Current Psychiatry

History: ‘A zillion racing thoughts’

Ms. R, age 44, is referred by her primary care physician. She complains of tenseness, irritability, avolition, and fatigue. She worries incessantly that her children will get sick, a catastrophe will befall her husband, or she’ll do something wrong. She says she sometimes feels as if she’s thinking “a zillion racing thoughts.”

Once fun-loving, outgoing, and energetic, Ms. R says she began feeling unusually anxious 3 years ago. A psychiatrist diagnosed bipolar disorder type II based on her racing thoughts, irritability, low energy, and history of mood swings. Over 2 years, the psychiatrist tried combining valproic acid with bupropion, citalopram, or extended-release venlafaxine, then tried lithium monotherapy. Nothing worked.

Frustrated, Ms. R left the psychiatrist and consulted her primary care physician, who prescribed gabapentin, 200 mg each morning and 300 mg at night; fluoxetine, 50 mg/d; and quetiapine, 12.5 mg/d. Ms. R noticed no improvement and stopped the medications after 6 weeks. The physician urged her to see another psychiatrist, and she presented to us 2 weeks after stopping the medications.

Ms. R also has been feeling depressed and irritable the past 4 months and has trouble falling and staying asleep at night. She sleeps 4 to 5 hours nightly, constantly feels tired, cannot concentrate, and overeats to try to alleviate her stress. She has gained 6 pounds over 2 to 3 months and weighs 160 lb; her body mass index of 26 indicates she is overweight.

She says her worries overwhelm her and cause heart palpitations and muscle tension in her neck and shoulders. She admits to feeling “worthless,” but denies suicidal thoughts.

Ms. R describes her husband and two teenage daughters as “very supportive,” but admits that her fatigue and irritability have strained these relationships; she says she snaps at them for minor things, such as coming to dinner 1 minute late. She misses her job, which she recently quit because of her decreasing ability to function.

At intake, Ms. R says she will not resume previous medications but will consider alternatives. She refuses psychotherapy because of time constraints and transportation problems but is willing to return every 2 weeks for medication checks. She says she adhered to every prescription over 3 years with no major side effects. She has never taken an antidepressant or anxiolytic without a mood stabilizer.

Ms. R reports no medical problems, past substance use, current or past psychotic symptoms, or psychiatric hospitalizations. Her family history shows depression in one first-degree relative and anxiety in others. Her Hamilton Anxiety Scale (HAM-A) score of 20 indicates moderate anxiety. Laboratory tests ordered by her primary care physician are normal.

poll here

The authors’ observations

Racing thoughts, irritable mood, decreased sleep, and concentration problems can point to GAD, mania associated with bipolar disorder type I, or hypomania suggesting bipolar disorder type I or II (Table 1).¹

We suspect GAD because:

• Ms. R’s thoughts “race” only when she worries
• her irritability and concentration problems seem more sustained than episodic
• she has difficulty falling and staying asleep, but her need for sleep has not decreased
• she complains of constant fatigue, whereas abnormally high energy characterizes bipolar disorder’s manic or hypomanic phase.

Does Ms. R have depression? Determining if the patient’s depressive symptoms are secondary to GAD or warrant a separate diagnosis can be difficult (Table 1). With Ms. R’s permission, we talked to her family, because collateral information often helps clarify the diagnosis. Her husband and daughters offered no significant new insights, however.

Table 1

Overlap among symptoms that suggest GAD, mania, or major depression

Treatment: Targeting the anxiety

To address Ms. R’s anxiety symptoms, we start buspirone, 5 mg tid, and titrate to 15 mg bid over 2 weeks. We choose buspirone—which is FDA-approved to treat GAD—because it is unlikely to cause a mood switch if bipolar disorder is causing Ms. R’s depression. We discuss with her the drug’s indications, benefits, and potential side effects (such as vertigo, headache, lightheadedness, and nausea).

At the first 2-week follow-up, Ms. R reports no side effects but little improvement. After another 2 weeks, she says she feels less anxiety, irritability, pain, and fewer racing thoughts. She reports less difficulty falling asleep, though she’s still sleeping only about 6 hours nightly. Her HAM-A score falls to 12, indicating mild anxiety.

Ms. R, however, says she still feels depressed, tired, distracted, unmotivated, and worthless. Her Hamilton Rating Scale for Depression (HAM-D) score of 16 indicates moderate depression.

poll here

The authors’ observations

The persistence of Ms. R’s depressive symptoms suggests comorbid major depressive disorder (MDD). In fact, MDD and GAD are considered the most common mood-anxiety comorbidities.²

Determining whether Ms. R has unipolar depression or bipolar disorder is extremely important, considering the treatment implications. In patients with bipolar disorder, any antidepressant can trigger mania or hypomania if used without a mood stabilizer. Some studies also have associated rare cases of suicidal behavior with antidepressant use.^3,4 Lifetime risk of suicide in bipolar disorder is approximately 20 times that in the general population.⁵

Although Ms. R’s history does not reveal a previous manic episode, ruling out hypomania is difficult because it usually does not impair work or social functioning. Hypomania often goes unreported because others hardly notice it. Collateral history can uncover clues to hypomania (See For Your Patient), but Ms. R’s husband and daughters say they have not seen such episodes.

On the other hand, normal behavior can be mistaken for hypomania. Ms. R’s previous psychiatrist and primary care physician might have misinterpreted Ms. R’s baseline extroverted personality as hypomanic behavior. Also, her over-whelming depressive and anxiety symptoms between depressive episodes made her normal moods appear hypomanic.

Compared with unipolar depression, bipolar depression is more frequently associated with psychomotor retardation, hypersomnia, early onset, and family history of bipolar disorder.⁶ Ms. R, however, suffered low energy, terminal insomnia, and late onset, and had no known family history of bipolar disorder.

The Mood Disorder Questionnaire, a scale of self-administered questions, can help screen for symptoms that suggest bipolar disorder. A positive questionnaire result demands further clinical evaluation.⁷

Box

Continued treatment: ‘normal’ again

In addition to the HAM-D, we also administer the Mood Disorder Questionnaire. Results suggest Ms. R does not have bipolar illness.

To address Ms. R’s depressive symptoms, we start the selective serotonin reuptake inhibitor escitalopram at a low dosage (5 mg/d) to avoid exacerbating her anxiety. We discuss the drug’s potential to induce mania, hypomania, or other adverse effects such as nausea, anxiety, sleep disturbance, headache, and sexual dysfunction. Buspirone is maintained at 15 mg bid.

Two weeks later, Ms. R reports some increase in energy and motivation. After another 2 weeks, she reports significantly improved mood and concentration. She consistently falls asleep at 10 PM and sleeps 8 hours each night. She also finds time to read and go out with her friends and she gets along more amicably with her daughters and husband.

One month later, we increase escitalopram to 10 mg/d, a normal therapeutic dosage. Ms. R continues to respond positively and reports no side effects. Two months after starting the antidepressant, her HAM-D score of 8 suggests normal mood. We decrease follow-up visits to once monthly.

At a subsequent visit, Ms. R tells us she wants to find a job. A month later, she says she is enjoying her new job in a department store. Over the next 6 months, she remains free of anxiety, depressive symptoms, hypomanic behavior, and side effects. She tells us it’s nice to feel “normal” again.

We reduce Ms. R’s appointments to every 3 months. After another year, we refer her back to her primary care physician at her request.

The authors’ observations

DSM-IV-TR¹ divides bipolar disorder into three categories:

• type I, in which the patient has had at least one manic episode with or without major depression
• type II, characterized by one or more major depressive episodes and at least one hypomanic episode
• cyclothymia, which is defined as fluctuation between hypomanic and minor depressive episodes.

Much is said about how underdiagnosis of bipolar disorder⁸ delays or prevents proper therapy with mood stabilizers, leading to suboptimal symptom resolution. As with Ms. R, however, an incorrect bipolar disorder diagnosis can be just as harmful. Three years of unnecessary and ineffective treatment worsened her anxiety and depressive symptoms and quality of life.

A comprehensive clinical interview supplemented with insights from family and friends can minimize the risk of misdiagnosis when patients present with symptoms that suggest bipolar disorder, depression, or GAD.

Differentiating between the following clinical features can also help you reach a diagnosis:

Sleep/energy level. Mania/hypomania is characterized by decreased need for sleep; patients often feel energetic even after 2 to 4 hours of sleep. Both depression and GAD diminish energy level, although mood is more depressed in depression. Patients with GAD have trouble falling asleep, while those with depression awaken early or have hypersomnia.

Behavior. Patients in the manic phase of bipolar disorder engage in risky, pleasurable activities with high potential for painful consequences. This drastic behavior change is not seen in depression or GAD (Table 2).

Table 2

Differentiating symptoms common to GAD, major depression, and mania

Related resources

• Depression and Bipolar Support Alliance. www.dbsalliance.org.
• Anxiety Disorders Association of America. www.adaa.org.

Drug brand names

• Bupropion • Wellbutrin
• Buspirone • BuSpar
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Quetiapine • Seroquel
• Valproic acid • Depakene
• Venlafaxine • Effexor

Disclosures

Dr. Williams is a speaker for Wyeth.

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

History: ‘A zillion racing thoughts’

Ms. R, age 44, is referred by her primary care physician. She complains of tenseness, irritability, avolition, and fatigue. She worries incessantly that her children will get sick, a catastrophe will befall her husband, or she’ll do something wrong. She says she sometimes feels as if she’s thinking “a zillion racing thoughts.”

Once fun-loving, outgoing, and energetic, Ms. R says she began feeling unusually anxious 3 years ago. A psychiatrist diagnosed bipolar disorder type II based on her racing thoughts, irritability, low energy, and history of mood swings. Over 2 years, the psychiatrist tried combining valproic acid with bupropion, citalopram, or extended-release venlafaxine, then tried lithium monotherapy. Nothing worked.

Frustrated, Ms. R left the psychiatrist and consulted her primary care physician, who prescribed gabapentin, 200 mg each morning and 300 mg at night; fluoxetine, 50 mg/d; and quetiapine, 12.5 mg/d. Ms. R noticed no improvement and stopped the medications after 6 weeks. The physician urged her to see another psychiatrist, and she presented to us 2 weeks after stopping the medications.

Ms. R also has been feeling depressed and irritable the past 4 months and has trouble falling and staying asleep at night. She sleeps 4 to 5 hours nightly, constantly feels tired, cannot concentrate, and overeats to try to alleviate her stress. She has gained 6 pounds over 2 to 3 months and weighs 160 lb; her body mass index of 26 indicates she is overweight.

She says her worries overwhelm her and cause heart palpitations and muscle tension in her neck and shoulders. She admits to feeling “worthless,” but denies suicidal thoughts.

Ms. R describes her husband and two teenage daughters as “very supportive,” but admits that her fatigue and irritability have strained these relationships; she says she snaps at them for minor things, such as coming to dinner 1 minute late. She misses her job, which she recently quit because of her decreasing ability to function.

At intake, Ms. R says she will not resume previous medications but will consider alternatives. She refuses psychotherapy because of time constraints and transportation problems but is willing to return every 2 weeks for medication checks. She says she adhered to every prescription over 3 years with no major side effects. She has never taken an antidepressant or anxiolytic without a mood stabilizer.

Ms. R reports no medical problems, past substance use, current or past psychotic symptoms, or psychiatric hospitalizations. Her family history shows depression in one first-degree relative and anxiety in others. Her Hamilton Anxiety Scale (HAM-A) score of 20 indicates moderate anxiety. Laboratory tests ordered by her primary care physician are normal.

poll here

The authors’ observations

Racing thoughts, irritable mood, decreased sleep, and concentration problems can point to GAD, mania associated with bipolar disorder type I, or hypomania suggesting bipolar disorder type I or II (Table 1).¹

We suspect GAD because:

• Ms. R’s thoughts “race” only when she worries
• her irritability and concentration problems seem more sustained than episodic
• she has difficulty falling and staying asleep, but her need for sleep has not decreased
• she complains of constant fatigue, whereas abnormally high energy characterizes bipolar disorder’s manic or hypomanic phase.

Does Ms. R have depression? Determining if the patient’s depressive symptoms are secondary to GAD or warrant a separate diagnosis can be difficult (Table 1). With Ms. R’s permission, we talked to her family, because collateral information often helps clarify the diagnosis. Her husband and daughters offered no significant new insights, however.

Table 1

Overlap among symptoms that suggest GAD, mania, or major depression

Treatment: Targeting the anxiety

To address Ms. R’s anxiety symptoms, we start buspirone, 5 mg tid, and titrate to 15 mg bid over 2 weeks. We choose buspirone—which is FDA-approved to treat GAD—because it is unlikely to cause a mood switch if bipolar disorder is causing Ms. R’s depression. We discuss with her the drug’s indications, benefits, and potential side effects (such as vertigo, headache, lightheadedness, and nausea).

At the first 2-week follow-up, Ms. R reports no side effects but little improvement. After another 2 weeks, she says she feels less anxiety, irritability, pain, and fewer racing thoughts. She reports less difficulty falling asleep, though she’s still sleeping only about 6 hours nightly. Her HAM-A score falls to 12, indicating mild anxiety.

Ms. R, however, says she still feels depressed, tired, distracted, unmotivated, and worthless. Her Hamilton Rating Scale for Depression (HAM-D) score of 16 indicates moderate depression.

poll here

The authors’ observations

The persistence of Ms. R’s depressive symptoms suggests comorbid major depressive disorder (MDD). In fact, MDD and GAD are considered the most common mood-anxiety comorbidities.²

Determining whether Ms. R has unipolar depression or bipolar disorder is extremely important, considering the treatment implications. In patients with bipolar disorder, any antidepressant can trigger mania or hypomania if used without a mood stabilizer. Some studies also have associated rare cases of suicidal behavior with antidepressant use.^3,4 Lifetime risk of suicide in bipolar disorder is approximately 20 times that in the general population.⁵

Although Ms. R’s history does not reveal a previous manic episode, ruling out hypomania is difficult because it usually does not impair work or social functioning. Hypomania often goes unreported because others hardly notice it. Collateral history can uncover clues to hypomania (See For Your Patient), but Ms. R’s husband and daughters say they have not seen such episodes.

On the other hand, normal behavior can be mistaken for hypomania. Ms. R’s previous psychiatrist and primary care physician might have misinterpreted Ms. R’s baseline extroverted personality as hypomanic behavior. Also, her over-whelming depressive and anxiety symptoms between depressive episodes made her normal moods appear hypomanic.

Compared with unipolar depression, bipolar depression is more frequently associated with psychomotor retardation, hypersomnia, early onset, and family history of bipolar disorder.⁶ Ms. R, however, suffered low energy, terminal insomnia, and late onset, and had no known family history of bipolar disorder.

The Mood Disorder Questionnaire, a scale of self-administered questions, can help screen for symptoms that suggest bipolar disorder. A positive questionnaire result demands further clinical evaluation.⁷

Box

Continued treatment: ‘normal’ again

In addition to the HAM-D, we also administer the Mood Disorder Questionnaire. Results suggest Ms. R does not have bipolar illness.

To address Ms. R’s depressive symptoms, we start the selective serotonin reuptake inhibitor escitalopram at a low dosage (5 mg/d) to avoid exacerbating her anxiety. We discuss the drug’s potential to induce mania, hypomania, or other adverse effects such as nausea, anxiety, sleep disturbance, headache, and sexual dysfunction. Buspirone is maintained at 15 mg bid.

Two weeks later, Ms. R reports some increase in energy and motivation. After another 2 weeks, she reports significantly improved mood and concentration. She consistently falls asleep at 10 PM and sleeps 8 hours each night. She also finds time to read and go out with her friends and she gets along more amicably with her daughters and husband.

One month later, we increase escitalopram to 10 mg/d, a normal therapeutic dosage. Ms. R continues to respond positively and reports no side effects. Two months after starting the antidepressant, her HAM-D score of 8 suggests normal mood. We decrease follow-up visits to once monthly.

At a subsequent visit, Ms. R tells us she wants to find a job. A month later, she says she is enjoying her new job in a department store. Over the next 6 months, she remains free of anxiety, depressive symptoms, hypomanic behavior, and side effects. She tells us it’s nice to feel “normal” again.

We reduce Ms. R’s appointments to every 3 months. After another year, we refer her back to her primary care physician at her request.

The authors’ observations

DSM-IV-TR¹ divides bipolar disorder into three categories:

• type I, in which the patient has had at least one manic episode with or without major depression
• type II, characterized by one or more major depressive episodes and at least one hypomanic episode
• cyclothymia, which is defined as fluctuation between hypomanic and minor depressive episodes.

Much is said about how underdiagnosis of bipolar disorder⁸ delays or prevents proper therapy with mood stabilizers, leading to suboptimal symptom resolution. As with Ms. R, however, an incorrect bipolar disorder diagnosis can be just as harmful. Three years of unnecessary and ineffective treatment worsened her anxiety and depressive symptoms and quality of life.

A comprehensive clinical interview supplemented with insights from family and friends can minimize the risk of misdiagnosis when patients present with symptoms that suggest bipolar disorder, depression, or GAD.

Differentiating between the following clinical features can also help you reach a diagnosis:

Sleep/energy level. Mania/hypomania is characterized by decreased need for sleep; patients often feel energetic even after 2 to 4 hours of sleep. Both depression and GAD diminish energy level, although mood is more depressed in depression. Patients with GAD have trouble falling asleep, while those with depression awaken early or have hypersomnia.

Behavior. Patients in the manic phase of bipolar disorder engage in risky, pleasurable activities with high potential for painful consequences. This drastic behavior change is not seen in depression or GAD (Table 2).

Table 2

Differentiating symptoms common to GAD, major depression, and mania

Related resources

• Depression and Bipolar Support Alliance. www.dbsalliance.org.
• Anxiety Disorders Association of America. www.adaa.org.

Drug brand names

• Bupropion • Wellbutrin
• Buspirone • BuSpar
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Quetiapine • Seroquel
• Valproic acid • Depakene
• Venlafaxine • Effexor

Disclosures

Dr. Williams is a speaker for Wyeth.

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

History: ‘A zillion racing thoughts’

Ms. R, age 44, is referred by her primary care physician. She complains of tenseness, irritability, avolition, and fatigue. She worries incessantly that her children will get sick, a catastrophe will befall her husband, or she’ll do something wrong. She says she sometimes feels as if she’s thinking “a zillion racing thoughts.”

Once fun-loving, outgoing, and energetic, Ms. R says she began feeling unusually anxious 3 years ago. A psychiatrist diagnosed bipolar disorder type II based on her racing thoughts, irritability, low energy, and history of mood swings. Over 2 years, the psychiatrist tried combining valproic acid with bupropion, citalopram, or extended-release venlafaxine, then tried lithium monotherapy. Nothing worked.

Frustrated, Ms. R left the psychiatrist and consulted her primary care physician, who prescribed gabapentin, 200 mg each morning and 300 mg at night; fluoxetine, 50 mg/d; and quetiapine, 12.5 mg/d. Ms. R noticed no improvement and stopped the medications after 6 weeks. The physician urged her to see another psychiatrist, and she presented to us 2 weeks after stopping the medications.

Ms. R also has been feeling depressed and irritable the past 4 months and has trouble falling and staying asleep at night. She sleeps 4 to 5 hours nightly, constantly feels tired, cannot concentrate, and overeats to try to alleviate her stress. She has gained 6 pounds over 2 to 3 months and weighs 160 lb; her body mass index of 26 indicates she is overweight.

She says her worries overwhelm her and cause heart palpitations and muscle tension in her neck and shoulders. She admits to feeling “worthless,” but denies suicidal thoughts.

Ms. R describes her husband and two teenage daughters as “very supportive,” but admits that her fatigue and irritability have strained these relationships; she says she snaps at them for minor things, such as coming to dinner 1 minute late. She misses her job, which she recently quit because of her decreasing ability to function.

At intake, Ms. R says she will not resume previous medications but will consider alternatives. She refuses psychotherapy because of time constraints and transportation problems but is willing to return every 2 weeks for medication checks. She says she adhered to every prescription over 3 years with no major side effects. She has never taken an antidepressant or anxiolytic without a mood stabilizer.

Ms. R reports no medical problems, past substance use, current or past psychotic symptoms, or psychiatric hospitalizations. Her family history shows depression in one first-degree relative and anxiety in others. Her Hamilton Anxiety Scale (HAM-A) score of 20 indicates moderate anxiety. Laboratory tests ordered by her primary care physician are normal.

poll here

The authors’ observations

Racing thoughts, irritable mood, decreased sleep, and concentration problems can point to GAD, mania associated with bipolar disorder type I, or hypomania suggesting bipolar disorder type I or II (Table 1).¹

We suspect GAD because:

• Ms. R’s thoughts “race” only when she worries
• her irritability and concentration problems seem more sustained than episodic
• she has difficulty falling and staying asleep, but her need for sleep has not decreased
• she complains of constant fatigue, whereas abnormally high energy characterizes bipolar disorder’s manic or hypomanic phase.

Does Ms. R have depression? Determining if the patient’s depressive symptoms are secondary to GAD or warrant a separate diagnosis can be difficult (Table 1). With Ms. R’s permission, we talked to her family, because collateral information often helps clarify the diagnosis. Her husband and daughters offered no significant new insights, however.

Table 1

Overlap among symptoms that suggest GAD, mania, or major depression

Treatment: Targeting the anxiety

To address Ms. R’s anxiety symptoms, we start buspirone, 5 mg tid, and titrate to 15 mg bid over 2 weeks. We choose buspirone—which is FDA-approved to treat GAD—because it is unlikely to cause a mood switch if bipolar disorder is causing Ms. R’s depression. We discuss with her the drug’s indications, benefits, and potential side effects (such as vertigo, headache, lightheadedness, and nausea).

At the first 2-week follow-up, Ms. R reports no side effects but little improvement. After another 2 weeks, she says she feels less anxiety, irritability, pain, and fewer racing thoughts. She reports less difficulty falling asleep, though she’s still sleeping only about 6 hours nightly. Her HAM-A score falls to 12, indicating mild anxiety.

Ms. R, however, says she still feels depressed, tired, distracted, unmotivated, and worthless. Her Hamilton Rating Scale for Depression (HAM-D) score of 16 indicates moderate depression.

poll here

The authors’ observations

The persistence of Ms. R’s depressive symptoms suggests comorbid major depressive disorder (MDD). In fact, MDD and GAD are considered the most common mood-anxiety comorbidities.²

Determining whether Ms. R has unipolar depression or bipolar disorder is extremely important, considering the treatment implications. In patients with bipolar disorder, any antidepressant can trigger mania or hypomania if used without a mood stabilizer. Some studies also have associated rare cases of suicidal behavior with antidepressant use.^3,4 Lifetime risk of suicide in bipolar disorder is approximately 20 times that in the general population.⁵

Although Ms. R’s history does not reveal a previous manic episode, ruling out hypomania is difficult because it usually does not impair work or social functioning. Hypomania often goes unreported because others hardly notice it. Collateral history can uncover clues to hypomania (See For Your Patient), but Ms. R’s husband and daughters say they have not seen such episodes.

On the other hand, normal behavior can be mistaken for hypomania. Ms. R’s previous psychiatrist and primary care physician might have misinterpreted Ms. R’s baseline extroverted personality as hypomanic behavior. Also, her over-whelming depressive and anxiety symptoms between depressive episodes made her normal moods appear hypomanic.

Compared with unipolar depression, bipolar depression is more frequently associated with psychomotor retardation, hypersomnia, early onset, and family history of bipolar disorder.⁶ Ms. R, however, suffered low energy, terminal insomnia, and late onset, and had no known family history of bipolar disorder.

The Mood Disorder Questionnaire, a scale of self-administered questions, can help screen for symptoms that suggest bipolar disorder. A positive questionnaire result demands further clinical evaluation.⁷

Box

Continued treatment: ‘normal’ again

In addition to the HAM-D, we also administer the Mood Disorder Questionnaire. Results suggest Ms. R does not have bipolar illness.

To address Ms. R’s depressive symptoms, we start the selective serotonin reuptake inhibitor escitalopram at a low dosage (5 mg/d) to avoid exacerbating her anxiety. We discuss the drug’s potential to induce mania, hypomania, or other adverse effects such as nausea, anxiety, sleep disturbance, headache, and sexual dysfunction. Buspirone is maintained at 15 mg bid.

Two weeks later, Ms. R reports some increase in energy and motivation. After another 2 weeks, she reports significantly improved mood and concentration. She consistently falls asleep at 10 PM and sleeps 8 hours each night. She also finds time to read and go out with her friends and she gets along more amicably with her daughters and husband.

One month later, we increase escitalopram to 10 mg/d, a normal therapeutic dosage. Ms. R continues to respond positively and reports no side effects. Two months after starting the antidepressant, her HAM-D score of 8 suggests normal mood. We decrease follow-up visits to once monthly.

At a subsequent visit, Ms. R tells us she wants to find a job. A month later, she says she is enjoying her new job in a department store. Over the next 6 months, she remains free of anxiety, depressive symptoms, hypomanic behavior, and side effects. She tells us it’s nice to feel “normal” again.

We reduce Ms. R’s appointments to every 3 months. After another year, we refer her back to her primary care physician at her request.

The authors’ observations

DSM-IV-TR¹ divides bipolar disorder into three categories:

• type I, in which the patient has had at least one manic episode with or without major depression
• type II, characterized by one or more major depressive episodes and at least one hypomanic episode
• cyclothymia, which is defined as fluctuation between hypomanic and minor depressive episodes.

Much is said about how underdiagnosis of bipolar disorder⁸ delays or prevents proper therapy with mood stabilizers, leading to suboptimal symptom resolution. As with Ms. R, however, an incorrect bipolar disorder diagnosis can be just as harmful. Three years of unnecessary and ineffective treatment worsened her anxiety and depressive symptoms and quality of life.

A comprehensive clinical interview supplemented with insights from family and friends can minimize the risk of misdiagnosis when patients present with symptoms that suggest bipolar disorder, depression, or GAD.

Differentiating between the following clinical features can also help you reach a diagnosis:

Sleep/energy level. Mania/hypomania is characterized by decreased need for sleep; patients often feel energetic even after 2 to 4 hours of sleep. Both depression and GAD diminish energy level, although mood is more depressed in depression. Patients with GAD have trouble falling asleep, while those with depression awaken early or have hypersomnia.

Behavior. Patients in the manic phase of bipolar disorder engage in risky, pleasurable activities with high potential for painful consequences. This drastic behavior change is not seen in depression or GAD (Table 2).

Table 2

Differentiating symptoms common to GAD, major depression, and mania

Related resources

• Depression and Bipolar Support Alliance. www.dbsalliance.org.
• Anxiety Disorders Association of America. www.adaa.org.

Drug brand names

• Bupropion • Wellbutrin
• Buspirone • BuSpar
• Escitalopram • Lexapro
• Fluoxetine • Prozac
• Gabapentin • Neurontin
• Quetiapine • Seroquel
• Valproic acid • Depakene
• Venlafaxine • Effexor

Disclosures

Dr. Williams is a speaker for Wyeth.

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

Police find Mr. B, age 45, at home after he called 911 to report that he killed his wife. Covered in blood, he confesses immediately and is holding the knife he used to stab her. Police arrest him without resistance and charge him with murder.

Three months later, Mr. B presents for a sanity evaluation. He has a history of schizoaffective disorder and has required three past psychiatric hospitalizations. Urine and serum toxicology studies the day of the killing were negative for alcohol and drugs.

Was Mr. B legally sane or insane when he committed this offense? As psychiatrists, we are often called on to assess competence to stand trial and sanity at the time of a crime. In a previous article (Current Psychiatry, June 2006), we described how to evaluate whether a mentally ill criminal court defendant is competent to stand trial. This article introduces the process for conducting a sanity evaluation.

What is sanity?

“Sanity” is a legal—not clinical—term related to a plea of “not guilty by reason of insanity.” A sanity evaluation—a mental health professional’s specialized assessment—may be entered into evidence at a criminal trial to help a judge or jury determine whether a defendant is criminally responsible for an alleged offense.

Approximately 1 in every 100 defendants charged with a felony raise an insanity defense.¹ A criminal defendant who pleads not guilty by reason of insanity asserts that he committed the offense and asks the court to find him not culpable because of his mental state when the offense occurred. Competence to stand trial, by comparison, focuses on the defendant’s present mental state (Table 1).

Before starting a sanity evaluation, determine the standard that applies in the jurisdiction where the alleged offense occurred. Federal and state courts have restricted insanity standards the past 20 years. Some states, including Idaho and Nevada, abolished the insanity defense. Others adopted “guilty but mentally ill” standards, which hold mentally-ill defendants criminally responsible for their actions.²

All insanity standards require that the defendant had a mental disease or defect at the time of the offense, but the terms “mental disease” and “mental defect” do not equate with particular DSM-IV-TR “mental disorders.” Rather, courts can interpret which diagnoses qualify for determining sanity.

Courts usually rule that serious psychotic and mood disorders qualify as a mental disease and mental retardation qualifies as a mental defect. Mental disorders that usually do not qualify include personality disorders, paraphilias, and voluntary intoxication.

Table 1

How competency and sanity assessments differ

History of insanity defense

Many early codes of law provided exceptions to criminal responsibility for the mentally ill. Modern insanity standards are based on English common law (Table 2).

Table 2

From ‘wild beast’ to ‘irresistible impulse’: Milestones in the insanity defense

To be found insane under the wild beast standard, the defendant had to be “totally deprived of his understanding and memory, so as to not know what he is doing, no more than an infant, a brute or a wild beast.”³

‘Irresistible impulse.’ The “irresistible impulse” standard was first used successfully in 1840 in the trial of Edward Oxford, who attempted to assassinate Queen Victoria. In Regina v. Oxford, the court recognized that “if some controlling disease was…the acting power within him which he could not resist, then he will not be responsible.”⁴

The M’Naughten rule—perhaps the most famous standard—was established in 1843. M’Naughten suffered from paranoid delusions that the prime minister of England was plotting against him; he planned to kill the prime minister but mistakenly killed his secretary. The examiners who evaluated M’Naughten testified that he was insane, and the jury concurred. The public and royal family were incensed, however, and appellate judges reviewed the verdict and insanity standard.

The appeals court issued the M’Naughten rule,⁵ by which a mentally ill defendant may be considered insane if, at the time of the act, he:

• did not understand the nature and quality of the act
  
• or did not know the wrongfulness of the act.
  

• appreciate the criminality of his act
  
• or conform his conduct to the requirements of the law.
  

How to evaluate insanity

Prepare. Review the defendant’s medical/psychiatric records and materials pertaining to the offense, including the police report and other legal or medical documents. Indications of a prior psychiatric diagnosis may support or rebut the presence of a mental disease or defect at the time account of the of the alleged offense.

To assess the defendant’s mental state at the time of the act, note any recorded observations of his or her behavior during or around that time. You may wish to collect this information from collateral sources, as well. Look for bizarre behavior or other evidence that the defendant suffered from delusions, hallucinations, or other symptoms of a severe mental disease or defect.

Police records may contain:

• reports by witnesses, victims, and police officers about the defendant’s statements or behavior during or soon after the offense
  
• a defendant’s statement to the arresting officers.
  

Interview the defendant. Next, conduct a thorough standard psychiatric interview in person. Inform the defendant that the interview is not confidential, and that any information he or she provides may be included in a written report to the court or disclosed during trial testimony.

Consider psychiatric symptoms the defendant experienced during the offense, medication adherence, and use of alcohol or other mood-altering substances. Remember that voluntary intoxication does not provide grounds for an insanity defense, even in states that allow the irresistible impulse defense.

Obtain a detailed account of the event from the defendant. Look for:

• symptoms of a mental disease or defect when the offense occurred
  
• the defendant’s knowledge (or lack thereof) that the offense was wrong at that time (Table 3)
  

Signs that a defendant knew an act was wrong

Indications that the defendant was aware at the time of the offense that his actions were wrong may include:

• behaviors during or immediately after the event, such as hiding evidence, lying to authorities, or fleeing the scene
  
• a rational motive such as jealousy, revenge, or personal gain.
  

Caveats. The defendant’s mental status during the interview may differ vastly from that at the time of the offense. Don’t be swayed if a defendant with a history of psychosis now appears symptom-free. Recent treatment may explain his or her lack of symptoms. Also be aware that the defendant may be malingering mental illness to support an insanity defense and escape criminal responsibility.⁷

Outcomes. Approximately 15% to 25% of criminal defendants who plead insanity are adjudicated insane. Technically, a defendant who is found legally insane has been acquitted of the offense. The insanity defense is less likely to succeed in jury than in nonjury trials.⁸

Although the defendant may not be punished once acquitted, he or she may be committed to a mental institution to ensure treatment compliance and protect the public.

Table 4

Irresistible impulse test for sanity: A modern interpretation

Case continued: seeing red

When you interview Mr. B 3 months after his arrest, he is not psychotic. He says he ran out of his medications 6 months before he killed his wife and resumed taking them while in jail awaiting trial.

Mr. B relates that in the months before the offense he grew concerned that his wife was involved in “ritualistic sexual perversions” commanded by the devil. He tried to discuss this with his mother-in-law and minister but did not get a satisfactory response.

On the evening of the killing, Mr. B was particularly agitated while waiting for his wife to return home from work. She walked in wearing a red sweater, which indicated to him that she had had sex with 17 different men at work that day. To save her from eternal damnation for adultery, Mr. B believed he had to stab her 17 times before sunrise.

He becomes tearful during the interview and says he wishes he “could go back in time and fix things.”

Mr. B. shows clear evidence of a severe mental disease during the offense (psychosis, medication nonadherence) without a personality or substance use disorder.

Factors that indicate he did not know his actions were wrong at the time of the event include:

• his delusional belief that he was saving his wife from damnation
  
• lack of a rational motive
  
• lack of effort to conceal the offense
  
• his ready confession to 911 operators and police officers
  
• his cooperation with police.
  

Mr. B’s attempts at alternate solutions (discussions with clergy and his mother-in-law) and the perceived deadline (the need to kill his wife before sunrise to prevent damnation) indicate that he had an irresistible impulse.

Open to interpretation

As this case suggests, a defendant’s sanity or insanity is determined by many factors and is often open to interpretation. In court, the prosecution and defense aim to answer two complex questions:

• Did the defendant suffer from a mental illness? (This may be clear in patients with schizophrenia but more difficult to determine in others, such as in substance-induced mood disorder.)
  
• Did this mental illness alter the defendant’s judgment to such a degree that he or she no longer knew the offense was wrongful?
  

Recent cases. Despite her plea of not guilty by reason of insanity, Andrea Yates was convicted of murder in June 2002 for drowning her five children in the bathtub of their home. Though most would agree the Texas housewife suffered from a severe mental illness, prosecutors convinced the jury that she knew the wrongfulness of her actions. An appeal was granted earlier this year, and Yates returned to court in June.

Also this year, the U.S. Supreme Court heard a case contesting Arizona’s insanity defense on grounds that it violated a defendant’s right to due process. In late June, the court sided with the state, continuing to allow each to state to establish its own insanity defense standard.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org,
  
• Giorgi-Guarnieri D, Janofsky J, Keram E, et al. AAPL practice guideline for forensic psychiatric evaluation of defendants raising the insanity defense. J Am Acad Psychiatry Law 2002;30(2 suppl):S3-40.
  
• Noffsinger SG, Resnick PJ. Insanity defense evaluations. Directions in Psychiatry 1999;19:325-38.
  

Police find Mr. B, age 45, at home after he called 911 to report that he killed his wife. Covered in blood, he confesses immediately and is holding the knife he used to stab her. Police arrest him without resistance and charge him with murder.

Three months later, Mr. B presents for a sanity evaluation. He has a history of schizoaffective disorder and has required three past psychiatric hospitalizations. Urine and serum toxicology studies the day of the killing were negative for alcohol and drugs.

Was Mr. B legally sane or insane when he committed this offense? As psychiatrists, we are often called on to assess competence to stand trial and sanity at the time of a crime. In a previous article (Current Psychiatry, June 2006), we described how to evaluate whether a mentally ill criminal court defendant is competent to stand trial. This article introduces the process for conducting a sanity evaluation.

What is sanity?

“Sanity” is a legal—not clinical—term related to a plea of “not guilty by reason of insanity.” A sanity evaluation—a mental health professional’s specialized assessment—may be entered into evidence at a criminal trial to help a judge or jury determine whether a defendant is criminally responsible for an alleged offense.

Approximately 1 in every 100 defendants charged with a felony raise an insanity defense.¹ A criminal defendant who pleads not guilty by reason of insanity asserts that he committed the offense and asks the court to find him not culpable because of his mental state when the offense occurred. Competence to stand trial, by comparison, focuses on the defendant’s present mental state (Table 1).

Before starting a sanity evaluation, determine the standard that applies in the jurisdiction where the alleged offense occurred. Federal and state courts have restricted insanity standards the past 20 years. Some states, including Idaho and Nevada, abolished the insanity defense. Others adopted “guilty but mentally ill” standards, which hold mentally-ill defendants criminally responsible for their actions.²

All insanity standards require that the defendant had a mental disease or defect at the time of the offense, but the terms “mental disease” and “mental defect” do not equate with particular DSM-IV-TR “mental disorders.” Rather, courts can interpret which diagnoses qualify for determining sanity.

Courts usually rule that serious psychotic and mood disorders qualify as a mental disease and mental retardation qualifies as a mental defect. Mental disorders that usually do not qualify include personality disorders, paraphilias, and voluntary intoxication.

Table 1

How competency and sanity assessments differ

History of insanity defense

Many early codes of law provided exceptions to criminal responsibility for the mentally ill. Modern insanity standards are based on English common law (Table 2).

Table 2

From ‘wild beast’ to ‘irresistible impulse’: Milestones in the insanity defense

To be found insane under the wild beast standard, the defendant had to be “totally deprived of his understanding and memory, so as to not know what he is doing, no more than an infant, a brute or a wild beast.”³

‘Irresistible impulse.’ The “irresistible impulse” standard was first used successfully in 1840 in the trial of Edward Oxford, who attempted to assassinate Queen Victoria. In Regina v. Oxford, the court recognized that “if some controlling disease was…the acting power within him which he could not resist, then he will not be responsible.”⁴

The M’Naughten rule—perhaps the most famous standard—was established in 1843. M’Naughten suffered from paranoid delusions that the prime minister of England was plotting against him; he planned to kill the prime minister but mistakenly killed his secretary. The examiners who evaluated M’Naughten testified that he was insane, and the jury concurred. The public and royal family were incensed, however, and appellate judges reviewed the verdict and insanity standard.

The appeals court issued the M’Naughten rule,⁵ by which a mentally ill defendant may be considered insane if, at the time of the act, he:

• did not understand the nature and quality of the act
  
• or did not know the wrongfulness of the act.
  

• appreciate the criminality of his act
  
• or conform his conduct to the requirements of the law.
  

How to evaluate insanity

Prepare. Review the defendant’s medical/psychiatric records and materials pertaining to the offense, including the police report and other legal or medical documents. Indications of a prior psychiatric diagnosis may support or rebut the presence of a mental disease or defect at the time account of the of the alleged offense.

To assess the defendant’s mental state at the time of the act, note any recorded observations of his or her behavior during or around that time. You may wish to collect this information from collateral sources, as well. Look for bizarre behavior or other evidence that the defendant suffered from delusions, hallucinations, or other symptoms of a severe mental disease or defect.

Police records may contain:

• reports by witnesses, victims, and police officers about the defendant’s statements or behavior during or soon after the offense
  
• a defendant’s statement to the arresting officers.
  

Interview the defendant. Next, conduct a thorough standard psychiatric interview in person. Inform the defendant that the interview is not confidential, and that any information he or she provides may be included in a written report to the court or disclosed during trial testimony.

Consider psychiatric symptoms the defendant experienced during the offense, medication adherence, and use of alcohol or other mood-altering substances. Remember that voluntary intoxication does not provide grounds for an insanity defense, even in states that allow the irresistible impulse defense.

Obtain a detailed account of the event from the defendant. Look for:

• symptoms of a mental disease or defect when the offense occurred
  
• the defendant’s knowledge (or lack thereof) that the offense was wrong at that time (Table 3)
  

Signs that a defendant knew an act was wrong

Indications that the defendant was aware at the time of the offense that his actions were wrong may include:

• behaviors during or immediately after the event, such as hiding evidence, lying to authorities, or fleeing the scene
  
• a rational motive such as jealousy, revenge, or personal gain.
  

Caveats. The defendant’s mental status during the interview may differ vastly from that at the time of the offense. Don’t be swayed if a defendant with a history of psychosis now appears symptom-free. Recent treatment may explain his or her lack of symptoms. Also be aware that the defendant may be malingering mental illness to support an insanity defense and escape criminal responsibility.⁷

Outcomes. Approximately 15% to 25% of criminal defendants who plead insanity are adjudicated insane. Technically, a defendant who is found legally insane has been acquitted of the offense. The insanity defense is less likely to succeed in jury than in nonjury trials.⁸

Although the defendant may not be punished once acquitted, he or she may be committed to a mental institution to ensure treatment compliance and protect the public.

Table 4

Irresistible impulse test for sanity: A modern interpretation

Case continued: seeing red

When you interview Mr. B 3 months after his arrest, he is not psychotic. He says he ran out of his medications 6 months before he killed his wife and resumed taking them while in jail awaiting trial.

Mr. B relates that in the months before the offense he grew concerned that his wife was involved in “ritualistic sexual perversions” commanded by the devil. He tried to discuss this with his mother-in-law and minister but did not get a satisfactory response.

On the evening of the killing, Mr. B was particularly agitated while waiting for his wife to return home from work. She walked in wearing a red sweater, which indicated to him that she had had sex with 17 different men at work that day. To save her from eternal damnation for adultery, Mr. B believed he had to stab her 17 times before sunrise.

He becomes tearful during the interview and says he wishes he “could go back in time and fix things.”

Mr. B. shows clear evidence of a severe mental disease during the offense (psychosis, medication nonadherence) without a personality or substance use disorder.

Factors that indicate he did not know his actions were wrong at the time of the event include:

• his delusional belief that he was saving his wife from damnation
  
• lack of a rational motive
  
• lack of effort to conceal the offense
  
• his ready confession to 911 operators and police officers
  
• his cooperation with police.
  

Mr. B’s attempts at alternate solutions (discussions with clergy and his mother-in-law) and the perceived deadline (the need to kill his wife before sunrise to prevent damnation) indicate that he had an irresistible impulse.

Open to interpretation

As this case suggests, a defendant’s sanity or insanity is determined by many factors and is often open to interpretation. In court, the prosecution and defense aim to answer two complex questions:

• Did the defendant suffer from a mental illness? (This may be clear in patients with schizophrenia but more difficult to determine in others, such as in substance-induced mood disorder.)
  
• Did this mental illness alter the defendant’s judgment to such a degree that he or she no longer knew the offense was wrongful?
  

Recent cases. Despite her plea of not guilty by reason of insanity, Andrea Yates was convicted of murder in June 2002 for drowning her five children in the bathtub of their home. Though most would agree the Texas housewife suffered from a severe mental illness, prosecutors convinced the jury that she knew the wrongfulness of her actions. An appeal was granted earlier this year, and Yates returned to court in June.

Also this year, the U.S. Supreme Court heard a case contesting Arizona’s insanity defense on grounds that it violated a defendant’s right to due process. In late June, the court sided with the state, continuing to allow each to state to establish its own insanity defense standard.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org,
  
• Giorgi-Guarnieri D, Janofsky J, Keram E, et al. AAPL practice guideline for forensic psychiatric evaluation of defendants raising the insanity defense. J Am Acad Psychiatry Law 2002;30(2 suppl):S3-40.
  
• Noffsinger SG, Resnick PJ. Insanity defense evaluations. Directions in Psychiatry 1999;19:325-38.
  

Police find Mr. B, age 45, at home after he called 911 to report that he killed his wife. Covered in blood, he confesses immediately and is holding the knife he used to stab her. Police arrest him without resistance and charge him with murder.

Three months later, Mr. B presents for a sanity evaluation. He has a history of schizoaffective disorder and has required three past psychiatric hospitalizations. Urine and serum toxicology studies the day of the killing were negative for alcohol and drugs.

Was Mr. B legally sane or insane when he committed this offense? As psychiatrists, we are often called on to assess competence to stand trial and sanity at the time of a crime. In a previous article (Current Psychiatry, June 2006), we described how to evaluate whether a mentally ill criminal court defendant is competent to stand trial. This article introduces the process for conducting a sanity evaluation.

What is sanity?

“Sanity” is a legal—not clinical—term related to a plea of “not guilty by reason of insanity.” A sanity evaluation—a mental health professional’s specialized assessment—may be entered into evidence at a criminal trial to help a judge or jury determine whether a defendant is criminally responsible for an alleged offense.

Approximately 1 in every 100 defendants charged with a felony raise an insanity defense.¹ A criminal defendant who pleads not guilty by reason of insanity asserts that he committed the offense and asks the court to find him not culpable because of his mental state when the offense occurred. Competence to stand trial, by comparison, focuses on the defendant’s present mental state (Table 1).

Before starting a sanity evaluation, determine the standard that applies in the jurisdiction where the alleged offense occurred. Federal and state courts have restricted insanity standards the past 20 years. Some states, including Idaho and Nevada, abolished the insanity defense. Others adopted “guilty but mentally ill” standards, which hold mentally-ill defendants criminally responsible for their actions.²

All insanity standards require that the defendant had a mental disease or defect at the time of the offense, but the terms “mental disease” and “mental defect” do not equate with particular DSM-IV-TR “mental disorders.” Rather, courts can interpret which diagnoses qualify for determining sanity.

Courts usually rule that serious psychotic and mood disorders qualify as a mental disease and mental retardation qualifies as a mental defect. Mental disorders that usually do not qualify include personality disorders, paraphilias, and voluntary intoxication.

Table 1

How competency and sanity assessments differ

History of insanity defense

Many early codes of law provided exceptions to criminal responsibility for the mentally ill. Modern insanity standards are based on English common law (Table 2).

Table 2

From ‘wild beast’ to ‘irresistible impulse’: Milestones in the insanity defense

To be found insane under the wild beast standard, the defendant had to be “totally deprived of his understanding and memory, so as to not know what he is doing, no more than an infant, a brute or a wild beast.”³

‘Irresistible impulse.’ The “irresistible impulse” standard was first used successfully in 1840 in the trial of Edward Oxford, who attempted to assassinate Queen Victoria. In Regina v. Oxford, the court recognized that “if some controlling disease was…the acting power within him which he could not resist, then he will not be responsible.”⁴

The M’Naughten rule—perhaps the most famous standard—was established in 1843. M’Naughten suffered from paranoid delusions that the prime minister of England was plotting against him; he planned to kill the prime minister but mistakenly killed his secretary. The examiners who evaluated M’Naughten testified that he was insane, and the jury concurred. The public and royal family were incensed, however, and appellate judges reviewed the verdict and insanity standard.

The appeals court issued the M’Naughten rule,⁵ by which a mentally ill defendant may be considered insane if, at the time of the act, he:

• did not understand the nature and quality of the act
  
• or did not know the wrongfulness of the act.
  

• appreciate the criminality of his act
  
• or conform his conduct to the requirements of the law.
  

How to evaluate insanity

Prepare. Review the defendant’s medical/psychiatric records and materials pertaining to the offense, including the police report and other legal or medical documents. Indications of a prior psychiatric diagnosis may support or rebut the presence of a mental disease or defect at the time account of the of the alleged offense.

To assess the defendant’s mental state at the time of the act, note any recorded observations of his or her behavior during or around that time. You may wish to collect this information from collateral sources, as well. Look for bizarre behavior or other evidence that the defendant suffered from delusions, hallucinations, or other symptoms of a severe mental disease or defect.

Police records may contain:

• reports by witnesses, victims, and police officers about the defendant’s statements or behavior during or soon after the offense
  
• a defendant’s statement to the arresting officers.
  

Interview the defendant. Next, conduct a thorough standard psychiatric interview in person. Inform the defendant that the interview is not confidential, and that any information he or she provides may be included in a written report to the court or disclosed during trial testimony.

Consider psychiatric symptoms the defendant experienced during the offense, medication adherence, and use of alcohol or other mood-altering substances. Remember that voluntary intoxication does not provide grounds for an insanity defense, even in states that allow the irresistible impulse defense.

Obtain a detailed account of the event from the defendant. Look for:

• symptoms of a mental disease or defect when the offense occurred
  
• the defendant’s knowledge (or lack thereof) that the offense was wrong at that time (Table 3)
  

Signs that a defendant knew an act was wrong

Indications that the defendant was aware at the time of the offense that his actions were wrong may include:

• behaviors during or immediately after the event, such as hiding evidence, lying to authorities, or fleeing the scene
  
• a rational motive such as jealousy, revenge, or personal gain.
  

Caveats. The defendant’s mental status during the interview may differ vastly from that at the time of the offense. Don’t be swayed if a defendant with a history of psychosis now appears symptom-free. Recent treatment may explain his or her lack of symptoms. Also be aware that the defendant may be malingering mental illness to support an insanity defense and escape criminal responsibility.⁷

Outcomes. Approximately 15% to 25% of criminal defendants who plead insanity are adjudicated insane. Technically, a defendant who is found legally insane has been acquitted of the offense. The insanity defense is less likely to succeed in jury than in nonjury trials.⁸

Although the defendant may not be punished once acquitted, he or she may be committed to a mental institution to ensure treatment compliance and protect the public.

Table 4

Irresistible impulse test for sanity: A modern interpretation

Case continued: seeing red

When you interview Mr. B 3 months after his arrest, he is not psychotic. He says he ran out of his medications 6 months before he killed his wife and resumed taking them while in jail awaiting trial.

Mr. B relates that in the months before the offense he grew concerned that his wife was involved in “ritualistic sexual perversions” commanded by the devil. He tried to discuss this with his mother-in-law and minister but did not get a satisfactory response.

On the evening of the killing, Mr. B was particularly agitated while waiting for his wife to return home from work. She walked in wearing a red sweater, which indicated to him that she had had sex with 17 different men at work that day. To save her from eternal damnation for adultery, Mr. B believed he had to stab her 17 times before sunrise.

He becomes tearful during the interview and says he wishes he “could go back in time and fix things.”

Mr. B. shows clear evidence of a severe mental disease during the offense (psychosis, medication nonadherence) without a personality or substance use disorder.

Factors that indicate he did not know his actions were wrong at the time of the event include:

• his delusional belief that he was saving his wife from damnation
  
• lack of a rational motive
  
• lack of effort to conceal the offense
  
• his ready confession to 911 operators and police officers
  
• his cooperation with police.
  

Mr. B’s attempts at alternate solutions (discussions with clergy and his mother-in-law) and the perceived deadline (the need to kill his wife before sunrise to prevent damnation) indicate that he had an irresistible impulse.

Open to interpretation

As this case suggests, a defendant’s sanity or insanity is determined by many factors and is often open to interpretation. In court, the prosecution and defense aim to answer two complex questions:

• Did the defendant suffer from a mental illness? (This may be clear in patients with schizophrenia but more difficult to determine in others, such as in substance-induced mood disorder.)
  
• Did this mental illness alter the defendant’s judgment to such a degree that he or she no longer knew the offense was wrongful?
  

Recent cases. Despite her plea of not guilty by reason of insanity, Andrea Yates was convicted of murder in June 2002 for drowning her five children in the bathtub of their home. Though most would agree the Texas housewife suffered from a severe mental illness, prosecutors convinced the jury that she knew the wrongfulness of her actions. An appeal was granted earlier this year, and Yates returned to court in June.

Also this year, the U.S. Supreme Court heard a case contesting Arizona’s insanity defense on grounds that it violated a defendant’s right to due process. In late June, the court sided with the state, continuing to allow each to state to establish its own insanity defense standard.

Related resources

• American Academy of Psychiatry and the Law. www.aapl.org,
  
• Giorgi-Guarnieri D, Janofsky J, Keram E, et al. AAPL practice guideline for forensic psychiatric evaluation of defendants raising the insanity defense. J Am Acad Psychiatry Law 2002;30(2 suppl):S3-40.
  
• Noffsinger SG, Resnick PJ. Insanity defense evaluations. Directions in Psychiatry 1999;19:325-38.
  

Women become dependent more rapidly than men after initial cocaine, opioid, or alcohol use and may be more sensitive to drugs’ adverse health effects.¹ And although men and women relapse to substance use at similar rates, ovulating women may be particularly vulnerable to relapse at certain times of the month.

Understanding the hormonal influences that increase women’s relapse risk can help you intervene more effectively. This article describes:

• how women’s relapse patterns differ from men’s
  
• why psychotherapy and hormone regulation may be preferred for relapse prevention in women with substance use disorders.
  

Case report: will she relapse again?

Ms. H, age 46, is in her third month of an alcohol and drug residential rehabilitation program. She has a 10-year history of alcohol and crack cocaine dependence and is battling cravings to use again. These feelings are usually triggered by being in places or with people associated with her drug use, but this time she is committed to staying sober.

She started smoking cigarettes in her teens and using drugs and alcohol in her mid 20s. She feels that her dependency has been out of control in the 10 years since her son was born.

She has tried to quit many times on her own but has managed no more than 1 month of abstinence. She often has relapsed in response to feeling anxious or depressed about being unemployed or after arguing with her partner.

Mechanisms of relapse

Dopamine release is essential for encoding learned associations. When a drug is used in the early dependency state, dopamine release produces pleasure that reinforces continued drug use. Once the behavior is learned, environmental stimuli can trigger dopamine and turn on the brain circuits for this familiar, highly rewarding behavior. Dopamine also is the primary cause of long-lasting brain changes that make it difficult for substance-dependent persons such as Ms. H to control desire for the drug.²

Early relapse—caused by dopamine’s and other neurotransmitters’ effects on various brain regions—is triggered by environmental stimuli such as:

• re-exposure to a small amount of the drug
  
• exposure to an environment or cues associated with past drug use
  
• exposure to stressful events.
  

Table 1

3 stages of relapse and their neurobiologic components

Emotions, stress trigger relapse

Ms. H. reports increased irritability and impulsivity along with depressed mood—especially during the 3 to 4 days preceding her menstrual period. Her periods are regular, and these mood symptoms recur each month. She does not meet criteria for major depressive disorder.

Emotional reactions play a larger role in relapse for women than for men. Women report higher levels of craving and depressed mood during abstinence and experience stronger urges to drink and smoke when depressed. Women also are more likely to report substance use relapse in response to specific stressful events, disappointments, or depressed mood.¹ This is consistent with evidence that women have heightened physiologic responses to social rejection and social stressors.⁵

A lower density of brain serotonin transporter has been associated with a higher risk of depression in women. Because estrogen and progesterone affect expression of the serotonin transporter, changes in these hormone levels might alter the risk of depression.⁶ Thus, ovarian hormones’ effect on the serotonin system may contribute to the higher rate of emotionally triggered relapse in women versus men.

Menstrual cycle phases. How men and women respond to stress may contribute to differences in their relapse behaviors (Table 2).

During the first 2 weeks of the menstrual cycle—the follicular phase—women show lower physiologic reactivity (as seen in blood pressure and catecholamine measurements) and lower cortisol responsiveness than men do in response to psychosocial stress. Estrogen contributes to this effect by attenuating sympathoadrenal responsiveness.⁵

During the latter 2 weeks of the menstrual cycle—the luteal phase—the ovulating woman’s hypothalamic-pituitary-adrenal (HPA) axis response increases and increases her sensitivity to stress. In this phase, progesterone’s presence reverses estrogen’s effect and makes the brain more reactive to emotions and stressors.

Higher stress responsiveness is associated with increased cocaine craving.^7,8 A 20-year literature review of the role of substance abuse in depression indicates that HPA axis responsiveness of depressed women exceeds that of depressed men.⁹

Summary. Women may be more susceptible than men to emotionally triggered relapse, especially during the menstrual cycle’s luteal phase. Women may also be more susceptible than men to relapse in response to nicotine and cocaine cues.

Table 2

Substance use relapse patterns: Women versus men

Menstruation and relapse patterns

Research into a correlation between menstrual cycle phases and dependency behavior is in its infancy. Early nicotine, alcohol, and stimulant addiction studies have shown inconsistent results.

Nicotine. A naturalistic study of women smokers ages 20 to 39 showed that they smoked more cigarettes per day during the late luteal phase, but their nicotine boost and mood states were similar throughout the menstrual cycle.¹⁰

Some—but not all—studies suggest that nicotine withdrawal symptoms increase during the luteal phase.^11,12 In an outpatient study designed to assess hormonal effects on nicotine response, 30 female smokers acutely abstinent of nicotine were randomly assigned by menstrual cycle phase to receive transdermal nicotine or a placebo patch. Both premenstrual and nicotine withdrawal symptoms intensified in the women’s late luteal phase, compared with the follicular phase.¹²

Conversely, the same researchers found that menstrual cycle phase did not affect withdrawal symptoms in 21 nicotine-dependent female inpatients, even though premenstrual changes occurred in the late luteal phase.

As the authors observed, drawing conclusions can be difficult when menstrual cycle hormone withdrawal and nicotine withdrawal symptoms overlap.^12-16

Alcohol. Premenstrual syndrome (PMS) increases a woman’s risk of alcohol abuse. Alcohol and allopregnenolone—progesterone’s neuroactive metabolite—both facilitate gamma-aminobutyric acid ionotropic type A (GABAA) receptor activity. Thus, women with PMS and alcohol dependence may have a genetically more-sensitive GABAA system.¹⁷ Unfortunately, aside from one study that shows increased alcohol intake during the luteal phase, no studies have examined alcohol withdrawal, craving, and relapse across the menstrual cycle.¹⁸

Stimulants. Stimulant craving and relapse have not been examined in women at different menstrual cycle phases. Some authors speculate that women may have a higher subjective response to stimulants during the early follicular phase—when estrogen levels are higher and progesterone levels are lower—compared with the luteal phase.¹⁹

Sex hormones and relapse

Estrogen. Preclinical studies suggest that estrogen facilitates substance dependence by enhancing dopaminergic activity (Table 3).^1,20-26 Because reinstatement (the animal model of relapse) is driven partially by dopaminergic activity in the striatum, one could hypothesize that:

• estrogen’s dopamine-enhancing effects facilitate dependence
  
• women with stimulant dependence are at higher risk of relapse in the follicular phase—when estrogen levels are higher—than in the luteal phase.
  

Table 3

Preclinical findings: How hormones may influence addictive behavior

Treatment implications

Psychotherapy. Evidence suggests that emotions and mood states may play a larger role in triggering substance abuse relapse in women than in men. Psychotherapy and residential treatment therefore are particularly important components of women’s treatment.

In a 6-month follow-up outpatient study of cocaine dependence, women responded better than men did to behavioral treatment, even though the women had more-severe disorders at entry.^27,28

A more-recent inpatient study followed 64 men and 37 women hospitalized for treatment of cocaine dependence. Researchers compared the patients’ drug use histories, psychiatric diagnoses, and Addiction Severity Index (ASI) scores during hospitalization and their cocaine use and ASI scores 6 months later. In initial evaluations, women had significantly more-severe family and social problems. At follow-up, however, significantly more women than men were abstinent from cocaine use, and their family/social problems had diminshed.²⁸

Notably, a recent functional MRI study comparing 17 male and 10 female abstinent cocaine-dependent subjects indicated that the women more often used verbal coping strategies to decrease cocaine craving.²⁹ This finding supports the potential benefit of psychotherapy to prevent relapse in women with a history of substance dependence.

Hormone regulation. For many women, continuous oral contraceptives (OCPs) can improve affect variability across the menstrual cycle and diminish negative mood. Others, however, experience negative changes in mood or affect while taking OCPs. Risk factors for a negative response include:

• history of depression or other psychological distress symptoms
  
• dysmenorrhea
  
• PMS
  
• history of pregnancy-related mood symptoms
  
• family history of OCP-related mood complaints
  
• being in the postpartum
  
• age 30
  

Continuous OCPs can be given so that women have only two to three menstrual periods per year. Formulations with ethinyl estradiol and norethindrone—such as Necon 0.5/35 or 1.0/35—may stabilize mood more effectively than others.

Give a 2-month trial, then re-evaluate progress. Because of the increased risk of clotting, only nonsmokers and women without a history of blood clots should take OCPs.

Case report: Fighting the cravings

Eight months ago, when Ms. H was still using cocaine, her primary care physician prescribed fluoxetine, 20 mg/d, for depressive symptoms. Her mood has not improved, nor has her menstrual cycle-related depression or irritability. She asks if anything else might stop her premenstrual cravings.

Because of Ms. H’s reported PMS, we counsel her to be especially vigilant for alcohol cravings around the luteal and late luteal phases of her menstrual cycle (Table 4). We discuss with her:

• the need to watch for signs of relapse
  
• the importance of aggressive treatment, including psychotherapy, group therapy, and residential treatment, as needed.
  

She agrees to a 2-month trial, and we schedule a follow-up appointment to re-evaluate her progress.

Table 4

Interventions to prevent relapse in women with addiction disorders

• Carroll ME, Lynch WJ, Roth ME, et al. Sex and estrogen influence drug abuse. Trends Pharmacol Sci 2004;25(5):273-9.
  
• Roth ME, Cosgrove KP, Carroll ME. Sex differences in the vulnerability to drug abuse: a review of preclinical studies. Neurosci Biobehav Rev 2004;28(6):533-46.
  
• Everitt BJ, Robbins TW. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nat Neurosci 2005;8(11):1481-9.
  

• Fluoxetine • Prozac
  
• Ethinyl estradiol and norethindrone oral contraceptive • Necon, others
  

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

Women become dependent more rapidly than men after initial cocaine, opioid, or alcohol use and may be more sensitive to drugs’ adverse health effects.¹ And although men and women relapse to substance use at similar rates, ovulating women may be particularly vulnerable to relapse at certain times of the month.

Understanding the hormonal influences that increase women’s relapse risk can help you intervene more effectively. This article describes:

• how women’s relapse patterns differ from men’s
  
• why psychotherapy and hormone regulation may be preferred for relapse prevention in women with substance use disorders.
  

Case report: will she relapse again?

Ms. H, age 46, is in her third month of an alcohol and drug residential rehabilitation program. She has a 10-year history of alcohol and crack cocaine dependence and is battling cravings to use again. These feelings are usually triggered by being in places or with people associated with her drug use, but this time she is committed to staying sober.

She started smoking cigarettes in her teens and using drugs and alcohol in her mid 20s. She feels that her dependency has been out of control in the 10 years since her son was born.

She has tried to quit many times on her own but has managed no more than 1 month of abstinence. She often has relapsed in response to feeling anxious or depressed about being unemployed or after arguing with her partner.

Mechanisms of relapse

Dopamine release is essential for encoding learned associations. When a drug is used in the early dependency state, dopamine release produces pleasure that reinforces continued drug use. Once the behavior is learned, environmental stimuli can trigger dopamine and turn on the brain circuits for this familiar, highly rewarding behavior. Dopamine also is the primary cause of long-lasting brain changes that make it difficult for substance-dependent persons such as Ms. H to control desire for the drug.²

Early relapse—caused by dopamine’s and other neurotransmitters’ effects on various brain regions—is triggered by environmental stimuli such as:

• re-exposure to a small amount of the drug
  
• exposure to an environment or cues associated with past drug use
  
• exposure to stressful events.
  

Table 1

3 stages of relapse and their neurobiologic components

Emotions, stress trigger relapse

Ms. H. reports increased irritability and impulsivity along with depressed mood—especially during the 3 to 4 days preceding her menstrual period. Her periods are regular, and these mood symptoms recur each month. She does not meet criteria for major depressive disorder.

Emotional reactions play a larger role in relapse for women than for men. Women report higher levels of craving and depressed mood during abstinence and experience stronger urges to drink and smoke when depressed. Women also are more likely to report substance use relapse in response to specific stressful events, disappointments, or depressed mood.¹ This is consistent with evidence that women have heightened physiologic responses to social rejection and social stressors.⁵

A lower density of brain serotonin transporter has been associated with a higher risk of depression in women. Because estrogen and progesterone affect expression of the serotonin transporter, changes in these hormone levels might alter the risk of depression.⁶ Thus, ovarian hormones’ effect on the serotonin system may contribute to the higher rate of emotionally triggered relapse in women versus men.

Menstrual cycle phases. How men and women respond to stress may contribute to differences in their relapse behaviors (Table 2).

During the first 2 weeks of the menstrual cycle—the follicular phase—women show lower physiologic reactivity (as seen in blood pressure and catecholamine measurements) and lower cortisol responsiveness than men do in response to psychosocial stress. Estrogen contributes to this effect by attenuating sympathoadrenal responsiveness.⁵

During the latter 2 weeks of the menstrual cycle—the luteal phase—the ovulating woman’s hypothalamic-pituitary-adrenal (HPA) axis response increases and increases her sensitivity to stress. In this phase, progesterone’s presence reverses estrogen’s effect and makes the brain more reactive to emotions and stressors.

Higher stress responsiveness is associated with increased cocaine craving.^7,8 A 20-year literature review of the role of substance abuse in depression indicates that HPA axis responsiveness of depressed women exceeds that of depressed men.⁹

Summary. Women may be more susceptible than men to emotionally triggered relapse, especially during the menstrual cycle’s luteal phase. Women may also be more susceptible than men to relapse in response to nicotine and cocaine cues.

Table 2

Substance use relapse patterns: Women versus men

Menstruation and relapse patterns

Research into a correlation between menstrual cycle phases and dependency behavior is in its infancy. Early nicotine, alcohol, and stimulant addiction studies have shown inconsistent results.

Nicotine. A naturalistic study of women smokers ages 20 to 39 showed that they smoked more cigarettes per day during the late luteal phase, but their nicotine boost and mood states were similar throughout the menstrual cycle.¹⁰

Some—but not all—studies suggest that nicotine withdrawal symptoms increase during the luteal phase.^11,12 In an outpatient study designed to assess hormonal effects on nicotine response, 30 female smokers acutely abstinent of nicotine were randomly assigned by menstrual cycle phase to receive transdermal nicotine or a placebo patch. Both premenstrual and nicotine withdrawal symptoms intensified in the women’s late luteal phase, compared with the follicular phase.¹²

Conversely, the same researchers found that menstrual cycle phase did not affect withdrawal symptoms in 21 nicotine-dependent female inpatients, even though premenstrual changes occurred in the late luteal phase.

As the authors observed, drawing conclusions can be difficult when menstrual cycle hormone withdrawal and nicotine withdrawal symptoms overlap.^12-16

Alcohol. Premenstrual syndrome (PMS) increases a woman’s risk of alcohol abuse. Alcohol and allopregnenolone—progesterone’s neuroactive metabolite—both facilitate gamma-aminobutyric acid ionotropic type A (GABAA) receptor activity. Thus, women with PMS and alcohol dependence may have a genetically more-sensitive GABAA system.¹⁷ Unfortunately, aside from one study that shows increased alcohol intake during the luteal phase, no studies have examined alcohol withdrawal, craving, and relapse across the menstrual cycle.¹⁸

Stimulants. Stimulant craving and relapse have not been examined in women at different menstrual cycle phases. Some authors speculate that women may have a higher subjective response to stimulants during the early follicular phase—when estrogen levels are higher and progesterone levels are lower—compared with the luteal phase.¹⁹

Sex hormones and relapse

Estrogen. Preclinical studies suggest that estrogen facilitates substance dependence by enhancing dopaminergic activity (Table 3).^1,20-26 Because reinstatement (the animal model of relapse) is driven partially by dopaminergic activity in the striatum, one could hypothesize that:

• estrogen’s dopamine-enhancing effects facilitate dependence
  
• women with stimulant dependence are at higher risk of relapse in the follicular phase—when estrogen levels are higher—than in the luteal phase.
  

Table 3

Preclinical findings: How hormones may influence addictive behavior

Treatment implications

Psychotherapy. Evidence suggests that emotions and mood states may play a larger role in triggering substance abuse relapse in women than in men. Psychotherapy and residential treatment therefore are particularly important components of women’s treatment.

In a 6-month follow-up outpatient study of cocaine dependence, women responded better than men did to behavioral treatment, even though the women had more-severe disorders at entry.^27,28

A more-recent inpatient study followed 64 men and 37 women hospitalized for treatment of cocaine dependence. Researchers compared the patients’ drug use histories, psychiatric diagnoses, and Addiction Severity Index (ASI) scores during hospitalization and their cocaine use and ASI scores 6 months later. In initial evaluations, women had significantly more-severe family and social problems. At follow-up, however, significantly more women than men were abstinent from cocaine use, and their family/social problems had diminshed.²⁸

Notably, a recent functional MRI study comparing 17 male and 10 female abstinent cocaine-dependent subjects indicated that the women more often used verbal coping strategies to decrease cocaine craving.²⁹ This finding supports the potential benefit of psychotherapy to prevent relapse in women with a history of substance dependence.

Hormone regulation. For many women, continuous oral contraceptives (OCPs) can improve affect variability across the menstrual cycle and diminish negative mood. Others, however, experience negative changes in mood or affect while taking OCPs. Risk factors for a negative response include:

• history of depression or other psychological distress symptoms
  
• dysmenorrhea
  
• PMS
  
• history of pregnancy-related mood symptoms
  
• family history of OCP-related mood complaints
  
• being in the postpartum
  
• age 30
  

Continuous OCPs can be given so that women have only two to three menstrual periods per year. Formulations with ethinyl estradiol and norethindrone—such as Necon 0.5/35 or 1.0/35—may stabilize mood more effectively than others.

Give a 2-month trial, then re-evaluate progress. Because of the increased risk of clotting, only nonsmokers and women without a history of blood clots should take OCPs.

Case report: Fighting the cravings

Eight months ago, when Ms. H was still using cocaine, her primary care physician prescribed fluoxetine, 20 mg/d, for depressive symptoms. Her mood has not improved, nor has her menstrual cycle-related depression or irritability. She asks if anything else might stop her premenstrual cravings.

Because of Ms. H’s reported PMS, we counsel her to be especially vigilant for alcohol cravings around the luteal and late luteal phases of her menstrual cycle (Table 4). We discuss with her:

• the need to watch for signs of relapse
  
• the importance of aggressive treatment, including psychotherapy, group therapy, and residential treatment, as needed.
  

She agrees to a 2-month trial, and we schedule a follow-up appointment to re-evaluate her progress.

Table 4

Interventions to prevent relapse in women with addiction disorders

• Carroll ME, Lynch WJ, Roth ME, et al. Sex and estrogen influence drug abuse. Trends Pharmacol Sci 2004;25(5):273-9.
  
• Roth ME, Cosgrove KP, Carroll ME. Sex differences in the vulnerability to drug abuse: a review of preclinical studies. Neurosci Biobehav Rev 2004;28(6):533-46.
  
• Everitt BJ, Robbins TW. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nat Neurosci 2005;8(11):1481-9.
  

• Fluoxetine • Prozac
  
• Ethinyl estradiol and norethindrone oral contraceptive • Necon, others
  

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

Women become dependent more rapidly than men after initial cocaine, opioid, or alcohol use and may be more sensitive to drugs’ adverse health effects.¹ And although men and women relapse to substance use at similar rates, ovulating women may be particularly vulnerable to relapse at certain times of the month.

Understanding the hormonal influences that increase women’s relapse risk can help you intervene more effectively. This article describes:

• how women’s relapse patterns differ from men’s
  
• why psychotherapy and hormone regulation may be preferred for relapse prevention in women with substance use disorders.
  

Case report: will she relapse again?

Ms. H, age 46, is in her third month of an alcohol and drug residential rehabilitation program. She has a 10-year history of alcohol and crack cocaine dependence and is battling cravings to use again. These feelings are usually triggered by being in places or with people associated with her drug use, but this time she is committed to staying sober.

She started smoking cigarettes in her teens and using drugs and alcohol in her mid 20s. She feels that her dependency has been out of control in the 10 years since her son was born.

She has tried to quit many times on her own but has managed no more than 1 month of abstinence. She often has relapsed in response to feeling anxious or depressed about being unemployed or after arguing with her partner.

Mechanisms of relapse

Dopamine release is essential for encoding learned associations. When a drug is used in the early dependency state, dopamine release produces pleasure that reinforces continued drug use. Once the behavior is learned, environmental stimuli can trigger dopamine and turn on the brain circuits for this familiar, highly rewarding behavior. Dopamine also is the primary cause of long-lasting brain changes that make it difficult for substance-dependent persons such as Ms. H to control desire for the drug.²

Early relapse—caused by dopamine’s and other neurotransmitters’ effects on various brain regions—is triggered by environmental stimuli such as:

• re-exposure to a small amount of the drug
  
• exposure to an environment or cues associated with past drug use
  
• exposure to stressful events.
  

Table 1

3 stages of relapse and their neurobiologic components

Emotions, stress trigger relapse

Ms. H. reports increased irritability and impulsivity along with depressed mood—especially during the 3 to 4 days preceding her menstrual period. Her periods are regular, and these mood symptoms recur each month. She does not meet criteria for major depressive disorder.

Emotional reactions play a larger role in relapse for women than for men. Women report higher levels of craving and depressed mood during abstinence and experience stronger urges to drink and smoke when depressed. Women also are more likely to report substance use relapse in response to specific stressful events, disappointments, or depressed mood.¹ This is consistent with evidence that women have heightened physiologic responses to social rejection and social stressors.⁵

A lower density of brain serotonin transporter has been associated with a higher risk of depression in women. Because estrogen and progesterone affect expression of the serotonin transporter, changes in these hormone levels might alter the risk of depression.⁶ Thus, ovarian hormones’ effect on the serotonin system may contribute to the higher rate of emotionally triggered relapse in women versus men.

Menstrual cycle phases. How men and women respond to stress may contribute to differences in their relapse behaviors (Table 2).

During the first 2 weeks of the menstrual cycle—the follicular phase—women show lower physiologic reactivity (as seen in blood pressure and catecholamine measurements) and lower cortisol responsiveness than men do in response to psychosocial stress. Estrogen contributes to this effect by attenuating sympathoadrenal responsiveness.⁵

During the latter 2 weeks of the menstrual cycle—the luteal phase—the ovulating woman’s hypothalamic-pituitary-adrenal (HPA) axis response increases and increases her sensitivity to stress. In this phase, progesterone’s presence reverses estrogen’s effect and makes the brain more reactive to emotions and stressors.

Higher stress responsiveness is associated with increased cocaine craving.^7,8 A 20-year literature review of the role of substance abuse in depression indicates that HPA axis responsiveness of depressed women exceeds that of depressed men.⁹

Summary. Women may be more susceptible than men to emotionally triggered relapse, especially during the menstrual cycle’s luteal phase. Women may also be more susceptible than men to relapse in response to nicotine and cocaine cues.

Table 2

Substance use relapse patterns: Women versus men

Menstruation and relapse patterns

Research into a correlation between menstrual cycle phases and dependency behavior is in its infancy. Early nicotine, alcohol, and stimulant addiction studies have shown inconsistent results.

Nicotine. A naturalistic study of women smokers ages 20 to 39 showed that they smoked more cigarettes per day during the late luteal phase, but their nicotine boost and mood states were similar throughout the menstrual cycle.¹⁰

Some—but not all—studies suggest that nicotine withdrawal symptoms increase during the luteal phase.^11,12 In an outpatient study designed to assess hormonal effects on nicotine response, 30 female smokers acutely abstinent of nicotine were randomly assigned by menstrual cycle phase to receive transdermal nicotine or a placebo patch. Both premenstrual and nicotine withdrawal symptoms intensified in the women’s late luteal phase, compared with the follicular phase.¹²

Conversely, the same researchers found that menstrual cycle phase did not affect withdrawal symptoms in 21 nicotine-dependent female inpatients, even though premenstrual changes occurred in the late luteal phase.

As the authors observed, drawing conclusions can be difficult when menstrual cycle hormone withdrawal and nicotine withdrawal symptoms overlap.^12-16

Alcohol. Premenstrual syndrome (PMS) increases a woman’s risk of alcohol abuse. Alcohol and allopregnenolone—progesterone’s neuroactive metabolite—both facilitate gamma-aminobutyric acid ionotropic type A (GABAA) receptor activity. Thus, women with PMS and alcohol dependence may have a genetically more-sensitive GABAA system.¹⁷ Unfortunately, aside from one study that shows increased alcohol intake during the luteal phase, no studies have examined alcohol withdrawal, craving, and relapse across the menstrual cycle.¹⁸

Stimulants. Stimulant craving and relapse have not been examined in women at different menstrual cycle phases. Some authors speculate that women may have a higher subjective response to stimulants during the early follicular phase—when estrogen levels are higher and progesterone levels are lower—compared with the luteal phase.¹⁹

Sex hormones and relapse

Estrogen. Preclinical studies suggest that estrogen facilitates substance dependence by enhancing dopaminergic activity (Table 3).^1,20-26 Because reinstatement (the animal model of relapse) is driven partially by dopaminergic activity in the striatum, one could hypothesize that:

• estrogen’s dopamine-enhancing effects facilitate dependence
  
• women with stimulant dependence are at higher risk of relapse in the follicular phase—when estrogen levels are higher—than in the luteal phase.
  

Table 3

Preclinical findings: How hormones may influence addictive behavior

Treatment implications

Psychotherapy. Evidence suggests that emotions and mood states may play a larger role in triggering substance abuse relapse in women than in men. Psychotherapy and residential treatment therefore are particularly important components of women’s treatment.

In a 6-month follow-up outpatient study of cocaine dependence, women responded better than men did to behavioral treatment, even though the women had more-severe disorders at entry.^27,28

A more-recent inpatient study followed 64 men and 37 women hospitalized for treatment of cocaine dependence. Researchers compared the patients’ drug use histories, psychiatric diagnoses, and Addiction Severity Index (ASI) scores during hospitalization and their cocaine use and ASI scores 6 months later. In initial evaluations, women had significantly more-severe family and social problems. At follow-up, however, significantly more women than men were abstinent from cocaine use, and their family/social problems had diminshed.²⁸

Notably, a recent functional MRI study comparing 17 male and 10 female abstinent cocaine-dependent subjects indicated that the women more often used verbal coping strategies to decrease cocaine craving.²⁹ This finding supports the potential benefit of psychotherapy to prevent relapse in women with a history of substance dependence.

Hormone regulation. For many women, continuous oral contraceptives (OCPs) can improve affect variability across the menstrual cycle and diminish negative mood. Others, however, experience negative changes in mood or affect while taking OCPs. Risk factors for a negative response include:

• history of depression or other psychological distress symptoms
  
• dysmenorrhea
  
• PMS
  
• history of pregnancy-related mood symptoms
  
• family history of OCP-related mood complaints
  
• being in the postpartum
  
• age 30
  

Continuous OCPs can be given so that women have only two to three menstrual periods per year. Formulations with ethinyl estradiol and norethindrone—such as Necon 0.5/35 or 1.0/35—may stabilize mood more effectively than others.

Give a 2-month trial, then re-evaluate progress. Because of the increased risk of clotting, only nonsmokers and women without a history of blood clots should take OCPs.

Case report: Fighting the cravings

Eight months ago, when Ms. H was still using cocaine, her primary care physician prescribed fluoxetine, 20 mg/d, for depressive symptoms. Her mood has not improved, nor has her menstrual cycle-related depression or irritability. She asks if anything else might stop her premenstrual cravings.

Because of Ms. H’s reported PMS, we counsel her to be especially vigilant for alcohol cravings around the luteal and late luteal phases of her menstrual cycle (Table 4). We discuss with her:

• the need to watch for signs of relapse
  
• the importance of aggressive treatment, including psychotherapy, group therapy, and residential treatment, as needed.
  

She agrees to a 2-month trial, and we schedule a follow-up appointment to re-evaluate her progress.

Table 4

Interventions to prevent relapse in women with addiction disorders

• Carroll ME, Lynch WJ, Roth ME, et al. Sex and estrogen influence drug abuse. Trends Pharmacol Sci 2004;25(5):273-9.
  
• Roth ME, Cosgrove KP, Carroll ME. Sex differences in the vulnerability to drug abuse: a review of preclinical studies. Neurosci Biobehav Rev 2004;28(6):533-46.
  
• Everitt BJ, Robbins TW. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nat Neurosci 2005;8(11):1481-9.
  

• Fluoxetine • Prozac
  
• Ethinyl estradiol and norethindrone oral contraceptive • Necon, others
  

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

Whether you are in training or an experienced practitioner, you need more than a rudimentary understanding of cognitive-behavioral therapy (CBT). This easy-to-use psychotherapy has broad empiric support, is a first-choice treatment,¹ and can help patients cope with depression, anxiety, and other psychological problems.

Psychiatrists who learn CBT well can alleviate many patients’ distress by creatively applying its tools and techniques. For example, the cognitive approach to panic disorder compares favorably to medication^1-3 (Box).

Aaron beck’s CBT

Negative thoughts, biased processing. The greater your fidelity to CBT’s guiding principles (Table 1), the more effective the therapy becomes.⁴ Beck designed CBT to address his observation that depressed persons hold unrealistically negative views about themselves, the world, and the future.^5,6 A distorted information-processing system prevents them from correcting underlying negative beliefs. Negative thoughts predominate their cognitions and seem to arise spontaneously, reflexively, and unremittingly. These “automatic thoughts,” as he called them, reflect underlying themes about the self that can be identified as:

• intermediate beliefs (conditional assumptions, attitudes, and rules)
  
• core beliefs (fundamental, often global, and absolute rules).⁷
  

Guiding principles of cognitive-behavioral therapy

• external (environmental) stress that carries symbolic value
  
• internal (physiologic) stress that activates the affective valence of the underlying schema.^1,5,6
  

CBT’s scientific method. CBT teaches a person the skills to identify this cognitive material and to recognize biases that affect how he or she processes information. You can help patients understand:

• the bidirectional relationship between thoughts, feelings, and behaviors
  
• that they can influence their emotions by changing their thoughts and behavior.
  

You provide empiric tools to help them explore the validity or usefulness of their thoughts and the impact of their behaviors. When patients disprove a negative cognition through this process of “experiential disconfirmation,” you help them to change that cognition. Homework is a key ingredient (Table 2); patients who do their CBT homework are more likely to improve than those who don’t.⁸

Table 2

Structure of a typical CBT session

Evaluating cognitive distortions

Thought records. Automatic thoughts are the cognitive content that runs through our minds moment to moment and that we can access by asking ourselves, “What was going through my mind when I felt (emotion)?” Automatic thoughts can exist as:

• verbal messages (“I can’t believe this!” or “I’m such a loser”)
  
• or images (“I picture my boss screaming at me”).
  

Self-monitoring also facilitates “decentering,” or viewing one’s emotional experience from a distance, which may be crucial to therapeutic success.⁹ By using Socratic questioning (Table 3) and guided discovery, you teach patients to evaluate their automatic thoughts as hypotheses to be tested.

If patients discover that their automatic thoughts are inaccurate, you can help them construct more-balanced or alternate appraisals. Conversely, hypothesis testing may help generate new solutions if the process validates the patient’s initial interpretation of a situation.¹⁰

Table 3

Examples of Socratic and non-Socratic questioning

• overgeneralization (“Nothing ever works out for me”)
  
• all-or-nothing thinking (“I failed again” [after getting 95% on an exam])
  
• mind-reading (“My boss thinks I’m incompetent”)
  
• catastrophization (“My heart is racing; I think I’m having a heart attack!”).¹¹
  

• attitudes (“Weakness is contemptible”)
  
• rules (“I will not let others take advantage of me”)
  
• conditional assumptions (“If I let others take advantage of me, I’m a thoroughly weak person”).
  

Framing the intermediate belief as a conditional assumption can help accomplish this goal. Presumably, the patient was distressed about loaning money to his friend. When pressed, he says he didn’t want to lend the money but felt he couldn’t say no. He identifies his automatic thought as “I’ve been taken advantage of.” Asked what this means if it is true, he replies, “If I get taken advantage of, it means I’m weak.”

Core beliefs are deeper cognitive structures that are not always immediately accessible, although they may occasionally emerge spontaneously as automatic thoughts. They are overgeneralized, absolute statements that fall into one of two categories:

• affiliation (“I am bad,” “I am unlovable”)
  
• competence/vulnerability (“I am weak,” “I am helpless”).
  

Very often, intermediate and core beliefs must be defined in a measurable way before you can help the patient test them. For the man feeling distressed about loaning money, for example, you might ask him to define “being taken advantage of ” or define “weak” by listing all the characteristics he associates with this label.

Restructuring negative beliefs

A variety of techniques can be used to restructure negative beliefs.

• Cost-benefit analysis involves exploring advantages and disadvantages of maintaining a negative belief or a more-balanced alternate belief.
  
• Core belief logs¹² can track day-to-day evidence that suggests a core belief is not 100% true. You and the patient can scrutinize evidence that supports the core belief and reframe the evidence in a more-rational manner.
  
• Life review^10,12 involves asking the patient to re-evaluate a core belief ’s historical underpinnings and to reframe these events from an adult perspective.
  

• rational-emotional role play
  
• empty chair or two-chair dialogue
  
• restructuring early memories with directed imagery.
  

Adjunctive Behavioral Strategies

Behavioral interventions are used in CBT to combat anergia, increase socialization, diminish avoidance, and accumulate data to challenge negative beliefs. Common strategies are designed to enhance self-esteem and confidence and build therapeutic momentum as patients gain energy, feel better, and disconfirm negative beliefs.

Activity monitoring and scheduling. Instruct anergic or avoidant patients to monitor daily activities for the week and to rate the degree of pleasure and accomplishment each activity yields on a scale of 1 to 10. As patients become aware of how much time they spend on low-yield activities, help them gradually replace low-yield with higher-yield activities.

Schedule into the week behavioral goals patients identified at the beginning of therapy. Schedule avoided tasks such as household chores, and link them to pleasurable activities as rewards. To evaluate the accuracy of their thinking, ask patients to predict how much pleasure or mastery they will achieve with scheduled activities, then compare their predictions with actual results.

Also ask patients to anticipate obstacles to achieving their goals, to challenge those obstacles, and to develop contingency plans. Reviewing the patient’s week and its bright spots can disconfirm negatively biased recall such as, “My week was terrible,” or, “I don’t have the energy to do anything anymore.”¹³

Graded task assignments. When scheduling activities, improve success rates by helping patients break down large, unrealistic goals into smaller, more manageable pieces. Ask them to consider realistically what they can accomplish now, not what they could have accomplished before they became ill.

Exposure. Anxious patients avoid feared situations because of catastrophic beliefs that experiencing those situations will harm them. A man with panic disorder may avoid exercise, for example, because he perceives lightheadedness and rapid heart rate as signs of imminent heart attack. Avoiding exercise to prevent the feared symptoms perpetuates his catastrophic beliefs.

Exposure to feared symptoms—while initially arousing high anxiety—allows the patient to experientially disconfirm his beliefs. As he remains well after lightheadedness and rapid heart rate are induced interoceptively (by climbing several flights of stairs, for example), he comes to recognize the situational symptoms as manifestations of anxiety rather than evidence of life-threatening illness.^2,3

In vivo exposure entails confronting the patient with the avoided object or situation. For example, you may show a woman with needle phobia pictures of needles, followed by actual needles themselves, then ask her to touch a needle, hold a needle, etc., until her anxiety gradually diminishes.

Imaginal exposure involves asking the patient to imagine himself in a feared situation and manipulating the images to build his sense of mastery. If he stops the image at the moment of highest arousal, instruct him to “continue to play the film forward” by asking, “What happens next?” This approach shows him that he can cope with difficult situations.

Related resources

For clinicians

• Persons JB. Cognitive therapy in practice: a case formulation approach. New York: WW Norton and Co.; 1989.
  
• Academy of Cognitive Therapy. Training, certification as a cognitive therapist. www.academyofct.org.
  
• Behavior Online. Gathering site for mental health professionals. www.behavior.net.
  
• MySelfHelp.com. Interactive programs and moderated discussion designed as treatment adjuncts for patients with depression, stress, eating disorders, etc. Funded by the National Institute of Mental Health ($20/month program access fee). www.MySelfHelp.com.
  

• Antony M, Swinson R. When perfect isn’t good enough. Oakland, CA: New Harbinger Press; 1998.
  
• Antony M, Swinson R. The shyness and social anxiety workbook. Oakland, CA: New Harbinger Press; 2000.
  
• Young J, Klosko J. Reinventing your life: how to break free from negative life patterns. New York: Dutton; 1993.
  
• Davis M, Eshelman E, McKay M. The relaxation and stress reduction workbook. New York: New Harbinger Press; 1995.
  

Whether you are in training or an experienced practitioner, you need more than a rudimentary understanding of cognitive-behavioral therapy (CBT). This easy-to-use psychotherapy has broad empiric support, is a first-choice treatment,¹ and can help patients cope with depression, anxiety, and other psychological problems.

Psychiatrists who learn CBT well can alleviate many patients’ distress by creatively applying its tools and techniques. For example, the cognitive approach to panic disorder compares favorably to medication^1-3 (Box).

Aaron beck’s CBT

Negative thoughts, biased processing. The greater your fidelity to CBT’s guiding principles (Table 1), the more effective the therapy becomes.⁴ Beck designed CBT to address his observation that depressed persons hold unrealistically negative views about themselves, the world, and the future.^5,6 A distorted information-processing system prevents them from correcting underlying negative beliefs. Negative thoughts predominate their cognitions and seem to arise spontaneously, reflexively, and unremittingly. These “automatic thoughts,” as he called them, reflect underlying themes about the self that can be identified as:

• intermediate beliefs (conditional assumptions, attitudes, and rules)
  
• core beliefs (fundamental, often global, and absolute rules).⁷
  

Guiding principles of cognitive-behavioral therapy

• external (environmental) stress that carries symbolic value
  
• internal (physiologic) stress that activates the affective valence of the underlying schema.^1,5,6
  

CBT’s scientific method. CBT teaches a person the skills to identify this cognitive material and to recognize biases that affect how he or she processes information. You can help patients understand:

• the bidirectional relationship between thoughts, feelings, and behaviors
  
• that they can influence their emotions by changing their thoughts and behavior.
  

You provide empiric tools to help them explore the validity or usefulness of their thoughts and the impact of their behaviors. When patients disprove a negative cognition through this process of “experiential disconfirmation,” you help them to change that cognition. Homework is a key ingredient (Table 2); patients who do their CBT homework are more likely to improve than those who don’t.⁸

Table 2

Structure of a typical CBT session

Evaluating cognitive distortions

Thought records. Automatic thoughts are the cognitive content that runs through our minds moment to moment and that we can access by asking ourselves, “What was going through my mind when I felt (emotion)?” Automatic thoughts can exist as:

• verbal messages (“I can’t believe this!” or “I’m such a loser”)
  
• or images (“I picture my boss screaming at me”).
  

Self-monitoring also facilitates “decentering,” or viewing one’s emotional experience from a distance, which may be crucial to therapeutic success.⁹ By using Socratic questioning (Table 3) and guided discovery, you teach patients to evaluate their automatic thoughts as hypotheses to be tested.

If patients discover that their automatic thoughts are inaccurate, you can help them construct more-balanced or alternate appraisals. Conversely, hypothesis testing may help generate new solutions if the process validates the patient’s initial interpretation of a situation.¹⁰

Table 3

Examples of Socratic and non-Socratic questioning

• overgeneralization (“Nothing ever works out for me”)
  
• all-or-nothing thinking (“I failed again” [after getting 95% on an exam])
  
• mind-reading (“My boss thinks I’m incompetent”)
  
• catastrophization (“My heart is racing; I think I’m having a heart attack!”).¹¹
  

• attitudes (“Weakness is contemptible”)
  
• rules (“I will not let others take advantage of me”)
  
• conditional assumptions (“If I let others take advantage of me, I’m a thoroughly weak person”).
  

Framing the intermediate belief as a conditional assumption can help accomplish this goal. Presumably, the patient was distressed about loaning money to his friend. When pressed, he says he didn’t want to lend the money but felt he couldn’t say no. He identifies his automatic thought as “I’ve been taken advantage of.” Asked what this means if it is true, he replies, “If I get taken advantage of, it means I’m weak.”

Core beliefs are deeper cognitive structures that are not always immediately accessible, although they may occasionally emerge spontaneously as automatic thoughts. They are overgeneralized, absolute statements that fall into one of two categories:

• affiliation (“I am bad,” “I am unlovable”)
  
• competence/vulnerability (“I am weak,” “I am helpless”).
  

Very often, intermediate and core beliefs must be defined in a measurable way before you can help the patient test them. For the man feeling distressed about loaning money, for example, you might ask him to define “being taken advantage of ” or define “weak” by listing all the characteristics he associates with this label.

Restructuring negative beliefs

A variety of techniques can be used to restructure negative beliefs.

• Cost-benefit analysis involves exploring advantages and disadvantages of maintaining a negative belief or a more-balanced alternate belief.
  
• Core belief logs¹² can track day-to-day evidence that suggests a core belief is not 100% true. You and the patient can scrutinize evidence that supports the core belief and reframe the evidence in a more-rational manner.
  
• Life review^10,12 involves asking the patient to re-evaluate a core belief ’s historical underpinnings and to reframe these events from an adult perspective.
  

• rational-emotional role play
  
• empty chair or two-chair dialogue
  
• restructuring early memories with directed imagery.
  

Adjunctive Behavioral Strategies

Behavioral interventions are used in CBT to combat anergia, increase socialization, diminish avoidance, and accumulate data to challenge negative beliefs. Common strategies are designed to enhance self-esteem and confidence and build therapeutic momentum as patients gain energy, feel better, and disconfirm negative beliefs.

Activity monitoring and scheduling. Instruct anergic or avoidant patients to monitor daily activities for the week and to rate the degree of pleasure and accomplishment each activity yields on a scale of 1 to 10. As patients become aware of how much time they spend on low-yield activities, help them gradually replace low-yield with higher-yield activities.

Schedule into the week behavioral goals patients identified at the beginning of therapy. Schedule avoided tasks such as household chores, and link them to pleasurable activities as rewards. To evaluate the accuracy of their thinking, ask patients to predict how much pleasure or mastery they will achieve with scheduled activities, then compare their predictions with actual results.

Also ask patients to anticipate obstacles to achieving their goals, to challenge those obstacles, and to develop contingency plans. Reviewing the patient’s week and its bright spots can disconfirm negatively biased recall such as, “My week was terrible,” or, “I don’t have the energy to do anything anymore.”¹³

Graded task assignments. When scheduling activities, improve success rates by helping patients break down large, unrealistic goals into smaller, more manageable pieces. Ask them to consider realistically what they can accomplish now, not what they could have accomplished before they became ill.

Exposure. Anxious patients avoid feared situations because of catastrophic beliefs that experiencing those situations will harm them. A man with panic disorder may avoid exercise, for example, because he perceives lightheadedness and rapid heart rate as signs of imminent heart attack. Avoiding exercise to prevent the feared symptoms perpetuates his catastrophic beliefs.

Exposure to feared symptoms—while initially arousing high anxiety—allows the patient to experientially disconfirm his beliefs. As he remains well after lightheadedness and rapid heart rate are induced interoceptively (by climbing several flights of stairs, for example), he comes to recognize the situational symptoms as manifestations of anxiety rather than evidence of life-threatening illness.^2,3

In vivo exposure entails confronting the patient with the avoided object or situation. For example, you may show a woman with needle phobia pictures of needles, followed by actual needles themselves, then ask her to touch a needle, hold a needle, etc., until her anxiety gradually diminishes.

Imaginal exposure involves asking the patient to imagine himself in a feared situation and manipulating the images to build his sense of mastery. If he stops the image at the moment of highest arousal, instruct him to “continue to play the film forward” by asking, “What happens next?” This approach shows him that he can cope with difficult situations.

Related resources

For clinicians

• Persons JB. Cognitive therapy in practice: a case formulation approach. New York: WW Norton and Co.; 1989.
  
• Academy of Cognitive Therapy. Training, certification as a cognitive therapist. www.academyofct.org.
  
• Behavior Online. Gathering site for mental health professionals. www.behavior.net.
  
• MySelfHelp.com. Interactive programs and moderated discussion designed as treatment adjuncts for patients with depression, stress, eating disorders, etc. Funded by the National Institute of Mental Health ($20/month program access fee). www.MySelfHelp.com.
  

• Antony M, Swinson R. When perfect isn’t good enough. Oakland, CA: New Harbinger Press; 1998.
  
• Antony M, Swinson R. The shyness and social anxiety workbook. Oakland, CA: New Harbinger Press; 2000.
  
• Young J, Klosko J. Reinventing your life: how to break free from negative life patterns. New York: Dutton; 1993.
  
• Davis M, Eshelman E, McKay M. The relaxation and stress reduction workbook. New York: New Harbinger Press; 1995.
  

Whether you are in training or an experienced practitioner, you need more than a rudimentary understanding of cognitive-behavioral therapy (CBT). This easy-to-use psychotherapy has broad empiric support, is a first-choice treatment,¹ and can help patients cope with depression, anxiety, and other psychological problems.

Psychiatrists who learn CBT well can alleviate many patients’ distress by creatively applying its tools and techniques. For example, the cognitive approach to panic disorder compares favorably to medication^1-3 (Box).

Aaron beck’s CBT

Negative thoughts, biased processing. The greater your fidelity to CBT’s guiding principles (Table 1), the more effective the therapy becomes.⁴ Beck designed CBT to address his observation that depressed persons hold unrealistically negative views about themselves, the world, and the future.^5,6 A distorted information-processing system prevents them from correcting underlying negative beliefs. Negative thoughts predominate their cognitions and seem to arise spontaneously, reflexively, and unremittingly. These “automatic thoughts,” as he called them, reflect underlying themes about the self that can be identified as:

• intermediate beliefs (conditional assumptions, attitudes, and rules)
  
• core beliefs (fundamental, often global, and absolute rules).⁷
  

Guiding principles of cognitive-behavioral therapy

• external (environmental) stress that carries symbolic value
  
• internal (physiologic) stress that activates the affective valence of the underlying schema.^1,5,6
  

CBT’s scientific method. CBT teaches a person the skills to identify this cognitive material and to recognize biases that affect how he or she processes information. You can help patients understand:

• the bidirectional relationship between thoughts, feelings, and behaviors
  
• that they can influence their emotions by changing their thoughts and behavior.
  

You provide empiric tools to help them explore the validity or usefulness of their thoughts and the impact of their behaviors. When patients disprove a negative cognition through this process of “experiential disconfirmation,” you help them to change that cognition. Homework is a key ingredient (Table 2); patients who do their CBT homework are more likely to improve than those who don’t.⁸

Table 2

Structure of a typical CBT session

Evaluating cognitive distortions

Thought records. Automatic thoughts are the cognitive content that runs through our minds moment to moment and that we can access by asking ourselves, “What was going through my mind when I felt (emotion)?” Automatic thoughts can exist as:

• verbal messages (“I can’t believe this!” or “I’m such a loser”)
  
• or images (“I picture my boss screaming at me”).
  

Self-monitoring also facilitates “decentering,” or viewing one’s emotional experience from a distance, which may be crucial to therapeutic success.⁹ By using Socratic questioning (Table 3) and guided discovery, you teach patients to evaluate their automatic thoughts as hypotheses to be tested.

If patients discover that their automatic thoughts are inaccurate, you can help them construct more-balanced or alternate appraisals. Conversely, hypothesis testing may help generate new solutions if the process validates the patient’s initial interpretation of a situation.¹⁰

Table 3

Examples of Socratic and non-Socratic questioning

• overgeneralization (“Nothing ever works out for me”)
  
• all-or-nothing thinking (“I failed again” [after getting 95% on an exam])
  
• mind-reading (“My boss thinks I’m incompetent”)
  
• catastrophization (“My heart is racing; I think I’m having a heart attack!”).¹¹
  

• attitudes (“Weakness is contemptible”)
  
• rules (“I will not let others take advantage of me”)
  
• conditional assumptions (“If I let others take advantage of me, I’m a thoroughly weak person”).
  

Framing the intermediate belief as a conditional assumption can help accomplish this goal. Presumably, the patient was distressed about loaning money to his friend. When pressed, he says he didn’t want to lend the money but felt he couldn’t say no. He identifies his automatic thought as “I’ve been taken advantage of.” Asked what this means if it is true, he replies, “If I get taken advantage of, it means I’m weak.”

Core beliefs are deeper cognitive structures that are not always immediately accessible, although they may occasionally emerge spontaneously as automatic thoughts. They are overgeneralized, absolute statements that fall into one of two categories:

• affiliation (“I am bad,” “I am unlovable”)
  
• competence/vulnerability (“I am weak,” “I am helpless”).
  

Very often, intermediate and core beliefs must be defined in a measurable way before you can help the patient test them. For the man feeling distressed about loaning money, for example, you might ask him to define “being taken advantage of ” or define “weak” by listing all the characteristics he associates with this label.

Restructuring negative beliefs

A variety of techniques can be used to restructure negative beliefs.

• Cost-benefit analysis involves exploring advantages and disadvantages of maintaining a negative belief or a more-balanced alternate belief.
  
• Core belief logs¹² can track day-to-day evidence that suggests a core belief is not 100% true. You and the patient can scrutinize evidence that supports the core belief and reframe the evidence in a more-rational manner.
  
• Life review^10,12 involves asking the patient to re-evaluate a core belief ’s historical underpinnings and to reframe these events from an adult perspective.
  

• rational-emotional role play
  
• empty chair or two-chair dialogue
  
• restructuring early memories with directed imagery.
  

Adjunctive Behavioral Strategies

Behavioral interventions are used in CBT to combat anergia, increase socialization, diminish avoidance, and accumulate data to challenge negative beliefs. Common strategies are designed to enhance self-esteem and confidence and build therapeutic momentum as patients gain energy, feel better, and disconfirm negative beliefs.

Activity monitoring and scheduling. Instruct anergic or avoidant patients to monitor daily activities for the week and to rate the degree of pleasure and accomplishment each activity yields on a scale of 1 to 10. As patients become aware of how much time they spend on low-yield activities, help them gradually replace low-yield with higher-yield activities.

Schedule into the week behavioral goals patients identified at the beginning of therapy. Schedule avoided tasks such as household chores, and link them to pleasurable activities as rewards. To evaluate the accuracy of their thinking, ask patients to predict how much pleasure or mastery they will achieve with scheduled activities, then compare their predictions with actual results.

Also ask patients to anticipate obstacles to achieving their goals, to challenge those obstacles, and to develop contingency plans. Reviewing the patient’s week and its bright spots can disconfirm negatively biased recall such as, “My week was terrible,” or, “I don’t have the energy to do anything anymore.”¹³

Graded task assignments. When scheduling activities, improve success rates by helping patients break down large, unrealistic goals into smaller, more manageable pieces. Ask them to consider realistically what they can accomplish now, not what they could have accomplished before they became ill.

Exposure. Anxious patients avoid feared situations because of catastrophic beliefs that experiencing those situations will harm them. A man with panic disorder may avoid exercise, for example, because he perceives lightheadedness and rapid heart rate as signs of imminent heart attack. Avoiding exercise to prevent the feared symptoms perpetuates his catastrophic beliefs.

Exposure to feared symptoms—while initially arousing high anxiety—allows the patient to experientially disconfirm his beliefs. As he remains well after lightheadedness and rapid heart rate are induced interoceptively (by climbing several flights of stairs, for example), he comes to recognize the situational symptoms as manifestations of anxiety rather than evidence of life-threatening illness.^2,3

In vivo exposure entails confronting the patient with the avoided object or situation. For example, you may show a woman with needle phobia pictures of needles, followed by actual needles themselves, then ask her to touch a needle, hold a needle, etc., until her anxiety gradually diminishes.

Imaginal exposure involves asking the patient to imagine himself in a feared situation and manipulating the images to build his sense of mastery. If he stops the image at the moment of highest arousal, instruct him to “continue to play the film forward” by asking, “What happens next?” This approach shows him that he can cope with difficult situations.

Related resources

For clinicians

• Persons JB. Cognitive therapy in practice: a case formulation approach. New York: WW Norton and Co.; 1989.
  
• Academy of Cognitive Therapy. Training, certification as a cognitive therapist. www.academyofct.org.
  
• Behavior Online. Gathering site for mental health professionals. www.behavior.net.
  
• MySelfHelp.com. Interactive programs and moderated discussion designed as treatment adjuncts for patients with depression, stress, eating disorders, etc. Funded by the National Institute of Mental Health ($20/month program access fee). www.MySelfHelp.com.
  

• Antony M, Swinson R. When perfect isn’t good enough. Oakland, CA: New Harbinger Press; 1998.
  
• Antony M, Swinson R. The shyness and social anxiety workbook. Oakland, CA: New Harbinger Press; 2000.
  
• Young J, Klosko J. Reinventing your life: how to break free from negative life patterns. New York: Dutton; 1993.
  
• Davis M, Eshelman E, McKay M. The relaxation and stress reduction workbook. New York: New Harbinger Press; 1995.
  

When you address sexuality, you open a window to the patient’s psychology. Talking about sex may illuminate important clues about the individual’s capacity to:

• give and receive pleasure
  
• love and be loved
  
• be psychologically intimate
  
• manage expected and unexpected changes throughout adulthood.¹
  

The opportunity to listen to sexual histories over time will help you become proficient in generating causal hypotheses and using them to help your patients.

Patients think—often erroneously—that all psychiatrists are knowledgeable, skillful, and interested in addressing sexual concerns. But psychiatric practice has turned away from clinical sexuality, and most of us learn on our own how to take a sexual history and to bring up relevant topics during subsequent sessions.

These activities are not particularly difficult,² but they often bump up against one or more clinician fears (Table 1).³ You can master these apprehensions by:

• identifying them in yourself
  
• thinking about them rationally
  
• learning about the broad range of human sexual expression
  
• understanding professional boundaries.⁴
  

Table 1

Clinicians’ 5 worst fears about taking sexual histories

Assessing sexual complaints

Sexual behavior—normal and abnormal, masturbatory and partnered—rests upon biological, psychological, and interpersonal elements, and cultural concepts of normality and morality.⁵ These four components also are the sources of sexual problems (Table 2).^6,7

To accurately assess individuals’ and couples’ sexual problems, we must consider the four components’ present and past contributions in every case. We may declare a hypothesis of cause after one or two sessions, but the explanation usually evolves and becomes more complex with time.⁸

Outside of sexuality clinics, we usually learn about a patient’s sexual complaint during therapy for another problem:

• Individuals may bring up cross-dressing, anxiety about possibly being homosexual, concern about violent sexual fantasies, or other issues of sexual identity. Sexual function concerns may include new difficulty attaining orgasm, aversion to intercourse, painful intercourse, too-rapid ejaculation, episodic inability to maintain an erection, or longstanding inability to ejaculate while with a partner.
  
• Couples may present with difficulty orchestrating their sexual lives. Their complaints may involve discrepancies in sexual desire, inability to bring a young wife to orgasm, cessation of sex, infidelity, dyspareunia, erectile dysfunction in a newly married couple in their 60s, or a wife’s distress over her husband’s use of Internet pornography.
  
• Referrals may come from a social agency about an individual whose sexual behavior clashes with social values or laws. Judges, lawyers, state boards, clergy, or medical chiefs-of-staff may request assistance with individuals who cross sexual boundaries at work, are accused of sex crimes, or have been sexually victimized.⁵
  

4 components of sexual behavior: Where sexual problems may arise

Ask about sexual identity

By the end of adolescence, most individuals have stably in place the three self labels that encompass sexual identity:

• gender identity—the degree of comfort with the self as masculine or feminine
  
• orientation—the gender of those who attract or repel us for romantic and sexual purposes
  
• intention—what we want to do with our bodies and our partners’ bodies during sexual behavior.⁹
  

Conventional sexual identities do not pose a countertransference problem for most professionals after they become accustomed to discussing sexual matters. But unconventional identities—such as a gender identity disorder, homosexuality, or a paraphilia—can cause anxiety and avoidance for sexually conventional psychiatrists.

Table 3

Ask about 3 components of sexual identity

Learn to ask about erotic fantasies, knowing that occasionally you will encounter behaviors or thoughts that are contrary to your own values. Knowing that you will encounter paraphilia enables you to anticipate and work through any private moral outrage before you meet the patient.³

Ask about sexual function

Desire, arousal, and orgasm are the three dimensions of sexual function listed in DSM-IV-TR. Sexual dysfunction may be classified as lifelong (since onset of sexual activity) or acquired (after a symptom-free period). If a patient’s sexual dysfunction is acquired, determine whether it occurs in all sexual encounters or is situational (with only one partner or present sometimes with a partner). These distinctions allow you to rationally pursue the cause (Table 4).

If a patient complains of loss of desire for sex, determine if it is manifested by:

• absence of sexual thoughts, fantasies, attractions, or masturbation (as might be seen in acquired hypogonadal states)
  
• lost motivation to approach his or her partner for sex (as commonly occurs when partners become alienated).¹⁰
  

Common sexual dysfunctions such as premature ejaculation, female anorgasmia, hypoactive sexual desire disorder, and arousal dysfunctions often have no significant genital findings. Erectile dysfunction in middle-aged and older men indicates the need to do a workup for early vascular disease and metabolic syndrome.

Desire versus arousal. Differentiating sexual desire and arousal can be complicated because they overlap, particularly during middle age or as individuals settle down with a consistent partner. Desire is also complicated by a vital gender difference.¹¹ Most women in monogamous relationships eventually notice that the arousal stimulated by sexual behavior precedes their intense desire for sex, whereas most men report that their desire for sex precedes their arousal through much of the life cycle. Understanding these concepts will shape your follow-up questions about desire and arousal experiences.

Table 4

Ask about 3 components of sexual function

Adult Sex Life: 6 Stages

Sexual dysfunction symptoms may be the same throughout the life cycle, but their meanings to patients vary dramatically. For example:

• A psychological stress that creates erectile dysfunction in a 60-year-old might not affect a 25-year-old because biological capacities for arousal are different at these life stages.
  
• Anorgasmia in a 22-year-old does not have the same psychological and biological sources as anorgasmia in a 62-year-old.
  

Stage 1: Sexual unfolding usually corresponds with adolescence and single adulthood. It is characterized by growing awareness of individual identity and functional characteristics and experiments in managing sexual drives, sexual opportunities, and relationships through masturbation and partner sex. It ends when a person depends on one partner for sexual expression.

Stage 2: Sexual equilibrium is established as part of a monogamous partnership. This equilibrium, which shapes the couple’s unique pattern of sexual expression, is formed by the interaction of their individual identity, desire, arousal, and orgasmic attainment characteristics.

The power of this interaction can be seen in previously functional men and women who quickly become dysfunctional in a new equilibrium because they discern their partner’s displeasure, lack of satisfaction, or lack of interest in particular sexual acts. Their perception of their partner’s unhappiness can quickly induce performance anxiety during sex, anger about sex, or a sense of hopelessness about getting one’s needs met.

The sexual equilibrium’s power is evident in previously dysfunctional individuals who quickly become comfortable and capable when they sense that their partners are pleased with them as partners. Inhibitions gradually lessen, and the couple’s sexual life begins on a good footing.

Stage 3: Preservation of sexual behavior refers to maintaining partnered sexual activity as life becomes more complex because of expected events such as pregnancy, rearing children, new job responsibilities, illness in parents, etc. The couple’s ability to preserve their sexual relationship rests on their capacity to:

• manage disappointment over emerging knowledge of the partner’s character
  
• resolve periodic nonsexual disagreements
  
• re-attain psychological intimacy
  
• understand how important sex is as a means to erase anger, reduce extramarital temptation, reaffirm the couple’s bond, and have fun.
  

Stage 4: The physiologic downturn in midlife for women begins during perimenopause and is characterized by diminished drive, vaginal dryness, and reduced vulvar and breast erotic sensitivity.¹² Men’s physiologic decline—usually apparent to them by their mid-50s—is characterized by reduced drive and less-firm penile tumescence.¹³

Stage 5: Aging effects emerge gradually as individuals move into their 60s. Both sexes usually find orgasm more difficult to attain. Women may say they have sex primarily to please their partners, and men may notice less consistent potency.

Both sexes rely on motivational aspects of desire to have sex, not on sex drive per se. A man may say he wants to have sex, for example, because “it is normal to want to have sex as long as the body is willing; it makes me feel manly.” Women who maintained natural vaginal lubrication during their 50s often now use lubricants.¹⁴

Stage 6: The era of serious illness—whether psychiatric or physical—can occur any time in the life cycle. Illnesses ranging from congestive heart failure to complicated grief can limit a person’s sexual activities. Some changes can increase the frequency of sex—such as hypomania or mania, the new appreciation of a now-impaired spouse, or substance abuse that decreases sexual restraints—but most serious illnesses diminish the patient’s or partner’s sexual desire and arousal.

When death, divorce, or other separations disrupt relationships and individuals find themselves unattached, they return to stage 1: unfolding. With new partners, they will have different desire, arousal, and orgasmic characteristics than they did when last unattached. Their next sexual equilibrium will be different from the one before.

Related resources

• Levine SB. Sexual life: a clinician’s guide. New York: Plenum; 1992.
  
• Risen CB. Listening to sexual stories. In: Levine SB, Risen CB, Althof SE (eds). Handbook of clinical sexuality for mental health professionals. New York: Brunner/Routledge; 2003:1-20.
  

When you address sexuality, you open a window to the patient’s psychology. Talking about sex may illuminate important clues about the individual’s capacity to:

• give and receive pleasure
  
• love and be loved
  
• be psychologically intimate
  
• manage expected and unexpected changes throughout adulthood.¹
  

The opportunity to listen to sexual histories over time will help you become proficient in generating causal hypotheses and using them to help your patients.

Patients think—often erroneously—that all psychiatrists are knowledgeable, skillful, and interested in addressing sexual concerns. But psychiatric practice has turned away from clinical sexuality, and most of us learn on our own how to take a sexual history and to bring up relevant topics during subsequent sessions.

These activities are not particularly difficult,² but they often bump up against one or more clinician fears (Table 1).³ You can master these apprehensions by:

• identifying them in yourself
  
• thinking about them rationally
  
• learning about the broad range of human sexual expression
  
• understanding professional boundaries.⁴
  

Table 1

Clinicians’ 5 worst fears about taking sexual histories

Assessing sexual complaints

Sexual behavior—normal and abnormal, masturbatory and partnered—rests upon biological, psychological, and interpersonal elements, and cultural concepts of normality and morality.⁵ These four components also are the sources of sexual problems (Table 2).^6,7

To accurately assess individuals’ and couples’ sexual problems, we must consider the four components’ present and past contributions in every case. We may declare a hypothesis of cause after one or two sessions, but the explanation usually evolves and becomes more complex with time.⁸

Outside of sexuality clinics, we usually learn about a patient’s sexual complaint during therapy for another problem:

• Individuals may bring up cross-dressing, anxiety about possibly being homosexual, concern about violent sexual fantasies, or other issues of sexual identity. Sexual function concerns may include new difficulty attaining orgasm, aversion to intercourse, painful intercourse, too-rapid ejaculation, episodic inability to maintain an erection, or longstanding inability to ejaculate while with a partner.
  
• Couples may present with difficulty orchestrating their sexual lives. Their complaints may involve discrepancies in sexual desire, inability to bring a young wife to orgasm, cessation of sex, infidelity, dyspareunia, erectile dysfunction in a newly married couple in their 60s, or a wife’s distress over her husband’s use of Internet pornography.
  
• Referrals may come from a social agency about an individual whose sexual behavior clashes with social values or laws. Judges, lawyers, state boards, clergy, or medical chiefs-of-staff may request assistance with individuals who cross sexual boundaries at work, are accused of sex crimes, or have been sexually victimized.⁵
  

4 components of sexual behavior: Where sexual problems may arise

Ask about sexual identity

By the end of adolescence, most individuals have stably in place the three self labels that encompass sexual identity:

• gender identity—the degree of comfort with the self as masculine or feminine
  
• orientation—the gender of those who attract or repel us for romantic and sexual purposes
  
• intention—what we want to do with our bodies and our partners’ bodies during sexual behavior.⁹
  

Conventional sexual identities do not pose a countertransference problem for most professionals after they become accustomed to discussing sexual matters. But unconventional identities—such as a gender identity disorder, homosexuality, or a paraphilia—can cause anxiety and avoidance for sexually conventional psychiatrists.

Table 3

Ask about 3 components of sexual identity

Learn to ask about erotic fantasies, knowing that occasionally you will encounter behaviors or thoughts that are contrary to your own values. Knowing that you will encounter paraphilia enables you to anticipate and work through any private moral outrage before you meet the patient.³

Ask about sexual function

Desire, arousal, and orgasm are the three dimensions of sexual function listed in DSM-IV-TR. Sexual dysfunction may be classified as lifelong (since onset of sexual activity) or acquired (after a symptom-free period). If a patient’s sexual dysfunction is acquired, determine whether it occurs in all sexual encounters or is situational (with only one partner or present sometimes with a partner). These distinctions allow you to rationally pursue the cause (Table 4).

If a patient complains of loss of desire for sex, determine if it is manifested by:

• absence of sexual thoughts, fantasies, attractions, or masturbation (as might be seen in acquired hypogonadal states)
  
• lost motivation to approach his or her partner for sex (as commonly occurs when partners become alienated).¹⁰
  

Common sexual dysfunctions such as premature ejaculation, female anorgasmia, hypoactive sexual desire disorder, and arousal dysfunctions often have no significant genital findings. Erectile dysfunction in middle-aged and older men indicates the need to do a workup for early vascular disease and metabolic syndrome.

Desire versus arousal. Differentiating sexual desire and arousal can be complicated because they overlap, particularly during middle age or as individuals settle down with a consistent partner. Desire is also complicated by a vital gender difference.¹¹ Most women in monogamous relationships eventually notice that the arousal stimulated by sexual behavior precedes their intense desire for sex, whereas most men report that their desire for sex precedes their arousal through much of the life cycle. Understanding these concepts will shape your follow-up questions about desire and arousal experiences.

Table 4

Ask about 3 components of sexual function

Adult Sex Life: 6 Stages

Sexual dysfunction symptoms may be the same throughout the life cycle, but their meanings to patients vary dramatically. For example:

• A psychological stress that creates erectile dysfunction in a 60-year-old might not affect a 25-year-old because biological capacities for arousal are different at these life stages.
  
• Anorgasmia in a 22-year-old does not have the same psychological and biological sources as anorgasmia in a 62-year-old.
  

Stage 1: Sexual unfolding usually corresponds with adolescence and single adulthood. It is characterized by growing awareness of individual identity and functional characteristics and experiments in managing sexual drives, sexual opportunities, and relationships through masturbation and partner sex. It ends when a person depends on one partner for sexual expression.

Stage 2: Sexual equilibrium is established as part of a monogamous partnership. This equilibrium, which shapes the couple’s unique pattern of sexual expression, is formed by the interaction of their individual identity, desire, arousal, and orgasmic attainment characteristics.

The power of this interaction can be seen in previously functional men and women who quickly become dysfunctional in a new equilibrium because they discern their partner’s displeasure, lack of satisfaction, or lack of interest in particular sexual acts. Their perception of their partner’s unhappiness can quickly induce performance anxiety during sex, anger about sex, or a sense of hopelessness about getting one’s needs met.

The sexual equilibrium’s power is evident in previously dysfunctional individuals who quickly become comfortable and capable when they sense that their partners are pleased with them as partners. Inhibitions gradually lessen, and the couple’s sexual life begins on a good footing.

Stage 3: Preservation of sexual behavior refers to maintaining partnered sexual activity as life becomes more complex because of expected events such as pregnancy, rearing children, new job responsibilities, illness in parents, etc. The couple’s ability to preserve their sexual relationship rests on their capacity to:

• manage disappointment over emerging knowledge of the partner’s character
  
• resolve periodic nonsexual disagreements
  
• re-attain psychological intimacy
  
• understand how important sex is as a means to erase anger, reduce extramarital temptation, reaffirm the couple’s bond, and have fun.
  

Stage 4: The physiologic downturn in midlife for women begins during perimenopause and is characterized by diminished drive, vaginal dryness, and reduced vulvar and breast erotic sensitivity.¹² Men’s physiologic decline—usually apparent to them by their mid-50s—is characterized by reduced drive and less-firm penile tumescence.¹³

Stage 5: Aging effects emerge gradually as individuals move into their 60s. Both sexes usually find orgasm more difficult to attain. Women may say they have sex primarily to please their partners, and men may notice less consistent potency.

Both sexes rely on motivational aspects of desire to have sex, not on sex drive per se. A man may say he wants to have sex, for example, because “it is normal to want to have sex as long as the body is willing; it makes me feel manly.” Women who maintained natural vaginal lubrication during their 50s often now use lubricants.¹⁴

Stage 6: The era of serious illness—whether psychiatric or physical—can occur any time in the life cycle. Illnesses ranging from congestive heart failure to complicated grief can limit a person’s sexual activities. Some changes can increase the frequency of sex—such as hypomania or mania, the new appreciation of a now-impaired spouse, or substance abuse that decreases sexual restraints—but most serious illnesses diminish the patient’s or partner’s sexual desire and arousal.

When death, divorce, or other separations disrupt relationships and individuals find themselves unattached, they return to stage 1: unfolding. With new partners, they will have different desire, arousal, and orgasmic characteristics than they did when last unattached. Their next sexual equilibrium will be different from the one before.

Related resources

• Levine SB. Sexual life: a clinician’s guide. New York: Plenum; 1992.
  
• Risen CB. Listening to sexual stories. In: Levine SB, Risen CB, Althof SE (eds). Handbook of clinical sexuality for mental health professionals. New York: Brunner/Routledge; 2003:1-20.
  

When you address sexuality, you open a window to the patient’s psychology. Talking about sex may illuminate important clues about the individual’s capacity to:

• give and receive pleasure
  
• love and be loved
  
• be psychologically intimate
  
• manage expected and unexpected changes throughout adulthood.¹
  

The opportunity to listen to sexual histories over time will help you become proficient in generating causal hypotheses and using them to help your patients.

Patients think—often erroneously—that all psychiatrists are knowledgeable, skillful, and interested in addressing sexual concerns. But psychiatric practice has turned away from clinical sexuality, and most of us learn on our own how to take a sexual history and to bring up relevant topics during subsequent sessions.

These activities are not particularly difficult,² but they often bump up against one or more clinician fears (Table 1).³ You can master these apprehensions by:

• identifying them in yourself
  
• thinking about them rationally
  
• learning about the broad range of human sexual expression
  
• understanding professional boundaries.⁴
  

Table 1

Clinicians’ 5 worst fears about taking sexual histories

Assessing sexual complaints

Sexual behavior—normal and abnormal, masturbatory and partnered—rests upon biological, psychological, and interpersonal elements, and cultural concepts of normality and morality.⁵ These four components also are the sources of sexual problems (Table 2).^6,7

To accurately assess individuals’ and couples’ sexual problems, we must consider the four components’ present and past contributions in every case. We may declare a hypothesis of cause after one or two sessions, but the explanation usually evolves and becomes more complex with time.⁸

Outside of sexuality clinics, we usually learn about a patient’s sexual complaint during therapy for another problem:

• Individuals may bring up cross-dressing, anxiety about possibly being homosexual, concern about violent sexual fantasies, or other issues of sexual identity. Sexual function concerns may include new difficulty attaining orgasm, aversion to intercourse, painful intercourse, too-rapid ejaculation, episodic inability to maintain an erection, or longstanding inability to ejaculate while with a partner.
  
• Couples may present with difficulty orchestrating their sexual lives. Their complaints may involve discrepancies in sexual desire, inability to bring a young wife to orgasm, cessation of sex, infidelity, dyspareunia, erectile dysfunction in a newly married couple in their 60s, or a wife’s distress over her husband’s use of Internet pornography.
  
• Referrals may come from a social agency about an individual whose sexual behavior clashes with social values or laws. Judges, lawyers, state boards, clergy, or medical chiefs-of-staff may request assistance with individuals who cross sexual boundaries at work, are accused of sex crimes, or have been sexually victimized.⁵
  

4 components of sexual behavior: Where sexual problems may arise

Ask about sexual identity

By the end of adolescence, most individuals have stably in place the three self labels that encompass sexual identity:

• gender identity—the degree of comfort with the self as masculine or feminine
  
• orientation—the gender of those who attract or repel us for romantic and sexual purposes
  
• intention—what we want to do with our bodies and our partners’ bodies during sexual behavior.⁹
  

Conventional sexual identities do not pose a countertransference problem for most professionals after they become accustomed to discussing sexual matters. But unconventional identities—such as a gender identity disorder, homosexuality, or a paraphilia—can cause anxiety and avoidance for sexually conventional psychiatrists.

Table 3

Ask about 3 components of sexual identity

Learn to ask about erotic fantasies, knowing that occasionally you will encounter behaviors or thoughts that are contrary to your own values. Knowing that you will encounter paraphilia enables you to anticipate and work through any private moral outrage before you meet the patient.³

Ask about sexual function

Desire, arousal, and orgasm are the three dimensions of sexual function listed in DSM-IV-TR. Sexual dysfunction may be classified as lifelong (since onset of sexual activity) or acquired (after a symptom-free period). If a patient’s sexual dysfunction is acquired, determine whether it occurs in all sexual encounters or is situational (with only one partner or present sometimes with a partner). These distinctions allow you to rationally pursue the cause (Table 4).

If a patient complains of loss of desire for sex, determine if it is manifested by:

• absence of sexual thoughts, fantasies, attractions, or masturbation (as might be seen in acquired hypogonadal states)
  
• lost motivation to approach his or her partner for sex (as commonly occurs when partners become alienated).¹⁰
  

Common sexual dysfunctions such as premature ejaculation, female anorgasmia, hypoactive sexual desire disorder, and arousal dysfunctions often have no significant genital findings. Erectile dysfunction in middle-aged and older men indicates the need to do a workup for early vascular disease and metabolic syndrome.

Desire versus arousal. Differentiating sexual desire and arousal can be complicated because they overlap, particularly during middle age or as individuals settle down with a consistent partner. Desire is also complicated by a vital gender difference.¹¹ Most women in monogamous relationships eventually notice that the arousal stimulated by sexual behavior precedes their intense desire for sex, whereas most men report that their desire for sex precedes their arousal through much of the life cycle. Understanding these concepts will shape your follow-up questions about desire and arousal experiences.

Table 4

Ask about 3 components of sexual function

Adult Sex Life: 6 Stages

Sexual dysfunction symptoms may be the same throughout the life cycle, but their meanings to patients vary dramatically. For example:

• A psychological stress that creates erectile dysfunction in a 60-year-old might not affect a 25-year-old because biological capacities for arousal are different at these life stages.
  
• Anorgasmia in a 22-year-old does not have the same psychological and biological sources as anorgasmia in a 62-year-old.
  

Stage 1: Sexual unfolding usually corresponds with adolescence and single adulthood. It is characterized by growing awareness of individual identity and functional characteristics and experiments in managing sexual drives, sexual opportunities, and relationships through masturbation and partner sex. It ends when a person depends on one partner for sexual expression.

Stage 2: Sexual equilibrium is established as part of a monogamous partnership. This equilibrium, which shapes the couple’s unique pattern of sexual expression, is formed by the interaction of their individual identity, desire, arousal, and orgasmic attainment characteristics.

The power of this interaction can be seen in previously functional men and women who quickly become dysfunctional in a new equilibrium because they discern their partner’s displeasure, lack of satisfaction, or lack of interest in particular sexual acts. Their perception of their partner’s unhappiness can quickly induce performance anxiety during sex, anger about sex, or a sense of hopelessness about getting one’s needs met.

The sexual equilibrium’s power is evident in previously dysfunctional individuals who quickly become comfortable and capable when they sense that their partners are pleased with them as partners. Inhibitions gradually lessen, and the couple’s sexual life begins on a good footing.

Stage 3: Preservation of sexual behavior refers to maintaining partnered sexual activity as life becomes more complex because of expected events such as pregnancy, rearing children, new job responsibilities, illness in parents, etc. The couple’s ability to preserve their sexual relationship rests on their capacity to:

• manage disappointment over emerging knowledge of the partner’s character
  
• resolve periodic nonsexual disagreements
  
• re-attain psychological intimacy
  
• understand how important sex is as a means to erase anger, reduce extramarital temptation, reaffirm the couple’s bond, and have fun.
  

Stage 4: The physiologic downturn in midlife for women begins during perimenopause and is characterized by diminished drive, vaginal dryness, and reduced vulvar and breast erotic sensitivity.¹² Men’s physiologic decline—usually apparent to them by their mid-50s—is characterized by reduced drive and less-firm penile tumescence.¹³

Stage 5: Aging effects emerge gradually as individuals move into their 60s. Both sexes usually find orgasm more difficult to attain. Women may say they have sex primarily to please their partners, and men may notice less consistent potency.

Both sexes rely on motivational aspects of desire to have sex, not on sex drive per se. A man may say he wants to have sex, for example, because “it is normal to want to have sex as long as the body is willing; it makes me feel manly.” Women who maintained natural vaginal lubrication during their 50s often now use lubricants.¹⁴

Stage 6: The era of serious illness—whether psychiatric or physical—can occur any time in the life cycle. Illnesses ranging from congestive heart failure to complicated grief can limit a person’s sexual activities. Some changes can increase the frequency of sex—such as hypomania or mania, the new appreciation of a now-impaired spouse, or substance abuse that decreases sexual restraints—but most serious illnesses diminish the patient’s or partner’s sexual desire and arousal.

When death, divorce, or other separations disrupt relationships and individuals find themselves unattached, they return to stage 1: unfolding. With new partners, they will have different desire, arousal, and orgasmic characteristics than they did when last unattached. Their next sexual equilibrium will be different from the one before.

Related resources

• Levine SB. Sexual life: a clinician’s guide. New York: Plenum; 1992.
  
• Risen CB. Listening to sexual stories. In: Levine SB, Risen CB, Althof SE (eds). Handbook of clinical sexuality for mental health professionals. New York: Brunner/Routledge; 2003:1-20.
  

Are e-alerts cluttering your in box?

These indispensable e-mails offer immediate access to current clinical articles. But with so many e-alerts and search services available, useless alerts and irrelevant search results can clog your client—in the bargain slowing access to the data you need.

This article explains how to customize your subscriptions and choose e-alerts that most closely meet your needs.

Which e-alert is best for you?

When new issues appear online, journals typically send out:

• Publication alerts, which provide a link to the journal’s home page or current table of contents.
• Tables of contents—or eTOCs. Whereas publication alerts contain a few links, eTOCs list the current issue’s full TOC with links to abstracts and full-text versions of each article.
• Content alerts, which consolidate links to new articles on a specific topic. Content alerts are sent each time a keyword on your interest list is included within a new article’s title, keywords, or abstract.
• Citation alerts when an article on your list is cited. This helps you track how often authors are citing an article and alerts you to other articles in your field of interest.
• Author alerts when an article by a selected author is published, helping you consolidate links to current data from thought leaders on a given topic. Author alerts also help you track articles you’ve published.
• Saved search alerts, which retrieve a prior search each time the publisher’s database is updated. This can help you avoid having to restart searches.

E-alerts usually are free, but a paid subscription to the journal often is required to access full-text articles.

Psychiatric journals offer many types of e-alerts:

• Archives of General Psychiatry offers free eTOCs, content, author, and saved search alerts, as well as links to “early release” articles that are published online before they appear in print.
• The American Journal of Psychiatry offers these alerts through HighWire Press as well as PDA services, which each month download TOCs, citations, and abstracts to your personal digital assistant. You need a (free) HighWire account to subscribe to these services.

Publisher alerts. Some journal publishers—including American Psychiatric Publishing, Elsevier, Karger, and Springer—offer free publisher alerts that announce online updates to all journals in their groups. Elsevier offers a range of e-alert services, including free issue, citation, and saved search alerts, and a quarterly alert listing the “25 hottest articles.”

Publisher alerts contain links to several journals in one message. You don’t need to subscribe to any one journal to receive a publisher alert, but the information is limited to that publisher’s journals. American Psychiatric Publishing’s alert, for example, offers links to The American Journal of Psychiatry and the publisher’s other journals, but you need a separate alert for Journal of Clinical Psychiatry.

Choosing an e-alert service

Independent e-alert services, which scan the medical literature for links to pertinent articles, offer substantially more links than do publication or group e-alerts

HighWire Press, a division of Stanford University Libraries, hosts a searchable repository of full-text online articles from more than 900 journals—many of which can be accessed at no charge. HighWire also offers:

• eTOCs
• CiteTrack, an alert on new journal content based on search criteria (topics/keywords, authors, or articles being referenced or cited)
• PDA Channels, which delivers alerts to Palm OS and Pocket PC handhelds
• RSS (really simple syndication) feeds—compilations of alerts and headlines from various publications that must be viewed using RSS Reader software
• Subscription alerts, which warn users a few weeks before that their subscription will expire.

PubMed Central. Users can open MyNCBI accounts to save searches and receive alerts for new content, authors, journals, and saved searches.

AMEDEO offers weekly updates of journals by topic and alerts providing information on various medical fields. AMEDEO’s “psychiatric disorders” link, however, lists articles only on depression and schizophrenia.

MDLinx offers daily updates of journal and medical news by specialty and subspecialty. “PsychLinx” provides links to psychiatry articles, by subspecialty or topic, and direct links to journals.

IngentaConnect sends users free monthly eTOCs from five journals. Institutions that purchase an institutional alerting license from IngentaConnect can receive unlimited new-issue alerts and free search alerts.

We find that using HighWire with PubMed Central offers an optimal yield of psychiatric articles. Paid alert services, such as Ovid or Web of Science, require an institutional or personal subscription and offer no significant advantage over free services.

You can customize your e-alert based on specialty and specific search criteria. By scrolling to “Alert Sources” on the HighWire site, for example, you can choose to scan all PubMed content (abstracts), all HighWire-hosted content (abstracts and full text), or psychiatry journals only by clicking on “View list by topic” and checking the “Psychiatry” box.

Remember that e-alerts—no matter how effective they are or how many you receive—cannot link you to every article you need. Web searches will be necessary at times.

Avoiding spam, viruses, other problems

Before you subscribe to an e-alert, ask these questions to prevent unwanted e-mails:

Is the e-alert secure? As with any online service, giving your e-mail address when subscribing to an e-alert could open your client to spam or—worse—a virus transmitted via an unwanted message.

To reduce the risk, update your subscription form as needed to confirm your identity, and change your password yearly to guard your privacy. Most publishers/services enforce privacy policies that ensure safe transmission.

Is the journal site easy to navigate? The site should offer advanced search capabilities that allow you to customize searches. Instructions or answers to frequently asked questions about alert frequency, managing and refining alerts, and other issues should be clear and accessible.

Will my search terms work? Use specific terms to filter information. Whereas a broad search term such as “bipolar disorder” would yield a long list of irrelevant articles, a more specific term such as “bipolar maintenance therapy” would substantially narrow the search. Adjust and refine your search terms and update your interest list as needed to ensure an optimal flow of information.

Is the journal’s Webmaster accessible? Contact the Webmaster if an e-alert is not meeting your needs or if you have suggestions for improvement. A link to the Webmaster should be listed on the “contact us” page.

Related resources

Cuddy C. HighWire Press and its journey to become the world’s largest full-text STM online journal collection. Journal of Electronic Resources in Medical Libraries 2005;2:1-13.

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

To comment on this article or share your experience with e-alerts, click here.

Are e-alerts cluttering your in box?

These indispensable e-mails offer immediate access to current clinical articles. But with so many e-alerts and search services available, useless alerts and irrelevant search results can clog your client—in the bargain slowing access to the data you need.

This article explains how to customize your subscriptions and choose e-alerts that most closely meet your needs.

Which e-alert is best for you?

When new issues appear online, journals typically send out:

• Publication alerts, which provide a link to the journal’s home page or current table of contents.
• Tables of contents—or eTOCs. Whereas publication alerts contain a few links, eTOCs list the current issue’s full TOC with links to abstracts and full-text versions of each article.
• Content alerts, which consolidate links to new articles on a specific topic. Content alerts are sent each time a keyword on your interest list is included within a new article’s title, keywords, or abstract.
• Citation alerts when an article on your list is cited. This helps you track how often authors are citing an article and alerts you to other articles in your field of interest.
• Author alerts when an article by a selected author is published, helping you consolidate links to current data from thought leaders on a given topic. Author alerts also help you track articles you’ve published.
• Saved search alerts, which retrieve a prior search each time the publisher’s database is updated. This can help you avoid having to restart searches.

E-alerts usually are free, but a paid subscription to the journal often is required to access full-text articles.

Psychiatric journals offer many types of e-alerts:

• Archives of General Psychiatry offers free eTOCs, content, author, and saved search alerts, as well as links to “early release” articles that are published online before they appear in print.
• The American Journal of Psychiatry offers these alerts through HighWire Press as well as PDA services, which each month download TOCs, citations, and abstracts to your personal digital assistant. You need a (free) HighWire account to subscribe to these services.

Publisher alerts. Some journal publishers—including American Psychiatric Publishing, Elsevier, Karger, and Springer—offer free publisher alerts that announce online updates to all journals in their groups. Elsevier offers a range of e-alert services, including free issue, citation, and saved search alerts, and a quarterly alert listing the “25 hottest articles.”

Publisher alerts contain links to several journals in one message. You don’t need to subscribe to any one journal to receive a publisher alert, but the information is limited to that publisher’s journals. American Psychiatric Publishing’s alert, for example, offers links to The American Journal of Psychiatry and the publisher’s other journals, but you need a separate alert for Journal of Clinical Psychiatry.

Choosing an e-alert service

Independent e-alert services, which scan the medical literature for links to pertinent articles, offer substantially more links than do publication or group e-alerts

HighWire Press, a division of Stanford University Libraries, hosts a searchable repository of full-text online articles from more than 900 journals—many of which can be accessed at no charge. HighWire also offers:

• eTOCs
• CiteTrack, an alert on new journal content based on search criteria (topics/keywords, authors, or articles being referenced or cited)
• PDA Channels, which delivers alerts to Palm OS and Pocket PC handhelds
• RSS (really simple syndication) feeds—compilations of alerts and headlines from various publications that must be viewed using RSS Reader software
• Subscription alerts, which warn users a few weeks before that their subscription will expire.

PubMed Central. Users can open MyNCBI accounts to save searches and receive alerts for new content, authors, journals, and saved searches.

AMEDEO offers weekly updates of journals by topic and alerts providing information on various medical fields. AMEDEO’s “psychiatric disorders” link, however, lists articles only on depression and schizophrenia.

MDLinx offers daily updates of journal and medical news by specialty and subspecialty. “PsychLinx” provides links to psychiatry articles, by subspecialty or topic, and direct links to journals.

IngentaConnect sends users free monthly eTOCs from five journals. Institutions that purchase an institutional alerting license from IngentaConnect can receive unlimited new-issue alerts and free search alerts.

We find that using HighWire with PubMed Central offers an optimal yield of psychiatric articles. Paid alert services, such as Ovid or Web of Science, require an institutional or personal subscription and offer no significant advantage over free services.

You can customize your e-alert based on specialty and specific search criteria. By scrolling to “Alert Sources” on the HighWire site, for example, you can choose to scan all PubMed content (abstracts), all HighWire-hosted content (abstracts and full text), or psychiatry journals only by clicking on “View list by topic” and checking the “Psychiatry” box.

Remember that e-alerts—no matter how effective they are or how many you receive—cannot link you to every article you need. Web searches will be necessary at times.

Avoiding spam, viruses, other problems

Before you subscribe to an e-alert, ask these questions to prevent unwanted e-mails:

Is the e-alert secure? As with any online service, giving your e-mail address when subscribing to an e-alert could open your client to spam or—worse—a virus transmitted via an unwanted message.

To reduce the risk, update your subscription form as needed to confirm your identity, and change your password yearly to guard your privacy. Most publishers/services enforce privacy policies that ensure safe transmission.

Is the journal site easy to navigate? The site should offer advanced search capabilities that allow you to customize searches. Instructions or answers to frequently asked questions about alert frequency, managing and refining alerts, and other issues should be clear and accessible.

Will my search terms work? Use specific terms to filter information. Whereas a broad search term such as “bipolar disorder” would yield a long list of irrelevant articles, a more specific term such as “bipolar maintenance therapy” would substantially narrow the search. Adjust and refine your search terms and update your interest list as needed to ensure an optimal flow of information.

Is the journal’s Webmaster accessible? Contact the Webmaster if an e-alert is not meeting your needs or if you have suggestions for improvement. A link to the Webmaster should be listed on the “contact us” page.

Related resources

Cuddy C. HighWire Press and its journey to become the world’s largest full-text STM online journal collection. Journal of Electronic Resources in Medical Libraries 2005;2:1-13.

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

To comment on this article or share your experience with e-alerts, click here.

Are e-alerts cluttering your in box?

These indispensable e-mails offer immediate access to current clinical articles. But with so many e-alerts and search services available, useless alerts and irrelevant search results can clog your client—in the bargain slowing access to the data you need.

This article explains how to customize your subscriptions and choose e-alerts that most closely meet your needs.

Which e-alert is best for you?

When new issues appear online, journals typically send out:

• Publication alerts, which provide a link to the journal’s home page or current table of contents.
• Tables of contents—or eTOCs. Whereas publication alerts contain a few links, eTOCs list the current issue’s full TOC with links to abstracts and full-text versions of each article.
• Content alerts, which consolidate links to new articles on a specific topic. Content alerts are sent each time a keyword on your interest list is included within a new article’s title, keywords, or abstract.
• Citation alerts when an article on your list is cited. This helps you track how often authors are citing an article and alerts you to other articles in your field of interest.
• Author alerts when an article by a selected author is published, helping you consolidate links to current data from thought leaders on a given topic. Author alerts also help you track articles you’ve published.
• Saved search alerts, which retrieve a prior search each time the publisher’s database is updated. This can help you avoid having to restart searches.

E-alerts usually are free, but a paid subscription to the journal often is required to access full-text articles.

Psychiatric journals offer many types of e-alerts:

• Archives of General Psychiatry offers free eTOCs, content, author, and saved search alerts, as well as links to “early release” articles that are published online before they appear in print.
• The American Journal of Psychiatry offers these alerts through HighWire Press as well as PDA services, which each month download TOCs, citations, and abstracts to your personal digital assistant. You need a (free) HighWire account to subscribe to these services.

Publisher alerts. Some journal publishers—including American Psychiatric Publishing, Elsevier, Karger, and Springer—offer free publisher alerts that announce online updates to all journals in their groups. Elsevier offers a range of e-alert services, including free issue, citation, and saved search alerts, and a quarterly alert listing the “25 hottest articles.”

Publisher alerts contain links to several journals in one message. You don’t need to subscribe to any one journal to receive a publisher alert, but the information is limited to that publisher’s journals. American Psychiatric Publishing’s alert, for example, offers links to The American Journal of Psychiatry and the publisher’s other journals, but you need a separate alert for Journal of Clinical Psychiatry.

Choosing an e-alert service

Independent e-alert services, which scan the medical literature for links to pertinent articles, offer substantially more links than do publication or group e-alerts

HighWire Press, a division of Stanford University Libraries, hosts a searchable repository of full-text online articles from more than 900 journals—many of which can be accessed at no charge. HighWire also offers:

• eTOCs
• CiteTrack, an alert on new journal content based on search criteria (topics/keywords, authors, or articles being referenced or cited)
• PDA Channels, which delivers alerts to Palm OS and Pocket PC handhelds
• RSS (really simple syndication) feeds—compilations of alerts and headlines from various publications that must be viewed using RSS Reader software
• Subscription alerts, which warn users a few weeks before that their subscription will expire.

PubMed Central. Users can open MyNCBI accounts to save searches and receive alerts for new content, authors, journals, and saved searches.

AMEDEO offers weekly updates of journals by topic and alerts providing information on various medical fields. AMEDEO’s “psychiatric disorders” link, however, lists articles only on depression and schizophrenia.

MDLinx offers daily updates of journal and medical news by specialty and subspecialty. “PsychLinx” provides links to psychiatry articles, by subspecialty or topic, and direct links to journals.

IngentaConnect sends users free monthly eTOCs from five journals. Institutions that purchase an institutional alerting license from IngentaConnect can receive unlimited new-issue alerts and free search alerts.

We find that using HighWire with PubMed Central offers an optimal yield of psychiatric articles. Paid alert services, such as Ovid or Web of Science, require an institutional or personal subscription and offer no significant advantage over free services.

You can customize your e-alert based on specialty and specific search criteria. By scrolling to “Alert Sources” on the HighWire site, for example, you can choose to scan all PubMed content (abstracts), all HighWire-hosted content (abstracts and full text), or psychiatry journals only by clicking on “View list by topic” and checking the “Psychiatry” box.

Remember that e-alerts—no matter how effective they are or how many you receive—cannot link you to every article you need. Web searches will be necessary at times.

Avoiding spam, viruses, other problems

Before you subscribe to an e-alert, ask these questions to prevent unwanted e-mails:

Is the e-alert secure? As with any online service, giving your e-mail address when subscribing to an e-alert could open your client to spam or—worse—a virus transmitted via an unwanted message.

To reduce the risk, update your subscription form as needed to confirm your identity, and change your password yearly to guard your privacy. Most publishers/services enforce privacy policies that ensure safe transmission.

Is the journal site easy to navigate? The site should offer advanced search capabilities that allow you to customize searches. Instructions or answers to frequently asked questions about alert frequency, managing and refining alerts, and other issues should be clear and accessible.

Will my search terms work? Use specific terms to filter information. Whereas a broad search term such as “bipolar disorder” would yield a long list of irrelevant articles, a more specific term such as “bipolar maintenance therapy” would substantially narrow the search. Adjust and refine your search terms and update your interest list as needed to ensure an optimal flow of information.

Is the journal’s Webmaster accessible? Contact the Webmaster if an e-alert is not meeting your needs or if you have suggestions for improvement. A link to the Webmaster should be listed on the “contact us” page.

Related resources

Cuddy C. HighWire Press and its journey to become the world’s largest full-text STM online journal collection. Journal of Electronic Resources in Medical Libraries 2005;2:1-13.

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

To comment on this article or share your experience with e-alerts, click here.

Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

Psychiatrists commonly treat persons whose first words during an office visit are: “I need something for…”—usually sleep problems, obesity, anxiety, or low energy.

Although these difficulties could point to a psychiatric or medical disorder, unhealthy behaviors such as poor sleep hygiene, substance abuse, lack of exercise, or inadequate diet often are to blame. Despite the patient’s expectations, medication might not be therapeutic or clinically indicated.

For such cases, I use my prescription pad to “prescribe” problem-focused, medically appropriate, nondrug treatments. Handwritten prescriptions reinforce the targeted behavioral change or lifestyle modification discussed during our session.

A written prescription doesn’t replace verbal recommendations, but I believe it provides concrete treatment instructions that lead to positive behavioral changes.

How behavioral ‘prescriptions’ work

Suppose a person with insomnia who drinks coffee and caffeinated sodas throughout the day requests sleep medication. I write a prescription for “doses” of coffee (“Drink no more than three cups a day”) and when the doses should be taken (“Do not take coffee or soda after 4 PM”).

If a patient is sedentary and gaining weight, I write a prescription to reduce calories (“Avoid eating cookies, cake, and ‘junk food’”) and to begin an easy, graded exercise program (“Start walking 30 minutes per day, four times per week”). For a patient whose anxiety symptoms do not improve after therapeutic medication trials, I prescribe relaxation techniques (“Practice deep-breathing exercises twice daily for the next 14 days”).

These written prescriptions include the date, patient’s name, and my signature. To guard against forgeries, I leave no blank spaces. I hand the prescription to the patient and instruct him or her to post it in a conspicuous place, such as the refrigerator door, coffee maker, or bathroom mirror. Most patients respond positively even though the prescription is not for medication, because it directly addresses their stated problem.

As with written orders for medications, I keep copies of behavioral/lifestyle prescriptions in the patient’s chart and refer to them when discussing adherence, to reinforce progress, and to adjust behavior modifications.

The prescription pad holds therapeutic power, but not all prescriptions we hand our patients need to be for medicine.

Patient education and timing are crucial to promoting a positive outcome after switching antipsychotics. Although little empiric evidence is available to guide these medication switches,^1-3 we find the following process helpful based on our clinical experience.

Think Before You Switch

Before switching antipsychotics, ask:

• Did the first antipsychotic have some effect on psychosis or mood or on associated symptoms, such as sleep, anxiety, or agitation? If so, anticipate and manage the benefits that will be lost while tapering off the antipsychotic.
  
• How stable is the patient?
  
• How much external monitoring or support is available? If the patient has limited external support, make the switch slowly and monitor the patient more closely.
  
• How urgent is the medication switch?
  
• Is the patient suffering severe adverse effects from the first antipsychotic?
  
• Is a high dosage of the new antipsychotic needed to manage positive symptoms?
  

Dos and Don’Ts Of Switching

If switching antipsychotics is necessary, follow these seven steps:

1. Don’t switch while the patient is unstable, particularly if you are switching because of side effects or for administrative reasons such as formulary restrictions or cost. Delay the switch until the patient is stable, if possible. For unstable patients who are inadequately controlled on the first antipsychotic, consider temporarily adding another antipsychotic and deferring the switch until the patient is more stable.
   
2. Explain the switch’s risks and benefits to the patient. Mention how long before the new drug begins to work and when side effects could surface. Also, give the patient a choice regarding alternate medications, when to switch, and how gradual the switch should be. A collaborative approach is more likely to be successful.
   
3. Make sure the patient’s family, case managers, or group home operators understand why you are switching antipsychotics. Instruct them to watch for worsening symptoms after the patient starts the new medication.
   
4. Stay in touch with the patient—by phone and in person—during and after the switch. Numerous factors—including the patient’s stability and whether family or friends are monitoring him—should guide frequency of contact.
   
5. Tell the patient to call you if a problem arises. Counsel the patient through minor or temporary side effects with the new antipsychotic.
   
6. Do not switch multiple medications at once, if possible, as this can destabilize the patient and make it difficult to assess the new medications’ benefits and adverse effects.
   
7. An adjuvant medication can reduce pharmacodynamic changes resulting from the switch. For example, consider adding a hypnotic and/or an anxiolytic when switching from a sedating to a nonsedating antipsychotic. When switching from an antipsychotic with significant anticholinergic properties—such as olanzapine or quetiapine—consider adding an anticholinergic that may be tapered off later.