Pearls

Discharging patients from a hospital or emergency department despite his (her) ongoing suicidal ideation is a clinical dilemma. Typically, these patients do not respond to hospital care and do not follow up after discharge. They often have a poorly treated illness and many unmet psychosocial and interpersonal needs.¹ These patients may communicate their suicidality as conditional, aimed at satisfying unmet needs; secondary gain; dependency needs; or remaining in the sick role. Faced with impending discharge, such a patient might increase the intensity of his suicidal statements or engage in behaviors that subvert discharge. Some go as far as to engage in behaviors with apparent suicidal intent soon after discharge.

A complicated decision

Such patients often are at a chronically elevated risk for suicide because of mood disorders, personality pathology, substance use disorder, or a history of serious suicide attempt.² Do not dismiss a patient’s suicidal statements; he is ill and may end his own life.

Managing these situations can put you under a variety of pressures: your own negative emotional and psychological reactions to the patient; pressure from staff to avoid admission or expedite discharge of the patient; and administrative pressure to efficiently manage resources.³ You’re faced with a difficult decision: Discharge a patient who might self-harm or commit suicide, or continue care that may be counterproductive.

We propose 6 steps that have helped us promote good clinical care while documenting the necessary information to manage risk in these complex situations.

1. Define and document the clinical situation. Summarize the clinical dilemma.

2. Assess and document current suicide risk.⁴ Conduct a formal suicide risk assessment; if necessary, reassess throughout care. Focus on dynamic risk factors; protective risk factors (static and dynamic); acute stressors (or lack thereof) that would increase their risk of suicide above their chronically elevated baseline; and access to lethal means—firearms, stockpiled medication, etc.

3. Document modified dynamic or protective factors. Review the dynamic risk and protective factors you have identified and how they have been modified by treatment to date. If dynamic factors have not been modified, indicate why and document the recommended plan to address these matters. You might not be able to provide relief, but you should be able to outline a plan for eventual relief.

4. Document the reasons continued care in the acute setting is not indicated. Reasons might include: the patient isn’t participating in recommended care or treatment; the patient isn’t improving, or is becoming worse, in the care environment; continued care is preventing or interfering with access to more effective care options; is counterproductive to the patient’s stated goals; or compromising the safety benefit of the structured care environment because the patient is not collaborating with his care team.

5. Document your discussion of discharge with the patient. Highlight attempts to engage the patient in adaptive problem solving. Work out a crisis or suicide safety plan and give the patient a copy and keep a copy in his (her) chart.

      If the patient refuses to engage in safety planning, document it in the chart. Note the absence of any conditions that might impair the patient’s volitional capacity to not end their life—intoxication, delirium, acute psychosis, etc. Explicitly frame the patient’s responsibility for his life. Discuss and document a follow-up plan and make direct contact with providers and social supports, documenting whether contacting these providers was successful.

6. Consult with a colleague. An informal non-visit consultation with a colleague demonstrates your recognition of the complexity of the situation and your due diligence in arriving at a discharge decision. Consultation often will result in useful additional strategies for managing or engaging the patient. A colleague’s agreement helps demonstrate that “average practitioner” and “prudent practitioner” standards of care have been met with respect to clinical decision-making.

Disclosure

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

Discharging patients from a hospital or emergency department despite his (her) ongoing suicidal ideation is a clinical dilemma. Typically, these patients do not respond to hospital care and do not follow up after discharge. They often have a poorly treated illness and many unmet psychosocial and interpersonal needs.¹ These patients may communicate their suicidality as conditional, aimed at satisfying unmet needs; secondary gain; dependency needs; or remaining in the sick role. Faced with impending discharge, such a patient might increase the intensity of his suicidal statements or engage in behaviors that subvert discharge. Some go as far as to engage in behaviors with apparent suicidal intent soon after discharge.

A complicated decision

Such patients often are at a chronically elevated risk for suicide because of mood disorders, personality pathology, substance use disorder, or a history of serious suicide attempt.² Do not dismiss a patient’s suicidal statements; he is ill and may end his own life.

Managing these situations can put you under a variety of pressures: your own negative emotional and psychological reactions to the patient; pressure from staff to avoid admission or expedite discharge of the patient; and administrative pressure to efficiently manage resources.³ You’re faced with a difficult decision: Discharge a patient who might self-harm or commit suicide, or continue care that may be counterproductive.

We propose 6 steps that have helped us promote good clinical care while documenting the necessary information to manage risk in these complex situations.

1. Define and document the clinical situation. Summarize the clinical dilemma.

2. Assess and document current suicide risk.⁴ Conduct a formal suicide risk assessment; if necessary, reassess throughout care. Focus on dynamic risk factors; protective risk factors (static and dynamic); acute stressors (or lack thereof) that would increase their risk of suicide above their chronically elevated baseline; and access to lethal means—firearms, stockpiled medication, etc.

3. Document modified dynamic or protective factors. Review the dynamic risk and protective factors you have identified and how they have been modified by treatment to date. If dynamic factors have not been modified, indicate why and document the recommended plan to address these matters. You might not be able to provide relief, but you should be able to outline a plan for eventual relief.

4. Document the reasons continued care in the acute setting is not indicated. Reasons might include: the patient isn’t participating in recommended care or treatment; the patient isn’t improving, or is becoming worse, in the care environment; continued care is preventing or interfering with access to more effective care options; is counterproductive to the patient’s stated goals; or compromising the safety benefit of the structured care environment because the patient is not collaborating with his care team.

5. Document your discussion of discharge with the patient. Highlight attempts to engage the patient in adaptive problem solving. Work out a crisis or suicide safety plan and give the patient a copy and keep a copy in his (her) chart.

      If the patient refuses to engage in safety planning, document it in the chart. Note the absence of any conditions that might impair the patient’s volitional capacity to not end their life—intoxication, delirium, acute psychosis, etc. Explicitly frame the patient’s responsibility for his life. Discuss and document a follow-up plan and make direct contact with providers and social supports, documenting whether contacting these providers was successful.

6. Consult with a colleague. An informal non-visit consultation with a colleague demonstrates your recognition of the complexity of the situation and your due diligence in arriving at a discharge decision. Consultation often will result in useful additional strategies for managing or engaging the patient. A colleague’s agreement helps demonstrate that “average practitioner” and “prudent practitioner” standards of care have been met with respect to clinical decision-making.

Disclosure

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

Discharging patients from a hospital or emergency department despite his (her) ongoing suicidal ideation is a clinical dilemma. Typically, these patients do not respond to hospital care and do not follow up after discharge. They often have a poorly treated illness and many unmet psychosocial and interpersonal needs.¹ These patients may communicate their suicidality as conditional, aimed at satisfying unmet needs; secondary gain; dependency needs; or remaining in the sick role. Faced with impending discharge, such a patient might increase the intensity of his suicidal statements or engage in behaviors that subvert discharge. Some go as far as to engage in behaviors with apparent suicidal intent soon after discharge.

A complicated decision

Such patients often are at a chronically elevated risk for suicide because of mood disorders, personality pathology, substance use disorder, or a history of serious suicide attempt.² Do not dismiss a patient’s suicidal statements; he is ill and may end his own life.

Managing these situations can put you under a variety of pressures: your own negative emotional and psychological reactions to the patient; pressure from staff to avoid admission or expedite discharge of the patient; and administrative pressure to efficiently manage resources.³ You’re faced with a difficult decision: Discharge a patient who might self-harm or commit suicide, or continue care that may be counterproductive.

We propose 6 steps that have helped us promote good clinical care while documenting the necessary information to manage risk in these complex situations.

1. Define and document the clinical situation. Summarize the clinical dilemma.

2. Assess and document current suicide risk.⁴ Conduct a formal suicide risk assessment; if necessary, reassess throughout care. Focus on dynamic risk factors; protective risk factors (static and dynamic); acute stressors (or lack thereof) that would increase their risk of suicide above their chronically elevated baseline; and access to lethal means—firearms, stockpiled medication, etc.

3. Document modified dynamic or protective factors. Review the dynamic risk and protective factors you have identified and how they have been modified by treatment to date. If dynamic factors have not been modified, indicate why and document the recommended plan to address these matters. You might not be able to provide relief, but you should be able to outline a plan for eventual relief.

4. Document the reasons continued care in the acute setting is not indicated. Reasons might include: the patient isn’t participating in recommended care or treatment; the patient isn’t improving, or is becoming worse, in the care environment; continued care is preventing or interfering with access to more effective care options; is counterproductive to the patient’s stated goals; or compromising the safety benefit of the structured care environment because the patient is not collaborating with his care team.

5. Document your discussion of discharge with the patient. Highlight attempts to engage the patient in adaptive problem solving. Work out a crisis or suicide safety plan and give the patient a copy and keep a copy in his (her) chart.

      If the patient refuses to engage in safety planning, document it in the chart. Note the absence of any conditions that might impair the patient’s volitional capacity to not end their life—intoxication, delirium, acute psychosis, etc. Explicitly frame the patient’s responsibility for his life. Discuss and document a follow-up plan and make direct contact with providers and social supports, documenting whether contacting these providers was successful.

6. Consult with a colleague. An informal non-visit consultation with a colleague demonstrates your recognition of the complexity of the situation and your due diligence in arriving at a discharge decision. Consultation often will result in useful additional strategies for managing or engaging the patient. A colleague’s agreement helps demonstrate that “average practitioner” and “prudent practitioner” standards of care have been met with respect to clinical decision-making.

Disclosure

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

Clinicians often are unaware of a patient’s misuse or abuse of easily accessible substances such as spices, herbs, and natural supplements. This can lead to misdiagnosed severe psychiatric disorders and, more alarmingly, unnecessary use of long-term psychotropics and psychiatric services.

Excessive ingestion of nutmeg (Myristica fragrans) can produce psychiatric symptoms because it contains myristicin, a psychoactive substance, in its aromatic oil.¹ It is structurally similar to other hallucinogenic compounds such as mescaline. The effects of nutmeg could be attributed to metabolic formation of amphetamine derivatives from its core ingredients: elemicin, myristicin, and safrole.^1-3 However, neither amphetamine derivatives nor core ingredients are detected in the urine of patients suspected of abusing nutmeg, which makes diagnosis challenging.

We present a case of nutmeg abuse leading to psychotic depression.

Nutmeg and depression

Mr. D, age 50, is admitted to our inpatient psychiatric unit with severe dysphoria, hopelessness, persecutory delusions, suicidal ideation, and a sense of impending doom for the third time in 2 years. At previous admissions, he was diagnosed with bipolar disorder.

During his first admission, Mr. D reported an intentional overdose by water intoxication; laboratory studies revealed  hyponatremia, liver dysfunction, abnormal cardiac markers, increased creatine kinase, and leukocytosis with neutrophilia. With supportive treatment, all parameters returned to the normal range within 7 days.

At his third admission, Mr. D describes an extensive history of nutmeg abuse. He reports achieving desirable psychoactive effects such as excitement, euphoria, enhanced sensory perceptions, and racing thoughts within a half hour of ingesting 1 teaspoon (5 g) of nutmeg; effects lasted for 6 hours. He reports that consuming 2 teaspoons (10 g) produced a “stronger” effect, and that 1 tablespoon (15 g) was associated with severe dysphoria, fear, psychosis, suicidal ideation, and behavior, which led to his psychiatric admissions. He denies any other substance use.

Urine drug screen and other routine laboratory investigations are negative. Symptoms resolve spontaneously within 3 days and he is managed without pharmacotherapy. The diagnosis is revised to substance-induced mood disorder with psychotic features. We provide psychoeducation about nutmeg’s psychoactive effects, and Mr. D is motivated to stop abusing nutmeg. Three years later he remains in good health.

Effects of nutmeg

Acute nutmeg intoxication produces anxiety, fear, and hallucinations, and generally is self-limited, with most symptoms resolving within 24 hours.² Chronic effects of nutmeg abuse resemble those of marijuana abuse (Table 1). Acute and long-term physical effects are listed in Table 2. 

Be alert for presentations of a ‘natural high’

Nutmeg, other spices, and herbs can be used by persons looking for a ”natural high”; as we saw with Mr. D, nutmeg abuse can present as a mood disorder resembling bipolar disorder. An acute, atypical presentation of mood changes or suicidal ideation should prompt you to investigate causes other than primary mood or psychotic disorders, and should include consideration of the effects of atypical drugs—and spices—of abuse.

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

Clinicians often are unaware of a patient’s misuse or abuse of easily accessible substances such as spices, herbs, and natural supplements. This can lead to misdiagnosed severe psychiatric disorders and, more alarmingly, unnecessary use of long-term psychotropics and psychiatric services.

Excessive ingestion of nutmeg (Myristica fragrans) can produce psychiatric symptoms because it contains myristicin, a psychoactive substance, in its aromatic oil.¹ It is structurally similar to other hallucinogenic compounds such as mescaline. The effects of nutmeg could be attributed to metabolic formation of amphetamine derivatives from its core ingredients: elemicin, myristicin, and safrole.^1-3 However, neither amphetamine derivatives nor core ingredients are detected in the urine of patients suspected of abusing nutmeg, which makes diagnosis challenging.

We present a case of nutmeg abuse leading to psychotic depression.

Nutmeg and depression

Mr. D, age 50, is admitted to our inpatient psychiatric unit with severe dysphoria, hopelessness, persecutory delusions, suicidal ideation, and a sense of impending doom for the third time in 2 years. At previous admissions, he was diagnosed with bipolar disorder.

During his first admission, Mr. D reported an intentional overdose by water intoxication; laboratory studies revealed  hyponatremia, liver dysfunction, abnormal cardiac markers, increased creatine kinase, and leukocytosis with neutrophilia. With supportive treatment, all parameters returned to the normal range within 7 days.

At his third admission, Mr. D describes an extensive history of nutmeg abuse. He reports achieving desirable psychoactive effects such as excitement, euphoria, enhanced sensory perceptions, and racing thoughts within a half hour of ingesting 1 teaspoon (5 g) of nutmeg; effects lasted for 6 hours. He reports that consuming 2 teaspoons (10 g) produced a “stronger” effect, and that 1 tablespoon (15 g) was associated with severe dysphoria, fear, psychosis, suicidal ideation, and behavior, which led to his psychiatric admissions. He denies any other substance use.

Urine drug screen and other routine laboratory investigations are negative. Symptoms resolve spontaneously within 3 days and he is managed without pharmacotherapy. The diagnosis is revised to substance-induced mood disorder with psychotic features. We provide psychoeducation about nutmeg’s psychoactive effects, and Mr. D is motivated to stop abusing nutmeg. Three years later he remains in good health.

Effects of nutmeg

Acute nutmeg intoxication produces anxiety, fear, and hallucinations, and generally is self-limited, with most symptoms resolving within 24 hours.² Chronic effects of nutmeg abuse resemble those of marijuana abuse (Table 1). Acute and long-term physical effects are listed in Table 2. 

Be alert for presentations of a ‘natural high’

Nutmeg, other spices, and herbs can be used by persons looking for a ”natural high”; as we saw with Mr. D, nutmeg abuse can present as a mood disorder resembling bipolar disorder. An acute, atypical presentation of mood changes or suicidal ideation should prompt you to investigate causes other than primary mood or psychotic disorders, and should include consideration of the effects of atypical drugs—and spices—of abuse.

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

Clinicians often are unaware of a patient’s misuse or abuse of easily accessible substances such as spices, herbs, and natural supplements. This can lead to misdiagnosed severe psychiatric disorders and, more alarmingly, unnecessary use of long-term psychotropics and psychiatric services.

Excessive ingestion of nutmeg (Myristica fragrans) can produce psychiatric symptoms because it contains myristicin, a psychoactive substance, in its aromatic oil.¹ It is structurally similar to other hallucinogenic compounds such as mescaline. The effects of nutmeg could be attributed to metabolic formation of amphetamine derivatives from its core ingredients: elemicin, myristicin, and safrole.^1-3 However, neither amphetamine derivatives nor core ingredients are detected in the urine of patients suspected of abusing nutmeg, which makes diagnosis challenging.

We present a case of nutmeg abuse leading to psychotic depression.

Nutmeg and depression

Mr. D, age 50, is admitted to our inpatient psychiatric unit with severe dysphoria, hopelessness, persecutory delusions, suicidal ideation, and a sense of impending doom for the third time in 2 years. At previous admissions, he was diagnosed with bipolar disorder.

During his first admission, Mr. D reported an intentional overdose by water intoxication; laboratory studies revealed  hyponatremia, liver dysfunction, abnormal cardiac markers, increased creatine kinase, and leukocytosis with neutrophilia. With supportive treatment, all parameters returned to the normal range within 7 days.

At his third admission, Mr. D describes an extensive history of nutmeg abuse. He reports achieving desirable psychoactive effects such as excitement, euphoria, enhanced sensory perceptions, and racing thoughts within a half hour of ingesting 1 teaspoon (5 g) of nutmeg; effects lasted for 6 hours. He reports that consuming 2 teaspoons (10 g) produced a “stronger” effect, and that 1 tablespoon (15 g) was associated with severe dysphoria, fear, psychosis, suicidal ideation, and behavior, which led to his psychiatric admissions. He denies any other substance use.

Urine drug screen and other routine laboratory investigations are negative. Symptoms resolve spontaneously within 3 days and he is managed without pharmacotherapy. The diagnosis is revised to substance-induced mood disorder with psychotic features. We provide psychoeducation about nutmeg’s psychoactive effects, and Mr. D is motivated to stop abusing nutmeg. Three years later he remains in good health.

Effects of nutmeg

Acute nutmeg intoxication produces anxiety, fear, and hallucinations, and generally is self-limited, with most symptoms resolving within 24 hours.² Chronic effects of nutmeg abuse resemble those of marijuana abuse (Table 1). Acute and long-term physical effects are listed in Table 2. 

Be alert for presentations of a ‘natural high’

Nutmeg, other spices, and herbs can be used by persons looking for a ”natural high”; as we saw with Mr. D, nutmeg abuse can present as a mood disorder resembling bipolar disorder. An acute, atypical presentation of mood changes or suicidal ideation should prompt you to investigate causes other than primary mood or psychotic disorders, and should include consideration of the effects of atypical drugs—and spices—of abuse.

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

Most children who head bang—rhythmic movement of the head against a solid object, marked by compulsive repetitiveness¹—usually are normal, healthy, well-cared-for children, in whom no cause for this activity can be determined. More common in boys than in girls, childhood head banging usually starts when the child is age 18 months, but he (she) should grow out of it by age 4.^1,2 Nevertheless, you should be prepared to provide careful, targeted evaluation when presented with a child who head bangs, and discuss with parents or caregivers the possibility of a nonphysiologic cause, such as disruptions or discord in the home.

First concern: Is this normal?

Although head banging is seen in 5% to 15% of healthy children,¹ children who are mentally retarded, blind, deaf, or autistic are more likely to participate in head banging.¹ There also may be a familial predisposition; head banging is more frequent among cousins of children who bang their heads.¹ Some studies have found that socioeconomic status, birth order, response to music, and motor development are correlated with head banging.¹

Leung and colleagues¹ propose that head banging is an integral part of normal development; a tension-releasing maneuver; an attention-seeking device; and a form of pain relief in response to acute illnesses. Fatigue, hunger, teething, or discomfort from a wet diaper can increase the tendency to head bang.

How does it happen?

Head banging generally occurs before sleep. The child will repeatedly bang his head—usually the frontal-parietal region—against a pillow, headboard, or railing of a crib 60 to 80 times per minute.¹ This repetitive motion may continue for a few minutes or as long as an hour. While head banging, the child does not seem to experience pain or discomfort, but may appear relaxed or happy. Although this habit appears alarming (calluses, bruises, abrasions, and contusions may occur—especially in children with mental retardation)^1,2, there rarely is significant head damage.

Talking to concerned parents

Head banging can be confused with typical temper tantrums, spasmus nutans (triad of pendular nystagmus, head nodding, and torticollis), and infantile myoclonic seizures (sudden dropping of the head and flexion of the arms).¹ Take a detailed history and careful evaluation of the parent-child relationship to uncover any underlying causes, such as an unhappy home environment (eg, divorce or neglect). A complete physical examination may reveal an ear infection, visual problems, deafness, cerebral palsy, mental retardation, or evidence of abuse.

Psychotropic medication is not recommended. Treatment options include:¹

•  treating underlying abnormalities, such as otitis media

•  padding the sides of the crib

•  providing auditory stimulation, including allowing the child to participate in rhythmic actions during the day³

•  fitting the child for a protective helmet.

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

Most children who head bang—rhythmic movement of the head against a solid object, marked by compulsive repetitiveness¹—usually are normal, healthy, well-cared-for children, in whom no cause for this activity can be determined. More common in boys than in girls, childhood head banging usually starts when the child is age 18 months, but he (she) should grow out of it by age 4.^1,2 Nevertheless, you should be prepared to provide careful, targeted evaluation when presented with a child who head bangs, and discuss with parents or caregivers the possibility of a nonphysiologic cause, such as disruptions or discord in the home.

First concern: Is this normal?

Although head banging is seen in 5% to 15% of healthy children,¹ children who are mentally retarded, blind, deaf, or autistic are more likely to participate in head banging.¹ There also may be a familial predisposition; head banging is more frequent among cousins of children who bang their heads.¹ Some studies have found that socioeconomic status, birth order, response to music, and motor development are correlated with head banging.¹

Leung and colleagues¹ propose that head banging is an integral part of normal development; a tension-releasing maneuver; an attention-seeking device; and a form of pain relief in response to acute illnesses. Fatigue, hunger, teething, or discomfort from a wet diaper can increase the tendency to head bang.

How does it happen?

Head banging generally occurs before sleep. The child will repeatedly bang his head—usually the frontal-parietal region—against a pillow, headboard, or railing of a crib 60 to 80 times per minute.¹ This repetitive motion may continue for a few minutes or as long as an hour. While head banging, the child does not seem to experience pain or discomfort, but may appear relaxed or happy. Although this habit appears alarming (calluses, bruises, abrasions, and contusions may occur—especially in children with mental retardation)^1,2, there rarely is significant head damage.

Talking to concerned parents

Head banging can be confused with typical temper tantrums, spasmus nutans (triad of pendular nystagmus, head nodding, and torticollis), and infantile myoclonic seizures (sudden dropping of the head and flexion of the arms).¹ Take a detailed history and careful evaluation of the parent-child relationship to uncover any underlying causes, such as an unhappy home environment (eg, divorce or neglect). A complete physical examination may reveal an ear infection, visual problems, deafness, cerebral palsy, mental retardation, or evidence of abuse.

Psychotropic medication is not recommended. Treatment options include:¹

•  treating underlying abnormalities, such as otitis media

•  padding the sides of the crib

•  providing auditory stimulation, including allowing the child to participate in rhythmic actions during the day³

•  fitting the child for a protective helmet.

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

Most children who head bang—rhythmic movement of the head against a solid object, marked by compulsive repetitiveness¹—usually are normal, healthy, well-cared-for children, in whom no cause for this activity can be determined. More common in boys than in girls, childhood head banging usually starts when the child is age 18 months, but he (she) should grow out of it by age 4.^1,2 Nevertheless, you should be prepared to provide careful, targeted evaluation when presented with a child who head bangs, and discuss with parents or caregivers the possibility of a nonphysiologic cause, such as disruptions or discord in the home.

First concern: Is this normal?

Although head banging is seen in 5% to 15% of healthy children,¹ children who are mentally retarded, blind, deaf, or autistic are more likely to participate in head banging.¹ There also may be a familial predisposition; head banging is more frequent among cousins of children who bang their heads.¹ Some studies have found that socioeconomic status, birth order, response to music, and motor development are correlated with head banging.¹

Leung and colleagues¹ propose that head banging is an integral part of normal development; a tension-releasing maneuver; an attention-seeking device; and a form of pain relief in response to acute illnesses. Fatigue, hunger, teething, or discomfort from a wet diaper can increase the tendency to head bang.

How does it happen?

Head banging generally occurs before sleep. The child will repeatedly bang his head—usually the frontal-parietal region—against a pillow, headboard, or railing of a crib 60 to 80 times per minute.¹ This repetitive motion may continue for a few minutes or as long as an hour. While head banging, the child does not seem to experience pain or discomfort, but may appear relaxed or happy. Although this habit appears alarming (calluses, bruises, abrasions, and contusions may occur—especially in children with mental retardation)^1,2, there rarely is significant head damage.

Talking to concerned parents

Head banging can be confused with typical temper tantrums, spasmus nutans (triad of pendular nystagmus, head nodding, and torticollis), and infantile myoclonic seizures (sudden dropping of the head and flexion of the arms).¹ Take a detailed history and careful evaluation of the parent-child relationship to uncover any underlying causes, such as an unhappy home environment (eg, divorce or neglect). A complete physical examination may reveal an ear infection, visual problems, deafness, cerebral palsy, mental retardation, or evidence of abuse.

Psychotropic medication is not recommended. Treatment options include:¹

•  treating underlying abnormalities, such as otitis media

•  padding the sides of the crib

•  providing auditory stimulation, including allowing the child to participate in rhythmic actions during the day³

•  fitting the child for a protective helmet.

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

There are a lack of research on, and strategies for dealing with, an insufficient response to antipsychotics. Treatment often is guided by what is described in published case reports or anecdotal evidence, rather than the findings of systematic studies.

We propose that a patient be considered “difficult-to-treat” or “treatment-resistant” after experiencing limited or negative responses to 3 different antipsychotics—with ≥1 being a second-generation antipsychotic (SGA)—that the patient has taken for at least 6 to 8 weeks at the maximum recommended dosage. Furthermore, switching to clozapine is an important strategy; do not consider it solely a last resort.

These 6 ‘D’s can remind you of other problems to consider when evaluating a treatment-resistant patient.

Diagnosis. Is the diagnosis, including the presence of comorbid conditions, accurate? Are significant psychosocial stressors undermining treatment response? Treat any comorbid conditions and consider instituting adjunctive psychosocial interventions, including cognitive-behavioral therapy.

Dosage. Have the patient try the maximum recommended dosage if he (she) can tolerate it. Equivalent dosages of antipsychotics are shown in the Table,^1,2 and can guide off-label use of higher dosages. Research does not support use of chlorpromazine equivalents >1,000 mg/d, and usually should not be employed. If using a higher than normal dosage, perform an ECG before the increase.³

Beneficial and adverse effects should be monitored carefully. Reduce the dosage after 3 months if the risk-benefit ratio does not justify the higher dosage.³

Duration. Try a treatment for at least 6 weeks at the maximum tolerated
dosage—even extending it to 12 weeks—before considering abandoning it because of insufficient response.

Drug interactions. Use a drug interaction tool to ensure drug-drug interactions are not reducing antipsychotic levels. A recent increase in smoking or decrease in caffeine intake can reduce the blood level of olanzapine and clozapine.⁴ Ultra-rapid metabolizers of cytochrome P450 isoenzymes may have a lower blood level of antipsychotic.

Consider pharmacogenetic testing in patients in whom you observe an unexpected lack of efficacy or adverse effects at customary dosages.

Double up. You might need to add another medication to the antipsychotic. Symptoms might help determine which medication to add:

• a combination of an SGA and a first-generation antipsychotic may be more effective than antipsychotic monotherapy⁵
• for prominent negative symptoms, consider using 2 SGAs of different potency together. Use caution when prescribing ziprasidone with another antipsychotic because this could prolong the QTc interval
• if a mood stabilizer is appropriate, consider lamotrigine because of its possible potentiating effect on SGAs⁶
• benzodiazepines can be used to reduce agitation or anxiety but are ineffective for psychosis.⁷

Drug levels. Measurement of the blood level of the drug is most useful when administering clozapine; focus on the clozapine, not on the norclozapine level that also is reported. Ensure a clozapine level of 350 to 600 ng/mL.

Therapeutic levels have been established for most antipsychotics (Table).^1,2 Occasionally, knowing these levels can be helpful in evaluating patients for potential problems with absorption and metabolism of the drug, and with nonadherence.

Disclosures

Drs. Faden and Pinninti report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Mago receives grant/research support from Bristol-Myers Squibb, Forest Institute, Genomind, and Shire.

There are a lack of research on, and strategies for dealing with, an insufficient response to antipsychotics. Treatment often is guided by what is described in published case reports or anecdotal evidence, rather than the findings of systematic studies.

We propose that a patient be considered “difficult-to-treat” or “treatment-resistant” after experiencing limited or negative responses to 3 different antipsychotics—with ≥1 being a second-generation antipsychotic (SGA)—that the patient has taken for at least 6 to 8 weeks at the maximum recommended dosage. Furthermore, switching to clozapine is an important strategy; do not consider it solely a last resort.

These 6 ‘D’s can remind you of other problems to consider when evaluating a treatment-resistant patient.

Diagnosis. Is the diagnosis, including the presence of comorbid conditions, accurate? Are significant psychosocial stressors undermining treatment response? Treat any comorbid conditions and consider instituting adjunctive psychosocial interventions, including cognitive-behavioral therapy.

Dosage. Have the patient try the maximum recommended dosage if he (she) can tolerate it. Equivalent dosages of antipsychotics are shown in the Table,^1,2 and can guide off-label use of higher dosages. Research does not support use of chlorpromazine equivalents >1,000 mg/d, and usually should not be employed. If using a higher than normal dosage, perform an ECG before the increase.³

Beneficial and adverse effects should be monitored carefully. Reduce the dosage after 3 months if the risk-benefit ratio does not justify the higher dosage.³

Duration. Try a treatment for at least 6 weeks at the maximum tolerated
dosage—even extending it to 12 weeks—before considering abandoning it because of insufficient response.

Drug interactions. Use a drug interaction tool to ensure drug-drug interactions are not reducing antipsychotic levels. A recent increase in smoking or decrease in caffeine intake can reduce the blood level of olanzapine and clozapine.⁴ Ultra-rapid metabolizers of cytochrome P450 isoenzymes may have a lower blood level of antipsychotic.

Consider pharmacogenetic testing in patients in whom you observe an unexpected lack of efficacy or adverse effects at customary dosages.

Double up. You might need to add another medication to the antipsychotic. Symptoms might help determine which medication to add:

• a combination of an SGA and a first-generation antipsychotic may be more effective than antipsychotic monotherapy⁵
• for prominent negative symptoms, consider using 2 SGAs of different potency together. Use caution when prescribing ziprasidone with another antipsychotic because this could prolong the QTc interval
• if a mood stabilizer is appropriate, consider lamotrigine because of its possible potentiating effect on SGAs⁶
• benzodiazepines can be used to reduce agitation or anxiety but are ineffective for psychosis.⁷

Drug levels. Measurement of the blood level of the drug is most useful when administering clozapine; focus on the clozapine, not on the norclozapine level that also is reported. Ensure a clozapine level of 350 to 600 ng/mL.

Therapeutic levels have been established for most antipsychotics (Table).^1,2 Occasionally, knowing these levels can be helpful in evaluating patients for potential problems with absorption and metabolism of the drug, and with nonadherence.

Disclosures

Drs. Faden and Pinninti report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Mago receives grant/research support from Bristol-Myers Squibb, Forest Institute, Genomind, and Shire.

There are a lack of research on, and strategies for dealing with, an insufficient response to antipsychotics. Treatment often is guided by what is described in published case reports or anecdotal evidence, rather than the findings of systematic studies.

We propose that a patient be considered “difficult-to-treat” or “treatment-resistant” after experiencing limited or negative responses to 3 different antipsychotics—with ≥1 being a second-generation antipsychotic (SGA)—that the patient has taken for at least 6 to 8 weeks at the maximum recommended dosage. Furthermore, switching to clozapine is an important strategy; do not consider it solely a last resort.

These 6 ‘D’s can remind you of other problems to consider when evaluating a treatment-resistant patient.

Diagnosis. Is the diagnosis, including the presence of comorbid conditions, accurate? Are significant psychosocial stressors undermining treatment response? Treat any comorbid conditions and consider instituting adjunctive psychosocial interventions, including cognitive-behavioral therapy.

Dosage. Have the patient try the maximum recommended dosage if he (she) can tolerate it. Equivalent dosages of antipsychotics are shown in the Table,^1,2 and can guide off-label use of higher dosages. Research does not support use of chlorpromazine equivalents >1,000 mg/d, and usually should not be employed. If using a higher than normal dosage, perform an ECG before the increase.³

Beneficial and adverse effects should be monitored carefully. Reduce the dosage after 3 months if the risk-benefit ratio does not justify the higher dosage.³

Duration. Try a treatment for at least 6 weeks at the maximum tolerated
dosage—even extending it to 12 weeks—before considering abandoning it because of insufficient response.

Drug interactions. Use a drug interaction tool to ensure drug-drug interactions are not reducing antipsychotic levels. A recent increase in smoking or decrease in caffeine intake can reduce the blood level of olanzapine and clozapine.⁴ Ultra-rapid metabolizers of cytochrome P450 isoenzymes may have a lower blood level of antipsychotic.

Consider pharmacogenetic testing in patients in whom you observe an unexpected lack of efficacy or adverse effects at customary dosages.

Double up. You might need to add another medication to the antipsychotic. Symptoms might help determine which medication to add:

• a combination of an SGA and a first-generation antipsychotic may be more effective than antipsychotic monotherapy⁵
• for prominent negative symptoms, consider using 2 SGAs of different potency together. Use caution when prescribing ziprasidone with another antipsychotic because this could prolong the QTc interval
• if a mood stabilizer is appropriate, consider lamotrigine because of its possible potentiating effect on SGAs⁶
• benzodiazepines can be used to reduce agitation or anxiety but are ineffective for psychosis.⁷

Drug levels. Measurement of the blood level of the drug is most useful when administering clozapine; focus on the clozapine, not on the norclozapine level that also is reported. Ensure a clozapine level of 350 to 600 ng/mL.

Therapeutic levels have been established for most antipsychotics (Table).^1,2 Occasionally, knowing these levels can be helpful in evaluating patients for potential problems with absorption and metabolism of the drug, and with nonadherence.

Disclosures

Drs. Faden and Pinninti report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Mago receives grant/research support from Bristol-Myers Squibb, Forest Institute, Genomind, and Shire.

Psychiatrists often are required to obtain basic sexual information as part of a thorough clinical assessment.¹ Although a detailed sexual health assessment comprises multiple elaborate domains,² it’s important that mental health professionals remember a set of topics and related questions (Table) that can help investigate, diagnose, and treat sexual dysfunction, and contribute to a biopsychosocial formulation of your patient’s sexuality. The BIOTEACHERS mnemonic can remind you what to ask when taking a patient’s sexual history; it is not intended to be an alternative to a comprehensive sexual health evaluation.

Each letter stands for a component of the sexual assessment. The grouped letters of the acronym break down into different relevant areas that aid in remembering each category.

BIO

Background of the problem or the patient’s biophysical state

Identity

Orientation

BIO gathers basic medical information, then creates an opportunity to understand the patient’s gender identity. This step allows for nonjudgmental discussions about the patient’s sexual orientation.

TEACH

Thoughts of a sexual nature

Erotic desire or sexual interest

Arousal

Climax during sex

How often

TEACH incorporates a common chronology of sexual response and activity, starting with sexual thoughts, feelings of erotic desire, development of sexual arousal, ability and quality of a patient’s orgasm, as well as frequency of sexual activity.

ERS

Education

Repertoire or relationship dynamics

Self-stimulation

ERS comprises somewhat more complicated subjects: education (questions about a person’s sexual awareness and communication style); formal sexual knowledge; and health practices. These areas of questioning also normalize discussion of the patient’s sexual repertoire (what activities he [she] does and avoids), reviews qualities of the sexual relationship, and broaches the issue of self-stimulation.

Remember: All discussions of sexuality should be appropriate to the clinical context and considerate of the deeply personal nature of the information.

Disclosure

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

Acknowledgement

The authors thank Sallie Foley, LMSW, Daniela Wittmann, LMSW, and the University of Michigan Sexual Health Certificate program for their assistance.

Psychiatrists often are required to obtain basic sexual information as part of a thorough clinical assessment.¹ Although a detailed sexual health assessment comprises multiple elaborate domains,² it’s important that mental health professionals remember a set of topics and related questions (Table) that can help investigate, diagnose, and treat sexual dysfunction, and contribute to a biopsychosocial formulation of your patient’s sexuality. The BIOTEACHERS mnemonic can remind you what to ask when taking a patient’s sexual history; it is not intended to be an alternative to a comprehensive sexual health evaluation.

Each letter stands for a component of the sexual assessment. The grouped letters of the acronym break down into different relevant areas that aid in remembering each category.

BIO

Background of the problem or the patient’s biophysical state

Identity

Orientation

BIO gathers basic medical information, then creates an opportunity to understand the patient’s gender identity. This step allows for nonjudgmental discussions about the patient’s sexual orientation.

TEACH

Thoughts of a sexual nature

Erotic desire or sexual interest

Arousal

Climax during sex

How often

TEACH incorporates a common chronology of sexual response and activity, starting with sexual thoughts, feelings of erotic desire, development of sexual arousal, ability and quality of a patient’s orgasm, as well as frequency of sexual activity.

ERS

Education

Repertoire or relationship dynamics

Self-stimulation

ERS comprises somewhat more complicated subjects: education (questions about a person’s sexual awareness and communication style); formal sexual knowledge; and health practices. These areas of questioning also normalize discussion of the patient’s sexual repertoire (what activities he [she] does and avoids), reviews qualities of the sexual relationship, and broaches the issue of self-stimulation.

Remember: All discussions of sexuality should be appropriate to the clinical context and considerate of the deeply personal nature of the information.

Disclosure

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

Acknowledgement

The authors thank Sallie Foley, LMSW, Daniela Wittmann, LMSW, and the University of Michigan Sexual Health Certificate program for their assistance.

Psychiatrists often are required to obtain basic sexual information as part of a thorough clinical assessment.¹ Although a detailed sexual health assessment comprises multiple elaborate domains,² it’s important that mental health professionals remember a set of topics and related questions (Table) that can help investigate, diagnose, and treat sexual dysfunction, and contribute to a biopsychosocial formulation of your patient’s sexuality. The BIOTEACHERS mnemonic can remind you what to ask when taking a patient’s sexual history; it is not intended to be an alternative to a comprehensive sexual health evaluation.

Each letter stands for a component of the sexual assessment. The grouped letters of the acronym break down into different relevant areas that aid in remembering each category.

BIO

Background of the problem or the patient’s biophysical state

Identity

Orientation

BIO gathers basic medical information, then creates an opportunity to understand the patient’s gender identity. This step allows for nonjudgmental discussions about the patient’s sexual orientation.

TEACH

Thoughts of a sexual nature

Erotic desire or sexual interest

Arousal

Climax during sex

How often

TEACH incorporates a common chronology of sexual response and activity, starting with sexual thoughts, feelings of erotic desire, development of sexual arousal, ability and quality of a patient’s orgasm, as well as frequency of sexual activity.

ERS

Education

Repertoire or relationship dynamics

Self-stimulation

ERS comprises somewhat more complicated subjects: education (questions about a person’s sexual awareness and communication style); formal sexual knowledge; and health practices. These areas of questioning also normalize discussion of the patient’s sexual repertoire (what activities he [she] does and avoids), reviews qualities of the sexual relationship, and broaches the issue of self-stimulation.

Remember: All discussions of sexuality should be appropriate to the clinical context and considerate of the deeply personal nature of the information.

Disclosure

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

Acknowledgement

The authors thank Sallie Foley, LMSW, Daniela Wittmann, LMSW, and the University of Michigan Sexual Health Certificate program for their assistance.

In private practice, government, and (especially) academically affiliated settings, chart notations that are neither erroneous nor accurate but just imprecise are seen regularly. Academic supervisors may overlook these ambiguous notations by medical students and residents because of their regularity; others may be actively taught by supervisors who use ambiguous notations themselves.

In my experience, the most frequently seen imprecisions are in diagnoses of personality disorders: for example, the terms “clusters” and “deferred,” and the symptomatic overlap between antisocial personality disorder (APD) and substance abuse. Least helpful are qualifying phrases added to substance abuse diagnoses, along with an abundance of abbreviations. The latter occurs despite efforts by the U.S. Department of Veteran Affairs and other agencies to standardize acceptable lists of abbreviations. Many imprecisions could qualify for highlighting; here are 5 of the most unhelpful:

Clusters. Personality disorders are grouped into 3 “clusters,” according to similar characteristics (eg, Cluster A includes paranoid, schizoid, and schizotypal personality disorders and focuses on patients’ oddities and eccentricities). The need for identifying “clusters” could be debated, but a “cluster” is not a diagnosis. A psychiatric evaluation that notes “Cluster B traits” in lieu of a specific personality disorder is not informative, especially to a nonpsychiatric clinician. Which Cluster B traits apply? Is the patient unstable? Self-absorbed? Needy? Dramatic? Criminal? Assaultive?

In complicated or ambiguous cases, the diagnosis of a personality disorder not otherwise specified is appropriate, indicating that traits need to be clarified.

Deferred. This notation frequently is seen under axis II, and often is carried through the medical record for months or years. Psychiatrists are reluctant to diagnose a personality disorder because of the pejorative nature a diagnosis conveys. Nevertheless, by the second or third visit—after 2 or 3 hours of interview contact—it should be evident whether a personality disorder exists. If none does, “no diagnosis” should be documented. This notation can be adjusted if such evidence comes to light.

APD (or APD traits). This diagnosis often is made mistakenly when the root problem is in fact a substance abuse disorder. A multi-decade study of alcoholism and antisocial personality attributes in university students illustrated this phenomenon.¹

To be a successful substance abuser—that is, to satisfy the overwhelming urge to drink or use drugs—it’s essential to lie, cheat, and steal. Substance abusers might become belligerent when intoxicated. They might be arrested in bar fights, drive while intoxicated, and buy illegal substances. The result is incarceration, a common consequence of substance abuse and of APD. The latter diagnosis should be made only if the patient has exhibited a pattern of criminal behavior—often starting in adolescence—irrespective of substance abuse, such as breaking and entering, robbery, or assault with a deadly weapon.

Substance abusers often feel guilt and self-loathing for their “weakness,” and cannot gain control over their addiction; the APD patient, on the other hand, feels entitled to plunder and often justifies his (her) actions by attributing fault to the victim.

Keep in mind that many APD patients also are substance abusers; both diagnoses should be listed in the chart when that is the determination. Recognize that substance abuse and APD are distinct entities that should not be confused by the common denominator of having spent time in jail.

Early, late, full remission. These qualifiers often are appended to substance abuse disorders, but they do not convey useful information. How early is “early”? How late is “late”? Perhaps the most misleading term is “full” or “partial” remission,
because there is no clear definition of either.

If one is referring to length of time sober or a reduction in volume consumed, noting the date of the last use is more helpful—eg, “alcohol abuse in remission since summer of 2012.” If “partial” remission means the patient has reduced his intake, then that is not remission. The reduction can be specified—eg, “alcohol abuse, reduced to 1 or 2 beers per weekend.”

Abbreviations. Psychiatric evaluations should contain only standard, well-known medical shorthand (such as MSE for mental status exam). The military may be the biggest offender, devising acronyms and abbreviations for everything.

Two examples of abbreviations that I see in military psychiatric progress notes are AEB (“as evidenced by”) and LLGD (“linear, logical, and goal-directed”). Psychiatrists have a leg up on deciphering abbreviations in psychiatric notes; other providers might be compelled to resort to consultation. That wastes more time than typing out the words and results in frustration and lost productivity.

In private practice, government, and (especially) academically affiliated settings, chart notations that are neither erroneous nor accurate but just imprecise are seen regularly. Academic supervisors may overlook these ambiguous notations by medical students and residents because of their regularity; others may be actively taught by supervisors who use ambiguous notations themselves.

In my experience, the most frequently seen imprecisions are in diagnoses of personality disorders: for example, the terms “clusters” and “deferred,” and the symptomatic overlap between antisocial personality disorder (APD) and substance abuse. Least helpful are qualifying phrases added to substance abuse diagnoses, along with an abundance of abbreviations. The latter occurs despite efforts by the U.S. Department of Veteran Affairs and other agencies to standardize acceptable lists of abbreviations. Many imprecisions could qualify for highlighting; here are 5 of the most unhelpful:

Clusters. Personality disorders are grouped into 3 “clusters,” according to similar characteristics (eg, Cluster A includes paranoid, schizoid, and schizotypal personality disorders and focuses on patients’ oddities and eccentricities). The need for identifying “clusters” could be debated, but a “cluster” is not a diagnosis. A psychiatric evaluation that notes “Cluster B traits” in lieu of a specific personality disorder is not informative, especially to a nonpsychiatric clinician. Which Cluster B traits apply? Is the patient unstable? Self-absorbed? Needy? Dramatic? Criminal? Assaultive?

In complicated or ambiguous cases, the diagnosis of a personality disorder not otherwise specified is appropriate, indicating that traits need to be clarified.

Deferred. This notation frequently is seen under axis II, and often is carried through the medical record for months or years. Psychiatrists are reluctant to diagnose a personality disorder because of the pejorative nature a diagnosis conveys. Nevertheless, by the second or third visit—after 2 or 3 hours of interview contact—it should be evident whether a personality disorder exists. If none does, “no diagnosis” should be documented. This notation can be adjusted if such evidence comes to light.

APD (or APD traits). This diagnosis often is made mistakenly when the root problem is in fact a substance abuse disorder. A multi-decade study of alcoholism and antisocial personality attributes in university students illustrated this phenomenon.¹

To be a successful substance abuser—that is, to satisfy the overwhelming urge to drink or use drugs—it’s essential to lie, cheat, and steal. Substance abusers might become belligerent when intoxicated. They might be arrested in bar fights, drive while intoxicated, and buy illegal substances. The result is incarceration, a common consequence of substance abuse and of APD. The latter diagnosis should be made only if the patient has exhibited a pattern of criminal behavior—often starting in adolescence—irrespective of substance abuse, such as breaking and entering, robbery, or assault with a deadly weapon.

Substance abusers often feel guilt and self-loathing for their “weakness,” and cannot gain control over their addiction; the APD patient, on the other hand, feels entitled to plunder and often justifies his (her) actions by attributing fault to the victim.

Keep in mind that many APD patients also are substance abusers; both diagnoses should be listed in the chart when that is the determination. Recognize that substance abuse and APD are distinct entities that should not be confused by the common denominator of having spent time in jail.

Early, late, full remission. These qualifiers often are appended to substance abuse disorders, but they do not convey useful information. How early is “early”? How late is “late”? Perhaps the most misleading term is “full” or “partial” remission,
because there is no clear definition of either.

If one is referring to length of time sober or a reduction in volume consumed, noting the date of the last use is more helpful—eg, “alcohol abuse in remission since summer of 2012.” If “partial” remission means the patient has reduced his intake, then that is not remission. The reduction can be specified—eg, “alcohol abuse, reduced to 1 or 2 beers per weekend.”

Abbreviations. Psychiatric evaluations should contain only standard, well-known medical shorthand (such as MSE for mental status exam). The military may be the biggest offender, devising acronyms and abbreviations for everything.

Two examples of abbreviations that I see in military psychiatric progress notes are AEB (“as evidenced by”) and LLGD (“linear, logical, and goal-directed”). Psychiatrists have a leg up on deciphering abbreviations in psychiatric notes; other providers might be compelled to resort to consultation. That wastes more time than typing out the words and results in frustration and lost productivity.

In private practice, government, and (especially) academically affiliated settings, chart notations that are neither erroneous nor accurate but just imprecise are seen regularly. Academic supervisors may overlook these ambiguous notations by medical students and residents because of their regularity; others may be actively taught by supervisors who use ambiguous notations themselves.

In my experience, the most frequently seen imprecisions are in diagnoses of personality disorders: for example, the terms “clusters” and “deferred,” and the symptomatic overlap between antisocial personality disorder (APD) and substance abuse. Least helpful are qualifying phrases added to substance abuse diagnoses, along with an abundance of abbreviations. The latter occurs despite efforts by the U.S. Department of Veteran Affairs and other agencies to standardize acceptable lists of abbreviations. Many imprecisions could qualify for highlighting; here are 5 of the most unhelpful:

Clusters. Personality disorders are grouped into 3 “clusters,” according to similar characteristics (eg, Cluster A includes paranoid, schizoid, and schizotypal personality disorders and focuses on patients’ oddities and eccentricities). The need for identifying “clusters” could be debated, but a “cluster” is not a diagnosis. A psychiatric evaluation that notes “Cluster B traits” in lieu of a specific personality disorder is not informative, especially to a nonpsychiatric clinician. Which Cluster B traits apply? Is the patient unstable? Self-absorbed? Needy? Dramatic? Criminal? Assaultive?

In complicated or ambiguous cases, the diagnosis of a personality disorder not otherwise specified is appropriate, indicating that traits need to be clarified.

Deferred. This notation frequently is seen under axis II, and often is carried through the medical record for months or years. Psychiatrists are reluctant to diagnose a personality disorder because of the pejorative nature a diagnosis conveys. Nevertheless, by the second or third visit—after 2 or 3 hours of interview contact—it should be evident whether a personality disorder exists. If none does, “no diagnosis” should be documented. This notation can be adjusted if such evidence comes to light.

APD (or APD traits). This diagnosis often is made mistakenly when the root problem is in fact a substance abuse disorder. A multi-decade study of alcoholism and antisocial personality attributes in university students illustrated this phenomenon.¹

To be a successful substance abuser—that is, to satisfy the overwhelming urge to drink or use drugs—it’s essential to lie, cheat, and steal. Substance abusers might become belligerent when intoxicated. They might be arrested in bar fights, drive while intoxicated, and buy illegal substances. The result is incarceration, a common consequence of substance abuse and of APD. The latter diagnosis should be made only if the patient has exhibited a pattern of criminal behavior—often starting in adolescence—irrespective of substance abuse, such as breaking and entering, robbery, or assault with a deadly weapon.

Substance abusers often feel guilt and self-loathing for their “weakness,” and cannot gain control over their addiction; the APD patient, on the other hand, feels entitled to plunder and often justifies his (her) actions by attributing fault to the victim.

Keep in mind that many APD patients also are substance abusers; both diagnoses should be listed in the chart when that is the determination. Recognize that substance abuse and APD are distinct entities that should not be confused by the common denominator of having spent time in jail.

Early, late, full remission. These qualifiers often are appended to substance abuse disorders, but they do not convey useful information. How early is “early”? How late is “late”? Perhaps the most misleading term is “full” or “partial” remission,
because there is no clear definition of either.

If one is referring to length of time sober or a reduction in volume consumed, noting the date of the last use is more helpful—eg, “alcohol abuse in remission since summer of 2012.” If “partial” remission means the patient has reduced his intake, then that is not remission. The reduction can be specified—eg, “alcohol abuse, reduced to 1 or 2 beers per weekend.”

Abbreviations. Psychiatric evaluations should contain only standard, well-known medical shorthand (such as MSE for mental status exam). The military may be the biggest offender, devising acronyms and abbreviations for everything.

Two examples of abbreviations that I see in military psychiatric progress notes are AEB (“as evidenced by”) and LLGD (“linear, logical, and goal-directed”). Psychiatrists have a leg up on deciphering abbreviations in psychiatric notes; other providers might be compelled to resort to consultation. That wastes more time than typing out the words and results in frustration and lost productivity.