Evidence-Based Reviews

The Positive and Negative Syndrome Scale (PANSS) is moving from research into clinical practice as demand grows for objective rating scales. We see the PANSS becoming a treatment and planning tool for psychiatry, just as the electrocardiogram evolved into a measure of cardiac status in medical practice.

Based on our experience in co-authoring (LA Opler) and using the PANSS, we describe how you can use it to:

• identify psychotic symptoms for targeted treatment
  
• predict with greater accuracy how patients will respond to the treatment you provide.
  

Standardized Assessments

The PANSS first gained stature in studies that established the efficacy of second-generation antipsychotics (SGAs).^1-6 But its authors⁷ also envisioned the scale as a useful tool to help practicing clinicians treat patients with schizophrenia and other psychotic disorders.

Twenty years of experience has shown the PANSS to be a reliable and valid severity symptom scale for schizophrenia, bipolar disorder, and other serious mental illnesses. It is particularly useful to track changes in positive and negative symptoms.⁸

Traditionally, psychiatric evaluation has been impressionistic and subjective, but standardized tools provide a common language while introducing objective, empiric measures of clinical status. Because patients with mental disorders are treated by providers from psychiatry, psychology, social work, nursing, and other mental health disciplines, having standardized benchmarks to assess symptom severity can facilitate an integrated approach. And because the PANSS has been translated into some 40 languages and is being adopted in clinical settings worldwide, it provides a universal means of communicating information about a patient’s clinical status.

Panss Scoring System

The PANSS includes 30 items, each rated from 1 (absent) to 7 (extreme). In theory, a patient rated “absent” (or 1) on all items would receive a total score of 30, and a patient rated “extreme” (or 7) on all items would receive a total score of 210. In the real world, though, no one sees these extremes. Stable outpatients usually score 60 to 80. Inpatients’ scores rarely exceed 80 to 150, even in “treatment refractory” cases.

The 30 items are arranged as 7 positive symptom subscale items (P1-P7), 7 negative symptom subscale items (N1-N7), and 16 general psychopathology symptom items (G1-G16) (Table 1). Each item has a definition and a basis for rating. The first question you need to answer when rating a patient is whether the item is absent or present.

How it works. For example, the PANSS defines delusions as “beliefs that are unfounded, unrealistic, and idiosyncratic,” and the basis for rating is “thought content expressed during the interview and its influence on the patient’s social relations and behavior as reported from primary care workers or family.” If the definition does not apply to your patient, you rate this item 1 or absent. If the definition does apply, “anchoring points” for each level of severity are provided (Table 2), and you decide which anchoring point best describes the patient’s functioning during the interview and the preceding week.

Time required. In research, gathering informant information, conducting the interview, and generating reliable ratings takes 45 to 60 minutes. In clinical settings, if you know your patient and can function as informant and interviewer, you probably can obtain accurate ratings in 30 to 45 minutes.

Ideally, you would use the Structured Clinical Interview for the PANSS (SCI-PANSS), though clinicians who know this instrument well may prefer a less structured interview that covers all areas of inquiry. Accurate PANSS scores are easy to generate on all 30 items by combining information from the interview with information about how the patient has functioned in the past week.

PANSS ratings are not meant to be obtained after every patient contact but rather as often as needed to guide clinical treatment. For example, you might obtain a PANSS rating:

• when an inpatient is first admitted
  
• before starting a new medication
  
• weeks or months later to gauge the new treatment’s effect.
  

Training is vital to becoming a reliable PANSS rater and is offered at venues such as the American Psychiatric Association’s annual meeting. Other options include workshops or self-training materials from The PANSS Institute (see Related resources).

The PANSS manual—a complete individual kit costs approximately $200—or licenses to use multiple copies are available from the copyright holder, MultiHealth Systems, Inc. (see Related resources).

Table 1

Subscales of the 30-item Positive and Negative Syndrome Scale (PANSS)

7 Positive symptom subscale items	7 Negative symptom subscale items
P1. Delusions	N1. Blunted affect
P2. Conceptual disorganization	N2. Emotional withdrawal
P3. Hallucinatory behavior	N3. Poor rapport
P4. Excitement	N4. Passive/apathetic social withdrawal
P5. Grandiosity	N5. Difficulty in abstract thinking
P6. Suspiciousness/persecution	N6. Lack of spontaneity and flow of conversation
P7. Hostility	N7. Stereotyped thinking
16 General psychopathology symptoms
G1. Somatic concern	G9. Unusual thought content
G2. Anxiety	G10. Disorientation
G3. Guilt feelings	G11. Poor attention
G4. Tension	G12. Lack of judgment and insight
G5. Mannerisms and posturing	G13. Disturbance of volition
G6. Depression	G14. Poor impulse control
G7. Motor retardation	G15. Preoccupation
G8. Uncooperativeness	G16. Active social avoidance

 

Table 2

7 levels of severity on the PANSS for characterizing delusions

Severity level (“anchoring point”)	Description of patient function
1 - Absent	The definition does not apply
2 - Minimal	Questionable pathology; the patient may be at the upper extreme of normal limits
3 - Mild	Presence of one or two delusions that are vague, uncrystallized, and not tenaciously held. The delusions do not interfere with the patient’s thinking, social relations, or behavior
4 - Moderate	Presence of either a kaleidoscopic array of poorly formed, unstable delusions, or a few well-formed delusions that occasionally interfere with the patient’s thinking, social relations, or behavior
5 - Moderate severe	Presence of numerous well-formed delusions that are tenaciously held and occasionally interfere with the patient’s thinking, social relations, or behavior
6 - Severe	Presence of a stable set of delusions that are crystallized, possibly systematized, tenaciously held, and clearly interfere with the patient’s thinking, social relations, or behavior
7 - Extreme	Presence of a stable set of delusions that are either highly systematized or very numerous, and that dominate major facets of the patient’s life. This behavior frequently results in inappropriate and irresponsible action that may jeopardize the safety of the patient or others

Gauging Symptom Severity

Treatment planning. Clinicians at the Rochester (New York) Psychiatric Center use the PANSS to assess symptom severity in inpatients with schizophrenia and other psychotic disorders.

Within 1 week of admission, patients are evaluated on the 30 items by a team of experienced PANSS raters. Symptoms identified by the PANSS become targets in individualized treatment plans. Follow-up PANSS assessments help determine if treatment has improved the selected symptoms.

Tracking patient progress. Florida State Hospital uses the PANSS to track progress of patients with serious mental illnesses. Data collected over 8 years from >19,000 PANSS assessments in a multilingual, multicultural population suggests that the PANSS:

• aids in decision making for medical and nonmedical aspects of care for individual patients
  
• can help determine if changes in agency prescribing practices affect patient symptom profiles and severity, one indicator of how policy and guidelines translate into patient care.⁹
  

Monitoring depression. In Geha Psychiatric Hospital in Tel Aviv, Israel, treatment outcomes improved when the PANSS was used to measure severity of symptoms—particularly depression—in an inpatient population of adolescents with schizophrenia.¹⁰ PANSS items can measure dysphoria, including anxiety, tension, and guilt feelings. Clinicians now routinely use the PANSS to assess patients’ symptoms at admission and for periodic follow-up.

Predicting Outcomes

The PANSS has been shown to predict course of illness and treatment response, functional outcomes (including aggression), and long-term outcomes (including deterioration). Adjusting treatments to achieve optimal PANSS scores also can help clinicians achieve remission of their patients’ psychotic symptoms (Box).^11,12

Box

Course of illness. Schizophrenia patients in a Tokyo hospital psychiatric ward were rated within 3 days of admission and at weekly intervals for 8 weeks. Baseline PANSS scores on the conceptual disorganization item and the total negative scale score predicted which patients would respond to antipsychotic treatment within 5 weeks.¹³

Functional outcomes. Steinert et al¹⁴ used the PANSS to rate 199 inpatients within 24 hours of admission into an acute psychiatric ward. After discharge, each patient was assessed retrospectively for aggressive behavior. The conceptual disorganization and hostility items from the positive sub-scale could predict violent behaviors during inpatient treatment with statistical significance.

Long-term outcomes. White et al¹⁵ assessed older schizophrenia inpatients, using the PANSS at baseline and after 1 year. The researchers looked specifically at the “activation factor”—six PANSS items including hostility, poor impulse control, excitement, uncooperativeness, poor rapport, and tension. Poor outcome and low discharge rates were directly correlated with high baseline scores on the PANSS activation factor (PANSS-AF).

Deterioration. Goetz et al¹⁶ showed that residual positive symptoms were significantly related to deteriorating course of illness, even when patients adhered to their medications. These results suggest that even subtle symptom elevations as measured by the PANSS can predict deterioration.

 

Related resources

• The PANSS Institute. Information on how to attain, maintain, and retain high reliability as a PANSS rater. www.panss.org.
  
• MultiHealth Systems, Inc. (publisher and copyright holder) to purchase the Positive and Negative Syndrome Scale (PANSS). www.mhs.com.
  
• Opler LA, Ramirez PM, Mougios VA. Measuring outcome in serious mental illness. In: IsHak WW, Burt T, Sederer L (eds). Outcome measurement in psychiatry: a critical review. Washington, DC: American Psychiatric Press; 2002.
  

Disclosures

Dr. Lewis A. Opler receives royalties from MultiHealth Systems, Inc. on sales of the Positive and Negative Syndrome Scale (PANSS) Manual, the Structured Clinical Interview for the PANSS (SCI-PANSS), and the Informant Questionnaire for the PANSS (IQ-PANSS).

Dr. Mark G. Opler is Executive Director of The PANSS Institute.

Acknowledgement

This work was supported in part by NIMH grant K24 MH01699 (DM).

The Positive and Negative Syndrome Scale (PANSS) is moving from research into clinical practice as demand grows for objective rating scales. We see the PANSS becoming a treatment and planning tool for psychiatry, just as the electrocardiogram evolved into a measure of cardiac status in medical practice.

Based on our experience in co-authoring (LA Opler) and using the PANSS, we describe how you can use it to:

• identify psychotic symptoms for targeted treatment
  
• predict with greater accuracy how patients will respond to the treatment you provide.
  

Standardized Assessments

The PANSS first gained stature in studies that established the efficacy of second-generation antipsychotics (SGAs).^1-6 But its authors⁷ also envisioned the scale as a useful tool to help practicing clinicians treat patients with schizophrenia and other psychotic disorders.

Twenty years of experience has shown the PANSS to be a reliable and valid severity symptom scale for schizophrenia, bipolar disorder, and other serious mental illnesses. It is particularly useful to track changes in positive and negative symptoms.⁸

Traditionally, psychiatric evaluation has been impressionistic and subjective, but standardized tools provide a common language while introducing objective, empiric measures of clinical status. Because patients with mental disorders are treated by providers from psychiatry, psychology, social work, nursing, and other mental health disciplines, having standardized benchmarks to assess symptom severity can facilitate an integrated approach. And because the PANSS has been translated into some 40 languages and is being adopted in clinical settings worldwide, it provides a universal means of communicating information about a patient’s clinical status.

Panss Scoring System

The PANSS includes 30 items, each rated from 1 (absent) to 7 (extreme). In theory, a patient rated “absent” (or 1) on all items would receive a total score of 30, and a patient rated “extreme” (or 7) on all items would receive a total score of 210. In the real world, though, no one sees these extremes. Stable outpatients usually score 60 to 80. Inpatients’ scores rarely exceed 80 to 150, even in “treatment refractory” cases.

The 30 items are arranged as 7 positive symptom subscale items (P1-P7), 7 negative symptom subscale items (N1-N7), and 16 general psychopathology symptom items (G1-G16) (Table 1). Each item has a definition and a basis for rating. The first question you need to answer when rating a patient is whether the item is absent or present.

How it works. For example, the PANSS defines delusions as “beliefs that are unfounded, unrealistic, and idiosyncratic,” and the basis for rating is “thought content expressed during the interview and its influence on the patient’s social relations and behavior as reported from primary care workers or family.” If the definition does not apply to your patient, you rate this item 1 or absent. If the definition does apply, “anchoring points” for each level of severity are provided (Table 2), and you decide which anchoring point best describes the patient’s functioning during the interview and the preceding week.

Time required. In research, gathering informant information, conducting the interview, and generating reliable ratings takes 45 to 60 minutes. In clinical settings, if you know your patient and can function as informant and interviewer, you probably can obtain accurate ratings in 30 to 45 minutes.

Ideally, you would use the Structured Clinical Interview for the PANSS (SCI-PANSS), though clinicians who know this instrument well may prefer a less structured interview that covers all areas of inquiry. Accurate PANSS scores are easy to generate on all 30 items by combining information from the interview with information about how the patient has functioned in the past week.

PANSS ratings are not meant to be obtained after every patient contact but rather as often as needed to guide clinical treatment. For example, you might obtain a PANSS rating:

• when an inpatient is first admitted
  
• before starting a new medication
  
• weeks or months later to gauge the new treatment’s effect.
  

Training is vital to becoming a reliable PANSS rater and is offered at venues such as the American Psychiatric Association’s annual meeting. Other options include workshops or self-training materials from The PANSS Institute (see Related resources).

The PANSS manual—a complete individual kit costs approximately $200—or licenses to use multiple copies are available from the copyright holder, MultiHealth Systems, Inc. (see Related resources).

Table 1

Subscales of the 30-item Positive and Negative Syndrome Scale (PANSS)

7 Positive symptom subscale items	7 Negative symptom subscale items
P1. Delusions	N1. Blunted affect
P2. Conceptual disorganization	N2. Emotional withdrawal
P3. Hallucinatory behavior	N3. Poor rapport
P4. Excitement	N4. Passive/apathetic social withdrawal
P5. Grandiosity	N5. Difficulty in abstract thinking
P6. Suspiciousness/persecution	N6. Lack of spontaneity and flow of conversation
P7. Hostility	N7. Stereotyped thinking
16 General psychopathology symptoms
G1. Somatic concern	G9. Unusual thought content
G2. Anxiety	G10. Disorientation
G3. Guilt feelings	G11. Poor attention
G4. Tension	G12. Lack of judgment and insight
G5. Mannerisms and posturing	G13. Disturbance of volition
G6. Depression	G14. Poor impulse control
G7. Motor retardation	G15. Preoccupation
G8. Uncooperativeness	G16. Active social avoidance

 

Table 2

7 levels of severity on the PANSS for characterizing delusions

Severity level (“anchoring point”)	Description of patient function
1 - Absent	The definition does not apply
2 - Minimal	Questionable pathology; the patient may be at the upper extreme of normal limits
3 - Mild	Presence of one or two delusions that are vague, uncrystallized, and not tenaciously held. The delusions do not interfere with the patient’s thinking, social relations, or behavior
4 - Moderate	Presence of either a kaleidoscopic array of poorly formed, unstable delusions, or a few well-formed delusions that occasionally interfere with the patient’s thinking, social relations, or behavior
5 - Moderate severe	Presence of numerous well-formed delusions that are tenaciously held and occasionally interfere with the patient’s thinking, social relations, or behavior
6 - Severe	Presence of a stable set of delusions that are crystallized, possibly systematized, tenaciously held, and clearly interfere with the patient’s thinking, social relations, or behavior
7 - Extreme	Presence of a stable set of delusions that are either highly systematized or very numerous, and that dominate major facets of the patient’s life. This behavior frequently results in inappropriate and irresponsible action that may jeopardize the safety of the patient or others

Gauging Symptom Severity

Treatment planning. Clinicians at the Rochester (New York) Psychiatric Center use the PANSS to assess symptom severity in inpatients with schizophrenia and other psychotic disorders.

Within 1 week of admission, patients are evaluated on the 30 items by a team of experienced PANSS raters. Symptoms identified by the PANSS become targets in individualized treatment plans. Follow-up PANSS assessments help determine if treatment has improved the selected symptoms.

Tracking patient progress. Florida State Hospital uses the PANSS to track progress of patients with serious mental illnesses. Data collected over 8 years from >19,000 PANSS assessments in a multilingual, multicultural population suggests that the PANSS:

• aids in decision making for medical and nonmedical aspects of care for individual patients
  
• can help determine if changes in agency prescribing practices affect patient symptom profiles and severity, one indicator of how policy and guidelines translate into patient care.⁹
  

Monitoring depression. In Geha Psychiatric Hospital in Tel Aviv, Israel, treatment outcomes improved when the PANSS was used to measure severity of symptoms—particularly depression—in an inpatient population of adolescents with schizophrenia.¹⁰ PANSS items can measure dysphoria, including anxiety, tension, and guilt feelings. Clinicians now routinely use the PANSS to assess patients’ symptoms at admission and for periodic follow-up.

Predicting Outcomes

The PANSS has been shown to predict course of illness and treatment response, functional outcomes (including aggression), and long-term outcomes (including deterioration). Adjusting treatments to achieve optimal PANSS scores also can help clinicians achieve remission of their patients’ psychotic symptoms (Box).^11,12

Box

Course of illness. Schizophrenia patients in a Tokyo hospital psychiatric ward were rated within 3 days of admission and at weekly intervals for 8 weeks. Baseline PANSS scores on the conceptual disorganization item and the total negative scale score predicted which patients would respond to antipsychotic treatment within 5 weeks.¹³

Functional outcomes. Steinert et al¹⁴ used the PANSS to rate 199 inpatients within 24 hours of admission into an acute psychiatric ward. After discharge, each patient was assessed retrospectively for aggressive behavior. The conceptual disorganization and hostility items from the positive sub-scale could predict violent behaviors during inpatient treatment with statistical significance.

Long-term outcomes. White et al¹⁵ assessed older schizophrenia inpatients, using the PANSS at baseline and after 1 year. The researchers looked specifically at the “activation factor”—six PANSS items including hostility, poor impulse control, excitement, uncooperativeness, poor rapport, and tension. Poor outcome and low discharge rates were directly correlated with high baseline scores on the PANSS activation factor (PANSS-AF).

Deterioration. Goetz et al¹⁶ showed that residual positive symptoms were significantly related to deteriorating course of illness, even when patients adhered to their medications. These results suggest that even subtle symptom elevations as measured by the PANSS can predict deterioration.

 

Related resources

• The PANSS Institute. Information on how to attain, maintain, and retain high reliability as a PANSS rater. www.panss.org.
  
• MultiHealth Systems, Inc. (publisher and copyright holder) to purchase the Positive and Negative Syndrome Scale (PANSS). www.mhs.com.
  
• Opler LA, Ramirez PM, Mougios VA. Measuring outcome in serious mental illness. In: IsHak WW, Burt T, Sederer L (eds). Outcome measurement in psychiatry: a critical review. Washington, DC: American Psychiatric Press; 2002.
  

Disclosures

Dr. Lewis A. Opler receives royalties from MultiHealth Systems, Inc. on sales of the Positive and Negative Syndrome Scale (PANSS) Manual, the Structured Clinical Interview for the PANSS (SCI-PANSS), and the Informant Questionnaire for the PANSS (IQ-PANSS).

Dr. Mark G. Opler is Executive Director of The PANSS Institute.

Acknowledgement

This work was supported in part by NIMH grant K24 MH01699 (DM).

The Positive and Negative Syndrome Scale (PANSS) is moving from research into clinical practice as demand grows for objective rating scales. We see the PANSS becoming a treatment and planning tool for psychiatry, just as the electrocardiogram evolved into a measure of cardiac status in medical practice.

Based on our experience in co-authoring (LA Opler) and using the PANSS, we describe how you can use it to:

• identify psychotic symptoms for targeted treatment
  
• predict with greater accuracy how patients will respond to the treatment you provide.
  

Standardized Assessments

The PANSS first gained stature in studies that established the efficacy of second-generation antipsychotics (SGAs).^1-6 But its authors⁷ also envisioned the scale as a useful tool to help practicing clinicians treat patients with schizophrenia and other psychotic disorders.

Twenty years of experience has shown the PANSS to be a reliable and valid severity symptom scale for schizophrenia, bipolar disorder, and other serious mental illnesses. It is particularly useful to track changes in positive and negative symptoms.⁸

Traditionally, psychiatric evaluation has been impressionistic and subjective, but standardized tools provide a common language while introducing objective, empiric measures of clinical status. Because patients with mental disorders are treated by providers from psychiatry, psychology, social work, nursing, and other mental health disciplines, having standardized benchmarks to assess symptom severity can facilitate an integrated approach. And because the PANSS has been translated into some 40 languages and is being adopted in clinical settings worldwide, it provides a universal means of communicating information about a patient’s clinical status.

Panss Scoring System

The PANSS includes 30 items, each rated from 1 (absent) to 7 (extreme). In theory, a patient rated “absent” (or 1) on all items would receive a total score of 30, and a patient rated “extreme” (or 7) on all items would receive a total score of 210. In the real world, though, no one sees these extremes. Stable outpatients usually score 60 to 80. Inpatients’ scores rarely exceed 80 to 150, even in “treatment refractory” cases.

The 30 items are arranged as 7 positive symptom subscale items (P1-P7), 7 negative symptom subscale items (N1-N7), and 16 general psychopathology symptom items (G1-G16) (Table 1). Each item has a definition and a basis for rating. The first question you need to answer when rating a patient is whether the item is absent or present.

How it works. For example, the PANSS defines delusions as “beliefs that are unfounded, unrealistic, and idiosyncratic,” and the basis for rating is “thought content expressed during the interview and its influence on the patient’s social relations and behavior as reported from primary care workers or family.” If the definition does not apply to your patient, you rate this item 1 or absent. If the definition does apply, “anchoring points” for each level of severity are provided (Table 2), and you decide which anchoring point best describes the patient’s functioning during the interview and the preceding week.

Time required. In research, gathering informant information, conducting the interview, and generating reliable ratings takes 45 to 60 minutes. In clinical settings, if you know your patient and can function as informant and interviewer, you probably can obtain accurate ratings in 30 to 45 minutes.

Ideally, you would use the Structured Clinical Interview for the PANSS (SCI-PANSS), though clinicians who know this instrument well may prefer a less structured interview that covers all areas of inquiry. Accurate PANSS scores are easy to generate on all 30 items by combining information from the interview with information about how the patient has functioned in the past week.

PANSS ratings are not meant to be obtained after every patient contact but rather as often as needed to guide clinical treatment. For example, you might obtain a PANSS rating:

• when an inpatient is first admitted
  
• before starting a new medication
  
• weeks or months later to gauge the new treatment’s effect.
  

Training is vital to becoming a reliable PANSS rater and is offered at venues such as the American Psychiatric Association’s annual meeting. Other options include workshops or self-training materials from The PANSS Institute (see Related resources).

The PANSS manual—a complete individual kit costs approximately $200—or licenses to use multiple copies are available from the copyright holder, MultiHealth Systems, Inc. (see Related resources).

Table 1

Subscales of the 30-item Positive and Negative Syndrome Scale (PANSS)

7 Positive symptom subscale items	7 Negative symptom subscale items
P1. Delusions	N1. Blunted affect
P2. Conceptual disorganization	N2. Emotional withdrawal
P3. Hallucinatory behavior	N3. Poor rapport
P4. Excitement	N4. Passive/apathetic social withdrawal
P5. Grandiosity	N5. Difficulty in abstract thinking
P6. Suspiciousness/persecution	N6. Lack of spontaneity and flow of conversation
P7. Hostility	N7. Stereotyped thinking
16 General psychopathology symptoms
G1. Somatic concern	G9. Unusual thought content
G2. Anxiety	G10. Disorientation
G3. Guilt feelings	G11. Poor attention
G4. Tension	G12. Lack of judgment and insight
G5. Mannerisms and posturing	G13. Disturbance of volition
G6. Depression	G14. Poor impulse control
G7. Motor retardation	G15. Preoccupation
G8. Uncooperativeness	G16. Active social avoidance

 

Table 2

7 levels of severity on the PANSS for characterizing delusions

Severity level (“anchoring point”)	Description of patient function
1 - Absent	The definition does not apply
2 - Minimal	Questionable pathology; the patient may be at the upper extreme of normal limits
3 - Mild	Presence of one or two delusions that are vague, uncrystallized, and not tenaciously held. The delusions do not interfere with the patient’s thinking, social relations, or behavior
4 - Moderate	Presence of either a kaleidoscopic array of poorly formed, unstable delusions, or a few well-formed delusions that occasionally interfere with the patient’s thinking, social relations, or behavior
5 - Moderate severe	Presence of numerous well-formed delusions that are tenaciously held and occasionally interfere with the patient’s thinking, social relations, or behavior
6 - Severe	Presence of a stable set of delusions that are crystallized, possibly systematized, tenaciously held, and clearly interfere with the patient’s thinking, social relations, or behavior
7 - Extreme	Presence of a stable set of delusions that are either highly systematized or very numerous, and that dominate major facets of the patient’s life. This behavior frequently results in inappropriate and irresponsible action that may jeopardize the safety of the patient or others

Gauging Symptom Severity

Treatment planning. Clinicians at the Rochester (New York) Psychiatric Center use the PANSS to assess symptom severity in inpatients with schizophrenia and other psychotic disorders.

Within 1 week of admission, patients are evaluated on the 30 items by a team of experienced PANSS raters. Symptoms identified by the PANSS become targets in individualized treatment plans. Follow-up PANSS assessments help determine if treatment has improved the selected symptoms.

Tracking patient progress. Florida State Hospital uses the PANSS to track progress of patients with serious mental illnesses. Data collected over 8 years from >19,000 PANSS assessments in a multilingual, multicultural population suggests that the PANSS:

• aids in decision making for medical and nonmedical aspects of care for individual patients
  
• can help determine if changes in agency prescribing practices affect patient symptom profiles and severity, one indicator of how policy and guidelines translate into patient care.⁹
  

Monitoring depression. In Geha Psychiatric Hospital in Tel Aviv, Israel, treatment outcomes improved when the PANSS was used to measure severity of symptoms—particularly depression—in an inpatient population of adolescents with schizophrenia.¹⁰ PANSS items can measure dysphoria, including anxiety, tension, and guilt feelings. Clinicians now routinely use the PANSS to assess patients’ symptoms at admission and for periodic follow-up.

Predicting Outcomes

The PANSS has been shown to predict course of illness and treatment response, functional outcomes (including aggression), and long-term outcomes (including deterioration). Adjusting treatments to achieve optimal PANSS scores also can help clinicians achieve remission of their patients’ psychotic symptoms (Box).^11,12

Box

Course of illness. Schizophrenia patients in a Tokyo hospital psychiatric ward were rated within 3 days of admission and at weekly intervals for 8 weeks. Baseline PANSS scores on the conceptual disorganization item and the total negative scale score predicted which patients would respond to antipsychotic treatment within 5 weeks.¹³

Functional outcomes. Steinert et al¹⁴ used the PANSS to rate 199 inpatients within 24 hours of admission into an acute psychiatric ward. After discharge, each patient was assessed retrospectively for aggressive behavior. The conceptual disorganization and hostility items from the positive sub-scale could predict violent behaviors during inpatient treatment with statistical significance.

Long-term outcomes. White et al¹⁵ assessed older schizophrenia inpatients, using the PANSS at baseline and after 1 year. The researchers looked specifically at the “activation factor”—six PANSS items including hostility, poor impulse control, excitement, uncooperativeness, poor rapport, and tension. Poor outcome and low discharge rates were directly correlated with high baseline scores on the PANSS activation factor (PANSS-AF).

Deterioration. Goetz et al¹⁶ showed that residual positive symptoms were significantly related to deteriorating course of illness, even when patients adhered to their medications. These results suggest that even subtle symptom elevations as measured by the PANSS can predict deterioration.

 

Related resources

• The PANSS Institute. Information on how to attain, maintain, and retain high reliability as a PANSS rater. www.panss.org.
  
• MultiHealth Systems, Inc. (publisher and copyright holder) to purchase the Positive and Negative Syndrome Scale (PANSS). www.mhs.com.
  
• Opler LA, Ramirez PM, Mougios VA. Measuring outcome in serious mental illness. In: IsHak WW, Burt T, Sederer L (eds). Outcome measurement in psychiatry: a critical review. Washington, DC: American Psychiatric Press; 2002.
  

Disclosures

Dr. Lewis A. Opler receives royalties from MultiHealth Systems, Inc. on sales of the Positive and Negative Syndrome Scale (PANSS) Manual, the Structured Clinical Interview for the PANSS (SCI-PANSS), and the Informant Questionnaire for the PANSS (IQ-PANSS).

Dr. Mark G. Opler is Executive Director of The PANSS Institute.

Acknowledgement

This work was supported in part by NIMH grant K24 MH01699 (DM).

Pegylated interferon-alpha with ribavirin is the most effective therapy for chronic hepatitis C infection,^1,2 but psychiatric patients often discontinue IFN-alpha because of its mood side effects.³ Most studies describe depressive states, although manic symptoms—irritability, aggression, anger, hostility, emotional lability, anxiety, panic attacks, and insomnia—also have been reported.^4-6

To help you manage adverse mood changes and prevent IFN-alpha treatment discontinuation in patients with hepatitis C, this article:

• reviews studies of patients with a history mood disorders who were treated with IFN-alpha
• explains how to recognize and treat IFN-alpha-induced mood disturbances when antidepressants are contraindicated.

Psychiatric Patients and IFN Therapy

Chronic hepatitis C infection is common among psychiatric patients. Routine screening among 1,556 patients admitted to a U.S. public psychiatric hospital across 3 years identified 133 patients (8.5%) who were positive for hepatitis C virus.⁷

Patients with psychopathologic symptoms before starting IFN therapy may suffer more-severe adverse psychiatric effects during treatment than those without psychopathology.⁸ In fact, mood disorders were considered an absolute contraindication to IFN therapy until recently.

Now that the National Institutes of Health (NIH) has recommended extending hepatitis C research and treatment to psychiatric patients, IFN-alpha-induced mental illness could become more common in clinical practice. Before the 2002 NIH consensus statement, patients with mental illness and substance use disorders—who represent >50% of candidates who need IFN therapy—were excluded from research protocols.

Safely using IFN. Some reports and studies suggest that patients with past or existing psychiatric disorders can be treated safely and effectively with IFN-alpha.

In a prospective open-label study, 29 of 31 patients with co-existing chronic hepatitis C and psychiatric illness completed 6 months of IFN therapy, 5 million units (MU) three times/week or 5 MU daily. Patients continued maintenance psychotropics during IFN treatment, and a psychiatrist monitored psychiatric symptoms.

Psychiatric illness worsened in four patients, and two discontinued IFN treatment. Serum alanine aminotransferase returned to normal in 22 patients (71%), and hepatitis C virus RNA cleared from the sera of 15 (48%).⁹

Another prospective study of 50 patients treated with IFN for chronic hepatitis found that those with a pre-existing mood or anxiety disorder were not more likely than others to discontinue IFN therapy.¹⁰

Unique to hepatitis therapy? IFN-induced mood disturbances are probably different in patients with chronic hepatitis C than in those receiving IFN for other diseases because of differences in regimens and effects of the underlying pathologies. For example, prescribing a preventative antidepressant before starting IFN treatment might help cancer patients but not patients with hepatitis C.¹¹

This distinction could be particularly important when giving IFN-alpha to patients who are vulnerable to psychiatric illness with impulsive features. To emphasize this point, we describe clinical features and treatment response in patients with hepatitis C who were treated in our department.

IFN-Alpha-Induced Moods

In our prospective study of 93 patients, 30 (32%) developed IFN-alpha-induced mood disorders during the first 12 weeks of treatment.¹² Contrary to previous studies focusing on depression, most of our patients had a mix of manic/hypomanic and depressive symptoms. Twenty-four (13 women and 11 men, mean age 43) accepted referral to a psychiatrist specializing in mood disorders to characterize their symptoms.

Mood characteristics. Using DSM-IV criteria, the psychiatrist determined that IFN-alpha induced both manic/hypomanic and depressive symptoms in many patients, and the manic/hypomanic features predominated. Five manic symptoms and three depressive symptoms were present in >50% of patients (Figure 1, Table 1).

Three patients presented with a manic episode,15 with hypomania with prevalent irritability and dysphoric features, and 6 with a mixed depressive state (major depressive episode with at least 3 hypomania symptoms).¹³ Four patients (17%) suffered a relapse of alcohol or cannabis abuse.

Nearly all (84%) reported paroxysmal anxiety, and all had emotional hyperreactivity that the psychiatrist described as a main symptom of a manic or mixed state.¹⁴ Most felt extremely impulsive and feared losing control. Two faced legal difficulties, and one was in prison.

The patients’ mean Montgomery-Åsburg Depression Rating Scale (MADRS) score was 16.12 (±1.6), indicating a mild to moderate depressive state. The highest-scoring items were inner tension, reduced sleep, reduced appetite, and lassitude (Figure 2).

Their mean Bech-Rafaelsen Mania Scale¹⁵ score was 14.33 (±1.3), indicating hypomanic or moderate manic symptoms. Hostility was by far the predominant manic symptom (mean score 3.2/4). Other manic symptom scores ranged from 0.2/4 to 2.1/4 (Figure 3).

Figure 1 Mood symptoms identified in 24 patients after 12 weeks of IFN-alpha treatment

IFN: Interferon

Source: Reference 12

Figure 2 Depressive symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12

 

Figure 3 Manic symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12Table 1

Most-prevalent IFN-induced mood symptoms in 24 patients treated for hepatitis C

5 manic symptoms (% of patients)	3 depressive symptoms (% of patients)
Irritability (100%)	Insomnia or hypersomnia (100%)
Racing thoughts (87%)	Poor appetite or weight loss (92%)
Distractibility (87%)	Psychomotor agitation or retardation (54%)
Insomnia (58%)
Agitation (70%)
IFN: Interferon
Source: Reference 12

Treatment. Given the predominance of manic/hypomanic symptoms, we treated the 24 patients with low-to-moderate dosages of an atypical antipsychotic (amisulpride, 100 to 600 mg/d). This medication—not available in the United States—would be similar to using risperidone, 1 to 6 mg/d. Low-dose benzodiazepines (clonazepam or alprazolam) were added as needed to manage insomnia. Antipsychotic treatment enabled 23 of 24 patients (96%) to continue antiviral therapy.

Five patients had received selective serotonin reuptake inhibitors (SSRIs) for 1 to 4 weeks before referral to the psychiatrist. Antidepressants worsened their mood symptoms, which included impulsivity, agitation, and insomnia. Emotional hyper-reactivity, irritability, hostility, and impulsiveness improved in all 5 patients within 1 to 2 weeks of stopping SSRIs and starting the atypical antipsychotic.

Discussion

Accurately characterizing IFN-induced mood states confirmed our published data showing a mix of manic/hypomanic and depressive symptoms in psychiatric patients treated for chronic hepatitis C. Irritability and hostility were the two most prominent symptoms.

These findings differ from those of investigations that identified depressive symptoms as the hallmark of IFN’s psychiatric side effects.⁶ Our data were thoroughly characterized according to DSM-IV-TR criteria, two mood-rating scales, and a psychiatrist experienced in mood disorders.

Why is mania missed? One possible explanation for these different findings is that IFN-alpha-induced fatigue and flu-like symptoms could be misinterpreted as depressive symptoms. Also, most researchers have used depression rating scales—but not mania scales—and have not considered other psychiatric diagnostics.¹⁶

Self-report questionnaires for evaluating depression also take into account somatic side effects, resulting in higher rating scores. Moreover, few studies have included clinical psychiatric interviews and even fewer diagnostic confirmation by a psychiatrist.

Finally, clinical experience indicates that patients who present with both manic/hypomanic and depressive symptoms are more likely to complain about depression than about manic symptoms. Therefore, clinicians may miss manic symptoms if they don’t actively seek them.

Irritability and hostility. Previous studies have described irritability, mood lability, and anger/hostility as frequent symptoms^4,5 but failed to consider them as possible manifestations of mania or hypomania. Many of our patients reported irritability severe enough to interfere with their work, social, and family relationships.

Hostility was the symptom with the highest score on the Bech-Rafaelsen Mania Scale. This objective evidence suggests that investigating the consequences to patients of increased irritability, impulsivity, or hostility might reveal some frightening behavior

How to treat these patients. Considerable evidence from characterizing IFN-induced side effects in patients with hepatitis C points to a syndrome of depressive and manic/hypomanic symptoms^13,17-19 that does not fulfill criteria for a mixed state. This disorder is not described in DSM-IV-TR and, unfortunately, usually is misdiagnosed as a depressive state.

Antidepressants can worsen depression by causing agitation and impulsivity and can increase risk of suicide.^17,18,20 By contrast, atypical antipsychotics have been shown to improve bipolar depression.^21,22

We used an atypical antipsychotic to treat patients with prevalent manic or hypomanic symptoms and those who did not respond to SSRIs. Their IFN-induced mood disorders improved rapidly on low dosages of amisulpride, and antiviral therapy discontinuation rates were low (1/24; 4%). By comparison, other studies have reported antiviral treatment discontinuation rates of 30% to 40% in patients taking antidepressants.^23,24

The atypical antipsychotic did not improve our patients’ fatigue and other neurovegetative symptoms, but antidepressants likewise do not improve these symptoms.⁸

Recommendations

This study leads us to warn clinicians that antidepressants can worsen IFN-alpha-induced mood disorders and to recommend that antipsychotics be considered:

• at least before you decide to discontinue a hepatitis C patient’s IFN-alpha therapy
• or in patients with high irritability and hostility.

To determine whether to use an antidepressant or antimanic agent as first-line treatment, carefully diagnose the patient’s symptoms as a manic/hypomanic state, depressive mixed state, or depression. Successful IFN therapy requires:

• psychological support
• medication for psychiatric adverse effects
• collaboration between the psychiatrist and hepatologist.

IFN-alpha-induced mood disorders are triggered exogenously, do not correspond to typical features of any classic psychiatric disorder, and require further study. IFN-induced impulsivity and hostility also need to be better characterized, particularly as more patients with pre-existing psychiatric disorders are treated for hepatitis C.

Related resources

• Lauer GM, Walker BD. Hepatitis C virus infection. N Engl J Med 2001;345(1):41-52.
• Onyike CU, Bonner JO, Lyketsos CG, Treisman GJ. Mania during treatment of chronic hepatitis C with pegylated interferon and ribavirin. Am J Psychiatry 2004;161:3.

 

Drug brand names

• Alprazolam • Xanax
• Amisulpride • (not available in the United States)
• Clonazepam • Klonopin
• Risperidone • Risperdal

Acknowledgment

This study was conducted with support from the Centre d’Investigation Clinique INSERM/CHU de Bordeaux.

Pegylated interferon-alpha with ribavirin is the most effective therapy for chronic hepatitis C infection,^1,2 but psychiatric patients often discontinue IFN-alpha because of its mood side effects.³ Most studies describe depressive states, although manic symptoms—irritability, aggression, anger, hostility, emotional lability, anxiety, panic attacks, and insomnia—also have been reported.^4-6

To help you manage adverse mood changes and prevent IFN-alpha treatment discontinuation in patients with hepatitis C, this article:

• reviews studies of patients with a history mood disorders who were treated with IFN-alpha
• explains how to recognize and treat IFN-alpha-induced mood disturbances when antidepressants are contraindicated.

Psychiatric Patients and IFN Therapy

Chronic hepatitis C infection is common among psychiatric patients. Routine screening among 1,556 patients admitted to a U.S. public psychiatric hospital across 3 years identified 133 patients (8.5%) who were positive for hepatitis C virus.⁷

Patients with psychopathologic symptoms before starting IFN therapy may suffer more-severe adverse psychiatric effects during treatment than those without psychopathology.⁸ In fact, mood disorders were considered an absolute contraindication to IFN therapy until recently.

Now that the National Institutes of Health (NIH) has recommended extending hepatitis C research and treatment to psychiatric patients, IFN-alpha-induced mental illness could become more common in clinical practice. Before the 2002 NIH consensus statement, patients with mental illness and substance use disorders—who represent >50% of candidates who need IFN therapy—were excluded from research protocols.

Safely using IFN. Some reports and studies suggest that patients with past or existing psychiatric disorders can be treated safely and effectively with IFN-alpha.

In a prospective open-label study, 29 of 31 patients with co-existing chronic hepatitis C and psychiatric illness completed 6 months of IFN therapy, 5 million units (MU) three times/week or 5 MU daily. Patients continued maintenance psychotropics during IFN treatment, and a psychiatrist monitored psychiatric symptoms.

Psychiatric illness worsened in four patients, and two discontinued IFN treatment. Serum alanine aminotransferase returned to normal in 22 patients (71%), and hepatitis C virus RNA cleared from the sera of 15 (48%).⁹

Another prospective study of 50 patients treated with IFN for chronic hepatitis found that those with a pre-existing mood or anxiety disorder were not more likely than others to discontinue IFN therapy.¹⁰

Unique to hepatitis therapy? IFN-induced mood disturbances are probably different in patients with chronic hepatitis C than in those receiving IFN for other diseases because of differences in regimens and effects of the underlying pathologies. For example, prescribing a preventative antidepressant before starting IFN treatment might help cancer patients but not patients with hepatitis C.¹¹

This distinction could be particularly important when giving IFN-alpha to patients who are vulnerable to psychiatric illness with impulsive features. To emphasize this point, we describe clinical features and treatment response in patients with hepatitis C who were treated in our department.

IFN-Alpha-Induced Moods

In our prospective study of 93 patients, 30 (32%) developed IFN-alpha-induced mood disorders during the first 12 weeks of treatment.¹² Contrary to previous studies focusing on depression, most of our patients had a mix of manic/hypomanic and depressive symptoms. Twenty-four (13 women and 11 men, mean age 43) accepted referral to a psychiatrist specializing in mood disorders to characterize their symptoms.

Mood characteristics. Using DSM-IV criteria, the psychiatrist determined that IFN-alpha induced both manic/hypomanic and depressive symptoms in many patients, and the manic/hypomanic features predominated. Five manic symptoms and three depressive symptoms were present in >50% of patients (Figure 1, Table 1).

Three patients presented with a manic episode,15 with hypomania with prevalent irritability and dysphoric features, and 6 with a mixed depressive state (major depressive episode with at least 3 hypomania symptoms).¹³ Four patients (17%) suffered a relapse of alcohol or cannabis abuse.

Nearly all (84%) reported paroxysmal anxiety, and all had emotional hyperreactivity that the psychiatrist described as a main symptom of a manic or mixed state.¹⁴ Most felt extremely impulsive and feared losing control. Two faced legal difficulties, and one was in prison.

The patients’ mean Montgomery-Åsburg Depression Rating Scale (MADRS) score was 16.12 (±1.6), indicating a mild to moderate depressive state. The highest-scoring items were inner tension, reduced sleep, reduced appetite, and lassitude (Figure 2).

Their mean Bech-Rafaelsen Mania Scale¹⁵ score was 14.33 (±1.3), indicating hypomanic or moderate manic symptoms. Hostility was by far the predominant manic symptom (mean score 3.2/4). Other manic symptom scores ranged from 0.2/4 to 2.1/4 (Figure 3).

Figure 1 Mood symptoms identified in 24 patients after 12 weeks of IFN-alpha treatment

IFN: Interferon

Source: Reference 12

Figure 2 Depressive symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12

 

Figure 3 Manic symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12Table 1

Most-prevalent IFN-induced mood symptoms in 24 patients treated for hepatitis C

5 manic symptoms (% of patients)	3 depressive symptoms (% of patients)
Irritability (100%)	Insomnia or hypersomnia (100%)
Racing thoughts (87%)	Poor appetite or weight loss (92%)
Distractibility (87%)	Psychomotor agitation or retardation (54%)
Insomnia (58%)
Agitation (70%)
IFN: Interferon
Source: Reference 12

Treatment. Given the predominance of manic/hypomanic symptoms, we treated the 24 patients with low-to-moderate dosages of an atypical antipsychotic (amisulpride, 100 to 600 mg/d). This medication—not available in the United States—would be similar to using risperidone, 1 to 6 mg/d. Low-dose benzodiazepines (clonazepam or alprazolam) were added as needed to manage insomnia. Antipsychotic treatment enabled 23 of 24 patients (96%) to continue antiviral therapy.

Five patients had received selective serotonin reuptake inhibitors (SSRIs) for 1 to 4 weeks before referral to the psychiatrist. Antidepressants worsened their mood symptoms, which included impulsivity, agitation, and insomnia. Emotional hyper-reactivity, irritability, hostility, and impulsiveness improved in all 5 patients within 1 to 2 weeks of stopping SSRIs and starting the atypical antipsychotic.

Discussion

Accurately characterizing IFN-induced mood states confirmed our published data showing a mix of manic/hypomanic and depressive symptoms in psychiatric patients treated for chronic hepatitis C. Irritability and hostility were the two most prominent symptoms.

These findings differ from those of investigations that identified depressive symptoms as the hallmark of IFN’s psychiatric side effects.⁶ Our data were thoroughly characterized according to DSM-IV-TR criteria, two mood-rating scales, and a psychiatrist experienced in mood disorders.

Why is mania missed? One possible explanation for these different findings is that IFN-alpha-induced fatigue and flu-like symptoms could be misinterpreted as depressive symptoms. Also, most researchers have used depression rating scales—but not mania scales—and have not considered other psychiatric diagnostics.¹⁶

Self-report questionnaires for evaluating depression also take into account somatic side effects, resulting in higher rating scores. Moreover, few studies have included clinical psychiatric interviews and even fewer diagnostic confirmation by a psychiatrist.

Finally, clinical experience indicates that patients who present with both manic/hypomanic and depressive symptoms are more likely to complain about depression than about manic symptoms. Therefore, clinicians may miss manic symptoms if they don’t actively seek them.

Irritability and hostility. Previous studies have described irritability, mood lability, and anger/hostility as frequent symptoms^4,5 but failed to consider them as possible manifestations of mania or hypomania. Many of our patients reported irritability severe enough to interfere with their work, social, and family relationships.

Hostility was the symptom with the highest score on the Bech-Rafaelsen Mania Scale. This objective evidence suggests that investigating the consequences to patients of increased irritability, impulsivity, or hostility might reveal some frightening behavior

How to treat these patients. Considerable evidence from characterizing IFN-induced side effects in patients with hepatitis C points to a syndrome of depressive and manic/hypomanic symptoms^13,17-19 that does not fulfill criteria for a mixed state. This disorder is not described in DSM-IV-TR and, unfortunately, usually is misdiagnosed as a depressive state.

Antidepressants can worsen depression by causing agitation and impulsivity and can increase risk of suicide.^17,18,20 By contrast, atypical antipsychotics have been shown to improve bipolar depression.^21,22

We used an atypical antipsychotic to treat patients with prevalent manic or hypomanic symptoms and those who did not respond to SSRIs. Their IFN-induced mood disorders improved rapidly on low dosages of amisulpride, and antiviral therapy discontinuation rates were low (1/24; 4%). By comparison, other studies have reported antiviral treatment discontinuation rates of 30% to 40% in patients taking antidepressants.^23,24

The atypical antipsychotic did not improve our patients’ fatigue and other neurovegetative symptoms, but antidepressants likewise do not improve these symptoms.⁸

Recommendations

This study leads us to warn clinicians that antidepressants can worsen IFN-alpha-induced mood disorders and to recommend that antipsychotics be considered:

• at least before you decide to discontinue a hepatitis C patient’s IFN-alpha therapy
• or in patients with high irritability and hostility.

To determine whether to use an antidepressant or antimanic agent as first-line treatment, carefully diagnose the patient’s symptoms as a manic/hypomanic state, depressive mixed state, or depression. Successful IFN therapy requires:

• psychological support
• medication for psychiatric adverse effects
• collaboration between the psychiatrist and hepatologist.

IFN-alpha-induced mood disorders are triggered exogenously, do not correspond to typical features of any classic psychiatric disorder, and require further study. IFN-induced impulsivity and hostility also need to be better characterized, particularly as more patients with pre-existing psychiatric disorders are treated for hepatitis C.

Related resources

• Lauer GM, Walker BD. Hepatitis C virus infection. N Engl J Med 2001;345(1):41-52.
• Onyike CU, Bonner JO, Lyketsos CG, Treisman GJ. Mania during treatment of chronic hepatitis C with pegylated interferon and ribavirin. Am J Psychiatry 2004;161:3.

 

Drug brand names

• Alprazolam • Xanax
• Amisulpride • (not available in the United States)
• Clonazepam • Klonopin
• Risperidone • Risperdal

Acknowledgment

This study was conducted with support from the Centre d’Investigation Clinique INSERM/CHU de Bordeaux.

Pegylated interferon-alpha with ribavirin is the most effective therapy for chronic hepatitis C infection,^1,2 but psychiatric patients often discontinue IFN-alpha because of its mood side effects.³ Most studies describe depressive states, although manic symptoms—irritability, aggression, anger, hostility, emotional lability, anxiety, panic attacks, and insomnia—also have been reported.^4-6

To help you manage adverse mood changes and prevent IFN-alpha treatment discontinuation in patients with hepatitis C, this article:

• reviews studies of patients with a history mood disorders who were treated with IFN-alpha
• explains how to recognize and treat IFN-alpha-induced mood disturbances when antidepressants are contraindicated.

Psychiatric Patients and IFN Therapy

Chronic hepatitis C infection is common among psychiatric patients. Routine screening among 1,556 patients admitted to a U.S. public psychiatric hospital across 3 years identified 133 patients (8.5%) who were positive for hepatitis C virus.⁷

Patients with psychopathologic symptoms before starting IFN therapy may suffer more-severe adverse psychiatric effects during treatment than those without psychopathology.⁸ In fact, mood disorders were considered an absolute contraindication to IFN therapy until recently.

Now that the National Institutes of Health (NIH) has recommended extending hepatitis C research and treatment to psychiatric patients, IFN-alpha-induced mental illness could become more common in clinical practice. Before the 2002 NIH consensus statement, patients with mental illness and substance use disorders—who represent >50% of candidates who need IFN therapy—were excluded from research protocols.

Safely using IFN. Some reports and studies suggest that patients with past or existing psychiatric disorders can be treated safely and effectively with IFN-alpha.

In a prospective open-label study, 29 of 31 patients with co-existing chronic hepatitis C and psychiatric illness completed 6 months of IFN therapy, 5 million units (MU) three times/week or 5 MU daily. Patients continued maintenance psychotropics during IFN treatment, and a psychiatrist monitored psychiatric symptoms.

Psychiatric illness worsened in four patients, and two discontinued IFN treatment. Serum alanine aminotransferase returned to normal in 22 patients (71%), and hepatitis C virus RNA cleared from the sera of 15 (48%).⁹

Another prospective study of 50 patients treated with IFN for chronic hepatitis found that those with a pre-existing mood or anxiety disorder were not more likely than others to discontinue IFN therapy.¹⁰

Unique to hepatitis therapy? IFN-induced mood disturbances are probably different in patients with chronic hepatitis C than in those receiving IFN for other diseases because of differences in regimens and effects of the underlying pathologies. For example, prescribing a preventative antidepressant before starting IFN treatment might help cancer patients but not patients with hepatitis C.¹¹

This distinction could be particularly important when giving IFN-alpha to patients who are vulnerable to psychiatric illness with impulsive features. To emphasize this point, we describe clinical features and treatment response in patients with hepatitis C who were treated in our department.

IFN-Alpha-Induced Moods

In our prospective study of 93 patients, 30 (32%) developed IFN-alpha-induced mood disorders during the first 12 weeks of treatment.¹² Contrary to previous studies focusing on depression, most of our patients had a mix of manic/hypomanic and depressive symptoms. Twenty-four (13 women and 11 men, mean age 43) accepted referral to a psychiatrist specializing in mood disorders to characterize their symptoms.

Mood characteristics. Using DSM-IV criteria, the psychiatrist determined that IFN-alpha induced both manic/hypomanic and depressive symptoms in many patients, and the manic/hypomanic features predominated. Five manic symptoms and three depressive symptoms were present in >50% of patients (Figure 1, Table 1).

Three patients presented with a manic episode,15 with hypomania with prevalent irritability and dysphoric features, and 6 with a mixed depressive state (major depressive episode with at least 3 hypomania symptoms).¹³ Four patients (17%) suffered a relapse of alcohol or cannabis abuse.

Nearly all (84%) reported paroxysmal anxiety, and all had emotional hyperreactivity that the psychiatrist described as a main symptom of a manic or mixed state.¹⁴ Most felt extremely impulsive and feared losing control. Two faced legal difficulties, and one was in prison.

The patients’ mean Montgomery-Åsburg Depression Rating Scale (MADRS) score was 16.12 (±1.6), indicating a mild to moderate depressive state. The highest-scoring items were inner tension, reduced sleep, reduced appetite, and lassitude (Figure 2).

Their mean Bech-Rafaelsen Mania Scale¹⁵ score was 14.33 (±1.3), indicating hypomanic or moderate manic symptoms. Hostility was by far the predominant manic symptom (mean score 3.2/4). Other manic symptom scores ranged from 0.2/4 to 2.1/4 (Figure 3).

Figure 1 Mood symptoms identified in 24 patients after 12 weeks of IFN-alpha treatment

IFN: Interferon

Source: Reference 12

Figure 2 Depressive symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12

 

Figure 3 Manic symptoms in 24 patients with IFN-induced mood disorder

IFN: Interferon

Source: Reference 12Table 1

Most-prevalent IFN-induced mood symptoms in 24 patients treated for hepatitis C

5 manic symptoms (% of patients)	3 depressive symptoms (% of patients)
Irritability (100%)	Insomnia or hypersomnia (100%)
Racing thoughts (87%)	Poor appetite or weight loss (92%)
Distractibility (87%)	Psychomotor agitation or retardation (54%)
Insomnia (58%)
Agitation (70%)
IFN: Interferon
Source: Reference 12

Treatment. Given the predominance of manic/hypomanic symptoms, we treated the 24 patients with low-to-moderate dosages of an atypical antipsychotic (amisulpride, 100 to 600 mg/d). This medication—not available in the United States—would be similar to using risperidone, 1 to 6 mg/d. Low-dose benzodiazepines (clonazepam or alprazolam) were added as needed to manage insomnia. Antipsychotic treatment enabled 23 of 24 patients (96%) to continue antiviral therapy.

Five patients had received selective serotonin reuptake inhibitors (SSRIs) for 1 to 4 weeks before referral to the psychiatrist. Antidepressants worsened their mood symptoms, which included impulsivity, agitation, and insomnia. Emotional hyper-reactivity, irritability, hostility, and impulsiveness improved in all 5 patients within 1 to 2 weeks of stopping SSRIs and starting the atypical antipsychotic.

Discussion

Accurately characterizing IFN-induced mood states confirmed our published data showing a mix of manic/hypomanic and depressive symptoms in psychiatric patients treated for chronic hepatitis C. Irritability and hostility were the two most prominent symptoms.

These findings differ from those of investigations that identified depressive symptoms as the hallmark of IFN’s psychiatric side effects.⁶ Our data were thoroughly characterized according to DSM-IV-TR criteria, two mood-rating scales, and a psychiatrist experienced in mood disorders.

Why is mania missed? One possible explanation for these different findings is that IFN-alpha-induced fatigue and flu-like symptoms could be misinterpreted as depressive symptoms. Also, most researchers have used depression rating scales—but not mania scales—and have not considered other psychiatric diagnostics.¹⁶

Self-report questionnaires for evaluating depression also take into account somatic side effects, resulting in higher rating scores. Moreover, few studies have included clinical psychiatric interviews and even fewer diagnostic confirmation by a psychiatrist.

Finally, clinical experience indicates that patients who present with both manic/hypomanic and depressive symptoms are more likely to complain about depression than about manic symptoms. Therefore, clinicians may miss manic symptoms if they don’t actively seek them.

Irritability and hostility. Previous studies have described irritability, mood lability, and anger/hostility as frequent symptoms^4,5 but failed to consider them as possible manifestations of mania or hypomania. Many of our patients reported irritability severe enough to interfere with their work, social, and family relationships.

Hostility was the symptom with the highest score on the Bech-Rafaelsen Mania Scale. This objective evidence suggests that investigating the consequences to patients of increased irritability, impulsivity, or hostility might reveal some frightening behavior

How to treat these patients. Considerable evidence from characterizing IFN-induced side effects in patients with hepatitis C points to a syndrome of depressive and manic/hypomanic symptoms^13,17-19 that does not fulfill criteria for a mixed state. This disorder is not described in DSM-IV-TR and, unfortunately, usually is misdiagnosed as a depressive state.

Antidepressants can worsen depression by causing agitation and impulsivity and can increase risk of suicide.^17,18,20 By contrast, atypical antipsychotics have been shown to improve bipolar depression.^21,22

We used an atypical antipsychotic to treat patients with prevalent manic or hypomanic symptoms and those who did not respond to SSRIs. Their IFN-induced mood disorders improved rapidly on low dosages of amisulpride, and antiviral therapy discontinuation rates were low (1/24; 4%). By comparison, other studies have reported antiviral treatment discontinuation rates of 30% to 40% in patients taking antidepressants.^23,24

The atypical antipsychotic did not improve our patients’ fatigue and other neurovegetative symptoms, but antidepressants likewise do not improve these symptoms.⁸

Recommendations

This study leads us to warn clinicians that antidepressants can worsen IFN-alpha-induced mood disorders and to recommend that antipsychotics be considered:

• at least before you decide to discontinue a hepatitis C patient’s IFN-alpha therapy
• or in patients with high irritability and hostility.

To determine whether to use an antidepressant or antimanic agent as first-line treatment, carefully diagnose the patient’s symptoms as a manic/hypomanic state, depressive mixed state, or depression. Successful IFN therapy requires:

• psychological support
• medication for psychiatric adverse effects
• collaboration between the psychiatrist and hepatologist.

IFN-alpha-induced mood disorders are triggered exogenously, do not correspond to typical features of any classic psychiatric disorder, and require further study. IFN-induced impulsivity and hostility also need to be better characterized, particularly as more patients with pre-existing psychiatric disorders are treated for hepatitis C.

Related resources

• Lauer GM, Walker BD. Hepatitis C virus infection. N Engl J Med 2001;345(1):41-52.
• Onyike CU, Bonner JO, Lyketsos CG, Treisman GJ. Mania during treatment of chronic hepatitis C with pegylated interferon and ribavirin. Am J Psychiatry 2004;161:3.

 

Drug brand names

• Alprazolam • Xanax
• Amisulpride • (not available in the United States)
• Clonazepam • Klonopin
• Risperidone • Risperdal

Acknowledgment

This study was conducted with support from the Centre d’Investigation Clinique INSERM/CHU de Bordeaux.

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

	Competency	Sanity
Presence of mental illness	Yes	Yes
Mental status	Current mental state	Mental state at the time of the offense
Purpose of evaluation	Ability to stand trial	Criminal responsibility
Variation in laws by jurisdiction	Minor variation	Great variation

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

Standard	Year	Description
Wild beast	1724	Most strict standard; required total deprivation of memory and understanding
Irresistible impulse	1840	More liberal standard; required that “…some controlling disease was…the acting power within him which he could not resist…”
M’Naughten rule	1843	Required that the defendant not know the nature/quality or the wrongfulness of the offense.
American Law Institute’s Model Penal Code standard	1955	Combined M’Naughten Rule with irresistible impulse
Federal Insanity Defense Reform Act	1984	Stricter standard that dropped the irresistible impulse standard after attempted assassination of President Reagan

‘Wild beast.’ The “wild beast” standard was established in 1724 in Rex v. Arnold. Arnold, the mentally-ill defendant, was found guilty after he shot and wounded Lord Onslow. Arnold’s death sentence was reduced to life in prison after Lord Onslow himself advocated for this change.

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.
  

United States law. Based on the M’Naughten rule and the irresistible impulse standard, the American Law Institute in 1955 issued the Model Penal Code insanity standard. It stated that a defendant is not responsible for his criminal conduct if, at the time of the offense as a result of mental disease or defect, he lacked substantial capacity to:

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

These standards were tightened in federal jurisdictions by the Federal Insanity Defense Reform Act of 1984—a reaction to John Hinckley’s insanity acquittal after he tried to assassinate President Ronald Reagan.

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.
  

These may give insight into the defendant’s mental state.

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)
  

Table 3

Signs that a defendant knew an act was wrong

Efforts to avoid detection	Wearing gloves or a mask during the offense
	Concealing a weapon
	Falsifying information (using an alias or creating a passport)
	Committing the act in the dark
Disposal of evidence	Washing away blood
	Removing fingerprints
	Discarding the weapon
	Hiding the body
Efforts to avoid apprehension	Fleeing
	Lying to authorities

Irresistible impulse? In jurisdictions with an irresistible impulse test, evaluate whether the defendant was able to refrain from the offense when it occurred (Table 4). Allow the defendant to provide an uninterrupted narrative of the event. Use follow-up questions to fill in gaps in the story and to determine the defendant’s motive. You may choose to confront the defendant with contradictory information obtained from collateral sources.⁶

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.
  

By contrast, psychotic justification for the offense—for example, a mother who kills her children because she believes she is saving them from the devil—may indicate that the defendant believed that the offense was wrong but morally justified.

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

Inability to defer the act
Inability to ignore specific instructions
Must not be caused by rage or intoxication
Magnitude, likelihood, and imminence of consequences if act is not performed
Attempted alternatives to the act
Genuineness of command hallucinations and the ability to ignore them

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.
  

On the other hand, Mr. B knew that murder is illegal and that killing one’s wife for infidelity (whether delusional or not) is not legal. These factors suggest that Mr. B knew that his actions were wrong at the time.

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?
  

States use subtle variations in language to indicate the strictness of their standards. Some may use “know” (a stricter standard) versus “appreciate” the wrongfulness of his or her actions. This difficult concept becomes more detailed if the defendant knew the act was wrongful but had an overriding moral justification (such as Mr. B’s desire to save his wife from damnation).

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

	Competency	Sanity
Presence of mental illness	Yes	Yes
Mental status	Current mental state	Mental state at the time of the offense
Purpose of evaluation	Ability to stand trial	Criminal responsibility
Variation in laws by jurisdiction	Minor variation	Great variation

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

Standard	Year	Description
Wild beast	1724	Most strict standard; required total deprivation of memory and understanding
Irresistible impulse	1840	More liberal standard; required that “…some controlling disease was…the acting power within him which he could not resist…”
M’Naughten rule	1843	Required that the defendant not know the nature/quality or the wrongfulness of the offense.
American Law Institute’s Model Penal Code standard	1955	Combined M’Naughten Rule with irresistible impulse
Federal Insanity Defense Reform Act	1984	Stricter standard that dropped the irresistible impulse standard after attempted assassination of President Reagan

‘Wild beast.’ The “wild beast” standard was established in 1724 in Rex v. Arnold. Arnold, the mentally-ill defendant, was found guilty after he shot and wounded Lord Onslow. Arnold’s death sentence was reduced to life in prison after Lord Onslow himself advocated for this change.

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.
  

United States law. Based on the M’Naughten rule and the irresistible impulse standard, the American Law Institute in 1955 issued the Model Penal Code insanity standard. It stated that a defendant is not responsible for his criminal conduct if, at the time of the offense as a result of mental disease or defect, he lacked substantial capacity to:

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

These standards were tightened in federal jurisdictions by the Federal Insanity Defense Reform Act of 1984—a reaction to John Hinckley’s insanity acquittal after he tried to assassinate President Ronald Reagan.

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.
  

These may give insight into the defendant’s mental state.

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)
  

Table 3

Signs that a defendant knew an act was wrong

Efforts to avoid detection	Wearing gloves or a mask during the offense
	Concealing a weapon
	Falsifying information (using an alias or creating a passport)
	Committing the act in the dark
Disposal of evidence	Washing away blood
	Removing fingerprints
	Discarding the weapon
	Hiding the body
Efforts to avoid apprehension	Fleeing
	Lying to authorities

Irresistible impulse? In jurisdictions with an irresistible impulse test, evaluate whether the defendant was able to refrain from the offense when it occurred (Table 4). Allow the defendant to provide an uninterrupted narrative of the event. Use follow-up questions to fill in gaps in the story and to determine the defendant’s motive. You may choose to confront the defendant with contradictory information obtained from collateral sources.⁶

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.
  

By contrast, psychotic justification for the offense—for example, a mother who kills her children because she believes she is saving them from the devil—may indicate that the defendant believed that the offense was wrong but morally justified.

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

Inability to defer the act
Inability to ignore specific instructions
Must not be caused by rage or intoxication
Magnitude, likelihood, and imminence of consequences if act is not performed
Attempted alternatives to the act
Genuineness of command hallucinations and the ability to ignore them

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.
  

On the other hand, Mr. B knew that murder is illegal and that killing one’s wife for infidelity (whether delusional or not) is not legal. These factors suggest that Mr. B knew that his actions were wrong at the time.

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?
  

States use subtle variations in language to indicate the strictness of their standards. Some may use “know” (a stricter standard) versus “appreciate” the wrongfulness of his or her actions. This difficult concept becomes more detailed if the defendant knew the act was wrongful but had an overriding moral justification (such as Mr. B’s desire to save his wife from damnation).

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

	Competency	Sanity
Presence of mental illness	Yes	Yes
Mental status	Current mental state	Mental state at the time of the offense
Purpose of evaluation	Ability to stand trial	Criminal responsibility
Variation in laws by jurisdiction	Minor variation	Great variation

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

Standard	Year	Description
Wild beast	1724	Most strict standard; required total deprivation of memory and understanding
Irresistible impulse	1840	More liberal standard; required that “…some controlling disease was…the acting power within him which he could not resist…”
M’Naughten rule	1843	Required that the defendant not know the nature/quality or the wrongfulness of the offense.
American Law Institute’s Model Penal Code standard	1955	Combined M’Naughten Rule with irresistible impulse
Federal Insanity Defense Reform Act	1984	Stricter standard that dropped the irresistible impulse standard after attempted assassination of President Reagan

‘Wild beast.’ The “wild beast” standard was established in 1724 in Rex v. Arnold. Arnold, the mentally-ill defendant, was found guilty after he shot and wounded Lord Onslow. Arnold’s death sentence was reduced to life in prison after Lord Onslow himself advocated for this change.

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.
  

United States law. Based on the M’Naughten rule and the irresistible impulse standard, the American Law Institute in 1955 issued the Model Penal Code insanity standard. It stated that a defendant is not responsible for his criminal conduct if, at the time of the offense as a result of mental disease or defect, he lacked substantial capacity to:

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

These standards were tightened in federal jurisdictions by the Federal Insanity Defense Reform Act of 1984—a reaction to John Hinckley’s insanity acquittal after he tried to assassinate President Ronald Reagan.

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.
  

These may give insight into the defendant’s mental state.

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)
  

Table 3

Signs that a defendant knew an act was wrong

Efforts to avoid detection	Wearing gloves or a mask during the offense
	Concealing a weapon
	Falsifying information (using an alias or creating a passport)
	Committing the act in the dark
Disposal of evidence	Washing away blood
	Removing fingerprints
	Discarding the weapon
	Hiding the body
Efforts to avoid apprehension	Fleeing
	Lying to authorities

Irresistible impulse? In jurisdictions with an irresistible impulse test, evaluate whether the defendant was able to refrain from the offense when it occurred (Table 4). Allow the defendant to provide an uninterrupted narrative of the event. Use follow-up questions to fill in gaps in the story and to determine the defendant’s motive. You may choose to confront the defendant with contradictory information obtained from collateral sources.⁶

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.
  

By contrast, psychotic justification for the offense—for example, a mother who kills her children because she believes she is saving them from the devil—may indicate that the defendant believed that the offense was wrong but morally justified.

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

Inability to defer the act
Inability to ignore specific instructions
Must not be caused by rage or intoxication
Magnitude, likelihood, and imminence of consequences if act is not performed
Attempted alternatives to the act
Genuineness of command hallucinations and the ability to ignore them

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.
  

On the other hand, Mr. B knew that murder is illegal and that killing one’s wife for infidelity (whether delusional or not) is not legal. These factors suggest that Mr. B knew that his actions were wrong at the time.

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?
  

States use subtle variations in language to indicate the strictness of their standards. Some may use “know” (a stricter standard) versus “appreciate” the wrongfulness of his or her actions. This difficult concept becomes more detailed if the defendant knew the act was wrongful but had an overriding moral justification (such as Mr. B’s desire to save his wife from damnation).

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.
  

These effects lead from craving to increased likelihood to engage in behaviors to procure the drug and ultimately to relapse (Table 1).^2-4

Table 1

3 stages of relapse and their neurobiologic components

Relapse stage	Key neurotransmitters	Brain regions involved
Early relapse triggered by:
• exposure to a small amount of the drug	Dopamine	Ventral tegmental area
		Nucleus accumbens core
		Prefrontal cortex
• environmental cues that re-trigger learned associations	Dopamine	Basolateral amygdala
		Nucleus accumbens core
• stressful events and disappointments	Norepinephrine, corticotropin-releasing factor	Extended amygdala
		Bed nucleus of the stria terminalis
Craving	Multiple, undetermined	Prefrontal cortex circuitry involving the anterior cingulate and orbitofrontal cortices
Relapse	Glutamate, dopamine	Prefrontal cortex
		Nucleus accumbens core
		Ventral pallidum
Source: References 2-4

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

Emotions and mood state play a greater role in driving relapse in women
Craving. Women have greater craving than men in response to nicotine and cocaine drug cues
Nicotine dependency. Women are more likely to relapse to cigarette use
Abstinence. Women have shorter abstinence periods after cocaine treatment
Residential treatment. Women have a better prognosis than men 6 months after residential cocaine treatment
Premenstrual hormone changes increase women’s relapse risk

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.
  

Progesterone. Progesterone’s effect on dopamine release is unclear. In humans, allopregnenolone may curb relapse during the height of the luteal phase but cause anxiety when its levels drop. Thus, allopregnenolone withdrawal may promote craving and relapse late in the luteal phase.¹⁷ Allopregnenolone’s possible effect on relapse has not been confirmed in human studies, however.

Table 3

Preclinical findings: How hormones may influence addictive behavior

Hormone	Neurobiologic effect	Mechanism	Behavioral effect
Estrogen	Facilitates dopamine	Decreases inhibitory GABAB activity, regulates D2 autoreceptor expression, alters dopamine reuptake, modulates glutamate activity	Enhances reward, self-administration, sensitization,* and stimulant dependence; facilitates reinstatement†
Progesterone	Facilitates dopamine when given intermittently; might facilitate or inhibit estrogen’s effects on dopamine	Unclear	Attenuates response to stress, anxiety, pain, aggressiveness
Allopregnenolone‡	Facilitates GABAA	GABAA-positive allosteric modulator, such as ethanol	Enhances ethanol consumption, promotes ethanol reinstatement
GABAA/GABAB: gamma-aminobutyric acid, ionotropic types A and B
* Sensitization: Repeated exposure to psychostimulants results in drug-seeking response to subsequent exposure, which plays an important role in addiction and craving.
† Reinstatement is the animal model of relapse.
‡ Progesterone’s neuroactive metabolite
Source: References 1, 20-26

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
  

Careful studies of relapse with continuous OCP hormone control are needed before we would recommend this treatment routinely. For individual women at risk for relapse, however, you might consider using continuous OCPs to stabilize hormone fluctuations in the late luteal phase.

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.
  

We continue fluoxetine, which has decreased alcohol consumption in some studies.³¹ In collaboration with her primary care physician, we also prescribe an oral contraceptive for Ms. H to take continuously to stabilize her mood across the menstrual cycle.

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

Track craving and mood symptoms in relation to the patient’s menstrual cycle
Educate her about triggers for relapse
Provide psychotherapy to bolster her coping strategies for stressful life events
Screen for comorbid mood or psychiatric disorders and treat them aggressively
Treat premenstrual mood symptoms with a selective serotonin reuptake inhibitor and/or by regulating hormone levels with a continuous oral contraceptive

Related resources

• 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.
  

Drug brand names

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

Disclosures

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.
  

These effects lead from craving to increased likelihood to engage in behaviors to procure the drug and ultimately to relapse (Table 1).^2-4

Table 1

3 stages of relapse and their neurobiologic components

Relapse stage	Key neurotransmitters	Brain regions involved
Early relapse triggered by:
• exposure to a small amount of the drug	Dopamine	Ventral tegmental area
		Nucleus accumbens core
		Prefrontal cortex
• environmental cues that re-trigger learned associations	Dopamine	Basolateral amygdala
		Nucleus accumbens core
• stressful events and disappointments	Norepinephrine, corticotropin-releasing factor	Extended amygdala
		Bed nucleus of the stria terminalis
Craving	Multiple, undetermined	Prefrontal cortex circuitry involving the anterior cingulate and orbitofrontal cortices
Relapse	Glutamate, dopamine	Prefrontal cortex
		Nucleus accumbens core
		Ventral pallidum
Source: References 2-4

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

Emotions and mood state play a greater role in driving relapse in women
Craving. Women have greater craving than men in response to nicotine and cocaine drug cues
Nicotine dependency. Women are more likely to relapse to cigarette use
Abstinence. Women have shorter abstinence periods after cocaine treatment
Residential treatment. Women have a better prognosis than men 6 months after residential cocaine treatment
Premenstrual hormone changes increase women’s relapse risk

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.
  

Progesterone. Progesterone’s effect on dopamine release is unclear. In humans, allopregnenolone may curb relapse during the height of the luteal phase but cause anxiety when its levels drop. Thus, allopregnenolone withdrawal may promote craving and relapse late in the luteal phase.¹⁷ Allopregnenolone’s possible effect on relapse has not been confirmed in human studies, however.

Table 3

Preclinical findings: How hormones may influence addictive behavior

Hormone	Neurobiologic effect	Mechanism	Behavioral effect
Estrogen	Facilitates dopamine	Decreases inhibitory GABAB activity, regulates D2 autoreceptor expression, alters dopamine reuptake, modulates glutamate activity	Enhances reward, self-administration, sensitization,* and stimulant dependence; facilitates reinstatement†
Progesterone	Facilitates dopamine when given intermittently; might facilitate or inhibit estrogen’s effects on dopamine	Unclear	Attenuates response to stress, anxiety, pain, aggressiveness
Allopregnenolone‡	Facilitates GABAA	GABAA-positive allosteric modulator, such as ethanol	Enhances ethanol consumption, promotes ethanol reinstatement
GABAA/GABAB: gamma-aminobutyric acid, ionotropic types A and B
* Sensitization: Repeated exposure to psychostimulants results in drug-seeking response to subsequent exposure, which plays an important role in addiction and craving.
† Reinstatement is the animal model of relapse.
‡ Progesterone’s neuroactive metabolite
Source: References 1, 20-26

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
  

Careful studies of relapse with continuous OCP hormone control are needed before we would recommend this treatment routinely. For individual women at risk for relapse, however, you might consider using continuous OCPs to stabilize hormone fluctuations in the late luteal phase.

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.
  

We continue fluoxetine, which has decreased alcohol consumption in some studies.³¹ In collaboration with her primary care physician, we also prescribe an oral contraceptive for Ms. H to take continuously to stabilize her mood across the menstrual cycle.

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

Track craving and mood symptoms in relation to the patient’s menstrual cycle
Educate her about triggers for relapse
Provide psychotherapy to bolster her coping strategies for stressful life events
Screen for comorbid mood or psychiatric disorders and treat them aggressively
Treat premenstrual mood symptoms with a selective serotonin reuptake inhibitor and/or by regulating hormone levels with a continuous oral contraceptive

Related resources

• 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.
  

Drug brand names

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

Disclosures

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.
  

These effects lead from craving to increased likelihood to engage in behaviors to procure the drug and ultimately to relapse (Table 1).^2-4

Table 1

3 stages of relapse and their neurobiologic components

Relapse stage	Key neurotransmitters	Brain regions involved
Early relapse triggered by:
• exposure to a small amount of the drug	Dopamine	Ventral tegmental area
		Nucleus accumbens core
		Prefrontal cortex
• environmental cues that re-trigger learned associations	Dopamine	Basolateral amygdala
		Nucleus accumbens core
• stressful events and disappointments	Norepinephrine, corticotropin-releasing factor	Extended amygdala
		Bed nucleus of the stria terminalis
Craving	Multiple, undetermined	Prefrontal cortex circuitry involving the anterior cingulate and orbitofrontal cortices
Relapse	Glutamate, dopamine	Prefrontal cortex
		Nucleus accumbens core
		Ventral pallidum
Source: References 2-4

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

Emotions and mood state play a greater role in driving relapse in women
Craving. Women have greater craving than men in response to nicotine and cocaine drug cues
Nicotine dependency. Women are more likely to relapse to cigarette use
Abstinence. Women have shorter abstinence periods after cocaine treatment
Residential treatment. Women have a better prognosis than men 6 months after residential cocaine treatment
Premenstrual hormone changes increase women’s relapse risk

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.
  

Progesterone. Progesterone’s effect on dopamine release is unclear. In humans, allopregnenolone may curb relapse during the height of the luteal phase but cause anxiety when its levels drop. Thus, allopregnenolone withdrawal may promote craving and relapse late in the luteal phase.¹⁷ Allopregnenolone’s possible effect on relapse has not been confirmed in human studies, however.

Table 3

Preclinical findings: How hormones may influence addictive behavior

Hormone	Neurobiologic effect	Mechanism	Behavioral effect
Estrogen	Facilitates dopamine	Decreases inhibitory GABAB activity, regulates D2 autoreceptor expression, alters dopamine reuptake, modulates glutamate activity	Enhances reward, self-administration, sensitization,* and stimulant dependence; facilitates reinstatement†
Progesterone	Facilitates dopamine when given intermittently; might facilitate or inhibit estrogen’s effects on dopamine	Unclear	Attenuates response to stress, anxiety, pain, aggressiveness
Allopregnenolone‡	Facilitates GABAA	GABAA-positive allosteric modulator, such as ethanol	Enhances ethanol consumption, promotes ethanol reinstatement
GABAA/GABAB: gamma-aminobutyric acid, ionotropic types A and B
* Sensitization: Repeated exposure to psychostimulants results in drug-seeking response to subsequent exposure, which plays an important role in addiction and craving.
† Reinstatement is the animal model of relapse.
‡ Progesterone’s neuroactive metabolite
Source: References 1, 20-26

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
  

Careful studies of relapse with continuous OCP hormone control are needed before we would recommend this treatment routinely. For individual women at risk for relapse, however, you might consider using continuous OCPs to stabilize hormone fluctuations in the late luteal phase.

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.
  

We continue fluoxetine, which has decreased alcohol consumption in some studies.³¹ In collaboration with her primary care physician, we also prescribe an oral contraceptive for Ms. H to take continuously to stabilize her mood across the menstrual cycle.

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

Track craving and mood symptoms in relation to the patient’s menstrual cycle
Educate her about triggers for relapse
Provide psychotherapy to bolster her coping strategies for stressful life events
Screen for comorbid mood or psychiatric disorders and treat them aggressively
Treat premenstrual mood symptoms with a selective serotonin reuptake inhibitor and/or by regulating hormone levels with a continuous oral contraceptive

Related resources

• 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.
  

Drug brand names

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

Disclosures

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
  

Box

Table 1

Guiding principles of cognitive-behavioral therapy

Therapist uses the cognitive model to create meaning Sessions are structured and goal-oriented Therapist works actively, using a problem-solving approach, to help the patient change and develop Patient acquires new skills through homework, practicing, and experiencing Sessions are time-limited and focus on collaborative empiricism Patient learns skills for self-change and becomes empowered

Activating schema content. Cognitive content and biased processing are elements of the individual’s schema, an integrated knowledge structure that influences what he/she remembers and how he/she processes and stores new experiences. Negative schema content remains latent during periods of normal mood, according to Beck, but can be activated by:

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

For example, a man becomes despondent when a girlfriend cancels a date (external stress) because this activates his pre-existing beliefs of worthlessness and memories of childhood abandonment. Premenstrual dysphoria caused by hormonal changes—an internal stress—can trigger negative beliefs associated with that mood state.

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.
  

Using behavioral experiments, you collaboratively teach patients to examine their thoughts as “hypotheses to be tested” rather than self-evident “truths.”⁶ You encourage them to think like scientists who are observing and evaluating their idiosyncratic internal experience.

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

Step	What therapist may say or do to introduce this step
Collaborate in setting the agenda	‘What would you like to put on the agenda for today’s session? If we could address one or two items, what would they be?’
Link to previous session via feedback	Review and comment on the patient’s feedback form
Check target symptoms	‘How would you rate your level of (depression, anxiety, etc.) this week on a scale of 0 to 100?’
	Therapist also can review standardized rating scales, such as Beck Depression Inventory II
Check medication	‘Are there any concerns this week about your medication?’
Review week/scheduling	‘Could you update me about your week?’
	‘What would be important to focus on this coming week?’
Review homework	‘Let’s have a look at the homework/self-help work you did this week’
Set new agenda items	‘This issue sounds important; would you like to add it to today’s agenda?’
Collaborate in developing new homework	‘I’d like to work on this further next week; let’s decide together what would be doable’
Feedback	‘How did you feel about today’s session?’
	‘Is there anything you would like to be sure to remember after you leave today?’
	‘Anything you want to put on the agenda for next 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”).
  

Teach patients to monitor their experiences by writing down their thoughts and feelings as well as the corresponding situations when they feel strong negative emotions. Compared with psychodynamic therapies—which emphasize retrospective reconstruction of childhood experience—self-monitoring with a “thought record” focuses on the present, is more accessible, and is less prone to recall bias.

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

Socratic questioning What evidence do you have to support this idea? How strongly do you believe this now? On a scale of 0 to 100%, where does your belief fall? Where do other people’s fall? How does this thought affect how you feel and act? Can you describe experiences when this thought was not completely true? If a close friend thought this way, what would you tell him or her? If you told a close friend about this thought, what would he or she say? When you have felt differently in the past, what would you have said about this thought? Are any distortions present in the thought you identified? Non-Socratic questioning Why are you being so hard on yourself? You say you are a total loser. Would a total loser have accomplished all the things you did this week? I’m sure that others don’t see you this way.

Labels for distorted thoughts. Help patients identify and label their cognitive distortions. These distortions are systematic biases in information processing that reinforce negativistic thinking in depression or catastrophic thinking in anxiety. Examples include:

• 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
  

Intermediate beliefs may emerge as automatic thoughts or be identified in thought records as consistent themes. These underlying beliefs represent idiosyncratic vulnerabilities that make a person susceptible to distress or decompensation in a given stressful situation. They take the form of:

• 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”).
  

A man with the above intermediate beliefs who acquiesces to a friend’s request for a loan might perceive that the friend has taken advantage of him. Emotionally, he may react with sadness, despair, or anger. You and he can evaluate these beliefs through a thought record and view them as hypotheses to be tested with behavioral experiments.

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”).
  

Core beliefs can be identified by using the downward arrow technique (Table 4). After an automatic thought is identified, repeatedly ask the patient, “If that were true, what would that say about you/others/the world?” or, “What would be the worst thing about that if it were true?”

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.
  

Automatic thoughts might be restructured quickly, but core beliefs may take months to begin to change. Techniques focused on rational reappraisal are usually not sufficient by themselves. Supplemental approaches that focus on activating and amplifying emotion can be integral to this process. Examples include:

• 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.
  

For patients

• 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
  

Box

Table 1

Guiding principles of cognitive-behavioral therapy

Therapist uses the cognitive model to create meaning Sessions are structured and goal-oriented Therapist works actively, using a problem-solving approach, to help the patient change and develop Patient acquires new skills through homework, practicing, and experiencing Sessions are time-limited and focus on collaborative empiricism Patient learns skills for self-change and becomes empowered

Activating schema content. Cognitive content and biased processing are elements of the individual’s schema, an integrated knowledge structure that influences what he/she remembers and how he/she processes and stores new experiences. Negative schema content remains latent during periods of normal mood, according to Beck, but can be activated by:

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

For example, a man becomes despondent when a girlfriend cancels a date (external stress) because this activates his pre-existing beliefs of worthlessness and memories of childhood abandonment. Premenstrual dysphoria caused by hormonal changes—an internal stress—can trigger negative beliefs associated with that mood state.

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.
  

Using behavioral experiments, you collaboratively teach patients to examine their thoughts as “hypotheses to be tested” rather than self-evident “truths.”⁶ You encourage them to think like scientists who are observing and evaluating their idiosyncratic internal experience.

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

Step	What therapist may say or do to introduce this step
Collaborate in setting the agenda	‘What would you like to put on the agenda for today’s session? If we could address one or two items, what would they be?’
Link to previous session via feedback	Review and comment on the patient’s feedback form
Check target symptoms	‘How would you rate your level of (depression, anxiety, etc.) this week on a scale of 0 to 100?’
	Therapist also can review standardized rating scales, such as Beck Depression Inventory II
Check medication	‘Are there any concerns this week about your medication?’
Review week/scheduling	‘Could you update me about your week?’
	‘What would be important to focus on this coming week?’
Review homework	‘Let’s have a look at the homework/self-help work you did this week’
Set new agenda items	‘This issue sounds important; would you like to add it to today’s agenda?’
Collaborate in developing new homework	‘I’d like to work on this further next week; let’s decide together what would be doable’
Feedback	‘How did you feel about today’s session?’
	‘Is there anything you would like to be sure to remember after you leave today?’
	‘Anything you want to put on the agenda for next 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”).
  

Teach patients to monitor their experiences by writing down their thoughts and feelings as well as the corresponding situations when they feel strong negative emotions. Compared with psychodynamic therapies—which emphasize retrospective reconstruction of childhood experience—self-monitoring with a “thought record” focuses on the present, is more accessible, and is less prone to recall bias.

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

Socratic questioning What evidence do you have to support this idea? How strongly do you believe this now? On a scale of 0 to 100%, where does your belief fall? Where do other people’s fall? How does this thought affect how you feel and act? Can you describe experiences when this thought was not completely true? If a close friend thought this way, what would you tell him or her? If you told a close friend about this thought, what would he or she say? When you have felt differently in the past, what would you have said about this thought? Are any distortions present in the thought you identified? Non-Socratic questioning Why are you being so hard on yourself? You say you are a total loser. Would a total loser have accomplished all the things you did this week? I’m sure that others don’t see you this way.

Labels for distorted thoughts. Help patients identify and label their cognitive distortions. These distortions are systematic biases in information processing that reinforce negativistic thinking in depression or catastrophic thinking in anxiety. Examples include:

• 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
  

Intermediate beliefs may emerge as automatic thoughts or be identified in thought records as consistent themes. These underlying beliefs represent idiosyncratic vulnerabilities that make a person susceptible to distress or decompensation in a given stressful situation. They take the form of:

• 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”).
  

A man with the above intermediate beliefs who acquiesces to a friend’s request for a loan might perceive that the friend has taken advantage of him. Emotionally, he may react with sadness, despair, or anger. You and he can evaluate these beliefs through a thought record and view them as hypotheses to be tested with behavioral experiments.

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”).
  

Core beliefs can be identified by using the downward arrow technique (Table 4). After an automatic thought is identified, repeatedly ask the patient, “If that were true, what would that say about you/others/the world?” or, “What would be the worst thing about that if it were true?”

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.
  

Automatic thoughts might be restructured quickly, but core beliefs may take months to begin to change. Techniques focused on rational reappraisal are usually not sufficient by themselves. Supplemental approaches that focus on activating and amplifying emotion can be integral to this process. Examples include:

• 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.
  

For patients

• 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
  

Box

Table 1

Guiding principles of cognitive-behavioral therapy

Therapist uses the cognitive model to create meaning Sessions are structured and goal-oriented Therapist works actively, using a problem-solving approach, to help the patient change and develop Patient acquires new skills through homework, practicing, and experiencing Sessions are time-limited and focus on collaborative empiricism Patient learns skills for self-change and becomes empowered

Activating schema content. Cognitive content and biased processing are elements of the individual’s schema, an integrated knowledge structure that influences what he/she remembers and how he/she processes and stores new experiences. Negative schema content remains latent during periods of normal mood, according to Beck, but can be activated by:

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

For example, a man becomes despondent when a girlfriend cancels a date (external stress) because this activates his pre-existing beliefs of worthlessness and memories of childhood abandonment. Premenstrual dysphoria caused by hormonal changes—an internal stress—can trigger negative beliefs associated with that mood state.

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.
  

Using behavioral experiments, you collaboratively teach patients to examine their thoughts as “hypotheses to be tested” rather than self-evident “truths.”⁶ You encourage them to think like scientists who are observing and evaluating their idiosyncratic internal experience.

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

Step	What therapist may say or do to introduce this step
Collaborate in setting the agenda	‘What would you like to put on the agenda for today’s session? If we could address one or two items, what would they be?’
Link to previous session via feedback	Review and comment on the patient’s feedback form
Check target symptoms	‘How would you rate your level of (depression, anxiety, etc.) this week on a scale of 0 to 100?’
	Therapist also can review standardized rating scales, such as Beck Depression Inventory II
Check medication	‘Are there any concerns this week about your medication?’
Review week/scheduling	‘Could you update me about your week?’
	‘What would be important to focus on this coming week?’
Review homework	‘Let’s have a look at the homework/self-help work you did this week’
Set new agenda items	‘This issue sounds important; would you like to add it to today’s agenda?’
Collaborate in developing new homework	‘I’d like to work on this further next week; let’s decide together what would be doable’
Feedback	‘How did you feel about today’s session?’
	‘Is there anything you would like to be sure to remember after you leave today?’
	‘Anything you want to put on the agenda for next 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”).
  

Teach patients to monitor their experiences by writing down their thoughts and feelings as well as the corresponding situations when they feel strong negative emotions. Compared with psychodynamic therapies—which emphasize retrospective reconstruction of childhood experience—self-monitoring with a “thought record” focuses on the present, is more accessible, and is less prone to recall bias.

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

Socratic questioning What evidence do you have to support this idea? How strongly do you believe this now? On a scale of 0 to 100%, where does your belief fall? Where do other people’s fall? How does this thought affect how you feel and act? Can you describe experiences when this thought was not completely true? If a close friend thought this way, what would you tell him or her? If you told a close friend about this thought, what would he or she say? When you have felt differently in the past, what would you have said about this thought? Are any distortions present in the thought you identified? Non-Socratic questioning Why are you being so hard on yourself? You say you are a total loser. Would a total loser have accomplished all the things you did this week? I’m sure that others don’t see you this way.

Labels for distorted thoughts. Help patients identify and label their cognitive distortions. These distortions are systematic biases in information processing that reinforce negativistic thinking in depression or catastrophic thinking in anxiety. Examples include:

• 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
  

Intermediate beliefs may emerge as automatic thoughts or be identified in thought records as consistent themes. These underlying beliefs represent idiosyncratic vulnerabilities that make a person susceptible to distress or decompensation in a given stressful situation. They take the form of:

• 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”).
  

A man with the above intermediate beliefs who acquiesces to a friend’s request for a loan might perceive that the friend has taken advantage of him. Emotionally, he may react with sadness, despair, or anger. You and he can evaluate these beliefs through a thought record and view them as hypotheses to be tested with behavioral experiments.

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”).
  

Core beliefs can be identified by using the downward arrow technique (Table 4). After an automatic thought is identified, repeatedly ask the patient, “If that were true, what would that say about you/others/the world?” or, “What would be the worst thing about that if it were true?”

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.
  

Automatic thoughts might be restructured quickly, but core beliefs may take months to begin to change. Techniques focused on rational reappraisal are usually not sufficient by themselves. Supplemental approaches that focus on activating and amplifying emotion can be integral to this process. Examples include:

• 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.
  

For patients

• 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

Personal or patient sexual arousal while talking about sex
Not knowing what questions to ask
Not knowing how to help with patients’ sexual problems
Sudden awareness of one’s own sexual concerns
Having the patient see our moral repugnance about certain sexual practices
Source: Reference 3

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
  

Table 2

4 components of sexual behavior: Where sexual problems may arise

Component	Related sexual problems (examples)
Biological elements	Congenital androgen receptor disorder,9 undiagnosed prolactinoma,10 medical disorders (such as multiple sclerosis), medication side effects, heroin abuse
Psychological elements	Developmental processes (neglect, lack of warmth, or physical and sexual abuse from childhood caretakers) or present states (affect disorder, paranoia)
Interpersonal elements	Lack of psychological intimacy, marital alienation, disapproval of spouse’s behavior (such as gambling or excessive shopping), disrespect for spouse’s parenting style, past infidelity
Cultural concepts of normality and morality	Inability to free oneself of antisexual religious attitudes, homophobia, or belief that masturbation or oral-genital contact is abnormal sexual behavior

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
  

As you take a sexual history, explore how the patient views his or her sexual identity. Assess whether the patient’s concerns indicate a gender identity disorder; whether his or her orientation is heterosexual, homosexual, or bisexual; and if the patient’s fantasies and behavior indicate paraphilic intentions (Table 3).

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

Component	Sample questions
Gender identify	Are you happy that you are a male (female)?
	Do you privately feel sufficiently masculine (feminine)?
Orientation	Are you sexually and romantically attracted primarily to males, females, or both?
Intention	Are your sexual fantasies focused on unconventional images involving sadism, masochism, exhibitionism, voyeurism, clothing, animals, or children?

 

Paraphilia. The most upsetting paraphilia to learn about is pedophilia. The patient typically is nervous about revealing his (or rarely her) fantasy focus on boys, girls, or both. Pedophiles may be exclusively interested in particular age groups—such as preschoolers or grade school children—or be preoccupied with children while also having more conventional adult sexual interests.

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
  

As medical doctors, psychiatrists can recognize organic causes from sexual symptom patterns, take a relevant medical history, order appropriate lab tests, and ensure that genital examinations are done when indicated. After gathering such information, you can decide on a suitable referral.

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

Component	Sample questions
Desire	Are you ever “horny”—that is, have spontaneous feelings of mild sexual arousal?
	Tell me what motivates you to have sexual behavior with your partner
Arousal	Explain what is it like for you during lovemaking.
	Do you get excited? Do you stay excited?
Orgasm	Please tell me about your concerns about attaining orgasm

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.
  

My experience in taking sexual histories indicates that adults pass through six sexual stages,¹ and sexual symptoms can have very different psychological, interpersonal, cultural, or biological sources, depending on the stage at which they appear.

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.
  

During this stage, then, sexual function cannot be separated from nonsexual psychological and interpersonal matters.

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

Personal or patient sexual arousal while talking about sex
Not knowing what questions to ask
Not knowing how to help with patients’ sexual problems
Sudden awareness of one’s own sexual concerns
Having the patient see our moral repugnance about certain sexual practices
Source: Reference 3

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
  

Table 2

4 components of sexual behavior: Where sexual problems may arise

Component	Related sexual problems (examples)
Biological elements	Congenital androgen receptor disorder,9 undiagnosed prolactinoma,10 medical disorders (such as multiple sclerosis), medication side effects, heroin abuse
Psychological elements	Developmental processes (neglect, lack of warmth, or physical and sexual abuse from childhood caretakers) or present states (affect disorder, paranoia)
Interpersonal elements	Lack of psychological intimacy, marital alienation, disapproval of spouse’s behavior (such as gambling or excessive shopping), disrespect for spouse’s parenting style, past infidelity
Cultural concepts of normality and morality	Inability to free oneself of antisexual religious attitudes, homophobia, or belief that masturbation or oral-genital contact is abnormal sexual behavior

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
  

As you take a sexual history, explore how the patient views his or her sexual identity. Assess whether the patient’s concerns indicate a gender identity disorder; whether his or her orientation is heterosexual, homosexual, or bisexual; and if the patient’s fantasies and behavior indicate paraphilic intentions (Table 3).

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

Component	Sample questions
Gender identify	Are you happy that you are a male (female)?
	Do you privately feel sufficiently masculine (feminine)?
Orientation	Are you sexually and romantically attracted primarily to males, females, or both?
Intention	Are your sexual fantasies focused on unconventional images involving sadism, masochism, exhibitionism, voyeurism, clothing, animals, or children?

 

Paraphilia. The most upsetting paraphilia to learn about is pedophilia. The patient typically is nervous about revealing his (or rarely her) fantasy focus on boys, girls, or both. Pedophiles may be exclusively interested in particular age groups—such as preschoolers or grade school children—or be preoccupied with children while also having more conventional adult sexual interests.

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
  

As medical doctors, psychiatrists can recognize organic causes from sexual symptom patterns, take a relevant medical history, order appropriate lab tests, and ensure that genital examinations are done when indicated. After gathering such information, you can decide on a suitable referral.

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

Component	Sample questions
Desire	Are you ever “horny”—that is, have spontaneous feelings of mild sexual arousal?
	Tell me what motivates you to have sexual behavior with your partner
Arousal	Explain what is it like for you during lovemaking.
	Do you get excited? Do you stay excited?
Orgasm	Please tell me about your concerns about attaining orgasm

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.
  

My experience in taking sexual histories indicates that adults pass through six sexual stages,¹ and sexual symptoms can have very different psychological, interpersonal, cultural, or biological sources, depending on the stage at which they appear.

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.
  

During this stage, then, sexual function cannot be separated from nonsexual psychological and interpersonal matters.

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

Personal or patient sexual arousal while talking about sex
Not knowing what questions to ask
Not knowing how to help with patients’ sexual problems
Sudden awareness of one’s own sexual concerns
Having the patient see our moral repugnance about certain sexual practices
Source: Reference 3

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
  

Table 2

4 components of sexual behavior: Where sexual problems may arise

Component	Related sexual problems (examples)
Biological elements	Congenital androgen receptor disorder,9 undiagnosed prolactinoma,10 medical disorders (such as multiple sclerosis), medication side effects, heroin abuse
Psychological elements	Developmental processes (neglect, lack of warmth, or physical and sexual abuse from childhood caretakers) or present states (affect disorder, paranoia)
Interpersonal elements	Lack of psychological intimacy, marital alienation, disapproval of spouse’s behavior (such as gambling or excessive shopping), disrespect for spouse’s parenting style, past infidelity
Cultural concepts of normality and morality	Inability to free oneself of antisexual religious attitudes, homophobia, or belief that masturbation or oral-genital contact is abnormal sexual behavior

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
  

As you take a sexual history, explore how the patient views his or her sexual identity. Assess whether the patient’s concerns indicate a gender identity disorder; whether his or her orientation is heterosexual, homosexual, or bisexual; and if the patient’s fantasies and behavior indicate paraphilic intentions (Table 3).

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

Component	Sample questions
Gender identify	Are you happy that you are a male (female)?
	Do you privately feel sufficiently masculine (feminine)?
Orientation	Are you sexually and romantically attracted primarily to males, females, or both?
Intention	Are your sexual fantasies focused on unconventional images involving sadism, masochism, exhibitionism, voyeurism, clothing, animals, or children?

 

Paraphilia. The most upsetting paraphilia to learn about is pedophilia. The patient typically is nervous about revealing his (or rarely her) fantasy focus on boys, girls, or both. Pedophiles may be exclusively interested in particular age groups—such as preschoolers or grade school children—or be preoccupied with children while also having more conventional adult sexual interests.

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
  

As medical doctors, psychiatrists can recognize organic causes from sexual symptom patterns, take a relevant medical history, order appropriate lab tests, and ensure that genital examinations are done when indicated. After gathering such information, you can decide on a suitable referral.

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

Component	Sample questions
Desire	Are you ever “horny”—that is, have spontaneous feelings of mild sexual arousal?
	Tell me what motivates you to have sexual behavior with your partner
Arousal	Explain what is it like for you during lovemaking.
	Do you get excited? Do you stay excited?
Orgasm	Please tell me about your concerns about attaining orgasm

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.
  

My experience in taking sexual histories indicates that adults pass through six sexual stages,¹ and sexual symptoms can have very different psychological, interpersonal, cultural, or biological sources, depending on the stage at which they appear.

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.
  

During this stage, then, sexual function cannot be separated from nonsexual psychological and interpersonal matters.

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.