompted, “Be sure to remember all of them.” After 10 seconds, the stimulus is removed, and the examinee is asked to recreate the figure.

Normative data indicate that even a patient who has a severe traumatic brain injury is able to recreate at least eight of the symbols. Although controversial, research indicates that a score of <9 symbols is predictive of malingering with 40% sensitivity and 100% specificity.¹¹

Critics argued that confounding variables (IQ, memory disorder, age) might skew the quantitative score. For that reason, the same group developed the Rey’s II Test, which includes a supplementary qualitative scoring system that emphasizes embellishment errors (eg, the wrong symbol) and ordering errors (eg, wrong row). The Rey’s II Test proved to be more sensitive (accurate classification of malingers): A cut-off score of ≥2 qualitative errors is predictive of malingering with 86% sensitivity and 100% specificity.¹²

Coin-in-the-Hand Test. Perhaps the simplest test to administer is the Coin-in-the-Hand, designed to seem—superficially—to be a challenging memory test.

The patient must guess in which hand the examiner is holding a coin. The patient is shown the coin for two seconds, and then asked to close his eyes and count back from 10. The patient then points to one of the two clenched hands.

This task is repeated 10 times; each time, the provider gives verbal feedback about the accuracy or inaccuracy of that attempt. Studies indicate that a patient who has a severe traumatic brain injury is able to score 85% correct. A score <85%, however, suggests feigning of symptoms (sensitivity, 92.5%; specificity 87.5%).¹³ Hanley and co-workers demonstrated that people who are simulating cognitive impairment had a mean accurate response of 4.1, whereas people who had true amnesia had a mean accurate response of 9.65.¹⁴

Persons who feign psychosis or mood symptoms often inaccurately believe that people with mental illness also have cognitive impairment. Both Rey’s test and the Coin-in-the-Hand Test capitalize on this misconception.

Mini-Mental State Examination. Research also has shown that the Folstein Mini-Mental State Examination (MMSE) can screen for malingered cognitive impairment. Powell compared 40 mental health clinicians who were instructed to feign psychosis and 40 patients with schizophrenia. Using the MMSE, the researchers found that the malingers more often gave approximate answers.¹⁵ Moreover, Myers argued that, when compared with Rey’s Test, the MMSE is superior for assessing malingered cognitive impairment because it has a higher positive predictive value (67%, compared with 43% for Rey’s Test) and a higher negative predictive value (93% and 89%).¹⁶

What can you do for these patients after diagnosis?

Malingering is not considered a psychiatric diagnosis; there are no indicated therapies with which to manage it—only guidelines. When you suspect a patient of malingering, you should avoid accusing him (her) of faking symptoms. Rather, when feasible, gently confront the person and provide the opportunity for him to explain his current behaviors. For example, you might say: “I’ve treated many patients with the symptoms that you’re reporting, but the details you provide are different, and don’t ring completely true. Is there anything else that could explain this?”¹⁷

Regardless of a patient’s challenging behaviors, it is important to remember that people who feign illness—whether partial malingering or pure malingering—often do need help. The assistance they require, however, might be best obtained from a housing agency, a chemical dependency program, or another social service—not from the ER. Identifying malingered behaviors saves time and money and shifts limited resources to people who have a legitimate mental health condition.

Last, despite an empathetic approach, some malingering patients continue to feign symptoms—as Mr. K did.

CASE CONTINUED

Although the psychiatrist on call considered forsaking the police to escort Mr. K out of the ER, he eventually agreed to leave the hospital on his own, stating, “My death is going to be on your hands.”

Eight days later, Mr. K visited the ER at a different hospital, endorsing chronic pain and demanding narcotics.

Bottom Line

As the number of people seeking care in the emergency room (ER) has increased, so has the number of those who feign symptoms for secondary gain. No single factor is indicative of malingering, and no objective tests exist to diagnose it definitively. Furthermore, there are no indicated therapies with which to manage malingering—only guidelines. Keep in mind that people who feign illness, whether partial or pure malingering, often do need help—although not the services of an ER.

Related Resources

• Miller Forensic Assessment of Symptoms Test (M-FAST). Psychological Assessment Resources, Inc. www4.parinc.com (enter “M-FAST” in search field).
• Duffy S. Malingering psychological symptoms: An empirical review. Illinois State University, Department of Psychology. http://psychology.illinoisstate.edu/cc/Comps/Duffy%20-%20Malingering.pdf. Accessed September 10, 2013.

Drug Brand Names

Quetiapine • Seroquel

Disclosure

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

Featured Audio
M. Cait Brady, MD, shares strategies for assessing malingering. Dr. Brady is a Third-Year Resident in General Psychiatry, University of California, Davis Medical Center - Sacramento, Sacramento, California.

The authors of “Atypical antipsychotics during pregnancy” (Current Psychiatry, July 2013, pp. 12-18) incorrectly state that all atypical antipsychotics are FDA Pregnancy Category C except for clozapine. In fact, lurasidone (Latuda) is FDA Pregnancy Category B. I was disappointed that the authors did not address this distinction; I find it puzzling why such a new medication, with such little data available, was able to obtain a FDA Pregnancy Category B label.  

Laura Gilley, MD
Child and Adolescent Psychiatrist
Clinical Instructor
University of Utah
Salt Lake City, Utah

Drs. Robakis and Williams share clinically relevant information on an important issue in “Atypical antipsychotics during pregnancy.” For the most part, their information is current, but some facts need to be updated: Notably, olanzapine is now approved for use in the treatment of bipolar I disorder in children age 13 to 17¹ and paliperidone also is approved for the treatment of schizophrenia in children age 12 to 17.²

As we move forward with development of novel drugs, we will, I hope, create safer options for pregnant patients. Until then, clinically useful discussions of available evidence and risk/benefit analyses are greatly appreciated.

Deepak Prabhakar, MD, MPH
Attending Psychiatrist
Behavioral Health Services
Henry Ford Health System
Detroit, Michigan

References

1. Christian R, Saavedra L, Gaynes BN, et al. Future research needs for first- and second-generation antipsychotics for children and young adults. http://effectivehealthcare.ahrq.gov/ehc/products/147/835/CER39_Antipsychotics-Children-Young-Adults_20120221.pdf. Accessed August 13, 2012.

2. Invega {package insert}. Titusville, NJ: Janssen Pharmaceuticals Inc.; 2013.

The authors of “Atypical antipsychotics during pregnancy” (Current Psychiatry, July 2013, pp. 12-18) incorrectly state that all atypical antipsychotics are FDA Pregnancy Category C except for clozapine. In fact, lurasidone (Latuda) is FDA Pregnancy Category B. I was disappointed that the authors did not address this distinction; I find it puzzling why such a new medication, with such little data available, was able to obtain a FDA Pregnancy Category B label.  

Laura Gilley, MD
Child and Adolescent Psychiatrist
Clinical Instructor
University of Utah
Salt Lake City, Utah

Drs. Robakis and Williams share clinically relevant information on an important issue in “Atypical antipsychotics during pregnancy.” For the most part, their information is current, but some facts need to be updated: Notably, olanzapine is now approved for use in the treatment of bipolar I disorder in children age 13 to 17¹ and paliperidone also is approved for the treatment of schizophrenia in children age 12 to 17.²

As we move forward with development of novel drugs, we will, I hope, create safer options for pregnant patients. Until then, clinically useful discussions of available evidence and risk/benefit analyses are greatly appreciated.

Deepak Prabhakar, MD, MPH
Attending Psychiatrist
Behavioral Health Services
Henry Ford Health System
Detroit, Michigan

References

1. Christian R, Saavedra L, Gaynes BN, et al. Future research needs for first- and second-generation antipsychotics for children and young adults. http://effectivehealthcare.ahrq.gov/ehc/products/147/835/CER39_Antipsychotics-Children-Young-Adults_20120221.pdf. Accessed August 13, 2012.

2. Invega {package insert}. Titusville, NJ: Janssen Pharmaceuticals Inc.; 2013.

The authors of “Atypical antipsychotics during pregnancy” (Current Psychiatry, July 2013, pp. 12-18) incorrectly state that all atypical antipsychotics are FDA Pregnancy Category C except for clozapine. In fact, lurasidone (Latuda) is FDA Pregnancy Category B. I was disappointed that the authors did not address this distinction; I find it puzzling why such a new medication, with such little data available, was able to obtain a FDA Pregnancy Category B label.  

Laura Gilley, MD
Child and Adolescent Psychiatrist
Clinical Instructor
University of Utah
Salt Lake City, Utah

Drs. Robakis and Williams share clinically relevant information on an important issue in “Atypical antipsychotics during pregnancy.” For the most part, their information is current, but some facts need to be updated: Notably, olanzapine is now approved for use in the treatment of bipolar I disorder in children age 13 to 17¹ and paliperidone also is approved for the treatment of schizophrenia in children age 12 to 17.²

As we move forward with development of novel drugs, we will, I hope, create safer options for pregnant patients. Until then, clinically useful discussions of available evidence and risk/benefit analyses are greatly appreciated.

Deepak Prabhakar, MD, MPH
Attending Psychiatrist
Behavioral Health Services
Henry Ford Health System
Detroit, Michigan

References

1. Christian R, Saavedra L, Gaynes BN, et al. Future research needs for first- and second-generation antipsychotics for children and young adults. http://effectivehealthcare.ahrq.gov/ehc/products/147/835/CER39_Antipsychotics-Children-Young-Adults_20120221.pdf. Accessed August 13, 2012.

2. Invega {package insert}. Titusville, NJ: Janssen Pharmaceuticals Inc.; 2013.

For a relatively young medical discipline like psychiatry, the history of discovery of biological therapeutics is replete with twists and turns, the pace of which will likely not abate. These discoveries can be initiated by both observant clinicians and dedicated researchers.

As I contemplated the scientific saga of developing somatic and pharmaceutical treatments for major psychiatric disorders, I recognized several interesting themes: serendipity, evolution, paradigm shifts, and radical breakthroughs. Consider the following examples of those themes.

Neuromodulation

Electroconvulsive therapy (ECT), the original neuromodulation therapy, was discovered (serendipity) when Meduna, mistakenly thinking that schizophrenia and epilepsy are “antagonistic,” used camphor and, later, metrazol, to induce seizures to treat schizophrenia. Later, Cerletti and Bini switched the seizure induction to electricity (evolution), and the use of ECT spread, like a seizure, around the world after their initial report. Later, unilateral ECT and pulse wave ECT were developed to reduce the incidence of side effects (further evolution).

In contemporary psychiatry, a paradigm shift in neuromodulation techniques has emerged over the past decade with the development of an array of novel neuromodulation techniques,¹ some of which do not induce seizures or touch the scalp with electrodes—or even use electricity. These techniques include vagus nerve stimulation, repetitive transcranial magnetic stimulation, epidural cortical stimulation, focused ultrasound, low-field magnetic stimulation, transcranial direct current stimulation, and magnetic seizure therapy. Currently (pun intended!), radical breakthroughs with significant therapeutic promise are being developed, such as optogenetic stimulation and deep brain stimulation.

Antipsychotics

One of the most momentous serendipitous discoveries in psychiatry (one that should have won the Nobel Prize in Medicine or Physiology, like the discovery of penicillin) was the phenothiazine drug chlorpromazine, first used as an adjunct to surgical anesthesia in the late 1940s and early 1950s.² Chlorpromazine eliminated psychotic symptoms in many patients (refuting centuries of dogma that madness is irreversible), led to
deinstitutionalization and community care of patients who suffer a serious psychiatric disorder, and reduced psychiatric beds from 50% of all hospital beds in the United States to about 5% today. Numerous phenothiazines were developed (evolution) followed by six non-phenothiazine classes (paradigm shift).

Another truly felicitous serendipity was the discovery of the first atypical antipsychotic, clozapine (synthesized in 1959, the same year that the antipsychotic thioridazine [Mellaril] was synthesized), which was initially shelved because it did not cause extrapyramidal symptoms (EPS); at the time, EPS were erroneously thought to be indispensable for antipsychotic efficacy! The discovery of clozapine led to the development of the nine atypical antipsychotics that have largely replaced the first-generation agents (paradigm shift) and that mimic clozapine’s far stronger binding of serotonin 5-HT2A receptors than binding of dopamine D2 receptors, thus reducing the occurrence of neurologic movement disorders (ie, EPS).

Clozapine led to a radical breakthrough when it proved to have efficacy in schizophrenia that is refractory to first-generation antipsychotics (the CATIE study showed the same efficacy for second-generation antipsychotics). A follow-up breakthrough was the
discovery of the efficacy of clozapine on suicidality, a significant cause of mortality in patients with schizophrenia.

A recently reported treatment for schizophrenia might be a potentially radical breakthrough. In a pilot study, researchers reported very rapid and significant improvement in positive and negative symptoms (and even anxiety and depressive symptoms, and within 4 hours and persisting for 4 weeks!³), using the antihypertensive sodium nitroprusside, administered IV. Here is another paradigm shift—in drug delivery, similar to what was seen with IV ketamine, which led to a radical breakthrough in treating drug-resistant depression.

Interestingly, the N-methyl-d-aspartate (NMDA) receptor is playing a key role in radical breakthroughs in schizophrenia and depression. A glycine transporter I inhibitor (which potentiates what is strongly suspected to be a hypofunctional NMDA receptor in schizophrenia) is undergoing further study for the treatment of negative and residual symptoms of schizophrenia, after a promising initial trial. This promises to be a radical breakthrough in addressing a major unmet need in psychiatry: treating negative symptoms of schizophrenia.

Antidepressants

Serendipity played a role in the discovery of the first antidepressant, iproniazid, a monoamine oxidase inhibitor (MAOI) that was used to treat tuberculosis in the 1940s and 1950s; medical staff in sanitariums noticed that the drug elevated the mood of depressed tuberculosis patients. Several other clinically useful MAOIs were then developed (evolution).

When the first tricyclic antidepressant (TCA), imipramine, was synthesized, it was intended to be an antipsychotic but—serendipitously—turned out to be a strong antidepressant. A paradigm shift from MAOIs to TCAs then occurred through the 1970s and 1980s, prompted by concerns over adverse effects caused by the interaction of MAOIs and foods that contain tyramine.

A mechanistic breakthrough occurred when the first selective serotonin reuptake inhibitor (SSRI), fluoxetine, was developed in the late 1980s, followed soon by several other SSRIs (evolution). This triggered another massive paradigm shift away from TCAs to SSRIs because of the low cardiotoxicity of SSRIs.

Evolution then led to the development of other heterocyclic antidepressants, such as nefazodone, mirtazapine, venlafaxine, and duloxetine.

The recent exciting (pun intended again!) discovery of the efficacy of the glutamate NMDA receptor-antagonist ketamine for severe, treatment-resistant depression represents a radical breakthrough in the rapidity of remission (within 1 or 2 hours of IV administration) of depression and suicidal impulses. Until now, such rapid response was believed unattainable.

The ketamine treatment model also rep- resents several paradigm shifts: from mono- amines to glutamate; from the oral route to the IV route; from gradual (6 to 8 weeks) to abrupt (1 or 2 hours) resolution of symptoms; and from neurochemistry (monoamine neurotransmitters) to neuroplasticity (mammalian target of rapapmycin [mTOR] and brain- derived neurotrophic factor [BDNF]).

The saga will go on

Explosive growth in molecular neuroscience and deeper understanding of the pathophysiology of major psychiatric disorders bode well for an accelerating pace of radical breakthroughs in psychiatric therapies. The new revelation that symptoms of chronic neuropsychiatric disorders such as depression, mania, and schizophrenia can be re- versed within a few hours, instead of weeks, months, or years, is jubilant news for our long-suffering patients.

But even as science-driven breakthroughs accelerate and prompt paradigm shifts in treatment, we should never under-estimate the importance and value of serendipity in generating new insights that lead to the same transformative paradigm shifts in therapeutics. Scientists are equipped to make discoveries that are breakthroughs, but observant clinicians can make serendipitous discoveries that may reinvent the care of psychotic disorders. The discovery of psychiatric therapies can begin in a clinical setting—not just in the ivory tower of academia.

For a relatively young medical discipline like psychiatry, the history of discovery of biological therapeutics is replete with twists and turns, the pace of which will likely not abate. These discoveries can be initiated by both observant clinicians and dedicated researchers.

As I contemplated the scientific saga of developing somatic and pharmaceutical treatments for major psychiatric disorders, I recognized several interesting themes: serendipity, evolution, paradigm shifts, and radical breakthroughs. Consider the following examples of those themes.

Neuromodulation

Electroconvulsive therapy (ECT), the original neuromodulation therapy, was discovered (serendipity) when Meduna, mistakenly thinking that schizophrenia and epilepsy are “antagonistic,” used camphor and, later, metrazol, to induce seizures to treat schizophrenia. Later, Cerletti and Bini switched the seizure induction to electricity (evolution), and the use of ECT spread, like a seizure, around the world after their initial report. Later, unilateral ECT and pulse wave ECT were developed to reduce the incidence of side effects (further evolution).

In contemporary psychiatry, a paradigm shift in neuromodulation techniques has emerged over the past decade with the development of an array of novel neuromodulation techniques,¹ some of which do not induce seizures or touch the scalp with electrodes—or even use electricity. These techniques include vagus nerve stimulation, repetitive transcranial magnetic stimulation, epidural cortical stimulation, focused ultrasound, low-field magnetic stimulation, transcranial direct current stimulation, and magnetic seizure therapy. Currently (pun intended!), radical breakthroughs with significant therapeutic promise are being developed, such as optogenetic stimulation and deep brain stimulation.

Antipsychotics

One of the most momentous serendipitous discoveries in psychiatry (one that should have won the Nobel Prize in Medicine or Physiology, like the discovery of penicillin) was the phenothiazine drug chlorpromazine, first used as an adjunct to surgical anesthesia in the late 1940s and early 1950s.² Chlorpromazine eliminated psychotic symptoms in many patients (refuting centuries of dogma that madness is irreversible), led to
deinstitutionalization and community care of patients who suffer a serious psychiatric disorder, and reduced psychiatric beds from 50% of all hospital beds in the United States to about 5% today. Numerous phenothiazines were developed (evolution) followed by six non-phenothiazine classes (paradigm shift).

Another truly felicitous serendipity was the discovery of the first atypical antipsychotic, clozapine (synthesized in 1959, the same year that the antipsychotic thioridazine [Mellaril] was synthesized), which was initially shelved because it did not cause extrapyramidal symptoms (EPS); at the time, EPS were erroneously thought to be indispensable for antipsychotic efficacy! The discovery of clozapine led to the development of the nine atypical antipsychotics that have largely replaced the first-generation agents (paradigm shift) and that mimic clozapine’s far stronger binding of serotonin 5-HT2A receptors than binding of dopamine D2 receptors, thus reducing the occurrence of neurologic movement disorders (ie, EPS).

Clozapine led to a radical breakthrough when it proved to have efficacy in schizophrenia that is refractory to first-generation antipsychotics (the CATIE study showed the same efficacy for second-generation antipsychotics). A follow-up breakthrough was the
discovery of the efficacy of clozapine on suicidality, a significant cause of mortality in patients with schizophrenia.

A recently reported treatment for schizophrenia might be a potentially radical breakthrough. In a pilot study, researchers reported very rapid and significant improvement in positive and negative symptoms (and even anxiety and depressive symptoms, and within 4 hours and persisting for 4 weeks!³), using the antihypertensive sodium nitroprusside, administered IV. Here is another paradigm shift—in drug delivery, similar to what was seen with IV ketamine, which led to a radical breakthrough in treating drug-resistant depression.

Interestingly, the N-methyl-d-aspartate (NMDA) receptor is playing a key role in radical breakthroughs in schizophrenia and depression. A glycine transporter I inhibitor (which potentiates what is strongly suspected to be a hypofunctional NMDA receptor in schizophrenia) is undergoing further study for the treatment of negative and residual symptoms of schizophrenia, after a promising initial trial. This promises to be a radical breakthrough in addressing a major unmet need in psychiatry: treating negative symptoms of schizophrenia.

Antidepressants

Serendipity played a role in the discovery of the first antidepressant, iproniazid, a monoamine oxidase inhibitor (MAOI) that was used to treat tuberculosis in the 1940s and 1950s; medical staff in sanitariums noticed that the drug elevated the mood of depressed tuberculosis patients. Several other clinically useful MAOIs were then developed (evolution).

When the first tricyclic antidepressant (TCA), imipramine, was synthesized, it was intended to be an antipsychotic but—serendipitously—turned out to be a strong antidepressant. A paradigm shift from MAOIs to TCAs then occurred through the 1970s and 1980s, prompted by concerns over adverse effects caused by the interaction of MAOIs and foods that contain tyramine.

A mechanistic breakthrough occurred when the first selective serotonin reuptake inhibitor (SSRI), fluoxetine, was developed in the late 1980s, followed soon by several other SSRIs (evolution). This triggered another massive paradigm shift away from TCAs to SSRIs because of the low cardiotoxicity of SSRIs.

Evolution then led to the development of other heterocyclic antidepressants, such as nefazodone, mirtazapine, venlafaxine, and duloxetine.

The recent exciting (pun intended again!) discovery of the efficacy of the glutamate NMDA receptor-antagonist ketamine for severe, treatment-resistant depression represents a radical breakthrough in the rapidity of remission (within 1 or 2 hours of IV administration) of depression and suicidal impulses. Until now, such rapid response was believed unattainable.

The ketamine treatment model also rep- resents several paradigm shifts: from mono- amines to glutamate; from the oral route to the IV route; from gradual (6 to 8 weeks) to abrupt (1 or 2 hours) resolution of symptoms; and from neurochemistry (monoamine neurotransmitters) to neuroplasticity (mammalian target of rapapmycin [mTOR] and brain- derived neurotrophic factor [BDNF]).

The saga will go on

Explosive growth in molecular neuroscience and deeper understanding of the pathophysiology of major psychiatric disorders bode well for an accelerating pace of radical breakthroughs in psychiatric therapies. The new revelation that symptoms of chronic neuropsychiatric disorders such as depression, mania, and schizophrenia can be re- versed within a few hours, instead of weeks, months, or years, is jubilant news for our long-suffering patients.

But even as science-driven breakthroughs accelerate and prompt paradigm shifts in treatment, we should never under-estimate the importance and value of serendipity in generating new insights that lead to the same transformative paradigm shifts in therapeutics. Scientists are equipped to make discoveries that are breakthroughs, but observant clinicians can make serendipitous discoveries that may reinvent the care of psychotic disorders. The discovery of psychiatric therapies can begin in a clinical setting—not just in the ivory tower of academia.

For a relatively young medical discipline like psychiatry, the history of discovery of biological therapeutics is replete with twists and turns, the pace of which will likely not abate. These discoveries can be initiated by both observant clinicians and dedicated researchers.

As I contemplated the scientific saga of developing somatic and pharmaceutical treatments for major psychiatric disorders, I recognized several interesting themes: serendipity, evolution, paradigm shifts, and radical breakthroughs. Consider the following examples of those themes.

Neuromodulation

Electroconvulsive therapy (ECT), the original neuromodulation therapy, was discovered (serendipity) when Meduna, mistakenly thinking that schizophrenia and epilepsy are “antagonistic,” used camphor and, later, metrazol, to induce seizures to treat schizophrenia. Later, Cerletti and Bini switched the seizure induction to electricity (evolution), and the use of ECT spread, like a seizure, around the world after their initial report. Later, unilateral ECT and pulse wave ECT were developed to reduce the incidence of side effects (further evolution).

In contemporary psychiatry, a paradigm shift in neuromodulation techniques has emerged over the past decade with the development of an array of novel neuromodulation techniques,¹ some of which do not induce seizures or touch the scalp with electrodes—or even use electricity. These techniques include vagus nerve stimulation, repetitive transcranial magnetic stimulation, epidural cortical stimulation, focused ultrasound, low-field magnetic stimulation, transcranial direct current stimulation, and magnetic seizure therapy. Currently (pun intended!), radical breakthroughs with significant therapeutic promise are being developed, such as optogenetic stimulation and deep brain stimulation.

Antipsychotics

One of the most momentous serendipitous discoveries in psychiatry (one that should have won the Nobel Prize in Medicine or Physiology, like the discovery of penicillin) was the phenothiazine drug chlorpromazine, first used as an adjunct to surgical anesthesia in the late 1940s and early 1950s.² Chlorpromazine eliminated psychotic symptoms in many patients (refuting centuries of dogma that madness is irreversible), led to
deinstitutionalization and community care of patients who suffer a serious psychiatric disorder, and reduced psychiatric beds from 50% of all hospital beds in the United States to about 5% today. Numerous phenothiazines were developed (evolution) followed by six non-phenothiazine classes (paradigm shift).

Another truly felicitous serendipity was the discovery of the first atypical antipsychotic, clozapine (synthesized in 1959, the same year that the antipsychotic thioridazine [Mellaril] was synthesized), which was initially shelved because it did not cause extrapyramidal symptoms (EPS); at the time, EPS were erroneously thought to be indispensable for antipsychotic efficacy! The discovery of clozapine led to the development of the nine atypical antipsychotics that have largely replaced the first-generation agents (paradigm shift) and that mimic clozapine’s far stronger binding of serotonin 5-HT2A receptors than binding of dopamine D2 receptors, thus reducing the occurrence of neurologic movement disorders (ie, EPS).

Clozapine led to a radical breakthrough when it proved to have efficacy in schizophrenia that is refractory to first-generation antipsychotics (the CATIE study showed the same efficacy for second-generation antipsychotics). A follow-up breakthrough was the
discovery of the efficacy of clozapine on suicidality, a significant cause of mortality in patients with schizophrenia.

A recently reported treatment for schizophrenia might be a potentially radical breakthrough. In a pilot study, researchers reported very rapid and significant improvement in positive and negative symptoms (and even anxiety and depressive symptoms, and within 4 hours and persisting for 4 weeks!³), using the antihypertensive sodium nitroprusside, administered IV. Here is another paradigm shift—in drug delivery, similar to what was seen with IV ketamine, which led to a radical breakthrough in treating drug-resistant depression.

Interestingly, the N-methyl-d-aspartate (NMDA) receptor is playing a key role in radical breakthroughs in schizophrenia and depression. A glycine transporter I inhibitor (which potentiates what is strongly suspected to be a hypofunctional NMDA receptor in schizophrenia) is undergoing further study for the treatment of negative and residual symptoms of schizophrenia, after a promising initial trial. This promises to be a radical breakthrough in addressing a major unmet need in psychiatry: treating negative symptoms of schizophrenia.

Antidepressants

Serendipity played a role in the discovery of the first antidepressant, iproniazid, a monoamine oxidase inhibitor (MAOI) that was used to treat tuberculosis in the 1940s and 1950s; medical staff in sanitariums noticed that the drug elevated the mood of depressed tuberculosis patients. Several other clinically useful MAOIs were then developed (evolution).

When the first tricyclic antidepressant (TCA), imipramine, was synthesized, it was intended to be an antipsychotic but—serendipitously—turned out to be a strong antidepressant. A paradigm shift from MAOIs to TCAs then occurred through the 1970s and 1980s, prompted by concerns over adverse effects caused by the interaction of MAOIs and foods that contain tyramine.

A mechanistic breakthrough occurred when the first selective serotonin reuptake inhibitor (SSRI), fluoxetine, was developed in the late 1980s, followed soon by several other SSRIs (evolution). This triggered another massive paradigm shift away from TCAs to SSRIs because of the low cardiotoxicity of SSRIs.

Evolution then led to the development of other heterocyclic antidepressants, such as nefazodone, mirtazapine, venlafaxine, and duloxetine.

The recent exciting (pun intended again!) discovery of the efficacy of the glutamate NMDA receptor-antagonist ketamine for severe, treatment-resistant depression represents a radical breakthrough in the rapidity of remission (within 1 or 2 hours of IV administration) of depression and suicidal impulses. Until now, such rapid response was believed unattainable.

The ketamine treatment model also rep- resents several paradigm shifts: from mono- amines to glutamate; from the oral route to the IV route; from gradual (6 to 8 weeks) to abrupt (1 or 2 hours) resolution of symptoms; and from neurochemistry (monoamine neurotransmitters) to neuroplasticity (mammalian target of rapapmycin [mTOR] and brain- derived neurotrophic factor [BDNF]).

The saga will go on

Explosive growth in molecular neuroscience and deeper understanding of the pathophysiology of major psychiatric disorders bode well for an accelerating pace of radical breakthroughs in psychiatric therapies. The new revelation that symptoms of chronic neuropsychiatric disorders such as depression, mania, and schizophrenia can be re- versed within a few hours, instead of weeks, months, or years, is jubilant news for our long-suffering patients.

But even as science-driven breakthroughs accelerate and prompt paradigm shifts in treatment, we should never under-estimate the importance and value of serendipity in generating new insights that lead to the same transformative paradigm shifts in therapeutics. Scientists are equipped to make discoveries that are breakthroughs, but observant clinicians can make serendipitous discoveries that may reinvent the care of psychotic disorders. The discovery of psychiatric therapies can begin in a clinical setting—not just in the ivory tower of academia.

From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.

Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.¹ As a result, physicians and scientists are now more willing to explore AA’s mottos.

Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:

1.   “90 meetings in 90 days”

2.   “Keep it simple”

3.   “Denial is not just a river in Egypt”

4.   “Beware of people, places, and things”

5.   “A cucumber that has become a pickle cannot become a cucumber again”

Click here for another Pearl on alternatives to 12-step groups.

Disclosure

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

From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.

Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.¹ As a result, physicians and scientists are now more willing to explore AA’s mottos.

Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:

1.   “90 meetings in 90 days”

2.   “Keep it simple”

3.   “Denial is not just a river in Egypt”

4.   “Beware of people, places, and things”

5.   “A cucumber that has become a pickle cannot become a cucumber again”

Click here for another Pearl on alternatives to 12-step groups.

Disclosure

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

From “90 minutes in 90 days,” to “people, places, and things,” to “cucumbers and pickles,” Alcoholics Anonymous (AA) slogans have been influencing the public’s understanding of the addictive process for almost a century. Regrettably, these terms have, inadvertently, alienated the scientific community. The translation and subsequent use of AA slogans has been a valuable tool in engaging science experts with mutual-help fellowships such as AA.

Recent advances in the neurobiology and neurochemistry of addiction have validated several of the memorable sayings of AA.¹ As a result, physicians and scientists are now more willing to explore AA’s mottos.

Here are five well-known AA slogans that we have translated into medical terms and then briefly assessed in terms of their validity and relevance in today’s treatment of alcohol addiction:

1.   “90 meetings in 90 days”

2.   “Keep it simple”

3.   “Denial is not just a river in Egypt”

4.   “Beware of people, places, and things”

5.   “A cucumber that has become a pickle cannot become a cucumber again”

Click here for another Pearl on alternatives to 12-step groups.

Disclosure

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