Current Psychiatry

Psychological testing can help you clear up questions about psychiatric differential diagnosis and treatment planning, but only if your patients make and keep appointments for the tests you recommend.

Based on my observations as a psychologist who administers these tests, factors that undermine patient follow-through include patient or family resistance, prohibitive managed care policies, and limited availability of psychologists who perform testing. I suggest 7 practices that may enhance your patients’ adherence.

Familiarize yourself with best practices in psychological testing—including indications and contraindications—by consulting standard references,¹ taking a continuing education overview course, or attending in-service training with local psychologists.

Encourage your patient to find out if his health insurance covers the recommended testing. For example, few—if any—managed care plans cover testing for learning disorders, and some will not reimburse for testing when the primary rule-out diagnosis is attention-deficit/hyperactivity disorder. Plans may be more likely to cover testing when you frame the referral in terms of a differential diagnosis or need for clarity regarding treatment planning.

Maintain an updated list of well-regarded, established clinicians experienced in psychological testing. Children and adolescents should be evaluated by psychologists specializing in pediatric patients, and elderly adults should be seen by clinicians with experience in geriatric neuropsychology.

Educate patients about your reasons for the referral. Refer to earlier discussions when you and the patient were in broad agreement. You might say, for example, “You have wondered whether your forgetfulness is related to depression. Testing can help clarify this issue for us and move treatment forward.”

Remain empathic to characterologic resistance to psychological consultation. Patients with borderline personality disorder might experience a recommendation for testing as abandonment or coerced separation, narcissistic patients may fear humiliation or shame, and obsessive patients may become anxious about failing to “measure up” to some idealized standard of test performance.

Consult with the testing psychologist when you have questions about the clinical value of a formal referral or insurance coverage. Facilitate patient compliance by calling or forwarding the referral to the testing psychologist, who then can write a letter reminding the patient about the referral.

Provide reading materials about psychological testing in your waiting room to help demystify these procedures and encourage patient interest and adherence.

Psychological testing can help you clear up questions about psychiatric differential diagnosis and treatment planning, but only if your patients make and keep appointments for the tests you recommend.

Based on my observations as a psychologist who administers these tests, factors that undermine patient follow-through include patient or family resistance, prohibitive managed care policies, and limited availability of psychologists who perform testing. I suggest 7 practices that may enhance your patients’ adherence.

Familiarize yourself with best practices in psychological testing—including indications and contraindications—by consulting standard references,¹ taking a continuing education overview course, or attending in-service training with local psychologists.

Encourage your patient to find out if his health insurance covers the recommended testing. For example, few—if any—managed care plans cover testing for learning disorders, and some will not reimburse for testing when the primary rule-out diagnosis is attention-deficit/hyperactivity disorder. Plans may be more likely to cover testing when you frame the referral in terms of a differential diagnosis or need for clarity regarding treatment planning.

Maintain an updated list of well-regarded, established clinicians experienced in psychological testing. Children and adolescents should be evaluated by psychologists specializing in pediatric patients, and elderly adults should be seen by clinicians with experience in geriatric neuropsychology.

Educate patients about your reasons for the referral. Refer to earlier discussions when you and the patient were in broad agreement. You might say, for example, “You have wondered whether your forgetfulness is related to depression. Testing can help clarify this issue for us and move treatment forward.”

Remain empathic to characterologic resistance to psychological consultation. Patients with borderline personality disorder might experience a recommendation for testing as abandonment or coerced separation, narcissistic patients may fear humiliation or shame, and obsessive patients may become anxious about failing to “measure up” to some idealized standard of test performance.

Consult with the testing psychologist when you have questions about the clinical value of a formal referral or insurance coverage. Facilitate patient compliance by calling or forwarding the referral to the testing psychologist, who then can write a letter reminding the patient about the referral.

Provide reading materials about psychological testing in your waiting room to help demystify these procedures and encourage patient interest and adherence.

Psychological testing can help you clear up questions about psychiatric differential diagnosis and treatment planning, but only if your patients make and keep appointments for the tests you recommend.

Based on my observations as a psychologist who administers these tests, factors that undermine patient follow-through include patient or family resistance, prohibitive managed care policies, and limited availability of psychologists who perform testing. I suggest 7 practices that may enhance your patients’ adherence.

Familiarize yourself with best practices in psychological testing—including indications and contraindications—by consulting standard references,¹ taking a continuing education overview course, or attending in-service training with local psychologists.

Encourage your patient to find out if his health insurance covers the recommended testing. For example, few—if any—managed care plans cover testing for learning disorders, and some will not reimburse for testing when the primary rule-out diagnosis is attention-deficit/hyperactivity disorder. Plans may be more likely to cover testing when you frame the referral in terms of a differential diagnosis or need for clarity regarding treatment planning.

Maintain an updated list of well-regarded, established clinicians experienced in psychological testing. Children and adolescents should be evaluated by psychologists specializing in pediatric patients, and elderly adults should be seen by clinicians with experience in geriatric neuropsychology.

Educate patients about your reasons for the referral. Refer to earlier discussions when you and the patient were in broad agreement. You might say, for example, “You have wondered whether your forgetfulness is related to depression. Testing can help clarify this issue for us and move treatment forward.”

Remain empathic to characterologic resistance to psychological consultation. Patients with borderline personality disorder might experience a recommendation for testing as abandonment or coerced separation, narcissistic patients may fear humiliation or shame, and obsessive patients may become anxious about failing to “measure up” to some idealized standard of test performance.

Consult with the testing psychologist when you have questions about the clinical value of a formal referral or insurance coverage. Facilitate patient compliance by calling or forwarding the referral to the testing psychologist, who then can write a letter reminding the patient about the referral.

Provide reading materials about psychological testing in your waiting room to help demystify these procedures and encourage patient interest and adherence.

Principal Source: Roberts LM, Pattison H, Roalfe A, et al. Is subclinical thyroid dysfunction in the elderly associated with depression or cognitive dysfunction? Ann Intern Med. 2006;145:573-581.—Discussant: Y Pritham Raj, MD

Thyroid dysfunction enters the differential diagnosis for most mood, anxiety, thought, and cognitive disorders. Because more than one-half of the estimated 27 million Americans with hyperthyroidism or hypothyroidism are undiagnosed,¹ the American Thyroid Association recommends universal screening for thyroid dysfunction after age 35, with a recheck every 5 years. Although some clinicians feel this recommendation is excessive, strategic screening with a thyroid-stimulating hormone (TSH) test is important for patients with psychiatric illnesses.

If a patient’s TSH is abnormal, repeating the test while measuring the free thyroxine (T4) and in most cases the antithyroid peroxidase antibody (anti-TPO) has good clinical value. Anti-TPO antibodies are a useful biomarker for autoimmune thyroid disease, such as Hashimoto’s thyroiditis or Graves’ disease. If laboratory findings suggest the hypothyroid spectrum, a fasting lipid profile may help determine risk of adverse cardiovascular outcomes.

Therapy

Symptoms of hypothyroidism—indicated by an elevated TSH (usually >20 mU/L) and low T4—overlap with psychiatric illness (Table) but are easy to treat. Psychiatrists who are accustomed to calculating weight-based dosing of medications such as lithium and valproic acid may have little difficulty initiating levothyroxine replacement (typically 1.6 mcg/kg/day) for patients with overt hypothyroidism. Treating hyperthyroidism (low TSH and high T4) can be more complex and generally is left to an internist or endocrinologist. But how should you treat subclinical thyroid dysfunction?

Table

Hypothyroidism symptoms that indicate treatment

Treat or wait?

Subclinical hypothyroidism (SH)—in which T4 is normal—usually is a laboratory diagnosis defined in a spectrum:

• TSH of 4.5 to 10 mU/L is mild SH (80% of cases)
• TSH of 10 to 20 mU/L is more severe SH.

SH is a well-established risk factor for depression. One study found a nearly 3-fold higher lifetime prevalence of depression in young and middle-aged women with SH.² To the practicing psychiatrist, these results may sound like a mandate to treat all patients with SH—particularly those with depression. Consider, however, that in a prospective observational study the TSH of >37% of patients with SH returned to normal with observation alone.³ In fact, <27% of patients with SH went on to develop overt hypothyroidism during the study period, on average within 31.7 months.

A second study that would argue against treating patients with mild SH noted decreased cardiovascular and noncardio-vascular mortality among elderly patients with elevated TSH,⁴ implying that SH may be protective compared with the euthyroid state, at least among octogenarians.

Still, do mood, anxiety, or cognitive symptoms in SH patients merit earlier, more aggressive treatment? This question was addressed by a recent cross-sectional study that demonstrated no correlation between mood and SH.⁵ Although statistically significant associations were seen among anxiety, cognition, and elevated TSH, the magnitude of the associations lacked clinical relevance. This study was designed to further assess an earlier inconclusive review.⁶

Ultimately, treating SH—although easy to do—may have little impact on your patient’s overall mood and cognition until TSH is ≥10 mU/L.

Drug brand names

• Levothyroxine • Levoxyl, Synthroid
• Lithium • various
• Valproic acid • Depakene

Disclosure

Dr. Raj is a consultant to Alpharma and a speaker for AstraZeneca.

Principal Source: Roberts LM, Pattison H, Roalfe A, et al. Is subclinical thyroid dysfunction in the elderly associated with depression or cognitive dysfunction? Ann Intern Med. 2006;145:573-581.—Discussant: Y Pritham Raj, MD

Thyroid dysfunction enters the differential diagnosis for most mood, anxiety, thought, and cognitive disorders. Because more than one-half of the estimated 27 million Americans with hyperthyroidism or hypothyroidism are undiagnosed,¹ the American Thyroid Association recommends universal screening for thyroid dysfunction after age 35, with a recheck every 5 years. Although some clinicians feel this recommendation is excessive, strategic screening with a thyroid-stimulating hormone (TSH) test is important for patients with psychiatric illnesses.

If a patient’s TSH is abnormal, repeating the test while measuring the free thyroxine (T4) and in most cases the antithyroid peroxidase antibody (anti-TPO) has good clinical value. Anti-TPO antibodies are a useful biomarker for autoimmune thyroid disease, such as Hashimoto’s thyroiditis or Graves’ disease. If laboratory findings suggest the hypothyroid spectrum, a fasting lipid profile may help determine risk of adverse cardiovascular outcomes.

Therapy

Symptoms of hypothyroidism—indicated by an elevated TSH (usually >20 mU/L) and low T4—overlap with psychiatric illness (Table) but are easy to treat. Psychiatrists who are accustomed to calculating weight-based dosing of medications such as lithium and valproic acid may have little difficulty initiating levothyroxine replacement (typically 1.6 mcg/kg/day) for patients with overt hypothyroidism. Treating hyperthyroidism (low TSH and high T4) can be more complex and generally is left to an internist or endocrinologist. But how should you treat subclinical thyroid dysfunction?

Table

Hypothyroidism symptoms that indicate treatment

Treat or wait?

Subclinical hypothyroidism (SH)—in which T4 is normal—usually is a laboratory diagnosis defined in a spectrum:

• TSH of 4.5 to 10 mU/L is mild SH (80% of cases)
• TSH of 10 to 20 mU/L is more severe SH.

SH is a well-established risk factor for depression. One study found a nearly 3-fold higher lifetime prevalence of depression in young and middle-aged women with SH.² To the practicing psychiatrist, these results may sound like a mandate to treat all patients with SH—particularly those with depression. Consider, however, that in a prospective observational study the TSH of >37% of patients with SH returned to normal with observation alone.³ In fact, <27% of patients with SH went on to develop overt hypothyroidism during the study period, on average within 31.7 months.

A second study that would argue against treating patients with mild SH noted decreased cardiovascular and noncardio-vascular mortality among elderly patients with elevated TSH,⁴ implying that SH may be protective compared with the euthyroid state, at least among octogenarians.

Still, do mood, anxiety, or cognitive symptoms in SH patients merit earlier, more aggressive treatment? This question was addressed by a recent cross-sectional study that demonstrated no correlation between mood and SH.⁵ Although statistically significant associations were seen among anxiety, cognition, and elevated TSH, the magnitude of the associations lacked clinical relevance. This study was designed to further assess an earlier inconclusive review.⁶

Ultimately, treating SH—although easy to do—may have little impact on your patient’s overall mood and cognition until TSH is ≥10 mU/L.

Drug brand names

• Levothyroxine • Levoxyl, Synthroid
• Lithium • various
• Valproic acid • Depakene

Disclosure

Dr. Raj is a consultant to Alpharma and a speaker for AstraZeneca.

Principal Source: Roberts LM, Pattison H, Roalfe A, et al. Is subclinical thyroid dysfunction in the elderly associated with depression or cognitive dysfunction? Ann Intern Med. 2006;145:573-581.—Discussant: Y Pritham Raj, MD

Thyroid dysfunction enters the differential diagnosis for most mood, anxiety, thought, and cognitive disorders. Because more than one-half of the estimated 27 million Americans with hyperthyroidism or hypothyroidism are undiagnosed,¹ the American Thyroid Association recommends universal screening for thyroid dysfunction after age 35, with a recheck every 5 years. Although some clinicians feel this recommendation is excessive, strategic screening with a thyroid-stimulating hormone (TSH) test is important for patients with psychiatric illnesses.

If a patient’s TSH is abnormal, repeating the test while measuring the free thyroxine (T4) and in most cases the antithyroid peroxidase antibody (anti-TPO) has good clinical value. Anti-TPO antibodies are a useful biomarker for autoimmune thyroid disease, such as Hashimoto’s thyroiditis or Graves’ disease. If laboratory findings suggest the hypothyroid spectrum, a fasting lipid profile may help determine risk of adverse cardiovascular outcomes.

Therapy

Symptoms of hypothyroidism—indicated by an elevated TSH (usually >20 mU/L) and low T4—overlap with psychiatric illness (Table) but are easy to treat. Psychiatrists who are accustomed to calculating weight-based dosing of medications such as lithium and valproic acid may have little difficulty initiating levothyroxine replacement (typically 1.6 mcg/kg/day) for patients with overt hypothyroidism. Treating hyperthyroidism (low TSH and high T4) can be more complex and generally is left to an internist or endocrinologist. But how should you treat subclinical thyroid dysfunction?

Table

Hypothyroidism symptoms that indicate treatment

Treat or wait?

Subclinical hypothyroidism (SH)—in which T4 is normal—usually is a laboratory diagnosis defined in a spectrum:

• TSH of 4.5 to 10 mU/L is mild SH (80% of cases)
• TSH of 10 to 20 mU/L is more severe SH.

SH is a well-established risk factor for depression. One study found a nearly 3-fold higher lifetime prevalence of depression in young and middle-aged women with SH.² To the practicing psychiatrist, these results may sound like a mandate to treat all patients with SH—particularly those with depression. Consider, however, that in a prospective observational study the TSH of >37% of patients with SH returned to normal with observation alone.³ In fact, <27% of patients with SH went on to develop overt hypothyroidism during the study period, on average within 31.7 months.

A second study that would argue against treating patients with mild SH noted decreased cardiovascular and noncardio-vascular mortality among elderly patients with elevated TSH,⁴ implying that SH may be protective compared with the euthyroid state, at least among octogenarians.

Still, do mood, anxiety, or cognitive symptoms in SH patients merit earlier, more aggressive treatment? This question was addressed by a recent cross-sectional study that demonstrated no correlation between mood and SH.⁵ Although statistically significant associations were seen among anxiety, cognition, and elevated TSH, the magnitude of the associations lacked clinical relevance. This study was designed to further assess an earlier inconclusive review.⁶

Ultimately, treating SH—although easy to do—may have little impact on your patient’s overall mood and cognition until TSH is ≥10 mU/L.

Drug brand names

• Levothyroxine • Levoxyl, Synthroid
• Lithium • various
• Valproic acid • Depakene

Disclosure

Dr. Raj is a consultant to Alpharma and a speaker for AstraZeneca.

With advances in the understanding of stuttering and development of pharmacologic therapies,¹ modifications to the classification and treatment of this disorder are indicated. Research has shown that stuttering improves with pharmacologic therapy, and neurologic abnormalities have been identified.²

With DSM-V on the horizon, stuttering classification should be expanded to include an additional criterion of avoidance and/or anxiety around speaking situations related to stuttering.³ By adding this criterion, we recognize and can offer treatment to patients who do not have marked disturbances influency but experience avoidance and/or anxiety around certain feared words or situations.

We also recommend distinguishing childhood-onset, developmental stuttering—by far the predominant presentation—on Axis I separate from the adult-onset forms. Stuttering symptoms acquired as an adult—usually through neurologic injury⁴—are better coded under Axis III. Stuttering symptoms also rarely may be manifestations of conversion or malingering, and in cases such as this are better classified under these conditions.

As the understanding of stuttering leads toward a more physiologic etiology, clarification of DSM-V criteria will ensure that millions of individuals who stutter will have greater access to comprehensive care, including emerging pharmacologic therapies.

Gerald A. Maguire, MD, DFAPA

Victoria Huang, BA

C. Scott Huffman, MA
Department of psychiatry
School of medicine
University of California, Irvine

With advances in the understanding of stuttering and development of pharmacologic therapies,¹ modifications to the classification and treatment of this disorder are indicated. Research has shown that stuttering improves with pharmacologic therapy, and neurologic abnormalities have been identified.²

With DSM-V on the horizon, stuttering classification should be expanded to include an additional criterion of avoidance and/or anxiety around speaking situations related to stuttering.³ By adding this criterion, we recognize and can offer treatment to patients who do not have marked disturbances influency but experience avoidance and/or anxiety around certain feared words or situations.

We also recommend distinguishing childhood-onset, developmental stuttering—by far the predominant presentation—on Axis I separate from the adult-onset forms. Stuttering symptoms acquired as an adult—usually through neurologic injury⁴—are better coded under Axis III. Stuttering symptoms also rarely may be manifestations of conversion or malingering, and in cases such as this are better classified under these conditions.

As the understanding of stuttering leads toward a more physiologic etiology, clarification of DSM-V criteria will ensure that millions of individuals who stutter will have greater access to comprehensive care, including emerging pharmacologic therapies.

Gerald A. Maguire, MD, DFAPA

Victoria Huang, BA

C. Scott Huffman, MA
Department of psychiatry
School of medicine
University of California, Irvine

With advances in the understanding of stuttering and development of pharmacologic therapies,¹ modifications to the classification and treatment of this disorder are indicated. Research has shown that stuttering improves with pharmacologic therapy, and neurologic abnormalities have been identified.²

With DSM-V on the horizon, stuttering classification should be expanded to include an additional criterion of avoidance and/or anxiety around speaking situations related to stuttering.³ By adding this criterion, we recognize and can offer treatment to patients who do not have marked disturbances influency but experience avoidance and/or anxiety around certain feared words or situations.

We also recommend distinguishing childhood-onset, developmental stuttering—by far the predominant presentation—on Axis I separate from the adult-onset forms. Stuttering symptoms acquired as an adult—usually through neurologic injury⁴—are better coded under Axis III. Stuttering symptoms also rarely may be manifestations of conversion or malingering, and in cases such as this are better classified under these conditions.

As the understanding of stuttering leads toward a more physiologic etiology, clarification of DSM-V criteria will ensure that millions of individuals who stutter will have greater access to comprehensive care, including emerging pharmacologic therapies.

Gerald A. Maguire, MD, DFAPA

Victoria Huang, BA

C. Scott Huffman, MA
Department of psychiatry
School of medicine
University of California, Irvine

Dr. Henry Nasrallah’s editorial, “Should psychiatry list hubris in DSM-V?” (From the Editor, Current Psychiatry, December 2008), touches upon an important subject related to psychiatry’s place among medical specialties and the respect—or disrespect—our field gets. I shudder to think that “Excessive Nose Picking” could be listed in DSM-V with a fancy name such as “Rhinotelexomania” or “Excessive Nail Biting” with a sexy label such as “Onychophagia.” Psychiatry has been under attack for being pseudoscientific and not worthy of the respect that other medical specialties command. There is no need to add insult to injury.

Dissociative identity disorder (DID) is another controversial diagnosis that may have been very appealing to Hollywood moviemakers but does the field, patients, and their families a great disservice. Although DID is listed in DSM-IV-TR, criterion A—the presence of 2 or more distinct identities or personality states, each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self—is a definition rather than a useful guideline. Who, when, and how does this “presence” become present? What is the clinician’s role in the face of the first-person authority?

In other medical specialties, it is recommended—rather strongly encouraged—that the practitioner constantly challenge his or her basic assumptions about a possible diagnosis through a methodic process of inclusion, exclusion, and hypothesis testing. Gullibility, lack of scrutiny, lack of skepticism, and not having a high index of suspicion are signs of poor clinical practice. To use Donald Davidson’s words, the skeptic’s attempt to investigate dissociative phenomena—especially DID—is bound to break on the rocks of the first-person authority.¹

The antipsychiatry movement, despite its excesses, helped psychiatry do some introspection and look at its own excesses. It helped the field evolve from pseudoscientific psychoanalytic traditions to the evidence-based practices of today. The polarizing DID diagnosis is not only a difference of opinion between proponents and opponents, nor is it a harmless abstract controversy or just about “opinion” or “belief.” Patients and families are harmed by the diagnosis and the practice of its proponents.

For economy, I refer readers to the 2-part, 2004 review of DID in the Canadian Journal of Psychiatry, which came to following conclusions:

• there was no proof that DID results from childhood trauma
  
• DID could not be reliably diagnosed
  
• DID cases in children were almost never reported, and
  
• consistent evidence of blatant iatro genesis appeared in the practice of DID proponents.^2,3
  

The DID controversy is not a symmetrical argument of personal opinion vs another or 1 dogma vs another. Rather, it is like the Celestial Teapot parable of Bertrand Russell. An almost impossible belief persists because it can’t be proven wrong.

Numan Gharaibeh, MD
Principal psychiatrist
Western Connecticut Mental Health Network
Danbury, CT

Dr. Henry Nasrallah’s editorial, “Should psychiatry list hubris in DSM-V?” (From the Editor, Current Psychiatry, December 2008), touches upon an important subject related to psychiatry’s place among medical specialties and the respect—or disrespect—our field gets. I shudder to think that “Excessive Nose Picking” could be listed in DSM-V with a fancy name such as “Rhinotelexomania” or “Excessive Nail Biting” with a sexy label such as “Onychophagia.” Psychiatry has been under attack for being pseudoscientific and not worthy of the respect that other medical specialties command. There is no need to add insult to injury.

Dissociative identity disorder (DID) is another controversial diagnosis that may have been very appealing to Hollywood moviemakers but does the field, patients, and their families a great disservice. Although DID is listed in DSM-IV-TR, criterion A—the presence of 2 or more distinct identities or personality states, each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self—is a definition rather than a useful guideline. Who, when, and how does this “presence” become present? What is the clinician’s role in the face of the first-person authority?

In other medical specialties, it is recommended—rather strongly encouraged—that the practitioner constantly challenge his or her basic assumptions about a possible diagnosis through a methodic process of inclusion, exclusion, and hypothesis testing. Gullibility, lack of scrutiny, lack of skepticism, and not having a high index of suspicion are signs of poor clinical practice. To use Donald Davidson’s words, the skeptic’s attempt to investigate dissociative phenomena—especially DID—is bound to break on the rocks of the first-person authority.¹

The antipsychiatry movement, despite its excesses, helped psychiatry do some introspection and look at its own excesses. It helped the field evolve from pseudoscientific psychoanalytic traditions to the evidence-based practices of today. The polarizing DID diagnosis is not only a difference of opinion between proponents and opponents, nor is it a harmless abstract controversy or just about “opinion” or “belief.” Patients and families are harmed by the diagnosis and the practice of its proponents.

For economy, I refer readers to the 2-part, 2004 review of DID in the Canadian Journal of Psychiatry, which came to following conclusions:

• there was no proof that DID results from childhood trauma
  
• DID could not be reliably diagnosed
  
• DID cases in children were almost never reported, and
  
• consistent evidence of blatant iatro genesis appeared in the practice of DID proponents.^2,3
  

The DID controversy is not a symmetrical argument of personal opinion vs another or 1 dogma vs another. Rather, it is like the Celestial Teapot parable of Bertrand Russell. An almost impossible belief persists because it can’t be proven wrong.

Numan Gharaibeh, MD
Principal psychiatrist
Western Connecticut Mental Health Network
Danbury, CT

Dr. Henry Nasrallah’s editorial, “Should psychiatry list hubris in DSM-V?” (From the Editor, Current Psychiatry, December 2008), touches upon an important subject related to psychiatry’s place among medical specialties and the respect—or disrespect—our field gets. I shudder to think that “Excessive Nose Picking” could be listed in DSM-V with a fancy name such as “Rhinotelexomania” or “Excessive Nail Biting” with a sexy label such as “Onychophagia.” Psychiatry has been under attack for being pseudoscientific and not worthy of the respect that other medical specialties command. There is no need to add insult to injury.

Dissociative identity disorder (DID) is another controversial diagnosis that may have been very appealing to Hollywood moviemakers but does the field, patients, and their families a great disservice. Although DID is listed in DSM-IV-TR, criterion A—the presence of 2 or more distinct identities or personality states, each with its own relatively enduring pattern of perceiving, relating to, and thinking about the environment and self—is a definition rather than a useful guideline. Who, when, and how does this “presence” become present? What is the clinician’s role in the face of the first-person authority?

In other medical specialties, it is recommended—rather strongly encouraged—that the practitioner constantly challenge his or her basic assumptions about a possible diagnosis through a methodic process of inclusion, exclusion, and hypothesis testing. Gullibility, lack of scrutiny, lack of skepticism, and not having a high index of suspicion are signs of poor clinical practice. To use Donald Davidson’s words, the skeptic’s attempt to investigate dissociative phenomena—especially DID—is bound to break on the rocks of the first-person authority.¹

The antipsychiatry movement, despite its excesses, helped psychiatry do some introspection and look at its own excesses. It helped the field evolve from pseudoscientific psychoanalytic traditions to the evidence-based practices of today. The polarizing DID diagnosis is not only a difference of opinion between proponents and opponents, nor is it a harmless abstract controversy or just about “opinion” or “belief.” Patients and families are harmed by the diagnosis and the practice of its proponents.

For economy, I refer readers to the 2-part, 2004 review of DID in the Canadian Journal of Psychiatry, which came to following conclusions:

• there was no proof that DID results from childhood trauma
  
• DID could not be reliably diagnosed
  
• DID cases in children were almost never reported, and
  
• consistent evidence of blatant iatro genesis appeared in the practice of DID proponents.^2,3
  

The DID controversy is not a symmetrical argument of personal opinion vs another or 1 dogma vs another. Rather, it is like the Celestial Teapot parable of Bertrand Russell. An almost impossible belief persists because it can’t be proven wrong.

Numan Gharaibeh, MD
Principal psychiatrist
Western Connecticut Mental Health Network
Danbury, CT

In “Driving with dementia: How to assess safety behind the wheel” (Current Psychiatry, December 2008) the authors provided helpful suggestions on how to implement driving restrictions. The algorithm, however, relies too heavily on costly driving evaluations at the expense of clinical judgment.

Although the American Medical Association and the National Highway Traffic Safety Administration may not feel that a dementia diagnosis is sufficient to restrict driving, this opinion is not unanimous. In 2000 the American Academy of Neurology issued a practice parameter standard that patients with a Clinical Dementia Rating of 1 should not drive. This rating is equivalent to probable Alzheimer’s disease (AD) with mild impairment.¹

Furthermore, although the clockdrawing test, visuospatial copying tasks, and trail making test B might not have absolute utility in identifying those at risk of driving impairment, measures of attention and visuospatial skills have been found to correlate with on-road driving performance.²

Given that visuospatial testing evaluates an area of cognition that is necessary for driving and impairment of visuospatial functioning in AD is significantly correlated with anosognosia,³ a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone.

Ben Schoenbachler, MD
Assistant professor
Director, Memory Disorders Program
University of Louisville
Louisville, KY

References

1. Dubinsky RM, Stein AC, Lyons K. Practice parameter: risk of driving and Alzheimer’s disease (an evidence-based review): report of the quality standards subcommittee of the American Academy of Neurology. Neurology. 2000;54(12):2205-2211.

2. Reger MA, Welsh RK, Watson GS, et al. The relationship between neuropsychological functioning and driving ability in dementia: a meta-analysis. Neuropsychology. 2004;18(1):85-93.

3. Auchus AP, Goldstein FC, Green J, et al. Unawareness of cognitive impairments in Alzheimer’s disease. Neuropsychiatry Neuropsychol Behav Neurol. 1994;7:25-29.

The authors respond

We agree with Dr. Schoenbachler’s comment that “a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone,” and certainly do not wish readers to disregard the results of patient history, examination, or cognitive evaluation. Indeed, visuospatial testing has been shown to have moderate correlations with driving in the review that Dr. Schoenbachler cites. However, a recent systematic review¹ highlighted the inconsistency of this evidence and reported that only 6 of 11 analyses of the relationship between visuospatial skills and driving showed significant associations.

Although our article emphasized the limitations of evidence on the predictive value of the clinical evaluation of driving fitness, we encourage physicians to use their clinical judgment to decide when a patient’s cognitive deficits or behavioral symptoms preclude safe driving. The algorithm emphasizes the role of on-road testing in cases when the clinician is uncertain. When impairment is so severe or obvious that the patient clearly is unsafe to drive, in-depth testing is not needed. For less severe cases, clinicians will need to determine if they have enough information to decide or if an on-road assessment is warranted.

Mark Rapoport, MD

Carla Zucchero Sarracini, BA

Nathan Herrmann, MD
Department of psychiatry
University of Toronto
Sunnybrook Health Sciences Centre
Toronto, Ontario, Canada

Frank Molnar, MD
University of Ottawa
Ottawa Health Research Institute
Ottawa, Ontario, Canada

In “Driving with dementia: How to assess safety behind the wheel” (Current Psychiatry, December 2008) the authors provided helpful suggestions on how to implement driving restrictions. The algorithm, however, relies too heavily on costly driving evaluations at the expense of clinical judgment.

Although the American Medical Association and the National Highway Traffic Safety Administration may not feel that a dementia diagnosis is sufficient to restrict driving, this opinion is not unanimous. In 2000 the American Academy of Neurology issued a practice parameter standard that patients with a Clinical Dementia Rating of 1 should not drive. This rating is equivalent to probable Alzheimer’s disease (AD) with mild impairment.¹

Furthermore, although the clockdrawing test, visuospatial copying tasks, and trail making test B might not have absolute utility in identifying those at risk of driving impairment, measures of attention and visuospatial skills have been found to correlate with on-road driving performance.²

Given that visuospatial testing evaluates an area of cognition that is necessary for driving and impairment of visuospatial functioning in AD is significantly correlated with anosognosia,³ a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone.

Ben Schoenbachler, MD
Assistant professor
Director, Memory Disorders Program
University of Louisville
Louisville, KY

References

1. Dubinsky RM, Stein AC, Lyons K. Practice parameter: risk of driving and Alzheimer’s disease (an evidence-based review): report of the quality standards subcommittee of the American Academy of Neurology. Neurology. 2000;54(12):2205-2211.

2. Reger MA, Welsh RK, Watson GS, et al. The relationship between neuropsychological functioning and driving ability in dementia: a meta-analysis. Neuropsychology. 2004;18(1):85-93.

3. Auchus AP, Goldstein FC, Green J, et al. Unawareness of cognitive impairments in Alzheimer’s disease. Neuropsychiatry Neuropsychol Behav Neurol. 1994;7:25-29.

The authors respond

We agree with Dr. Schoenbachler’s comment that “a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone,” and certainly do not wish readers to disregard the results of patient history, examination, or cognitive evaluation. Indeed, visuospatial testing has been shown to have moderate correlations with driving in the review that Dr. Schoenbachler cites. However, a recent systematic review¹ highlighted the inconsistency of this evidence and reported that only 6 of 11 analyses of the relationship between visuospatial skills and driving showed significant associations.

Although our article emphasized the limitations of evidence on the predictive value of the clinical evaluation of driving fitness, we encourage physicians to use their clinical judgment to decide when a patient’s cognitive deficits or behavioral symptoms preclude safe driving. The algorithm emphasizes the role of on-road testing in cases when the clinician is uncertain. When impairment is so severe or obvious that the patient clearly is unsafe to drive, in-depth testing is not needed. For less severe cases, clinicians will need to determine if they have enough information to decide or if an on-road assessment is warranted.

Mark Rapoport, MD

Carla Zucchero Sarracini, BA

Nathan Herrmann, MD
Department of psychiatry
University of Toronto
Sunnybrook Health Sciences Centre
Toronto, Ontario, Canada

Frank Molnar, MD
University of Ottawa
Ottawa Health Research Institute
Ottawa, Ontario, Canada

In “Driving with dementia: How to assess safety behind the wheel” (Current Psychiatry, December 2008) the authors provided helpful suggestions on how to implement driving restrictions. The algorithm, however, relies too heavily on costly driving evaluations at the expense of clinical judgment.

Although the American Medical Association and the National Highway Traffic Safety Administration may not feel that a dementia diagnosis is sufficient to restrict driving, this opinion is not unanimous. In 2000 the American Academy of Neurology issued a practice parameter standard that patients with a Clinical Dementia Rating of 1 should not drive. This rating is equivalent to probable Alzheimer’s disease (AD) with mild impairment.¹

Furthermore, although the clockdrawing test, visuospatial copying tasks, and trail making test B might not have absolute utility in identifying those at risk of driving impairment, measures of attention and visuospatial skills have been found to correlate with on-road driving performance.²

Given that visuospatial testing evaluates an area of cognition that is necessary for driving and impairment of visuospatial functioning in AD is significantly correlated with anosognosia,³ a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone.

Ben Schoenbachler, MD
Assistant professor
Director, Memory Disorders Program
University of Louisville
Louisville, KY

References

1. Dubinsky RM, Stein AC, Lyons K. Practice parameter: risk of driving and Alzheimer’s disease (an evidence-based review): report of the quality standards subcommittee of the American Academy of Neurology. Neurology. 2000;54(12):2205-2211.

2. Reger MA, Welsh RK, Watson GS, et al. The relationship between neuropsychological functioning and driving ability in dementia: a meta-analysis. Neuropsychology. 2004;18(1):85-93.

3. Auchus AP, Goldstein FC, Green J, et al. Unawareness of cognitive impairments in Alzheimer’s disease. Neuropsychiatry Neuropsychol Behav Neurol. 1994;7:25-29.

The authors respond

We agree with Dr. Schoenbachler’s comment that “a prudent clinician may choose to restrict driving privileges based on bedside examination and clinical impression alone,” and certainly do not wish readers to disregard the results of patient history, examination, or cognitive evaluation. Indeed, visuospatial testing has been shown to have moderate correlations with driving in the review that Dr. Schoenbachler cites. However, a recent systematic review¹ highlighted the inconsistency of this evidence and reported that only 6 of 11 analyses of the relationship between visuospatial skills and driving showed significant associations.

Although our article emphasized the limitations of evidence on the predictive value of the clinical evaluation of driving fitness, we encourage physicians to use their clinical judgment to decide when a patient’s cognitive deficits or behavioral symptoms preclude safe driving. The algorithm emphasizes the role of on-road testing in cases when the clinician is uncertain. When impairment is so severe or obvious that the patient clearly is unsafe to drive, in-depth testing is not needed. For less severe cases, clinicians will need to determine if they have enough information to decide or if an on-road assessment is warranted.

Mark Rapoport, MD

Carla Zucchero Sarracini, BA

Nathan Herrmann, MD
Department of psychiatry
University of Toronto
Sunnybrook Health Sciences Centre
Toronto, Ontario, Canada

Frank Molnar, MD
University of Ottawa
Ottawa Health Research Institute
Ottawa, Ontario, Canada

Do you sometimes wonder what psychiatry’s future holds? Wonder no more: abundant clues point to exciting innovations in our field. Let me highlight 6 trends that will shape how we practice psychiatry.

1. Earlier diagnosis and early intervention. The past decade has witnessed a surge of progress in identifying individuals at high risk for psychosis or mood disorders. The “prodrome” has become a fertile area of research, with a focus on early “treatment” even before the clinical syndrome of schizophrenia or mania appears. The goal is to try to delay, modify, or ameliorate incipient serious mental illness by using both pharmacotherapy and psychotherapy.

2. A tsunami of genetic discoveries. Almost weekly, psychiatric geneticists are discovering genes associated with serious psychiatric disorders. Neuregulin 1, dysbindin, DISC1, DAOA (G72), PRODH, and COMT are among the many odd-sounding genes located on various chromosomes. These discoveries confirm the “complex genetics” of psychiatric disorders involving dozens—even hundreds—of susceptibility genes, in contrast to the “1 gene, 1 disease” Mendelian paradigm.

Ultimately, these genetic discoveries will provide clues to the molecular pathophysiology of major mental disorders, leading to the holy grail of psychiatric treatment: specific, biotechnology-driven, disease-modifying pharmacotherapeutics rather than merely symptom-control agents.

3. Neuroplasticity as treatment target. Over the past few years, structural atrophy of the brain at the cellular and molecular levels has been documented in psychosis, mania, depression, and anxiety. These findings have shifted our perspective of mental illness beyond the simplistic notions of “chemical imbalance.” The new model is progressive neuroplasticity changes in neurons, dendritic spines, neurite extensions, and synapses, (ie, the neuropil), with both grey and white matter reductions impairing brain connectivity and functioning.

In response, researchers are developing a neuro-protective paradigm to reverse neuroplastic changes as a new brain-repair strategy. Thus, therapeutic agents and their targets may include:

• caspase inhibitors to stop apoptosis
• neurogenesis stimulators to replenish neurons
• neurotropic enhancers to reverse deficits in various growth factors, such as nerve growth factor (NGF), brain-derived neurotropic factor (BDNF), vascular endothelial growth factor (VEGF), etc.
• antioxidants to neutralize excess free radicals
• glia-proliferation enhancers to rebuild white matter
• tumor necrosis factor-alpha (TNF-α) inhibitors to combat the inflammatory process reflected by high cytokine levels in psychotic and mood disorders.

Interestingly, many existing psychotropic agents have one or more of these neurotropic effects.

4. Neurostimulation for brain repair. Electroconvulsive therapy has been an effective (though sparingly used) psychiatric treatment for decades. Now, a new era of brain stimulation for psychiatric disorders is evolving with the FDA-approved modalities of repetitive transcranial magnetic stimulation (rTMS) and vagal nerve stimulation (VNS). But the next “big thing” may be deep-brain stimulation (DBS), which is becoming a routine treatment for neurologic conditions such as Parkinson’s disease. DBS has potential to provide major treatment breakthroughs, and DBS research is progressing rapidly.

Welcome, Dr. Goldberg

Dr. Goldberg

Joseph F. Goldberg, MD, has joined CURRENT PSYCHIATRY’s editorial board as Deputy Editor. Dr. Goldberg is associate clinical professor of psychiatry at Mount Sinai School of Medicine, New York, NY, and director of the affective disorders research program at Silver Hill Hospital, New Canaan, CT. He has published >100 peer-reviewed papers on bipolar disorder, his specialty in both research and clinical practice.

5. Pharmacogenomics in clinical practice. Psychiatrists are aware that inherited genetic variations (such as in cytochrome enzymes) can influence the body’s response to drugs. Thus, patients who are poor metabolizers often experience side effects at usual clinical doses and may discontinue medications that could help them. Similarly, fast metabolizers may fail to respond to drugs that should work and are labeled as “treatment-resistant.”

Pharmacogenetic screening in clinical practice soon will become routine—it already is at a few U.S. academic hospitals—and will enable psychiatrists to customize drug treatment to achieve better efficacy and tolerability for each patient. This will help us adapt therapies to address genetic variations within our ethnically diverse society.

6. Intertwining of physical and mental disorders. A comparatively high mortality rate from cardiovascular disease has been documented in persons with serious psychiatric disorders, especially schizophrenia, bipolar disorder, major depression, and anxiety. Similarly, persons with obesity, diabetes, dyslipidemia, and hypertension suffer from higher rates of psychiatric disorders. Inflammatory factors, in part secreted from visceral adipose tissue, appear to be a common pathway.

The optimal psychiatric practice is becoming a collaborative model of care between psychiatrists and family physicians, so that patients receive integrated, comprehensive physical and mental treatments.

What this all means. The journey to the future of psychiatric practice is underway. In many respects, the future is already here. I encourage you to join the excitement.

Do you sometimes wonder what psychiatry’s future holds? Wonder no more: abundant clues point to exciting innovations in our field. Let me highlight 6 trends that will shape how we practice psychiatry.

1. Earlier diagnosis and early intervention. The past decade has witnessed a surge of progress in identifying individuals at high risk for psychosis or mood disorders. The “prodrome” has become a fertile area of research, with a focus on early “treatment” even before the clinical syndrome of schizophrenia or mania appears. The goal is to try to delay, modify, or ameliorate incipient serious mental illness by using both pharmacotherapy and psychotherapy.

2. A tsunami of genetic discoveries. Almost weekly, psychiatric geneticists are discovering genes associated with serious psychiatric disorders. Neuregulin 1, dysbindin, DISC1, DAOA (G72), PRODH, and COMT are among the many odd-sounding genes located on various chromosomes. These discoveries confirm the “complex genetics” of psychiatric disorders involving dozens—even hundreds—of susceptibility genes, in contrast to the “1 gene, 1 disease” Mendelian paradigm.

Ultimately, these genetic discoveries will provide clues to the molecular pathophysiology of major mental disorders, leading to the holy grail of psychiatric treatment: specific, biotechnology-driven, disease-modifying pharmacotherapeutics rather than merely symptom-control agents.

3. Neuroplasticity as treatment target. Over the past few years, structural atrophy of the brain at the cellular and molecular levels has been documented in psychosis, mania, depression, and anxiety. These findings have shifted our perspective of mental illness beyond the simplistic notions of “chemical imbalance.” The new model is progressive neuroplasticity changes in neurons, dendritic spines, neurite extensions, and synapses, (ie, the neuropil), with both grey and white matter reductions impairing brain connectivity and functioning.

In response, researchers are developing a neuro-protective paradigm to reverse neuroplastic changes as a new brain-repair strategy. Thus, therapeutic agents and their targets may include:

• caspase inhibitors to stop apoptosis
• neurogenesis stimulators to replenish neurons
• neurotropic enhancers to reverse deficits in various growth factors, such as nerve growth factor (NGF), brain-derived neurotropic factor (BDNF), vascular endothelial growth factor (VEGF), etc.
• antioxidants to neutralize excess free radicals
• glia-proliferation enhancers to rebuild white matter
• tumor necrosis factor-alpha (TNF-α) inhibitors to combat the inflammatory process reflected by high cytokine levels in psychotic and mood disorders.

Interestingly, many existing psychotropic agents have one or more of these neurotropic effects.

4. Neurostimulation for brain repair. Electroconvulsive therapy has been an effective (though sparingly used) psychiatric treatment for decades. Now, a new era of brain stimulation for psychiatric disorders is evolving with the FDA-approved modalities of repetitive transcranial magnetic stimulation (rTMS) and vagal nerve stimulation (VNS). But the next “big thing” may be deep-brain stimulation (DBS), which is becoming a routine treatment for neurologic conditions such as Parkinson’s disease. DBS has potential to provide major treatment breakthroughs, and DBS research is progressing rapidly.

Welcome, Dr. Goldberg

Dr. Goldberg

Joseph F. Goldberg, MD, has joined CURRENT PSYCHIATRY’s editorial board as Deputy Editor. Dr. Goldberg is associate clinical professor of psychiatry at Mount Sinai School of Medicine, New York, NY, and director of the affective disorders research program at Silver Hill Hospital, New Canaan, CT. He has published >100 peer-reviewed papers on bipolar disorder, his specialty in both research and clinical practice.

5. Pharmacogenomics in clinical practice. Psychiatrists are aware that inherited genetic variations (such as in cytochrome enzymes) can influence the body’s response to drugs. Thus, patients who are poor metabolizers often experience side effects at usual clinical doses and may discontinue medications that could help them. Similarly, fast metabolizers may fail to respond to drugs that should work and are labeled as “treatment-resistant.”

Pharmacogenetic screening in clinical practice soon will become routine—it already is at a few U.S. academic hospitals—and will enable psychiatrists to customize drug treatment to achieve better efficacy and tolerability for each patient. This will help us adapt therapies to address genetic variations within our ethnically diverse society.

6. Intertwining of physical and mental disorders. A comparatively high mortality rate from cardiovascular disease has been documented in persons with serious psychiatric disorders, especially schizophrenia, bipolar disorder, major depression, and anxiety. Similarly, persons with obesity, diabetes, dyslipidemia, and hypertension suffer from higher rates of psychiatric disorders. Inflammatory factors, in part secreted from visceral adipose tissue, appear to be a common pathway.

The optimal psychiatric practice is becoming a collaborative model of care between psychiatrists and family physicians, so that patients receive integrated, comprehensive physical and mental treatments.

What this all means. The journey to the future of psychiatric practice is underway. In many respects, the future is already here. I encourage you to join the excitement.

Do you sometimes wonder what psychiatry’s future holds? Wonder no more: abundant clues point to exciting innovations in our field. Let me highlight 6 trends that will shape how we practice psychiatry.

1. Earlier diagnosis and early intervention. The past decade has witnessed a surge of progress in identifying individuals at high risk for psychosis or mood disorders. The “prodrome” has become a fertile area of research, with a focus on early “treatment” even before the clinical syndrome of schizophrenia or mania appears. The goal is to try to delay, modify, or ameliorate incipient serious mental illness by using both pharmacotherapy and psychotherapy.

2. A tsunami of genetic discoveries. Almost weekly, psychiatric geneticists are discovering genes associated with serious psychiatric disorders. Neuregulin 1, dysbindin, DISC1, DAOA (G72), PRODH, and COMT are among the many odd-sounding genes located on various chromosomes. These discoveries confirm the “complex genetics” of psychiatric disorders involving dozens—even hundreds—of susceptibility genes, in contrast to the “1 gene, 1 disease” Mendelian paradigm.

Ultimately, these genetic discoveries will provide clues to the molecular pathophysiology of major mental disorders, leading to the holy grail of psychiatric treatment: specific, biotechnology-driven, disease-modifying pharmacotherapeutics rather than merely symptom-control agents.

3. Neuroplasticity as treatment target. Over the past few years, structural atrophy of the brain at the cellular and molecular levels has been documented in psychosis, mania, depression, and anxiety. These findings have shifted our perspective of mental illness beyond the simplistic notions of “chemical imbalance.” The new model is progressive neuroplasticity changes in neurons, dendritic spines, neurite extensions, and synapses, (ie, the neuropil), with both grey and white matter reductions impairing brain connectivity and functioning.

In response, researchers are developing a neuro-protective paradigm to reverse neuroplastic changes as a new brain-repair strategy. Thus, therapeutic agents and their targets may include:

• caspase inhibitors to stop apoptosis
• neurogenesis stimulators to replenish neurons
• neurotropic enhancers to reverse deficits in various growth factors, such as nerve growth factor (NGF), brain-derived neurotropic factor (BDNF), vascular endothelial growth factor (VEGF), etc.
• antioxidants to neutralize excess free radicals
• glia-proliferation enhancers to rebuild white matter
• tumor necrosis factor-alpha (TNF-α) inhibitors to combat the inflammatory process reflected by high cytokine levels in psychotic and mood disorders.

Interestingly, many existing psychotropic agents have one or more of these neurotropic effects.

4. Neurostimulation for brain repair. Electroconvulsive therapy has been an effective (though sparingly used) psychiatric treatment for decades. Now, a new era of brain stimulation for psychiatric disorders is evolving with the FDA-approved modalities of repetitive transcranial magnetic stimulation (rTMS) and vagal nerve stimulation (VNS). But the next “big thing” may be deep-brain stimulation (DBS), which is becoming a routine treatment for neurologic conditions such as Parkinson’s disease. DBS has potential to provide major treatment breakthroughs, and DBS research is progressing rapidly.

Welcome, Dr. Goldberg

Dr. Goldberg

Joseph F. Goldberg, MD, has joined CURRENT PSYCHIATRY’s editorial board as Deputy Editor. Dr. Goldberg is associate clinical professor of psychiatry at Mount Sinai School of Medicine, New York, NY, and director of the affective disorders research program at Silver Hill Hospital, New Canaan, CT. He has published >100 peer-reviewed papers on bipolar disorder, his specialty in both research and clinical practice.

5. Pharmacogenomics in clinical practice. Psychiatrists are aware that inherited genetic variations (such as in cytochrome enzymes) can influence the body’s response to drugs. Thus, patients who are poor metabolizers often experience side effects at usual clinical doses and may discontinue medications that could help them. Similarly, fast metabolizers may fail to respond to drugs that should work and are labeled as “treatment-resistant.”

Pharmacogenetic screening in clinical practice soon will become routine—it already is at a few U.S. academic hospitals—and will enable psychiatrists to customize drug treatment to achieve better efficacy and tolerability for each patient. This will help us adapt therapies to address genetic variations within our ethnically diverse society.

6. Intertwining of physical and mental disorders. A comparatively high mortality rate from cardiovascular disease has been documented in persons with serious psychiatric disorders, especially schizophrenia, bipolar disorder, major depression, and anxiety. Similarly, persons with obesity, diabetes, dyslipidemia, and hypertension suffer from higher rates of psychiatric disorders. Inflammatory factors, in part secreted from visceral adipose tissue, appear to be a common pathway.

The optimal psychiatric practice is becoming a collaborative model of care between psychiatrists and family physicians, so that patients receive integrated, comprehensive physical and mental treatments.

What this all means. The journey to the future of psychiatric practice is underway. In many respects, the future is already here. I encourage you to join the excitement.

CASE ‘Sad, worried, and angry’

Mr. A, age 24, is referred to our university psychiatric clinic. He reports that he’s sad, worried, angry, and wants to hurt people. He endorses having chronic depressive episodes that last >2 weeks and consist of poor sleep, low energy, anhedonia, poor concentration, and psychomotor retardation.

He is developmentally disabled and has been living in a group home for almost 1 year. In former group homes, Mr. A threatened and assaulted other patients and staff. In 1 incident Mr. A broke a patient’s nose and was incarcerated for 4 days. With the help of a job coach, Mr. A has been working in a department store for 8 months. He was fired from other jobs because he threatened co-workers.

The author’s observations

Problem behaviors in patients with pervasive developmental disorders include aggression and self-injury. These behaviors may improve with behavioral or pharmacologic interventions.¹ For example, risperidone is FDA-approved to treat irritability associated with autistic disorder in children and adolescents age 5 to 16 years.² Violence has been reported in patients with pervasive developmental disorders, and such symptoms can lead to psychiatric referral.¹

HISTORY Difficult childhood

Mr. A’s medical history is unremarkable. He has no history of hypomania, mania, psychosis, substance use, tics, seizures, genetic illnesses, head trauma, or physical or sexual abuse. He has never attempted suicide nor been hospitalized for psychiatric illness.

With Mr. A’s permission, his mother is consulted. She says that as a child Mr. A would become extremely interested in various topics—including Pokémon, Magic cards, and video games—and had a strong desire to tell everyone the details of each. However, he rocked back and forth, had few friends, and would bite other children.

Mr. A has no history of language delay but received speech therapy during his childhood to help him “work on eye contact and social skills.” He is estranged from and angry with his father, who has difficulty accepting his son’s developmental disability.

At the time of referral, Mr. A is receiving paroxetine, 30 mg/d, for depression, risperidone, 1.5 mg/d, for aggression, and dextroamphetamine/amphetamine extended-release, 30 mg/d, for hyperactivity/inattention. The efficacy of these medications, which were prescribed by an outside psychiatrist, is unclear.

Table 1

Diagnostic criteria for Asperger’s disorder

Based on Mr. A’s impaired social interaction, repetitive interests and behaviors, and lack of language delay, Mr. A meets criteria for Asperger’s disorder (Table 1). He also meets criteria for major depressive disorder, recurrent, moderate.

The author’s observations

Psychosocial interventions for patients with an autism-spectrum disorder consist of educational, vocational, behavioral, and family interventions. Individual, group, and family psychotherapy may benefit patients with Asperger’s disorder who have comorbid depression.¹

TREATMENT A rocky start

At Mr. A’s initial assessment, the clinic psychiatrist increases risperidone to 1 mg twice daily to target aggression. Even after receiving this dosage for 1 month, however, Mr. A continues to display physical aggression toward peers in the group home whenever he becomes angry.

The psychiatrist refers Mr. A to a social worker for supportive therapy to help him cope with worry and chronic sadness. The social worker uses general cognitive-behavioral strategies for anxiety and aggression for 12 sessions over 8 months until scheduling conflicts end therapy. The efficacy of this therapy is minimal; Mr. A remains depressed, anxious, and aggressive. During this time, the psychiatrist increases paroxetine to 40 mg/d, but Mr. A continues to feel depressed after 1 month. Mr. A is cross-tapered to duloxetine, but continues to feel depressed after receiving duloxetine, 60 mg/d, for 1 month.

My first visit with Mr. A occurs 3 months after his last visit with the social worker. He states he does not remember anything from those sessions. Mr. A’s goals for therapy are to reduce anxiety, manage anger, and improve relationship skills.

I begin the first 4 months of Mr. A’s therapy with cognitive-behavioral interventions based on the Treatment of Adolescents Depression Study (TADS) manual.³ Although Mr. A is an adult, I choose a manual that targets adolescents because my clinical impression is that his cognitive developmental level is more like an adolescent’s than an adult’s.

I assign homework such as mood monitoring. I ask him to use a form from the TADS manual to rate his mood on a scale of 0 to 10 every morning, afternoon, and evening, and write down what he is doing that makes him feel that way at the time he rates his mood. Mr. A never completes any homework; during each session he states he “just forgot to do it.”

I discuss concepts such as goal setting, for a novel Mr. A says he wants to write, and relaxation strategies to address anger; in session, I work with him on filling out the “What Helps Me to Relax?” form from the TADS manual. Mr. A lists “play games,” “write my book,” “listen to music,” “go outside,” and “exercise” as strategies to help him relax. We also work on visual handouts—such as “Safety Plan” and “What Can I Do to Relax”—to post in his room.

Mr. A does not show up for 3 sessions. When I call the group home, a staff member tells me they were busy with other patients and forgot about Mr. A. I decide to call the group home the day before each appointment as a reminder. This increases Mr. A’s attendance rate.

During each session, Mr. A complains about the quality of the group home, the staff, and other patients. To get my own perspective of Mr. A’s living environment, I consider visiting his group home, similar to how a geriatric psychiatrist sees patients in a nursing home or an assertive community treatment team psychiatrist sees patients in their home environments. Because I am concerned about boundary crossings/violations, I first discuss this action with 2 psychotherapists not involved in Mr. A’s treatment. They recommend that I limit this action to a one-time visit.

I visit Mr. A’s group home 2 months after my first session with him. Located in front of a dairy farm in a rural part of the state about 1 hour from our clinic, the isolated facility has a secured keypad entry. When I meet Mr. A there, he says he feels as if he is in jail. I meet the staff and find them willing to help with various aspects of Mr. A’s treatment, such as discussing events, reporting behaviors, and helping carry out interventions.

For example, I ask staff to remind Mr. A of his relaxation strategies when he becomes angry. On the “Safety Plan” handout, I had Mr. A identify 5 people he could talk to when he becomes angry; I ask staff to remind him of those people when Mr. A becomes angry. I also ask staff to ask Mr. A every day if he is writing the novel he wants to complete. After my visit, Mr. A starts putting more effort into therapy. When I set a daily goal of working on his novel for 15 minutes, he starts bringing pages of his writings to sessions.

Table 2

Social skills training for patients with Asperger’s disorde

The author’s observations

In a study in rural Appalachia, telephone reminders increased attendance at psychiatric intake appointments.⁴ Calling the group home before each of Mr. A’s appointments took extra time out of my schedule but improved Mr. A’s attendance rate.

In residential treatment of children, Monahan notes that childcare workers could contribute useful observations and benefit from the therapist’s advice.⁵ Establishing rapport with the staff at Mr. A’s group home helped me proceed with therapy.

TREATMENT Social skills training

In the second 4 months of therapy, Mr. A changes jobs to become a greeter in a local video game store. He is happy, and group home staff members are pleased they no longer spend 2 hours each day transporting him to his previous job.

Soon after, during a reminder phone call, a staff member tells me that Mr. A’s brother and father were murdered the prior week. Three staff members attend Mr. A’s brother’s funeral, which he appreciates. Mr. A refuses to attend his father’s funeral because of continued anger toward him.

When I ask Mr. A if he wants to talk about the deaths, he declines. I subsequently spend half a session discussing strategies to address grief,⁶ such as imagining a conversation with his deceased brother.

I decide to review Mr. A’s therapy goals because he still has a lot of anger toward his recently deceased father. I am concerned he might discharge this anger onto a staff member, coworker, or fellow patient. Mr. A states he wants to focus on relationships, especially his anxiety around women. He discusses his anxiety with starting and maintaining conversations with women.

I begin role-playing in sessions by pretending to be a woman for Mr. A to speak with, but he feels this is silly. I teach him exercises from a social skills training workbook developed for patients with Asperger’s, such as “Starting a conversation,” “Staying on topic,” and “Making eye contact” (Table 2).⁷ Mr. A says group home staff members occasionally take him out to a nearby nightclub and encourage him to talk to women.

To see how Mr. A behaves in public, during our sessions I take him to different parts of the hospital, such as the gift shop, library, and deli. I instruct him to ask various women non-threatening questions, such as how much a certain entrée costs. I note his body language, such as tilting his head down and fidgeting during conversations. I provide him with immediate feedback, which slowly increases his awareness of these behaviors.

With Mr. A’s permission, I educate the group home staff about how to point out these behaviors when Mr. A is in public. I ask them to focus on body language and emphasize that Mr. A needs to apply what I teach him to other settings.

The author’s observations

Patients with Asperger’s disorder need specific training to build a repertoire of social skills.⁷ Teaching in real-life settings helps patients generalize these skills.¹

Zimmerman⁸ discusses how caregivers might have an unrealistic, “magical” view of psychotherapy and feel suspicious of the process. With Mr. A’s permission, I ask group home staff members to meet with me for 10 minutes at the end of each of Mr. A’s sessions to make them aware of what is happening with his therapy. I want them to feel that they are an important part of Mr. A’s therapy. These meetings may have alleviated staff members’ fears about my time with him. Even though Mr. A granted me permission to disclose all details of our sessions with the staff, I was careful to not disclose sensitive issues, such as the patient’s dreams and fantasies.

TREATMENT ‘Fear’

Mr. A rates his anxiety as a 4/10 whenever he speaks with women. To more specifically understand his underlying cognitions, I use Kendall’s FEAR plan (Table 3).⁹

I ask him to divide his automatic “E” thoughts into “she” and “I” thoughts. Examples of automatic “she” thoughts include “She probably won’t like me” and “She thinks I’m not cute.” Examples of automatic “I” thoughts include “I’m probably not smart enough for her” and “I think we won’t have anything in common.”

Table 3

The FEAR plan*

The author’s observations

Schwartz¹⁰ discusses countertransference challenges in nursing home patients, where therapists identify with patients’ hopelessness. Schwartz recommends addressing these challenges by thinking of realistic expectations. Even though a facility might be far from perfect, it may be “good enough.”

Mr. A’s group home was far from perfect and located in an isolated setting. Even so, I was able to help him complete psychotherapy at our clinic by adapting my practice to his needs, including:

• making reminder phone calls for appointments
  
• visiting the group home
  
• enlisting the help of caregivers with therapeutic techniques.
  

OUTCOME Improving

In the final 4 months of therapy, we continue to work on social skills lessons, practice exercises in the hospital, and the FEAR acronym. I continue to include caregivers in these efforts.

During 1 session, I tell Mr. A I will be leaving at the end of my fellowship. In the final month, I gradually transition him to a new therapist. I decided to transition him to a male therapist so Mr. A will continue to feel comfortable sharing his feelings, rather than shutting down from anxiety with a female therapist. As I end therapy, Mr. A is promoted to a cashier at the video game store and enrolls in classes to study for a General Education Development (GED) certificate.

Related resource

• National Institute of Mental Health. Autism spectrum disorders. www.nimh.nih.gov/health/publications/autism/complete-publication.shtml.
  

• Bupropion extended-release • Wellbutrin XL
  
• Dextroamphetamine/amphetamine extended-release • Adderall XR
  
• Duloxetine • Cymbalta
  
• Paroxetine • Paxil
  
• Risperidone • Risperdal
  
• Ziprasidone • Geodon
  

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

Acknowledgment

The author thanks Dr. Ann Lagges, PhD, for her assistance with this patient’s treatment.

CASE ‘Sad, worried, and angry’

Mr. A, age 24, is referred to our university psychiatric clinic. He reports that he’s sad, worried, angry, and wants to hurt people. He endorses having chronic depressive episodes that last >2 weeks and consist of poor sleep, low energy, anhedonia, poor concentration, and psychomotor retardation.

He is developmentally disabled and has been living in a group home for almost 1 year. In former group homes, Mr. A threatened and assaulted other patients and staff. In 1 incident Mr. A broke a patient’s nose and was incarcerated for 4 days. With the help of a job coach, Mr. A has been working in a department store for 8 months. He was fired from other jobs because he threatened co-workers.

The author’s observations

Problem behaviors in patients with pervasive developmental disorders include aggression and self-injury. These behaviors may improve with behavioral or pharmacologic interventions.¹ For example, risperidone is FDA-approved to treat irritability associated with autistic disorder in children and adolescents age 5 to 16 years.² Violence has been reported in patients with pervasive developmental disorders, and such symptoms can lead to psychiatric referral.¹

HISTORY Difficult childhood

Mr. A’s medical history is unremarkable. He has no history of hypomania, mania, psychosis, substance use, tics, seizures, genetic illnesses, head trauma, or physical or sexual abuse. He has never attempted suicide nor been hospitalized for psychiatric illness.

With Mr. A’s permission, his mother is consulted. She says that as a child Mr. A would become extremely interested in various topics—including Pokémon, Magic cards, and video games—and had a strong desire to tell everyone the details of each. However, he rocked back and forth, had few friends, and would bite other children.

Mr. A has no history of language delay but received speech therapy during his childhood to help him “work on eye contact and social skills.” He is estranged from and angry with his father, who has difficulty accepting his son’s developmental disability.

At the time of referral, Mr. A is receiving paroxetine, 30 mg/d, for depression, risperidone, 1.5 mg/d, for aggression, and dextroamphetamine/amphetamine extended-release, 30 mg/d, for hyperactivity/inattention. The efficacy of these medications, which were prescribed by an outside psychiatrist, is unclear.

Table 1

Diagnostic criteria for Asperger’s disorder

Based on Mr. A’s impaired social interaction, repetitive interests and behaviors, and lack of language delay, Mr. A meets criteria for Asperger’s disorder (Table 1). He also meets criteria for major depressive disorder, recurrent, moderate.

The author’s observations

Psychosocial interventions for patients with an autism-spectrum disorder consist of educational, vocational, behavioral, and family interventions. Individual, group, and family psychotherapy may benefit patients with Asperger’s disorder who have comorbid depression.¹

TREATMENT A rocky start

At Mr. A’s initial assessment, the clinic psychiatrist increases risperidone to 1 mg twice daily to target aggression. Even after receiving this dosage for 1 month, however, Mr. A continues to display physical aggression toward peers in the group home whenever he becomes angry.

The psychiatrist refers Mr. A to a social worker for supportive therapy to help him cope with worry and chronic sadness. The social worker uses general cognitive-behavioral strategies for anxiety and aggression for 12 sessions over 8 months until scheduling conflicts end therapy. The efficacy of this therapy is minimal; Mr. A remains depressed, anxious, and aggressive. During this time, the psychiatrist increases paroxetine to 40 mg/d, but Mr. A continues to feel depressed after 1 month. Mr. A is cross-tapered to duloxetine, but continues to feel depressed after receiving duloxetine, 60 mg/d, for 1 month.

My first visit with Mr. A occurs 3 months after his last visit with the social worker. He states he does not remember anything from those sessions. Mr. A’s goals for therapy are to reduce anxiety, manage anger, and improve relationship skills.

I begin the first 4 months of Mr. A’s therapy with cognitive-behavioral interventions based on the Treatment of Adolescents Depression Study (TADS) manual.³ Although Mr. A is an adult, I choose a manual that targets adolescents because my clinical impression is that his cognitive developmental level is more like an adolescent’s than an adult’s.

I assign homework such as mood monitoring. I ask him to use a form from the TADS manual to rate his mood on a scale of 0 to 10 every morning, afternoon, and evening, and write down what he is doing that makes him feel that way at the time he rates his mood. Mr. A never completes any homework; during each session he states he “just forgot to do it.”

I discuss concepts such as goal setting, for a novel Mr. A says he wants to write, and relaxation strategies to address anger; in session, I work with him on filling out the “What Helps Me to Relax?” form from the TADS manual. Mr. A lists “play games,” “write my book,” “listen to music,” “go outside,” and “exercise” as strategies to help him relax. We also work on visual handouts—such as “Safety Plan” and “What Can I Do to Relax”—to post in his room.

Mr. A does not show up for 3 sessions. When I call the group home, a staff member tells me they were busy with other patients and forgot about Mr. A. I decide to call the group home the day before each appointment as a reminder. This increases Mr. A’s attendance rate.

During each session, Mr. A complains about the quality of the group home, the staff, and other patients. To get my own perspective of Mr. A’s living environment, I consider visiting his group home, similar to how a geriatric psychiatrist sees patients in a nursing home or an assertive community treatment team psychiatrist sees patients in their home environments. Because I am concerned about boundary crossings/violations, I first discuss this action with 2 psychotherapists not involved in Mr. A’s treatment. They recommend that I limit this action to a one-time visit.

I visit Mr. A’s group home 2 months after my first session with him. Located in front of a dairy farm in a rural part of the state about 1 hour from our clinic, the isolated facility has a secured keypad entry. When I meet Mr. A there, he says he feels as if he is in jail. I meet the staff and find them willing to help with various aspects of Mr. A’s treatment, such as discussing events, reporting behaviors, and helping carry out interventions.

For example, I ask staff to remind Mr. A of his relaxation strategies when he becomes angry. On the “Safety Plan” handout, I had Mr. A identify 5 people he could talk to when he becomes angry; I ask staff to remind him of those people when Mr. A becomes angry. I also ask staff to ask Mr. A every day if he is writing the novel he wants to complete. After my visit, Mr. A starts putting more effort into therapy. When I set a daily goal of working on his novel for 15 minutes, he starts bringing pages of his writings to sessions.

Table 2

Social skills training for patients with Asperger’s disorde

The author’s observations

In a study in rural Appalachia, telephone reminders increased attendance at psychiatric intake appointments.⁴ Calling the group home before each of Mr. A’s appointments took extra time out of my schedule but improved Mr. A’s attendance rate.

In residential treatment of children, Monahan notes that childcare workers could contribute useful observations and benefit from the therapist’s advice.⁵ Establishing rapport with the staff at Mr. A’s group home helped me proceed with therapy.

TREATMENT Social skills training

In the second 4 months of therapy, Mr. A changes jobs to become a greeter in a local video game store. He is happy, and group home staff members are pleased they no longer spend 2 hours each day transporting him to his previous job.

Soon after, during a reminder phone call, a staff member tells me that Mr. A’s brother and father were murdered the prior week. Three staff members attend Mr. A’s brother’s funeral, which he appreciates. Mr. A refuses to attend his father’s funeral because of continued anger toward him.

When I ask Mr. A if he wants to talk about the deaths, he declines. I subsequently spend half a session discussing strategies to address grief,⁶ such as imagining a conversation with his deceased brother.

I decide to review Mr. A’s therapy goals because he still has a lot of anger toward his recently deceased father. I am concerned he might discharge this anger onto a staff member, coworker, or fellow patient. Mr. A states he wants to focus on relationships, especially his anxiety around women. He discusses his anxiety with starting and maintaining conversations with women.

I begin role-playing in sessions by pretending to be a woman for Mr. A to speak with, but he feels this is silly. I teach him exercises from a social skills training workbook developed for patients with Asperger’s, such as “Starting a conversation,” “Staying on topic,” and “Making eye contact” (Table 2).⁷ Mr. A says group home staff members occasionally take him out to a nearby nightclub and encourage him to talk to women.

To see how Mr. A behaves in public, during our sessions I take him to different parts of the hospital, such as the gift shop, library, and deli. I instruct him to ask various women non-threatening questions, such as how much a certain entrée costs. I note his body language, such as tilting his head down and fidgeting during conversations. I provide him with immediate feedback, which slowly increases his awareness of these behaviors.

With Mr. A’s permission, I educate the group home staff about how to point out these behaviors when Mr. A is in public. I ask them to focus on body language and emphasize that Mr. A needs to apply what I teach him to other settings.

The author’s observations

Patients with Asperger’s disorder need specific training to build a repertoire of social skills.⁷ Teaching in real-life settings helps patients generalize these skills.¹

Zimmerman⁸ discusses how caregivers might have an unrealistic, “magical” view of psychotherapy and feel suspicious of the process. With Mr. A’s permission, I ask group home staff members to meet with me for 10 minutes at the end of each of Mr. A’s sessions to make them aware of what is happening with his therapy. I want them to feel that they are an important part of Mr. A’s therapy. These meetings may have alleviated staff members’ fears about my time with him. Even though Mr. A granted me permission to disclose all details of our sessions with the staff, I was careful to not disclose sensitive issues, such as the patient’s dreams and fantasies.

TREATMENT ‘Fear’

Mr. A rates his anxiety as a 4/10 whenever he speaks with women. To more specifically understand his underlying cognitions, I use Kendall’s FEAR plan (Table 3).⁹

I ask him to divide his automatic “E” thoughts into “she” and “I” thoughts. Examples of automatic “she” thoughts include “She probably won’t like me” and “She thinks I’m not cute.” Examples of automatic “I” thoughts include “I’m probably not smart enough for her” and “I think we won’t have anything in common.”

Table 3

The FEAR plan*

The author’s observations

Schwartz¹⁰ discusses countertransference challenges in nursing home patients, where therapists identify with patients’ hopelessness. Schwartz recommends addressing these challenges by thinking of realistic expectations. Even though a facility might be far from perfect, it may be “good enough.”

Mr. A’s group home was far from perfect and located in an isolated setting. Even so, I was able to help him complete psychotherapy at our clinic by adapting my practice to his needs, including:

• making reminder phone calls for appointments
  
• visiting the group home
  
• enlisting the help of caregivers with therapeutic techniques.
  

OUTCOME Improving

In the final 4 months of therapy, we continue to work on social skills lessons, practice exercises in the hospital, and the FEAR acronym. I continue to include caregivers in these efforts.

During 1 session, I tell Mr. A I will be leaving at the end of my fellowship. In the final month, I gradually transition him to a new therapist. I decided to transition him to a male therapist so Mr. A will continue to feel comfortable sharing his feelings, rather than shutting down from anxiety with a female therapist. As I end therapy, Mr. A is promoted to a cashier at the video game store and enrolls in classes to study for a General Education Development (GED) certificate.

Related resource

• National Institute of Mental Health. Autism spectrum disorders. www.nimh.nih.gov/health/publications/autism/complete-publication.shtml.
  

• Bupropion extended-release • Wellbutrin XL
  
• Dextroamphetamine/amphetamine extended-release • Adderall XR
  
• Duloxetine • Cymbalta
  
• Paroxetine • Paxil
  
• Risperidone • Risperdal
  
• Ziprasidone • Geodon
  

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

Acknowledgment

The author thanks Dr. Ann Lagges, PhD, for her assistance with this patient’s treatment.

CASE ‘Sad, worried, and angry’

Mr. A, age 24, is referred to our university psychiatric clinic. He reports that he’s sad, worried, angry, and wants to hurt people. He endorses having chronic depressive episodes that last >2 weeks and consist of poor sleep, low energy, anhedonia, poor concentration, and psychomotor retardation.

He is developmentally disabled and has been living in a group home for almost 1 year. In former group homes, Mr. A threatened and assaulted other patients and staff. In 1 incident Mr. A broke a patient’s nose and was incarcerated for 4 days. With the help of a job coach, Mr. A has been working in a department store for 8 months. He was fired from other jobs because he threatened co-workers.

The author’s observations

Problem behaviors in patients with pervasive developmental disorders include aggression and self-injury. These behaviors may improve with behavioral or pharmacologic interventions.¹ For example, risperidone is FDA-approved to treat irritability associated with autistic disorder in children and adolescents age 5 to 16 years.² Violence has been reported in patients with pervasive developmental disorders, and such symptoms can lead to psychiatric referral.¹

HISTORY Difficult childhood

Mr. A’s medical history is unremarkable. He has no history of hypomania, mania, psychosis, substance use, tics, seizures, genetic illnesses, head trauma, or physical or sexual abuse. He has never attempted suicide nor been hospitalized for psychiatric illness.

With Mr. A’s permission, his mother is consulted. She says that as a child Mr. A would become extremely interested in various topics—including Pokémon, Magic cards, and video games—and had a strong desire to tell everyone the details of each. However, he rocked back and forth, had few friends, and would bite other children.

Mr. A has no history of language delay but received speech therapy during his childhood to help him “work on eye contact and social skills.” He is estranged from and angry with his father, who has difficulty accepting his son’s developmental disability.

At the time of referral, Mr. A is receiving paroxetine, 30 mg/d, for depression, risperidone, 1.5 mg/d, for aggression, and dextroamphetamine/amphetamine extended-release, 30 mg/d, for hyperactivity/inattention. The efficacy of these medications, which were prescribed by an outside psychiatrist, is unclear.

Table 1

Diagnostic criteria for Asperger’s disorder

Based on Mr. A’s impaired social interaction, repetitive interests and behaviors, and lack of language delay, Mr. A meets criteria for Asperger’s disorder (Table 1). He also meets criteria for major depressive disorder, recurrent, moderate.

The author’s observations

Psychosocial interventions for patients with an autism-spectrum disorder consist of educational, vocational, behavioral, and family interventions. Individual, group, and family psychotherapy may benefit patients with Asperger’s disorder who have comorbid depression.¹

TREATMENT A rocky start

At Mr. A’s initial assessment, the clinic psychiatrist increases risperidone to 1 mg twice daily to target aggression. Even after receiving this dosage for 1 month, however, Mr. A continues to display physical aggression toward peers in the group home whenever he becomes angry.

The psychiatrist refers Mr. A to a social worker for supportive therapy to help him cope with worry and chronic sadness. The social worker uses general cognitive-behavioral strategies for anxiety and aggression for 12 sessions over 8 months until scheduling conflicts end therapy. The efficacy of this therapy is minimal; Mr. A remains depressed, anxious, and aggressive. During this time, the psychiatrist increases paroxetine to 40 mg/d, but Mr. A continues to feel depressed after 1 month. Mr. A is cross-tapered to duloxetine, but continues to feel depressed after receiving duloxetine, 60 mg/d, for 1 month.

My first visit with Mr. A occurs 3 months after his last visit with the social worker. He states he does not remember anything from those sessions. Mr. A’s goals for therapy are to reduce anxiety, manage anger, and improve relationship skills.

I begin the first 4 months of Mr. A’s therapy with cognitive-behavioral interventions based on the Treatment of Adolescents Depression Study (TADS) manual.³ Although Mr. A is an adult, I choose a manual that targets adolescents because my clinical impression is that his cognitive developmental level is more like an adolescent’s than an adult’s.

I assign homework such as mood monitoring. I ask him to use a form from the TADS manual to rate his mood on a scale of 0 to 10 every morning, afternoon, and evening, and write down what he is doing that makes him feel that way at the time he rates his mood. Mr. A never completes any homework; during each session he states he “just forgot to do it.”

I discuss concepts such as goal setting, for a novel Mr. A says he wants to write, and relaxation strategies to address anger; in session, I work with him on filling out the “What Helps Me to Relax?” form from the TADS manual. Mr. A lists “play games,” “write my book,” “listen to music,” “go outside,” and “exercise” as strategies to help him relax. We also work on visual handouts—such as “Safety Plan” and “What Can I Do to Relax”—to post in his room.

Mr. A does not show up for 3 sessions. When I call the group home, a staff member tells me they were busy with other patients and forgot about Mr. A. I decide to call the group home the day before each appointment as a reminder. This increases Mr. A’s attendance rate.

During each session, Mr. A complains about the quality of the group home, the staff, and other patients. To get my own perspective of Mr. A’s living environment, I consider visiting his group home, similar to how a geriatric psychiatrist sees patients in a nursing home or an assertive community treatment team psychiatrist sees patients in their home environments. Because I am concerned about boundary crossings/violations, I first discuss this action with 2 psychotherapists not involved in Mr. A’s treatment. They recommend that I limit this action to a one-time visit.

I visit Mr. A’s group home 2 months after my first session with him. Located in front of a dairy farm in a rural part of the state about 1 hour from our clinic, the isolated facility has a secured keypad entry. When I meet Mr. A there, he says he feels as if he is in jail. I meet the staff and find them willing to help with various aspects of Mr. A’s treatment, such as discussing events, reporting behaviors, and helping carry out interventions.

For example, I ask staff to remind Mr. A of his relaxation strategies when he becomes angry. On the “Safety Plan” handout, I had Mr. A identify 5 people he could talk to when he becomes angry; I ask staff to remind him of those people when Mr. A becomes angry. I also ask staff to ask Mr. A every day if he is writing the novel he wants to complete. After my visit, Mr. A starts putting more effort into therapy. When I set a daily goal of working on his novel for 15 minutes, he starts bringing pages of his writings to sessions.

Table 2

Social skills training for patients with Asperger’s disorde

The author’s observations

In a study in rural Appalachia, telephone reminders increased attendance at psychiatric intake appointments.⁴ Calling the group home before each of Mr. A’s appointments took extra time out of my schedule but improved Mr. A’s attendance rate.

In residential treatment of children, Monahan notes that childcare workers could contribute useful observations and benefit from the therapist’s advice.⁵ Establishing rapport with the staff at Mr. A’s group home helped me proceed with therapy.

TREATMENT Social skills training

In the second 4 months of therapy, Mr. A changes jobs to become a greeter in a local video game store. He is happy, and group home staff members are pleased they no longer spend 2 hours each day transporting him to his previous job.

Soon after, during a reminder phone call, a staff member tells me that Mr. A’s brother and father were murdered the prior week. Three staff members attend Mr. A’s brother’s funeral, which he appreciates. Mr. A refuses to attend his father’s funeral because of continued anger toward him.

When I ask Mr. A if he wants to talk about the deaths, he declines. I subsequently spend half a session discussing strategies to address grief,⁶ such as imagining a conversation with his deceased brother.

I decide to review Mr. A’s therapy goals because he still has a lot of anger toward his recently deceased father. I am concerned he might discharge this anger onto a staff member, coworker, or fellow patient. Mr. A states he wants to focus on relationships, especially his anxiety around women. He discusses his anxiety with starting and maintaining conversations with women.

I begin role-playing in sessions by pretending to be a woman for Mr. A to speak with, but he feels this is silly. I teach him exercises from a social skills training workbook developed for patients with Asperger’s, such as “Starting a conversation,” “Staying on topic,” and “Making eye contact” (Table 2).⁷ Mr. A says group home staff members occasionally take him out to a nearby nightclub and encourage him to talk to women.

To see how Mr. A behaves in public, during our sessions I take him to different parts of the hospital, such as the gift shop, library, and deli. I instruct him to ask various women non-threatening questions, such as how much a certain entrée costs. I note his body language, such as tilting his head down and fidgeting during conversations. I provide him with immediate feedback, which slowly increases his awareness of these behaviors.

With Mr. A’s permission, I educate the group home staff about how to point out these behaviors when Mr. A is in public. I ask them to focus on body language and emphasize that Mr. A needs to apply what I teach him to other settings.

The author’s observations

Patients with Asperger’s disorder need specific training to build a repertoire of social skills.⁷ Teaching in real-life settings helps patients generalize these skills.¹

Zimmerman⁸ discusses how caregivers might have an unrealistic, “magical” view of psychotherapy and feel suspicious of the process. With Mr. A’s permission, I ask group home staff members to meet with me for 10 minutes at the end of each of Mr. A’s sessions to make them aware of what is happening with his therapy. I want them to feel that they are an important part of Mr. A’s therapy. These meetings may have alleviated staff members’ fears about my time with him. Even though Mr. A granted me permission to disclose all details of our sessions with the staff, I was careful to not disclose sensitive issues, such as the patient’s dreams and fantasies.

TREATMENT ‘Fear’

Mr. A rates his anxiety as a 4/10 whenever he speaks with women. To more specifically understand his underlying cognitions, I use Kendall’s FEAR plan (Table 3).⁹

I ask him to divide his automatic “E” thoughts into “she” and “I” thoughts. Examples of automatic “she” thoughts include “She probably won’t like me” and “She thinks I’m not cute.” Examples of automatic “I” thoughts include “I’m probably not smart enough for her” and “I think we won’t have anything in common.”

Table 3

The FEAR plan*

The author’s observations

Schwartz¹⁰ discusses countertransference challenges in nursing home patients, where therapists identify with patients’ hopelessness. Schwartz recommends addressing these challenges by thinking of realistic expectations. Even though a facility might be far from perfect, it may be “good enough.”

Mr. A’s group home was far from perfect and located in an isolated setting. Even so, I was able to help him complete psychotherapy at our clinic by adapting my practice to his needs, including:

• making reminder phone calls for appointments
  
• visiting the group home
  
• enlisting the help of caregivers with therapeutic techniques.
  

OUTCOME Improving

In the final 4 months of therapy, we continue to work on social skills lessons, practice exercises in the hospital, and the FEAR acronym. I continue to include caregivers in these efforts.

During 1 session, I tell Mr. A I will be leaving at the end of my fellowship. In the final month, I gradually transition him to a new therapist. I decided to transition him to a male therapist so Mr. A will continue to feel comfortable sharing his feelings, rather than shutting down from anxiety with a female therapist. As I end therapy, Mr. A is promoted to a cashier at the video game store and enrolls in classes to study for a General Education Development (GED) certificate.

Related resource

• National Institute of Mental Health. Autism spectrum disorders. www.nimh.nih.gov/health/publications/autism/complete-publication.shtml.
  

• Bupropion extended-release • Wellbutrin XL
  
• Dextroamphetamine/amphetamine extended-release • Adderall XR
  
• Duloxetine • Cymbalta
  
• Paroxetine • Paxil
  
• Risperidone • Risperdal
  
• Ziprasidone • Geodon
  

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

Acknowledgment

The author thanks Dr. Ann Lagges, PhD, for her assistance with this patient’s treatment.

A major challenge for the DSM-V committees as they revise the diagnostic “bible” of psychiatric disorders is to determine whether mental illnesses are diseases, disorders, or syndromes.

Here’s how my version of Webster’s dictionary defines these terms:

• Disease: A particular distinctive process in the body with a specific cause and characteristic symptoms.
• Disorder: Irregularity, disturbance, or interruption of normal functions.
• Syndrome: A number of symptoms occurring together and characterizing a specific disease.

Let’s consider 4 facts that may be relevant for this decision.

Probably not ‘diseases’

No objective laboratory test can differentiate 1 psychiatric malady from another, and this lack of specificity casts doubt on the disease model. However, many documented perturbations of normal brain functions are consistent with a disorder paradigm.

Symptom overlap

The signs and symptoms of psychiatric ailments overlap considerably. Depression and anxiety share many symptoms and frequently co-occur. Bipolar mania and schizophrenia share psychotic features, cognitive deficits, agitation, suicidality, aggressive behavior, etc. The obsessions of obsessive-compulsive disorder (OCD) resemble and sometimes morph into the fixed false beliefs (delusions) of psychosis, and OCD’s compulsions often characterize the behaviors of other psychiatric disorders, such as anorexia or bulimia nervosa.

Personality disorder features essentially are attenuated but enduring forms of Axis I conditions. Nearly all psychiatric illnesses have some degree of suicidality, insomnia, and addictive behavior. Posttraumatic stress disorder’s symptoms recapitulate those of numerous diagnostic categories, such as anxiety, depression, psychosis, negative symptoms, mania, OCD, impulsive behavior, and personality changes.

Common neurobiology

Most diagnostic categories in psychiatry share some neurobiologic features, such as:

• neurotransmitter pathways (serotonin, dopamine, norepinephrine, or glutamate)
• structural abnormalities on neuroimaging (cortical atrophy, ventriculomegaly, gray and/or white matter abnormalities) or
• genetic predispositions.

Medical and psychiatric comorbidities (migraine, chronic pain, diabetes, obesity, alcohol abuse, anxiety, eating disorders, and Axis II features) occur across all major psychiatric diagnoses.

Nonspecific medications

Psychotropics approved for treating 1 condition are frequently useful for others:

• Selective serotonin reuptake inhibitors initially were indicated for depression but soon were found to have efficacy for panic attacks, social phobia, OCD, bulimia, impulse dyscontrol, and fibromyalgia.
• Atypical antipsychotics indicated for schizophrenia have been found useful in bipolar mania, treatment-resistant OCD, treatment-resistant depression, borderline personality disorder, delirium, anxiety, etc.
• Anticonvulsants indicated for epilepsy later were approved for bipolar mania and then found to have uses in alcoholism and drug abuse, aggressive behavior, impulsivity, treatment-resistant anxiety, and psychosis.

The multiple efficacies of psychiatric drug classes strongly suggest shared pharmacotherapeutic responsiveness across psychiatric diagnoses, including those without any FDA-approved medication. They also render the opinionated and uninformed criticism of “off-label” prescribing practices hollow, effete, and counterproductive.

Back to definitions

So, should DSM-V committees define diagnostic categories as diseases, disorders, or syndromes? The state of knowledge points to disorders and syndromes rather than diseases. There very well could be a specific disease within a syndrome, but many phenotypes and genotypes manifest with similar clusters of psychiatric signs and symptoms. As research identifies each syndrome’s components, future DSM editions can systematically incorporate them and their specific pathophysiologies that converge into common neural and behavioral pathways.

Until neuroscience elucidates the pathogenesis of psychiatric diseases, wouldn’t it make sense to recognize 4 major syndromes: mood, anxiety, psychosis, and addiction? This might prompt the FDA to approve drugs for clusters of symptoms rather than for arbitrarily defined diagnostic categories that appear distinct but in fact share many signs and symptoms.

Psychiatrists, then, could reconceptualize how primary and secondary psychopathologic disorders can produce common symptoms that do not constitute a specific disease but do aggregate into treatable syndromes, the underpinning of which may be shared biological mechanisms.

A major challenge for the DSM-V committees as they revise the diagnostic “bible” of psychiatric disorders is to determine whether mental illnesses are diseases, disorders, or syndromes.

Here’s how my version of Webster’s dictionary defines these terms:

• Disease: A particular distinctive process in the body with a specific cause and characteristic symptoms.
• Disorder: Irregularity, disturbance, or interruption of normal functions.
• Syndrome: A number of symptoms occurring together and characterizing a specific disease.

Let’s consider 4 facts that may be relevant for this decision.

Probably not ‘diseases’

No objective laboratory test can differentiate 1 psychiatric malady from another, and this lack of specificity casts doubt on the disease model. However, many documented perturbations of normal brain functions are consistent with a disorder paradigm.

Symptom overlap

The signs and symptoms of psychiatric ailments overlap considerably. Depression and anxiety share many symptoms and frequently co-occur. Bipolar mania and schizophrenia share psychotic features, cognitive deficits, agitation, suicidality, aggressive behavior, etc. The obsessions of obsessive-compulsive disorder (OCD) resemble and sometimes morph into the fixed false beliefs (delusions) of psychosis, and OCD’s compulsions often characterize the behaviors of other psychiatric disorders, such as anorexia or bulimia nervosa.

Personality disorder features essentially are attenuated but enduring forms of Axis I conditions. Nearly all psychiatric illnesses have some degree of suicidality, insomnia, and addictive behavior. Posttraumatic stress disorder’s symptoms recapitulate those of numerous diagnostic categories, such as anxiety, depression, psychosis, negative symptoms, mania, OCD, impulsive behavior, and personality changes.

Common neurobiology

Most diagnostic categories in psychiatry share some neurobiologic features, such as:

• neurotransmitter pathways (serotonin, dopamine, norepinephrine, or glutamate)
• structural abnormalities on neuroimaging (cortical atrophy, ventriculomegaly, gray and/or white matter abnormalities) or
• genetic predispositions.

Medical and psychiatric comorbidities (migraine, chronic pain, diabetes, obesity, alcohol abuse, anxiety, eating disorders, and Axis II features) occur across all major psychiatric diagnoses.

Nonspecific medications

Psychotropics approved for treating 1 condition are frequently useful for others:

• Selective serotonin reuptake inhibitors initially were indicated for depression but soon were found to have efficacy for panic attacks, social phobia, OCD, bulimia, impulse dyscontrol, and fibromyalgia.
• Atypical antipsychotics indicated for schizophrenia have been found useful in bipolar mania, treatment-resistant OCD, treatment-resistant depression, borderline personality disorder, delirium, anxiety, etc.
• Anticonvulsants indicated for epilepsy later were approved for bipolar mania and then found to have uses in alcoholism and drug abuse, aggressive behavior, impulsivity, treatment-resistant anxiety, and psychosis.

The multiple efficacies of psychiatric drug classes strongly suggest shared pharmacotherapeutic responsiveness across psychiatric diagnoses, including those without any FDA-approved medication. They also render the opinionated and uninformed criticism of “off-label” prescribing practices hollow, effete, and counterproductive.

Back to definitions

So, should DSM-V committees define diagnostic categories as diseases, disorders, or syndromes? The state of knowledge points to disorders and syndromes rather than diseases. There very well could be a specific disease within a syndrome, but many phenotypes and genotypes manifest with similar clusters of psychiatric signs and symptoms. As research identifies each syndrome’s components, future DSM editions can systematically incorporate them and their specific pathophysiologies that converge into common neural and behavioral pathways.

Until neuroscience elucidates the pathogenesis of psychiatric diseases, wouldn’t it make sense to recognize 4 major syndromes: mood, anxiety, psychosis, and addiction? This might prompt the FDA to approve drugs for clusters of symptoms rather than for arbitrarily defined diagnostic categories that appear distinct but in fact share many signs and symptoms.

Psychiatrists, then, could reconceptualize how primary and secondary psychopathologic disorders can produce common symptoms that do not constitute a specific disease but do aggregate into treatable syndromes, the underpinning of which may be shared biological mechanisms.

A major challenge for the DSM-V committees as they revise the diagnostic “bible” of psychiatric disorders is to determine whether mental illnesses are diseases, disorders, or syndromes.

Here’s how my version of Webster’s dictionary defines these terms:

• Disease: A particular distinctive process in the body with a specific cause and characteristic symptoms.
• Disorder: Irregularity, disturbance, or interruption of normal functions.
• Syndrome: A number of symptoms occurring together and characterizing a specific disease.

Let’s consider 4 facts that may be relevant for this decision.

Probably not ‘diseases’

No objective laboratory test can differentiate 1 psychiatric malady from another, and this lack of specificity casts doubt on the disease model. However, many documented perturbations of normal brain functions are consistent with a disorder paradigm.

Symptom overlap

The signs and symptoms of psychiatric ailments overlap considerably. Depression and anxiety share many symptoms and frequently co-occur. Bipolar mania and schizophrenia share psychotic features, cognitive deficits, agitation, suicidality, aggressive behavior, etc. The obsessions of obsessive-compulsive disorder (OCD) resemble and sometimes morph into the fixed false beliefs (delusions) of psychosis, and OCD’s compulsions often characterize the behaviors of other psychiatric disorders, such as anorexia or bulimia nervosa.

Personality disorder features essentially are attenuated but enduring forms of Axis I conditions. Nearly all psychiatric illnesses have some degree of suicidality, insomnia, and addictive behavior. Posttraumatic stress disorder’s symptoms recapitulate those of numerous diagnostic categories, such as anxiety, depression, psychosis, negative symptoms, mania, OCD, impulsive behavior, and personality changes.

Common neurobiology

Most diagnostic categories in psychiatry share some neurobiologic features, such as:

• neurotransmitter pathways (serotonin, dopamine, norepinephrine, or glutamate)
• structural abnormalities on neuroimaging (cortical atrophy, ventriculomegaly, gray and/or white matter abnormalities) or
• genetic predispositions.

Medical and psychiatric comorbidities (migraine, chronic pain, diabetes, obesity, alcohol abuse, anxiety, eating disorders, and Axis II features) occur across all major psychiatric diagnoses.

Nonspecific medications

Psychotropics approved for treating 1 condition are frequently useful for others:

• Selective serotonin reuptake inhibitors initially were indicated for depression but soon were found to have efficacy for panic attacks, social phobia, OCD, bulimia, impulse dyscontrol, and fibromyalgia.
• Atypical antipsychotics indicated for schizophrenia have been found useful in bipolar mania, treatment-resistant OCD, treatment-resistant depression, borderline personality disorder, delirium, anxiety, etc.
• Anticonvulsants indicated for epilepsy later were approved for bipolar mania and then found to have uses in alcoholism and drug abuse, aggressive behavior, impulsivity, treatment-resistant anxiety, and psychosis.

The multiple efficacies of psychiatric drug classes strongly suggest shared pharmacotherapeutic responsiveness across psychiatric diagnoses, including those without any FDA-approved medication. They also render the opinionated and uninformed criticism of “off-label” prescribing practices hollow, effete, and counterproductive.

Back to definitions

So, should DSM-V committees define diagnostic categories as diseases, disorders, or syndromes? The state of knowledge points to disorders and syndromes rather than diseases. There very well could be a specific disease within a syndrome, but many phenotypes and genotypes manifest with similar clusters of psychiatric signs and symptoms. As research identifies each syndrome’s components, future DSM editions can systematically incorporate them and their specific pathophysiologies that converge into common neural and behavioral pathways.

Until neuroscience elucidates the pathogenesis of psychiatric diseases, wouldn’t it make sense to recognize 4 major syndromes: mood, anxiety, psychosis, and addiction? This might prompt the FDA to approve drugs for clusters of symptoms rather than for arbitrarily defined diagnostic categories that appear distinct but in fact share many signs and symptoms.

Psychiatrists, then, could reconceptualize how primary and secondary psychopathologic disorders can produce common symptoms that do not constitute a specific disease but do aggregate into treatable syndromes, the underpinning of which may be shared biological mechanisms.