Evidence-Based Reviews

Adults with gender identity disorder (GID)—commonly termed transsexualism—may seek psychiatric assessment and treatment for a variety of reasons. Some—but not all—might be candidates for hormone replacement therapies or sex reassignment surgery (SRS). For those with gender dysphoria, psychological assessment and psychotherapy are suggested and sometimes required.

Your role in the GID patient’s gender exploration and transition must be tailored to his or her gender identity and individual circumstances. For patients who are not candidates for surgery or cannot afford it, you may assist in exploring options for living with one’s gender identity.

WHAT IS GID?

Gender identity disorder is a rare, complex condition in which individuals of unambiguous genotype and phenotype identify with the opposite gender. One in 54,000 individuals are estimated to have GID:

• 75% are biologic males desiring reassignment to female gender (MTF)
  
• 25% are females desiring to be male (FTM).¹
  

Table 1

DSM-IV-TR criteria for gender identity disorder

ICD-10 diagnoses for gender identity disorder in adults

Epidemiologic studies of GID are rare, but in a survey by Rachlin et al⁴ of 23 MTFs and 70 FTMs:

• most underwent hormone therapy (64% of MTFs, 80% of FTMs) and/or name change (45% of MTFs, 72% of FTMs)
  
• none of the MTFs had breast augmentation, whereas 52% of FTMs had undergone mastectomy and reconstruction and another 33% were actively planning it
  
• 3% of FTMs had genital surgery, 16% were planning it, and 29% had decided definitely not to have it
  
• 9% of MTFs decided definitely not to have genital surgery; 23% had undergone genital surgery, and another 35% were actively planning it.
  

Biologic basis. GID’s cause remains unknown. Organic differences in brain anatomy have been identified in patients with GID. Zhou et al⁶ showed that the volume of the central subdivision of the bed nucleus of the stria terminalis (BSTc)—a brain area essential for sexual behavior—is larger in men than in women. A female-sized BSTc was found in MTF GID patients.

Research, mainly on biologic boys, indicates that GIDs are usually associated with behavioral difficulties, relationship problems with peers and parents, and—most notably—separation anxiety disorder.⁷ An audit of the files of 124 children and adolescents with GID showed that 42% experienced loss of one or both parents, mainly through separation.⁸

Psychiatric comorbidity. Studies using standardized diagnostic instruments to assess psychiatric comorbidity in GID are rare. A study of 31 patients with GID found that many met diagnostic criteria for lifetime psychiatric comorbidity, including:

• 71% for Axis I disorders (primarily mood and anxiety disorders)
  
• 42% for comorbid personality disorders, primarily a cluster B diagnosis
  
• 45% for substance-related disorders
  
• 6.5% for psychotic disorders
  
• 3.2% for eating disorders.⁹
  

TREATING PATIENTS WITH GID

Psychotherapy. GID treatment decisions are made without clear prospective data. Standards of care are determined by the World Professional Association for Transgender Health (WPATH).¹² Psychotherapy is often given before SRS but is not required. The therapist is left to determine the treatment terms and goals.

Your role in treating patients with GID goes beyond making an accurate diagnosis, identifying comorbid psychopathology, and instituting a treatment plan. Other tasks include:

• counseling the patient about the range of treatment options and their implications
  
• engaging in psychotherapy
  
• ascertaining eligibility and readiness for hormones and surgical therapy
  
• making formal recommendations to medical and surgical colleagues
  
• documenting the patient’s relevant history in a letter of recommendation
  
• educating support systems
  
• being available for follow-up.
  

Candidates for triadic therapy. For appropriately screened adults with severe GID, the therapeutic approach relies on triadic therapy:

• a 3-phase approach centered around real-life experience in the desired role
  
• hormones of the desired gender
  
• and surgery to change the genitalia and secondary sex characteristics.
  

HORMONE THERAPY

WPATH has established eligibility and readiness criteria for HRT in patients with GID (Table 3). Administering cross-sex hormones (testosterone in women; estrogens in men) brings about important physical changes as well as psychological relief. The prescribing physician need not be an endocrinologist but should become well-versed in relevant data.

Table 3

WPATH criteria for hormone replacement therapy*

Table 4

Sample hormonal regimens for transsexual patients*

Transdermal testosterone is an option for biologic females who are leery of injections.¹³ Patches result in stable testosterone levels in the male range but may cause skin irritation in >50% of patients. Use transdermal estrogen in males with clotting abnormalities or who are age >40.

Medical workup. Basic medical monitoring includes serial physical examinations, vital signs, weight measurements, laboratory assessment, and screening for pelvic malignancies.

For biologic males receiving estrogen, pretreatment laboratory assessment includes free testosterone, fasting glucose, liver function tests, and complete blood count, with reassessment at 6 and 12 months and annually thereafter. Obtain pretreatment prolactin levels and repeat annually. If hyperprolactinemia fails to develop within 3 years, no further measurements are necessary. Monitor for breast and prostate cancer, and instruct patients to perform self-breast exams. Following orchiectomy, estrogen doses can be reduced by one-third to one-half.

For biologic women receiving androgen, obtain pretreatment liver function tests and complete blood count, then reassess at 6 months, 12 months, and annually thereafter. Do yearly liver palpation examinations.

Physiologic changes. Biologic males treated with estrogens can expect breast growth, redistribution of fat in keeping with female habitus, decreased upper body strength, decreased body hair, retardation of male pattern balding, diminished testicular size, and decrease in erection firmness and frequency. MTF transsexuals require electrolysis to remove facial hair, as HRT does not do this.

Biologic females treated with testosterone can expect deepening of the voice, clitoral enlargement, mild breast atrophy, increased facial and body hair and male-pattern baldness, increased upper body strength, weight gain, and decreased hip fat.

With effective and continuous dosages, most changes begin in 2 to 4 months, start becoming irreversible in 6 to 12 months, start to level off in 2 years, and are mostly complete in 5 years. Men with insufficient breast growth following HRT may pursue breast augmentation surgery.

Voice changes. Hormone therapy generally is presumed to “masculinize” the voice of FTM transsexuals. In one series, after initiation of hormone therapy, 12 of 16 (75%) FTM transsexuals believed they had a voice that always would be considered masculine.^14,15

For MTF transsexuals, no surgical technique of pitch elevation is satisfactorily safe and effective. The most widely used—cricothyroid approximation—may not be long-lasting and can decrease range, loudness, and vocal quality.¹³

HRT COMPLICATIONS

Medical complications. Biologic males treated with estrogens and progestins may be at increased risk for blood clotting, benign pituitary prolactinomas, infertility, weight gain, liver disease, gallstones, somnolence, hypertension, and diabetes mellitus.

Biologic females treated with testosterone may be at increased risk for acne, cardiovascular disease from shifts of lipid profiles to male patterns, benign and malignant liver tumors, and hepatic dysfunction.

Psychiatric issues. Physical masculinization occurs much more rapidly and results in a more convincing opposite sex appearance in FTMs than feminization does in MTFs.^16,17 Behaving masculine may be more socially acceptable for women and therefore easier than it is for men to behave convincingly feminine without being characterized.

Cross-sex hormones contribute to the expression of sex-dimorphic behaviors in adulthood.^18,19 Estrogen appears to influence affect intensity, whereas androgens influence aggression and sexual motivation. Earlier studies established that untreated MTFs and FTMs do not differ in sex hormone levels from their biologic counterparts.^20,21

After 3 months of HRT, transsexuals’ sex hormones are in the range of their identified sex. FTMs treated with androgens become more prone to aggression and exhibit increased sexual motivation and arousability associated with an overall dampened affect. MTFs treated with estrogen show decreased irritability and sexual arousability.²²

SEX REASSIGNMENT SURGERY

The cost of SRS often is prohibitive. Patients may turn to the Internet or foreign venues for hormone therapy and surgical procedures. Thailand is a popular overseas destination, where the average cost for MTF surgery is approximately $6,000 to $9,000. In the United States the cost of counseling, hormones, electrolysis, and surgeries is typically $30,000 to $40,000.²³

Surgical options are not limited to genital reassignment but include mammoplasty (breast augmentation for MTF), chest reduction surgery (FTM), trachea shave surgery, forehead/brow ridge contouring, chin and jaw contouring, scalp advancement surgery, cheek implant surgery, alarplasty (nasal base resection to narrow a nose), and chin contouring.

Some insurance companies assert that transsexual procedures are not medically necessary and are declining coverage. WPATH contends that sex reassignment is effective and medically indicated in severe GID.

Postsurgical outcomes. Patients who are emotionally healthy, have adequate social support, and attain reasonable cosmetic results are most satisfied with life after SRS.²⁴ In studies of GID patients, the best predictor of postoperative psychopathology was poor surgical results.²⁵

FTMs are transformed through the use of hormones and generally are not perceived as visibly different from other men. Genital surgery is often seen as a final step in completing the transition to the identified gender.

FTMs may elect to have their female reproductive organs removed, along with construction of male external genitalia through phalloplasty or metoidioplasty. The decision to pursue surgery and the type of procedure depend on peer influence.²⁶ Although a phalloplasty does not provide a fully functioning and completely authentic-appearing penis, most FTMs report being satisfied with life after surgery and have few regrets.^27-31

Long-term postoperative follow-up by the surgeon and mental health professional is associated with good psychosocial outcome.

Legal considerations. An individual’s new surgically created gender can cause legal complications in jurisdictions that do not recognize the new gender. Some states are amending laws to make allowances for these advances in medical science.³²

Related resources

• World Professional Association For Transgender Health. (formerly the Harry Benjamin International Gender Dysphoria Association [HBIGDA]). www.hbigda.org. Includes a directory of transgender organizations.
  
• North American gender programs and service centers
  CAMH Gender Identity Clinic. Toronto, Ontario, Canada
  Gender Identity Project, New York, NY
  Gendercare Gender Clinic (Web clinic for gender variance). www.gendercare.com.
  Ingersoll Gender Center, Seattle, Washington
  Johns Hopkins Center for Sexual Health & Medicine, Baltimore, Maryland
  Program in Human Sexuality, Transgender Services at the University of Minnesota
  
• Sexology organizations and information
  American Association of Sex Educators, Counselors, and Therapists. www.aasect.org.
  Kinsey Institute at Indiana University. www.indiana.edu/%7Ekinsey.
  Sexuality Information and Education Council of the United States. www.siecus.org.
  Social Science Research Council. www.ssrc.org.
  Society for the Scientific Study of Sexuality. www.sexscience.org.
  

• Conjugated equine estrogens • Premarin
  
• Estradiol (oral) • Estrace
  
• Estradiol (transdermal) • Climara
  
• Medroxyprogesterone (oral) • Provera
  
• Medroxyprogesterone (IM) • Depo-Provera
  
• Micronized progesterone • Prometrium
  
• Spironolactone • Aldactone
  

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

Adults with gender identity disorder (GID)—commonly termed transsexualism—may seek psychiatric assessment and treatment for a variety of reasons. Some—but not all—might be candidates for hormone replacement therapies or sex reassignment surgery (SRS). For those with gender dysphoria, psychological assessment and psychotherapy are suggested and sometimes required.

Your role in the GID patient’s gender exploration and transition must be tailored to his or her gender identity and individual circumstances. For patients who are not candidates for surgery or cannot afford it, you may assist in exploring options for living with one’s gender identity.

WHAT IS GID?

Gender identity disorder is a rare, complex condition in which individuals of unambiguous genotype and phenotype identify with the opposite gender. One in 54,000 individuals are estimated to have GID:

• 75% are biologic males desiring reassignment to female gender (MTF)
  
• 25% are females desiring to be male (FTM).¹
  

Table 1

DSM-IV-TR criteria for gender identity disorder

ICD-10 diagnoses for gender identity disorder in adults

Epidemiologic studies of GID are rare, but in a survey by Rachlin et al⁴ of 23 MTFs and 70 FTMs:

• most underwent hormone therapy (64% of MTFs, 80% of FTMs) and/or name change (45% of MTFs, 72% of FTMs)
  
• none of the MTFs had breast augmentation, whereas 52% of FTMs had undergone mastectomy and reconstruction and another 33% were actively planning it
  
• 3% of FTMs had genital surgery, 16% were planning it, and 29% had decided definitely not to have it
  
• 9% of MTFs decided definitely not to have genital surgery; 23% had undergone genital surgery, and another 35% were actively planning it.
  

Biologic basis. GID’s cause remains unknown. Organic differences in brain anatomy have been identified in patients with GID. Zhou et al⁶ showed that the volume of the central subdivision of the bed nucleus of the stria terminalis (BSTc)—a brain area essential for sexual behavior—is larger in men than in women. A female-sized BSTc was found in MTF GID patients.

Research, mainly on biologic boys, indicates that GIDs are usually associated with behavioral difficulties, relationship problems with peers and parents, and—most notably—separation anxiety disorder.⁷ An audit of the files of 124 children and adolescents with GID showed that 42% experienced loss of one or both parents, mainly through separation.⁸

Psychiatric comorbidity. Studies using standardized diagnostic instruments to assess psychiatric comorbidity in GID are rare. A study of 31 patients with GID found that many met diagnostic criteria for lifetime psychiatric comorbidity, including:

• 71% for Axis I disorders (primarily mood and anxiety disorders)
  
• 42% for comorbid personality disorders, primarily a cluster B diagnosis
  
• 45% for substance-related disorders
  
• 6.5% for psychotic disorders
  
• 3.2% for eating disorders.⁹
  

TREATING PATIENTS WITH GID

Psychotherapy. GID treatment decisions are made without clear prospective data. Standards of care are determined by the World Professional Association for Transgender Health (WPATH).¹² Psychotherapy is often given before SRS but is not required. The therapist is left to determine the treatment terms and goals.

Your role in treating patients with GID goes beyond making an accurate diagnosis, identifying comorbid psychopathology, and instituting a treatment plan. Other tasks include:

• counseling the patient about the range of treatment options and their implications
  
• engaging in psychotherapy
  
• ascertaining eligibility and readiness for hormones and surgical therapy
  
• making formal recommendations to medical and surgical colleagues
  
• documenting the patient’s relevant history in a letter of recommendation
  
• educating support systems
  
• being available for follow-up.
  

Candidates for triadic therapy. For appropriately screened adults with severe GID, the therapeutic approach relies on triadic therapy:

• a 3-phase approach centered around real-life experience in the desired role
  
• hormones of the desired gender
  
• and surgery to change the genitalia and secondary sex characteristics.
  

HORMONE THERAPY

WPATH has established eligibility and readiness criteria for HRT in patients with GID (Table 3). Administering cross-sex hormones (testosterone in women; estrogens in men) brings about important physical changes as well as psychological relief. The prescribing physician need not be an endocrinologist but should become well-versed in relevant data.

Table 3

WPATH criteria for hormone replacement therapy*

Table 4

Sample hormonal regimens for transsexual patients*

Transdermal testosterone is an option for biologic females who are leery of injections.¹³ Patches result in stable testosterone levels in the male range but may cause skin irritation in >50% of patients. Use transdermal estrogen in males with clotting abnormalities or who are age >40.

Medical workup. Basic medical monitoring includes serial physical examinations, vital signs, weight measurements, laboratory assessment, and screening for pelvic malignancies.

For biologic males receiving estrogen, pretreatment laboratory assessment includes free testosterone, fasting glucose, liver function tests, and complete blood count, with reassessment at 6 and 12 months and annually thereafter. Obtain pretreatment prolactin levels and repeat annually. If hyperprolactinemia fails to develop within 3 years, no further measurements are necessary. Monitor for breast and prostate cancer, and instruct patients to perform self-breast exams. Following orchiectomy, estrogen doses can be reduced by one-third to one-half.

For biologic women receiving androgen, obtain pretreatment liver function tests and complete blood count, then reassess at 6 months, 12 months, and annually thereafter. Do yearly liver palpation examinations.

Physiologic changes. Biologic males treated with estrogens can expect breast growth, redistribution of fat in keeping with female habitus, decreased upper body strength, decreased body hair, retardation of male pattern balding, diminished testicular size, and decrease in erection firmness and frequency. MTF transsexuals require electrolysis to remove facial hair, as HRT does not do this.

Biologic females treated with testosterone can expect deepening of the voice, clitoral enlargement, mild breast atrophy, increased facial and body hair and male-pattern baldness, increased upper body strength, weight gain, and decreased hip fat.

With effective and continuous dosages, most changes begin in 2 to 4 months, start becoming irreversible in 6 to 12 months, start to level off in 2 years, and are mostly complete in 5 years. Men with insufficient breast growth following HRT may pursue breast augmentation surgery.

Voice changes. Hormone therapy generally is presumed to “masculinize” the voice of FTM transsexuals. In one series, after initiation of hormone therapy, 12 of 16 (75%) FTM transsexuals believed they had a voice that always would be considered masculine.^14,15

For MTF transsexuals, no surgical technique of pitch elevation is satisfactorily safe and effective. The most widely used—cricothyroid approximation—may not be long-lasting and can decrease range, loudness, and vocal quality.¹³

HRT COMPLICATIONS

Medical complications. Biologic males treated with estrogens and progestins may be at increased risk for blood clotting, benign pituitary prolactinomas, infertility, weight gain, liver disease, gallstones, somnolence, hypertension, and diabetes mellitus.

Biologic females treated with testosterone may be at increased risk for acne, cardiovascular disease from shifts of lipid profiles to male patterns, benign and malignant liver tumors, and hepatic dysfunction.

Psychiatric issues. Physical masculinization occurs much more rapidly and results in a more convincing opposite sex appearance in FTMs than feminization does in MTFs.^16,17 Behaving masculine may be more socially acceptable for women and therefore easier than it is for men to behave convincingly feminine without being characterized.

Cross-sex hormones contribute to the expression of sex-dimorphic behaviors in adulthood.^18,19 Estrogen appears to influence affect intensity, whereas androgens influence aggression and sexual motivation. Earlier studies established that untreated MTFs and FTMs do not differ in sex hormone levels from their biologic counterparts.^20,21

After 3 months of HRT, transsexuals’ sex hormones are in the range of their identified sex. FTMs treated with androgens become more prone to aggression and exhibit increased sexual motivation and arousability associated with an overall dampened affect. MTFs treated with estrogen show decreased irritability and sexual arousability.²²

SEX REASSIGNMENT SURGERY

The cost of SRS often is prohibitive. Patients may turn to the Internet or foreign venues for hormone therapy and surgical procedures. Thailand is a popular overseas destination, where the average cost for MTF surgery is approximately $6,000 to $9,000. In the United States the cost of counseling, hormones, electrolysis, and surgeries is typically $30,000 to $40,000.²³

Surgical options are not limited to genital reassignment but include mammoplasty (breast augmentation for MTF), chest reduction surgery (FTM), trachea shave surgery, forehead/brow ridge contouring, chin and jaw contouring, scalp advancement surgery, cheek implant surgery, alarplasty (nasal base resection to narrow a nose), and chin contouring.

Some insurance companies assert that transsexual procedures are not medically necessary and are declining coverage. WPATH contends that sex reassignment is effective and medically indicated in severe GID.

Postsurgical outcomes. Patients who are emotionally healthy, have adequate social support, and attain reasonable cosmetic results are most satisfied with life after SRS.²⁴ In studies of GID patients, the best predictor of postoperative psychopathology was poor surgical results.²⁵

FTMs are transformed through the use of hormones and generally are not perceived as visibly different from other men. Genital surgery is often seen as a final step in completing the transition to the identified gender.

FTMs may elect to have their female reproductive organs removed, along with construction of male external genitalia through phalloplasty or metoidioplasty. The decision to pursue surgery and the type of procedure depend on peer influence.²⁶ Although a phalloplasty does not provide a fully functioning and completely authentic-appearing penis, most FTMs report being satisfied with life after surgery and have few regrets.^27-31

Long-term postoperative follow-up by the surgeon and mental health professional is associated with good psychosocial outcome.

Legal considerations. An individual’s new surgically created gender can cause legal complications in jurisdictions that do not recognize the new gender. Some states are amending laws to make allowances for these advances in medical science.³²

Related resources

• World Professional Association For Transgender Health. (formerly the Harry Benjamin International Gender Dysphoria Association [HBIGDA]). www.hbigda.org. Includes a directory of transgender organizations.
  
• North American gender programs and service centers
  CAMH Gender Identity Clinic. Toronto, Ontario, Canada
  Gender Identity Project, New York, NY
  Gendercare Gender Clinic (Web clinic for gender variance). www.gendercare.com.
  Ingersoll Gender Center, Seattle, Washington
  Johns Hopkins Center for Sexual Health & Medicine, Baltimore, Maryland
  Program in Human Sexuality, Transgender Services at the University of Minnesota
  
• Sexology organizations and information
  American Association of Sex Educators, Counselors, and Therapists. www.aasect.org.
  Kinsey Institute at Indiana University. www.indiana.edu/%7Ekinsey.
  Sexuality Information and Education Council of the United States. www.siecus.org.
  Social Science Research Council. www.ssrc.org.
  Society for the Scientific Study of Sexuality. www.sexscience.org.
  

• Conjugated equine estrogens • Premarin
  
• Estradiol (oral) • Estrace
  
• Estradiol (transdermal) • Climara
  
• Medroxyprogesterone (oral) • Provera
  
• Medroxyprogesterone (IM) • Depo-Provera
  
• Micronized progesterone • Prometrium
  
• Spironolactone • Aldactone
  

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

Adults with gender identity disorder (GID)—commonly termed transsexualism—may seek psychiatric assessment and treatment for a variety of reasons. Some—but not all—might be candidates for hormone replacement therapies or sex reassignment surgery (SRS). For those with gender dysphoria, psychological assessment and psychotherapy are suggested and sometimes required.

Your role in the GID patient’s gender exploration and transition must be tailored to his or her gender identity and individual circumstances. For patients who are not candidates for surgery or cannot afford it, you may assist in exploring options for living with one’s gender identity.

WHAT IS GID?

Gender identity disorder is a rare, complex condition in which individuals of unambiguous genotype and phenotype identify with the opposite gender. One in 54,000 individuals are estimated to have GID:

• 75% are biologic males desiring reassignment to female gender (MTF)
  
• 25% are females desiring to be male (FTM).¹
  

Table 1

DSM-IV-TR criteria for gender identity disorder

ICD-10 diagnoses for gender identity disorder in adults

Epidemiologic studies of GID are rare, but in a survey by Rachlin et al⁴ of 23 MTFs and 70 FTMs:

• most underwent hormone therapy (64% of MTFs, 80% of FTMs) and/or name change (45% of MTFs, 72% of FTMs)
  
• none of the MTFs had breast augmentation, whereas 52% of FTMs had undergone mastectomy and reconstruction and another 33% were actively planning it
  
• 3% of FTMs had genital surgery, 16% were planning it, and 29% had decided definitely not to have it
  
• 9% of MTFs decided definitely not to have genital surgery; 23% had undergone genital surgery, and another 35% were actively planning it.
  

Biologic basis. GID’s cause remains unknown. Organic differences in brain anatomy have been identified in patients with GID. Zhou et al⁶ showed that the volume of the central subdivision of the bed nucleus of the stria terminalis (BSTc)—a brain area essential for sexual behavior—is larger in men than in women. A female-sized BSTc was found in MTF GID patients.

Research, mainly on biologic boys, indicates that GIDs are usually associated with behavioral difficulties, relationship problems with peers and parents, and—most notably—separation anxiety disorder.⁷ An audit of the files of 124 children and adolescents with GID showed that 42% experienced loss of one or both parents, mainly through separation.⁸

Psychiatric comorbidity. Studies using standardized diagnostic instruments to assess psychiatric comorbidity in GID are rare. A study of 31 patients with GID found that many met diagnostic criteria for lifetime psychiatric comorbidity, including:

• 71% for Axis I disorders (primarily mood and anxiety disorders)
  
• 42% for comorbid personality disorders, primarily a cluster B diagnosis
  
• 45% for substance-related disorders
  
• 6.5% for psychotic disorders
  
• 3.2% for eating disorders.⁹
  

TREATING PATIENTS WITH GID

Psychotherapy. GID treatment decisions are made without clear prospective data. Standards of care are determined by the World Professional Association for Transgender Health (WPATH).¹² Psychotherapy is often given before SRS but is not required. The therapist is left to determine the treatment terms and goals.

Your role in treating patients with GID goes beyond making an accurate diagnosis, identifying comorbid psychopathology, and instituting a treatment plan. Other tasks include:

• counseling the patient about the range of treatment options and their implications
  
• engaging in psychotherapy
  
• ascertaining eligibility and readiness for hormones and surgical therapy
  
• making formal recommendations to medical and surgical colleagues
  
• documenting the patient’s relevant history in a letter of recommendation
  
• educating support systems
  
• being available for follow-up.
  

Candidates for triadic therapy. For appropriately screened adults with severe GID, the therapeutic approach relies on triadic therapy:

• a 3-phase approach centered around real-life experience in the desired role
  
• hormones of the desired gender
  
• and surgery to change the genitalia and secondary sex characteristics.
  

HORMONE THERAPY

WPATH has established eligibility and readiness criteria for HRT in patients with GID (Table 3). Administering cross-sex hormones (testosterone in women; estrogens in men) brings about important physical changes as well as psychological relief. The prescribing physician need not be an endocrinologist but should become well-versed in relevant data.

Table 3

WPATH criteria for hormone replacement therapy*

Table 4

Sample hormonal regimens for transsexual patients*

Transdermal testosterone is an option for biologic females who are leery of injections.¹³ Patches result in stable testosterone levels in the male range but may cause skin irritation in >50% of patients. Use transdermal estrogen in males with clotting abnormalities or who are age >40.

Medical workup. Basic medical monitoring includes serial physical examinations, vital signs, weight measurements, laboratory assessment, and screening for pelvic malignancies.

For biologic males receiving estrogen, pretreatment laboratory assessment includes free testosterone, fasting glucose, liver function tests, and complete blood count, with reassessment at 6 and 12 months and annually thereafter. Obtain pretreatment prolactin levels and repeat annually. If hyperprolactinemia fails to develop within 3 years, no further measurements are necessary. Monitor for breast and prostate cancer, and instruct patients to perform self-breast exams. Following orchiectomy, estrogen doses can be reduced by one-third to one-half.

For biologic women receiving androgen, obtain pretreatment liver function tests and complete blood count, then reassess at 6 months, 12 months, and annually thereafter. Do yearly liver palpation examinations.

Physiologic changes. Biologic males treated with estrogens can expect breast growth, redistribution of fat in keeping with female habitus, decreased upper body strength, decreased body hair, retardation of male pattern balding, diminished testicular size, and decrease in erection firmness and frequency. MTF transsexuals require electrolysis to remove facial hair, as HRT does not do this.

Biologic females treated with testosterone can expect deepening of the voice, clitoral enlargement, mild breast atrophy, increased facial and body hair and male-pattern baldness, increased upper body strength, weight gain, and decreased hip fat.

With effective and continuous dosages, most changes begin in 2 to 4 months, start becoming irreversible in 6 to 12 months, start to level off in 2 years, and are mostly complete in 5 years. Men with insufficient breast growth following HRT may pursue breast augmentation surgery.

Voice changes. Hormone therapy generally is presumed to “masculinize” the voice of FTM transsexuals. In one series, after initiation of hormone therapy, 12 of 16 (75%) FTM transsexuals believed they had a voice that always would be considered masculine.^14,15

For MTF transsexuals, no surgical technique of pitch elevation is satisfactorily safe and effective. The most widely used—cricothyroid approximation—may not be long-lasting and can decrease range, loudness, and vocal quality.¹³

HRT COMPLICATIONS

Medical complications. Biologic males treated with estrogens and progestins may be at increased risk for blood clotting, benign pituitary prolactinomas, infertility, weight gain, liver disease, gallstones, somnolence, hypertension, and diabetes mellitus.

Biologic females treated with testosterone may be at increased risk for acne, cardiovascular disease from shifts of lipid profiles to male patterns, benign and malignant liver tumors, and hepatic dysfunction.

Psychiatric issues. Physical masculinization occurs much more rapidly and results in a more convincing opposite sex appearance in FTMs than feminization does in MTFs.^16,17 Behaving masculine may be more socially acceptable for women and therefore easier than it is for men to behave convincingly feminine without being characterized.

Cross-sex hormones contribute to the expression of sex-dimorphic behaviors in adulthood.^18,19 Estrogen appears to influence affect intensity, whereas androgens influence aggression and sexual motivation. Earlier studies established that untreated MTFs and FTMs do not differ in sex hormone levels from their biologic counterparts.^20,21

After 3 months of HRT, transsexuals’ sex hormones are in the range of their identified sex. FTMs treated with androgens become more prone to aggression and exhibit increased sexual motivation and arousability associated with an overall dampened affect. MTFs treated with estrogen show decreased irritability and sexual arousability.²²

SEX REASSIGNMENT SURGERY

The cost of SRS often is prohibitive. Patients may turn to the Internet or foreign venues for hormone therapy and surgical procedures. Thailand is a popular overseas destination, where the average cost for MTF surgery is approximately $6,000 to $9,000. In the United States the cost of counseling, hormones, electrolysis, and surgeries is typically $30,000 to $40,000.²³

Surgical options are not limited to genital reassignment but include mammoplasty (breast augmentation for MTF), chest reduction surgery (FTM), trachea shave surgery, forehead/brow ridge contouring, chin and jaw contouring, scalp advancement surgery, cheek implant surgery, alarplasty (nasal base resection to narrow a nose), and chin contouring.

Some insurance companies assert that transsexual procedures are not medically necessary and are declining coverage. WPATH contends that sex reassignment is effective and medically indicated in severe GID.

Postsurgical outcomes. Patients who are emotionally healthy, have adequate social support, and attain reasonable cosmetic results are most satisfied with life after SRS.²⁴ In studies of GID patients, the best predictor of postoperative psychopathology was poor surgical results.²⁵

FTMs are transformed through the use of hormones and generally are not perceived as visibly different from other men. Genital surgery is often seen as a final step in completing the transition to the identified gender.

FTMs may elect to have their female reproductive organs removed, along with construction of male external genitalia through phalloplasty or metoidioplasty. The decision to pursue surgery and the type of procedure depend on peer influence.²⁶ Although a phalloplasty does not provide a fully functioning and completely authentic-appearing penis, most FTMs report being satisfied with life after surgery and have few regrets.^27-31

Long-term postoperative follow-up by the surgeon and mental health professional is associated with good psychosocial outcome.

Legal considerations. An individual’s new surgically created gender can cause legal complications in jurisdictions that do not recognize the new gender. Some states are amending laws to make allowances for these advances in medical science.³²

Related resources

• World Professional Association For Transgender Health. (formerly the Harry Benjamin International Gender Dysphoria Association [HBIGDA]). www.hbigda.org. Includes a directory of transgender organizations.
  
• North American gender programs and service centers
  CAMH Gender Identity Clinic. Toronto, Ontario, Canada
  Gender Identity Project, New York, NY
  Gendercare Gender Clinic (Web clinic for gender variance). www.gendercare.com.
  Ingersoll Gender Center, Seattle, Washington
  Johns Hopkins Center for Sexual Health & Medicine, Baltimore, Maryland
  Program in Human Sexuality, Transgender Services at the University of Minnesota
  
• Sexology organizations and information
  American Association of Sex Educators, Counselors, and Therapists. www.aasect.org.
  Kinsey Institute at Indiana University. www.indiana.edu/%7Ekinsey.
  Sexuality Information and Education Council of the United States. www.siecus.org.
  Social Science Research Council. www.ssrc.org.
  Society for the Scientific Study of Sexuality. www.sexscience.org.
  

• Conjugated equine estrogens • Premarin
  
• Estradiol (oral) • Estrace
  
• Estradiol (transdermal) • Climara
  
• Medroxyprogesterone (oral) • Provera
  
• Medroxyprogesterone (IM) • Depo-Provera
  
• Micronized progesterone • Prometrium
  
• Spironolactone • Aldactone
  

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

When treating chronic psychotic disorders, U.S. psychiatrists generally prefer second-generation antipsychotics (SGAs) to first-generation antipsychotics (FGAs) because of widely held views^1,2 that SGAs:

• are more effective for negative and cognitive symptoms
• produce fewer troublesome side effects
• help patients realize a better quality of life.

These beliefs have been challenged by two large-scale, government-supported studies: the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) in the United States^3-6 and more recently the Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study (CUtLASS) from the United Kingdom.^7,8

CATIE and CUtLASS data suggest that the SGA advantage has been exaggerated, if in fact such an advantage exists. Other Current Psychiatry articles for the clinical practitioner have discussed the CATIE findings.^9-11 This article addresses the CUtLASS results in the context of the trial’s methodology, using information from the primary publications^7,8 and technical report.¹²

Cutlass study

Design. CUtLASS included 2 “bands” (Table 1):

• Band 1 compared the clinical usefulness and cost effectiveness of FGAs and SGAs in treating schizophrenia⁷
• Band 2 compared the effectiveness of clozapine versus other SGAs in treating refractory schizophrenia.⁸

CUtLASS Band 1 was not as extensive in scope as CATIE, and its design had some important differences (Table 2). Patients were referred for participation because their psychiatrists were considering a change in antipsychotic medication to address adverse effects or inadequate response. Fewer patients were recruited than expected—40% of the planned sample during 30 months of recruitment—but researchers considered the size sufficient to compare the effectiveness of FGAs and SGAs.

Patients were randomly assigned to treatment with an antipsychotic class, either:

• an FGA (1 of 11 options—including 5 depot formulations—chosen by the treating clinician)
• or an SGA (risperidone, olanzapine, quetiapine, or amisulpride, also chosen by the clinician).

Physicians and patients were not blinded to the medications used. They could choose medications within patients’ assigned classes and switch as needed in ways that mimicked clinical practice. Trained assessors, who were blinded to the medications being used, evaluated the patients after 12, 26, and 52 weeks.

Quality of life was the primary outcome measure.¹³ Secondary measures included symptoms, side effects, patient satisfaction, and cost of care.

Band 1 results. Patients assigned to the SGA or FGA classes showed no significant differences in quality of life measures or schizophrenia symptoms. If anything, the findings slightly favored the FGAs.

Patient satisfaction and overall cost of care were similar, and rates of extrapyramidal symptoms (EPS), tardive dyskinesia, and akathisia did not differ significantly.

Clozapine comparison. In CUtLASS band 2, a different sample of 136 schizophrenia patients who had responded poorly to ≥2 antipsychotics was randomly assigned to clozapine or one of the above four SGAs. During the 1-year comparison trial, clozapine:

• was found to be significantly more effective (P=0.01) in managing patients’ symptoms, as measured by total Positive and Negative Syndrome Scale (PANSS) score
• showed a trend (P=0.08) towards providing these treatment-resistant patients with a better quality of life.⁸

Table 1

Summary of CUtLASS trial design and results

Table 2

Comparing designs of the CUtLASS and CATIE schizophrenia trials

Comparing catie, cutlass data

The CUtLASS findings are not identical to those of CATIE phase 1¹⁴ but are remarkably similar: no differences in effectiveness were seen between FGAs and SGA when treating patients with chronic schizophrenia.^15,16

CUtLASS investigators concluded that “in people with schizophrenia whose medication is changed for clinical reasons, there is no disadvantage across 1 year in terms of quality of life, symptoms, or associated costs of care in using FGAs rather than nonclozapine SGAs.”⁷

By confirming CATIE’s results, is CUtLASS the final word on antipsychotic treatment of chronic schizophrenia? Or is it just another piece of the puzzle? CATIE and CUtLASS add much to our knowledge, but methodologic “flies in the ointment” plague all clinical trials. We must consider potential biases and confounding factors to properly interpret and apply their findings.

Although the CUtLASS trial was well-constructed and executed, its conclusions—like those of CATIE—merit careful scrutiny. Its patient recruitment methods and study design involved choices and compromises that are appropriate to evaluate^17,18 as we weigh CUtLASS’ contribution to the SGA/FGA debate (Table 3).

Table 3

‘Flies in the ointment’ of the CUtLASS trial design

Who was studied?

Selection questions. CUtLASS researchers had problems recruiting patients for their study, in part because clinicians were reluctant to expose their patients to a 50% probability of being assigned to an FGA. Only 40% of the targeted sample was recruited, and participating clinicians referred only 20% to 37% of their eligible patients to the study.¹² Thus, one could ask:

• Were enrolled subjects truly representative of the population from which they were drawn?
• Or did selection bias result in a disproportionate inclusion of individuals with certain characteristics?

Is it possible, for example, that clinicians preferentially referred medication-noncompliant patients to CUtLASS because they believed the benefits of depot FGAs—such as more assured adherence—would compensate for the potential benefits of SGAs—better efficacy/tolerability?¹⁹

Treatment resistance. Although patients were randomly assigned to FGAs or SGAs, a significantly greater proportion of those whose antipsychotics were being changed because of treatment resistance were assigned to receive SGAs. Treatment resistance was one reason that 88% of subjects in the SGA arm were referred to the trial, compared with 70% of subjects in the FGA arm (P<0.01).¹² The extent to which this differential assignment may have biased results against SGAs is unclear.

EPS risk. CUtLASS-1 patients had been ill a mean of 14 years and had low baseline EPS rates despite receiving long-term antipsychotics (primarily FGAs). Even so, FGAs and SGAs showed similar rates of akathisia and other EPS. Thus—as with the CATIE results—the extent to which CUtLASS-1 findings may apply beyond chronic schizophrenia patients at relatively low risk for EPS is unclear.^11,17

Impact of switching. Although patients were referred to CUtLASS because of adverse effects or inadequate response to one or more antipsychotics, they were only moderately ill (mean PANSS total score 72)²⁰ and probably were deriving some benefit from their baseline antipsychotics. Before randomization, 82% of patients were receiving an FGA and 19% an SGA. Consequently, a far larger percentage of patients in the SGA group had to switch to a different medication class as the trial began.

As observed in CATIE, switching antipsychotics often has short-term negative consequences for patients,²¹ although switching classes (as in CUtLASS) may have had a different impact than switching individual antipsychotics (as in CATIE). If unequal antipsychotic switching rates in the two arms differentially affected patients’ quality of life, we would expect to see this effect emerge at the 12-week assessment, which is precisely where the greatest difference in Quality of Life Scale (QLS)¹³ scores appeared.

The mean QLS score for patients in the SGA arm was 2.6 points lower than in the FGA group at 12 weeks. This difference disappeared and, in fact, reversed at 26 weeks, but this 12-week effect had a strong impact on results of the 52-week intent-to-treat analysis. CUtLASS—like CATIE—might exemplify the risks of switching patients from treatment with partially effective antipsychotics.²²

What was compared?

Classes vs individual drugs. The decision in CUtLASS-1 to compare antipsychotic classes rather than individual agents makes it difficult to interpret its findings. Antipsychotics are not homogeneous; clear differences exist within both the SGA and FGA classes in terms of individual agents’ efficacy and tolerability, and each SGA has a reasonably well-established and different side-effect profile.²³

Sulpiride was the most commonly used FGA in CUtLASS-1 (by 49% of FGA patients). Sulpiride has some unusual attributes—such as lower EPS liability—and is not available in the United States. Thus, including this agent might have affected how applicable CUtLASS findings are to clinical practice in the United States.

Oral vs depot delivery. Individuals assigned to an FGA could receive either oral or long-acting depot medication, whereas those assigned to an SGA could receive only oral medication. At baseline, 84 of 227 CUtLASS-1 participants were receiving a depot antipsychotic, which was discontinued during randomization in 72 patients. During the 1-year study, the number of patients receiving a depot antipsychotic tripled from 12 to 35, suggesting the usefulness of long-acting agents in this population.¹⁹

Cross-class switching. Although participating physicians and their patients were urged to stay within assigned antipsychotic classes at least for the first 12 weeks and ideally for 1 year, a high rate of cross-class switching occurred (Figure). At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead.

The CUtLASS authors’ assert that the trial refutes the hypothesis that using SGAs is superior to using FGAs in improving quality of life. This conclusion is difficult to justify when so many patients assigned to the FGA class actually were receiving SGAs. The conclusion is further weakened if differential switching rates put SGAs at a disadvantage in the first 12 weeks of the trial.

A more accurate conclusion of the intent-to-treat comparison appears in the technical report: “There was no statistically significant difference in terms of quality of life or symptoms over 1 year in commencing [italics added] conventional antipsychotic drugs rather than new atypical drugs.”¹²

Figure CUtLASS-1: Did switching rate affect trial outcome?

The high rate of cross-class medication switching in CUtLASS-1 may have weakened the study’s conclusion that virtually no difference in effectiveness exists between first- and second-generation antipsychotics. At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead. Not shown in the figure is that 4 of the total 55 patients who switched from FGAs to SGAs had switched back to FGAs by the 52-week assessment.

CUtLASS: Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study

FGA: First-generation antipsychotic

SGA: Second-generation antipsychotic

Source: Adapted from reference 7, Figure 1

Clinical implications

Notwithstanding these cautionary notes, CUtLASS-1 findings add to the questions raised by CATIE about the relative effectiveness of SGAs and FGAs. At a minimum, the data indicate that the SGA advantage has been overstated or oversimplified and that FGAs may be suitable options for meeting the needs of some patients with psychosis (particularly those at low risk for EPS).

Depot antipsychotics. CUtLASS also suggests a wider role for long-acting antipsychotics in chronic psychotic disorders, beyond treating patients with severe nonadherence.^19,23 The number of patients receiving long-acting agents tripled over the 1-year study.¹²

Clozapine. Both CATIE and CUtLASS-2 confirmed clozapine’s superior efficacy for patients with treatment-resistant psychotic illness (Table 4). CUtLASS-2 also reaffirmed the challenges of clozapine’s metabolic and other side effects, such as sedation, hypotension, and hypersalivation.

All-cause discontinuation was significantly higher (P<0.05) in patients taking clozapine (73%) than in those taking other SGAs (52%). Even so, clozapine-group patients achieved significantly greater symptom reduction and tended toward a higher quality of life than other SGA-group patients.

Table 4

Clinical ‘pearls’ from the CUtLASS trial data

Overview. In conclusion, one can reasonably conclude from analyzing the CATIE and CUtLASS data that:

• FGA-SGA differences are not as great as previously thought.
• Substantial differences exist among agents within both antipsychotic classes, particularly in side effect profiles.
• Neither study disproves the following presumed benefit of SGAs: that compared with FGAs, SGAs provide an equivalent antipsychotic effect and pose a lower risk of problems related to unmitigated dopamine blockade—such as EPS, dysphoria, bradyphrenia, neuroleptic-induced deficit syndrome, and tardive dyskinesia.¹¹
• To use antipsychotics effectively and optimize individual treatment, consider the CATIE and CUtLASS trials in the contexts of their designs and the results of other studies of patients with chronic schizophrenia.

Related resources

• Heres S, Davis J, Maino K, et al. Why olanzapine beats risperidone, risperidone beats quetiapine, and quetiapine beats olanzapine: An exploratory analysis of head-head comparison studies of second-generation antipsychotics. Am J Psychiatry 2006;163:185-94.

Drug brand names

• Clozapine • Clozaril
• Quetiapine • Seroquel
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

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

When treating chronic psychotic disorders, U.S. psychiatrists generally prefer second-generation antipsychotics (SGAs) to first-generation antipsychotics (FGAs) because of widely held views^1,2 that SGAs:

• are more effective for negative and cognitive symptoms
• produce fewer troublesome side effects
• help patients realize a better quality of life.

These beliefs have been challenged by two large-scale, government-supported studies: the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) in the United States^3-6 and more recently the Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study (CUtLASS) from the United Kingdom.^7,8

CATIE and CUtLASS data suggest that the SGA advantage has been exaggerated, if in fact such an advantage exists. Other Current Psychiatry articles for the clinical practitioner have discussed the CATIE findings.^9-11 This article addresses the CUtLASS results in the context of the trial’s methodology, using information from the primary publications^7,8 and technical report.¹²

Cutlass study

Design. CUtLASS included 2 “bands” (Table 1):

• Band 1 compared the clinical usefulness and cost effectiveness of FGAs and SGAs in treating schizophrenia⁷
• Band 2 compared the effectiveness of clozapine versus other SGAs in treating refractory schizophrenia.⁸

CUtLASS Band 1 was not as extensive in scope as CATIE, and its design had some important differences (Table 2). Patients were referred for participation because their psychiatrists were considering a change in antipsychotic medication to address adverse effects or inadequate response. Fewer patients were recruited than expected—40% of the planned sample during 30 months of recruitment—but researchers considered the size sufficient to compare the effectiveness of FGAs and SGAs.

Patients were randomly assigned to treatment with an antipsychotic class, either:

• an FGA (1 of 11 options—including 5 depot formulations—chosen by the treating clinician)
• or an SGA (risperidone, olanzapine, quetiapine, or amisulpride, also chosen by the clinician).

Physicians and patients were not blinded to the medications used. They could choose medications within patients’ assigned classes and switch as needed in ways that mimicked clinical practice. Trained assessors, who were blinded to the medications being used, evaluated the patients after 12, 26, and 52 weeks.

Quality of life was the primary outcome measure.¹³ Secondary measures included symptoms, side effects, patient satisfaction, and cost of care.

Band 1 results. Patients assigned to the SGA or FGA classes showed no significant differences in quality of life measures or schizophrenia symptoms. If anything, the findings slightly favored the FGAs.

Patient satisfaction and overall cost of care were similar, and rates of extrapyramidal symptoms (EPS), tardive dyskinesia, and akathisia did not differ significantly.

Clozapine comparison. In CUtLASS band 2, a different sample of 136 schizophrenia patients who had responded poorly to ≥2 antipsychotics was randomly assigned to clozapine or one of the above four SGAs. During the 1-year comparison trial, clozapine:

• was found to be significantly more effective (P=0.01) in managing patients’ symptoms, as measured by total Positive and Negative Syndrome Scale (PANSS) score
• showed a trend (P=0.08) towards providing these treatment-resistant patients with a better quality of life.⁸

Table 1

Summary of CUtLASS trial design and results

Table 2

Comparing designs of the CUtLASS and CATIE schizophrenia trials

Comparing catie, cutlass data

The CUtLASS findings are not identical to those of CATIE phase 1¹⁴ but are remarkably similar: no differences in effectiveness were seen between FGAs and SGA when treating patients with chronic schizophrenia.^15,16

CUtLASS investigators concluded that “in people with schizophrenia whose medication is changed for clinical reasons, there is no disadvantage across 1 year in terms of quality of life, symptoms, or associated costs of care in using FGAs rather than nonclozapine SGAs.”⁷

By confirming CATIE’s results, is CUtLASS the final word on antipsychotic treatment of chronic schizophrenia? Or is it just another piece of the puzzle? CATIE and CUtLASS add much to our knowledge, but methodologic “flies in the ointment” plague all clinical trials. We must consider potential biases and confounding factors to properly interpret and apply their findings.

Although the CUtLASS trial was well-constructed and executed, its conclusions—like those of CATIE—merit careful scrutiny. Its patient recruitment methods and study design involved choices and compromises that are appropriate to evaluate^17,18 as we weigh CUtLASS’ contribution to the SGA/FGA debate (Table 3).

Table 3

‘Flies in the ointment’ of the CUtLASS trial design

Who was studied?

Selection questions. CUtLASS researchers had problems recruiting patients for their study, in part because clinicians were reluctant to expose their patients to a 50% probability of being assigned to an FGA. Only 40% of the targeted sample was recruited, and participating clinicians referred only 20% to 37% of their eligible patients to the study.¹² Thus, one could ask:

• Were enrolled subjects truly representative of the population from which they were drawn?
• Or did selection bias result in a disproportionate inclusion of individuals with certain characteristics?

Is it possible, for example, that clinicians preferentially referred medication-noncompliant patients to CUtLASS because they believed the benefits of depot FGAs—such as more assured adherence—would compensate for the potential benefits of SGAs—better efficacy/tolerability?¹⁹

Treatment resistance. Although patients were randomly assigned to FGAs or SGAs, a significantly greater proportion of those whose antipsychotics were being changed because of treatment resistance were assigned to receive SGAs. Treatment resistance was one reason that 88% of subjects in the SGA arm were referred to the trial, compared with 70% of subjects in the FGA arm (P<0.01).¹² The extent to which this differential assignment may have biased results against SGAs is unclear.

EPS risk. CUtLASS-1 patients had been ill a mean of 14 years and had low baseline EPS rates despite receiving long-term antipsychotics (primarily FGAs). Even so, FGAs and SGAs showed similar rates of akathisia and other EPS. Thus—as with the CATIE results—the extent to which CUtLASS-1 findings may apply beyond chronic schizophrenia patients at relatively low risk for EPS is unclear.^11,17

Impact of switching. Although patients were referred to CUtLASS because of adverse effects or inadequate response to one or more antipsychotics, they were only moderately ill (mean PANSS total score 72)²⁰ and probably were deriving some benefit from their baseline antipsychotics. Before randomization, 82% of patients were receiving an FGA and 19% an SGA. Consequently, a far larger percentage of patients in the SGA group had to switch to a different medication class as the trial began.

As observed in CATIE, switching antipsychotics often has short-term negative consequences for patients,²¹ although switching classes (as in CUtLASS) may have had a different impact than switching individual antipsychotics (as in CATIE). If unequal antipsychotic switching rates in the two arms differentially affected patients’ quality of life, we would expect to see this effect emerge at the 12-week assessment, which is precisely where the greatest difference in Quality of Life Scale (QLS)¹³ scores appeared.

The mean QLS score for patients in the SGA arm was 2.6 points lower than in the FGA group at 12 weeks. This difference disappeared and, in fact, reversed at 26 weeks, but this 12-week effect had a strong impact on results of the 52-week intent-to-treat analysis. CUtLASS—like CATIE—might exemplify the risks of switching patients from treatment with partially effective antipsychotics.²²

What was compared?

Classes vs individual drugs. The decision in CUtLASS-1 to compare antipsychotic classes rather than individual agents makes it difficult to interpret its findings. Antipsychotics are not homogeneous; clear differences exist within both the SGA and FGA classes in terms of individual agents’ efficacy and tolerability, and each SGA has a reasonably well-established and different side-effect profile.²³

Sulpiride was the most commonly used FGA in CUtLASS-1 (by 49% of FGA patients). Sulpiride has some unusual attributes—such as lower EPS liability—and is not available in the United States. Thus, including this agent might have affected how applicable CUtLASS findings are to clinical practice in the United States.

Oral vs depot delivery. Individuals assigned to an FGA could receive either oral or long-acting depot medication, whereas those assigned to an SGA could receive only oral medication. At baseline, 84 of 227 CUtLASS-1 participants were receiving a depot antipsychotic, which was discontinued during randomization in 72 patients. During the 1-year study, the number of patients receiving a depot antipsychotic tripled from 12 to 35, suggesting the usefulness of long-acting agents in this population.¹⁹

Cross-class switching. Although participating physicians and their patients were urged to stay within assigned antipsychotic classes at least for the first 12 weeks and ideally for 1 year, a high rate of cross-class switching occurred (Figure). At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead.

The CUtLASS authors’ assert that the trial refutes the hypothesis that using SGAs is superior to using FGAs in improving quality of life. This conclusion is difficult to justify when so many patients assigned to the FGA class actually were receiving SGAs. The conclusion is further weakened if differential switching rates put SGAs at a disadvantage in the first 12 weeks of the trial.

A more accurate conclusion of the intent-to-treat comparison appears in the technical report: “There was no statistically significant difference in terms of quality of life or symptoms over 1 year in commencing [italics added] conventional antipsychotic drugs rather than new atypical drugs.”¹²

Figure CUtLASS-1: Did switching rate affect trial outcome?

The high rate of cross-class medication switching in CUtLASS-1 may have weakened the study’s conclusion that virtually no difference in effectiveness exists between first- and second-generation antipsychotics. At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead. Not shown in the figure is that 4 of the total 55 patients who switched from FGAs to SGAs had switched back to FGAs by the 52-week assessment.

CUtLASS: Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study

FGA: First-generation antipsychotic

SGA: Second-generation antipsychotic

Source: Adapted from reference 7, Figure 1

Clinical implications

Notwithstanding these cautionary notes, CUtLASS-1 findings add to the questions raised by CATIE about the relative effectiveness of SGAs and FGAs. At a minimum, the data indicate that the SGA advantage has been overstated or oversimplified and that FGAs may be suitable options for meeting the needs of some patients with psychosis (particularly those at low risk for EPS).

Depot antipsychotics. CUtLASS also suggests a wider role for long-acting antipsychotics in chronic psychotic disorders, beyond treating patients with severe nonadherence.^19,23 The number of patients receiving long-acting agents tripled over the 1-year study.¹²

Clozapine. Both CATIE and CUtLASS-2 confirmed clozapine’s superior efficacy for patients with treatment-resistant psychotic illness (Table 4). CUtLASS-2 also reaffirmed the challenges of clozapine’s metabolic and other side effects, such as sedation, hypotension, and hypersalivation.

All-cause discontinuation was significantly higher (P<0.05) in patients taking clozapine (73%) than in those taking other SGAs (52%). Even so, clozapine-group patients achieved significantly greater symptom reduction and tended toward a higher quality of life than other SGA-group patients.

Table 4

Clinical ‘pearls’ from the CUtLASS trial data

Overview. In conclusion, one can reasonably conclude from analyzing the CATIE and CUtLASS data that:

• FGA-SGA differences are not as great as previously thought.
• Substantial differences exist among agents within both antipsychotic classes, particularly in side effect profiles.
• Neither study disproves the following presumed benefit of SGAs: that compared with FGAs, SGAs provide an equivalent antipsychotic effect and pose a lower risk of problems related to unmitigated dopamine blockade—such as EPS, dysphoria, bradyphrenia, neuroleptic-induced deficit syndrome, and tardive dyskinesia.¹¹
• To use antipsychotics effectively and optimize individual treatment, consider the CATIE and CUtLASS trials in the contexts of their designs and the results of other studies of patients with chronic schizophrenia.

Related resources

• Heres S, Davis J, Maino K, et al. Why olanzapine beats risperidone, risperidone beats quetiapine, and quetiapine beats olanzapine: An exploratory analysis of head-head comparison studies of second-generation antipsychotics. Am J Psychiatry 2006;163:185-94.

Drug brand names

• Clozapine • Clozaril
• Quetiapine • Seroquel
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

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

When treating chronic psychotic disorders, U.S. psychiatrists generally prefer second-generation antipsychotics (SGAs) to first-generation antipsychotics (FGAs) because of widely held views^1,2 that SGAs:

• are more effective for negative and cognitive symptoms
• produce fewer troublesome side effects
• help patients realize a better quality of life.

These beliefs have been challenged by two large-scale, government-supported studies: the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) in the United States^3-6 and more recently the Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study (CUtLASS) from the United Kingdom.^7,8

CATIE and CUtLASS data suggest that the SGA advantage has been exaggerated, if in fact such an advantage exists. Other Current Psychiatry articles for the clinical practitioner have discussed the CATIE findings.^9-11 This article addresses the CUtLASS results in the context of the trial’s methodology, using information from the primary publications^7,8 and technical report.¹²

Cutlass study

Design. CUtLASS included 2 “bands” (Table 1):

• Band 1 compared the clinical usefulness and cost effectiveness of FGAs and SGAs in treating schizophrenia⁷
• Band 2 compared the effectiveness of clozapine versus other SGAs in treating refractory schizophrenia.⁸

CUtLASS Band 1 was not as extensive in scope as CATIE, and its design had some important differences (Table 2). Patients were referred for participation because their psychiatrists were considering a change in antipsychotic medication to address adverse effects or inadequate response. Fewer patients were recruited than expected—40% of the planned sample during 30 months of recruitment—but researchers considered the size sufficient to compare the effectiveness of FGAs and SGAs.

Patients were randomly assigned to treatment with an antipsychotic class, either:

• an FGA (1 of 11 options—including 5 depot formulations—chosen by the treating clinician)
• or an SGA (risperidone, olanzapine, quetiapine, or amisulpride, also chosen by the clinician).

Physicians and patients were not blinded to the medications used. They could choose medications within patients’ assigned classes and switch as needed in ways that mimicked clinical practice. Trained assessors, who were blinded to the medications being used, evaluated the patients after 12, 26, and 52 weeks.

Quality of life was the primary outcome measure.¹³ Secondary measures included symptoms, side effects, patient satisfaction, and cost of care.

Band 1 results. Patients assigned to the SGA or FGA classes showed no significant differences in quality of life measures or schizophrenia symptoms. If anything, the findings slightly favored the FGAs.

Patient satisfaction and overall cost of care were similar, and rates of extrapyramidal symptoms (EPS), tardive dyskinesia, and akathisia did not differ significantly.

Clozapine comparison. In CUtLASS band 2, a different sample of 136 schizophrenia patients who had responded poorly to ≥2 antipsychotics was randomly assigned to clozapine or one of the above four SGAs. During the 1-year comparison trial, clozapine:

• was found to be significantly more effective (P=0.01) in managing patients’ symptoms, as measured by total Positive and Negative Syndrome Scale (PANSS) score
• showed a trend (P=0.08) towards providing these treatment-resistant patients with a better quality of life.⁸

Table 1

Summary of CUtLASS trial design and results

Table 2

Comparing designs of the CUtLASS and CATIE schizophrenia trials

Comparing catie, cutlass data

The CUtLASS findings are not identical to those of CATIE phase 1¹⁴ but are remarkably similar: no differences in effectiveness were seen between FGAs and SGA when treating patients with chronic schizophrenia.^15,16

CUtLASS investigators concluded that “in people with schizophrenia whose medication is changed for clinical reasons, there is no disadvantage across 1 year in terms of quality of life, symptoms, or associated costs of care in using FGAs rather than nonclozapine SGAs.”⁷

By confirming CATIE’s results, is CUtLASS the final word on antipsychotic treatment of chronic schizophrenia? Or is it just another piece of the puzzle? CATIE and CUtLASS add much to our knowledge, but methodologic “flies in the ointment” plague all clinical trials. We must consider potential biases and confounding factors to properly interpret and apply their findings.

Although the CUtLASS trial was well-constructed and executed, its conclusions—like those of CATIE—merit careful scrutiny. Its patient recruitment methods and study design involved choices and compromises that are appropriate to evaluate^17,18 as we weigh CUtLASS’ contribution to the SGA/FGA debate (Table 3).

Table 3

‘Flies in the ointment’ of the CUtLASS trial design

Who was studied?

Selection questions. CUtLASS researchers had problems recruiting patients for their study, in part because clinicians were reluctant to expose their patients to a 50% probability of being assigned to an FGA. Only 40% of the targeted sample was recruited, and participating clinicians referred only 20% to 37% of their eligible patients to the study.¹² Thus, one could ask:

• Were enrolled subjects truly representative of the population from which they were drawn?
• Or did selection bias result in a disproportionate inclusion of individuals with certain characteristics?

Is it possible, for example, that clinicians preferentially referred medication-noncompliant patients to CUtLASS because they believed the benefits of depot FGAs—such as more assured adherence—would compensate for the potential benefits of SGAs—better efficacy/tolerability?¹⁹

Treatment resistance. Although patients were randomly assigned to FGAs or SGAs, a significantly greater proportion of those whose antipsychotics were being changed because of treatment resistance were assigned to receive SGAs. Treatment resistance was one reason that 88% of subjects in the SGA arm were referred to the trial, compared with 70% of subjects in the FGA arm (P<0.01).¹² The extent to which this differential assignment may have biased results against SGAs is unclear.

EPS risk. CUtLASS-1 patients had been ill a mean of 14 years and had low baseline EPS rates despite receiving long-term antipsychotics (primarily FGAs). Even so, FGAs and SGAs showed similar rates of akathisia and other EPS. Thus—as with the CATIE results—the extent to which CUtLASS-1 findings may apply beyond chronic schizophrenia patients at relatively low risk for EPS is unclear.^11,17

Impact of switching. Although patients were referred to CUtLASS because of adverse effects or inadequate response to one or more antipsychotics, they were only moderately ill (mean PANSS total score 72)²⁰ and probably were deriving some benefit from their baseline antipsychotics. Before randomization, 82% of patients were receiving an FGA and 19% an SGA. Consequently, a far larger percentage of patients in the SGA group had to switch to a different medication class as the trial began.

As observed in CATIE, switching antipsychotics often has short-term negative consequences for patients,²¹ although switching classes (as in CUtLASS) may have had a different impact than switching individual antipsychotics (as in CATIE). If unequal antipsychotic switching rates in the two arms differentially affected patients’ quality of life, we would expect to see this effect emerge at the 12-week assessment, which is precisely where the greatest difference in Quality of Life Scale (QLS)¹³ scores appeared.

The mean QLS score for patients in the SGA arm was 2.6 points lower than in the FGA group at 12 weeks. This difference disappeared and, in fact, reversed at 26 weeks, but this 12-week effect had a strong impact on results of the 52-week intent-to-treat analysis. CUtLASS—like CATIE—might exemplify the risks of switching patients from treatment with partially effective antipsychotics.²²

What was compared?

Classes vs individual drugs. The decision in CUtLASS-1 to compare antipsychotic classes rather than individual agents makes it difficult to interpret its findings. Antipsychotics are not homogeneous; clear differences exist within both the SGA and FGA classes in terms of individual agents’ efficacy and tolerability, and each SGA has a reasonably well-established and different side-effect profile.²³

Sulpiride was the most commonly used FGA in CUtLASS-1 (by 49% of FGA patients). Sulpiride has some unusual attributes—such as lower EPS liability—and is not available in the United States. Thus, including this agent might have affected how applicable CUtLASS findings are to clinical practice in the United States.

Oral vs depot delivery. Individuals assigned to an FGA could receive either oral or long-acting depot medication, whereas those assigned to an SGA could receive only oral medication. At baseline, 84 of 227 CUtLASS-1 participants were receiving a depot antipsychotic, which was discontinued during randomization in 72 patients. During the 1-year study, the number of patients receiving a depot antipsychotic tripled from 12 to 35, suggesting the usefulness of long-acting agents in this population.¹⁹

Cross-class switching. Although participating physicians and their patients were urged to stay within assigned antipsychotic classes at least for the first 12 weeks and ideally for 1 year, a high rate of cross-class switching occurred (Figure). At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead.

The CUtLASS authors’ assert that the trial refutes the hypothesis that using SGAs is superior to using FGAs in improving quality of life. This conclusion is difficult to justify when so many patients assigned to the FGA class actually were receiving SGAs. The conclusion is further weakened if differential switching rates put SGAs at a disadvantage in the first 12 weeks of the trial.

A more accurate conclusion of the intent-to-treat comparison appears in the technical report: “There was no statistically significant difference in terms of quality of life or symptoms over 1 year in commencing [italics added] conventional antipsychotic drugs rather than new atypical drugs.”¹²

Figure CUtLASS-1: Did switching rate affect trial outcome?

The high rate of cross-class medication switching in CUtLASS-1 may have weakened the study’s conclusion that virtually no difference in effectiveness exists between first- and second-generation antipsychotics. At the 52-week assessment, 51 of 118 patients (43%) in the intent-to-treat FGA group were receiving SGAs instead. Not shown in the figure is that 4 of the total 55 patients who switched from FGAs to SGAs had switched back to FGAs by the 52-week assessment.

CUtLASS: Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study

FGA: First-generation antipsychotic

SGA: Second-generation antipsychotic

Source: Adapted from reference 7, Figure 1

Clinical implications

Notwithstanding these cautionary notes, CUtLASS-1 findings add to the questions raised by CATIE about the relative effectiveness of SGAs and FGAs. At a minimum, the data indicate that the SGA advantage has been overstated or oversimplified and that FGAs may be suitable options for meeting the needs of some patients with psychosis (particularly those at low risk for EPS).

Depot antipsychotics. CUtLASS also suggests a wider role for long-acting antipsychotics in chronic psychotic disorders, beyond treating patients with severe nonadherence.^19,23 The number of patients receiving long-acting agents tripled over the 1-year study.¹²

Clozapine. Both CATIE and CUtLASS-2 confirmed clozapine’s superior efficacy for patients with treatment-resistant psychotic illness (Table 4). CUtLASS-2 also reaffirmed the challenges of clozapine’s metabolic and other side effects, such as sedation, hypotension, and hypersalivation.

All-cause discontinuation was significantly higher (P<0.05) in patients taking clozapine (73%) than in those taking other SGAs (52%). Even so, clozapine-group patients achieved significantly greater symptom reduction and tended toward a higher quality of life than other SGA-group patients.

Table 4

Clinical ‘pearls’ from the CUtLASS trial data

Overview. In conclusion, one can reasonably conclude from analyzing the CATIE and CUtLASS data that:

• FGA-SGA differences are not as great as previously thought.
• Substantial differences exist among agents within both antipsychotic classes, particularly in side effect profiles.
• Neither study disproves the following presumed benefit of SGAs: that compared with FGAs, SGAs provide an equivalent antipsychotic effect and pose a lower risk of problems related to unmitigated dopamine blockade—such as EPS, dysphoria, bradyphrenia, neuroleptic-induced deficit syndrome, and tardive dyskinesia.¹¹
• To use antipsychotics effectively and optimize individual treatment, consider the CATIE and CUtLASS trials in the contexts of their designs and the results of other studies of patients with chronic schizophrenia.

Related resources

• Heres S, Davis J, Maino K, et al. Why olanzapine beats risperidone, risperidone beats quetiapine, and quetiapine beats olanzapine: An exploratory analysis of head-head comparison studies of second-generation antipsychotics. Am J Psychiatry 2006;163:185-94.

Drug brand names

• Clozapine • Clozaril
• Quetiapine • Seroquel
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

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

Evidence grows that marijuana use can cause acute psychosis, bring forward in time a first schizophrenia episode, and worsen the prognosis of patients with psychotic disorders.

Roger, age 16, had been smoking marijuana on and off for about 2 years. His parents knew but believed this was a stage and not dangerous; they had tried marijuana in their youth without harm. Roger’s smoking had increased to several joints daily since he started a relationship with an older girl, who shared and encouraged his habit.

His parents became worried when Roger began making unusual comments, saying that food did not taste “right” and he thought someone was poisoning him. They brought Roger for psychiatric consultation at the recommendation of their family physician.

History and examination revealed that Roger had experienced vague persecutory ideas for several weeks but no systematized delusions or hallucinations. I told Roger and his parents he probably had a drug-induced psychosis and that symptoms would likely disappear without recurrence if he stopped using marijuana. At 2-weeks’ follow-up, he described no more psychotic experiences and said he now realized the danger for him of smoking marijuana. A review 1 month later showed Roger was doing well, and I discharged him after reinforcing the importance of abstinence. But his case didn’t end there.

Box 1

Two years later, I received a request for information about Roger’s episode from an acute inpatient facility. Roger had been admitted after an incident at the local mall in which he screamed at people and accused bystanders of trying to harm him. Despite using marijuana only occasionally, his behavior had been deteriorating and was becoming increasingly bizarre. The attending psychiatrist believed Roger had schizophrenia.

Clinicians regularly deal with patients such as Roger who suffer from a psychotic disorder and use marijuana. This is hardly surprising because marijuana is the most widely used illicit drug. In 2006, 5% of 12th graders in the United States reported using marijuana daily during the previous month, and 42% had tried it at least once.¹

Is psychotic patients’ use of marijuana a coincidence? Self-medication? Or could cannabis cause psychotic illness? This debate elicits strong views among community and professional groups. To help you provide up-to-date advice to patients and families, this review:

• describes the growing body of evidence on the mental health consequences of marijuana use
• seeks to help you detect and deal with the effects of marijuana use in clinical practice.

Marijuana and psychosis

Although the neurobiologic association is unclear (Box 1),^2-4 up to 15% of users report psychotic phenomena after consuming marijuana.⁵ Naturalistic and experimental studies have confirmed that marijuana can induce short-lived psychotic experiences.

In two parallel trials, 22 healthy individuals⁶ and 13 stable, antipsychotic-treated schizophrenia patients⁷ were given 2.5 mg and 5 mg intravenously of delta-9-tetrahydrocannabinol (delta-9-THC)—the primary psychoactive constituent of marijuana. Both groups developed dose-related, transient, schizophrenia-like symptoms and altered perceptions:

• Healthy volunteers showed the full range of psychotic symptoms. One individual said, “I thought you were giving me THC through the blood pressure machine and the sheets.”²
• Schizophrenia patients tended to report increases in the symptoms of their specific conditions. Those with paranoid illnesses, for example, reported an escalation in persecutory ideas.

Transient psychotic phenomena are not equivalent to a psychotic illness, however. To meet diagnostic criteria for a psychotic disorder, symptoms must be persistent and impair psychosocial functioning.

Early reports. Anecdotal clinical reports that marijuana use could cause psychosis emerged in the 1960s but were largely ignored. Many clinicians assumed that psychotic individuals used marijuana to relieve troubling symptoms (self-medication).

A 15-year, longitudinal study examined the incidence of schizophrenia in >50,000 Swedish conscripts and concluded that marijuana use during adolescence increased the risk of schizophrenia.⁸ Skeptics questioned the validity of the diagnosis and the etiologic role of other drugs in this study and suggested that prodromal symptoms might have led to marijuana use, rather than marijuana triggering the psychosis.

Recent evidence. Better-designed studies have shown that marijuana use increases the risk of psychosis later in life.

Adolescents who used marijuana by age 15 were more likely to develop a schizophreniform disorder by age 26 than nonusers, according to data from 759 New Zealanders who took part in a prospective, longitudinal, general population study. Marijuana use by age 15 was associated with a higher risk than later use (by age 18).⁹

A 3-year, longitudinal, population-based study from the Netherlands found marijuana use associated with increased risk of psychosis in 4,045 previously psychosis-free individuals. More than 50% of psychosis diagnoses could be attributed to marijuana use.¹⁰

Data from the 21-year longitudinal Christchurch Health and Development Study in New Zealand showed elevated rates of psychotic symptoms in young people with cannabis dependence at ages 18 and 21. The associations remained even after adjustments were made for previous psychotic symptoms and other confounding factors.¹¹

Follow-up analysis of data from the Swedish military conscripts study⁸ showed that the use of other psychoactive drugs or prodromal cases in the cohort did not explain the association between self-reported marijuana use and hospital admissions for schizophrenia and other psychoses.¹²

Box 2

Box 3

Researchers in Israel cross-linked a cohort of 9,724 youths aged 16 to 17 screened by the Israeli Draft Board with a national registry of psychiatric hospital admissions for schizophrenia in the following 4 to 15 years. Self-reported drug abuse (mostly marijuana) was higher in adolescents who were later hospitalized for schizophrenia (12.4%) than in those not hospitalized (5.9%).¹³

Box 4

Summary. A review of these 5 studies concluded that evidence supports the hypothesis that marijuana use acts as a risk factor in schizophrenia onset.¹⁴ Although marijuana use is not a “necessary” causal factor in psychotic illness—most users do not develop the disorder, and many persons with schizophrenia do not use marijuana—strong evidence indicates that it is one of many factors that can cause a psychotic illness (Box 2).^9-14

Who is at risk?

Can marijuana cause psychosis in any person or specifically in those at increased risk of psychosis? If the latter, then marijuana—rather than causing new, unanticipated cases—might bring forward schizophrenia onset in individuals who would have developed it later. This explanation is consistent with data showing that persons born in more-recent cohorts seem to have an earlier age of schizophrenia onset.¹⁵

Vulnerability for psychosis. Evidence strongly suggests that marijuana-induced psychotic symptoms are more prevalent among vulnerable or psychosis-prone individuals.

• When given 2.5 mg of delta-9-THC, 80% of 13 patients with well-controlled schizophrenia experienced high Positive and Negative Syndrome Scale scores, compared with 35% of 22 healthy controls.²
• Unusual perceptions or thought influence were more common following marijuana use in all participants in a naturalistic experiment, but much more so in “at risk” individuals who had previously described isolated psychotic symptoms.¹⁶
• Adolescents and young adults ages 14 to 24 who used marijuana and displayed high “psychoticism” scores at baseline had more than twice the risk of a psychosis outcome 4 years later than did those without high scores.¹⁷

Schizophrenia onset. Marijuana users who suffer a drug-induced psychosis are at very high risk of developing a psychotic illness later on. A ≥3-year follow-up study¹⁸ of 535 patients who had not been treated for psychotic problems before being diagnosed with marijuana-induced psychotic symptoms found that:

• marijuana-induced psychotic episodes often remitted quickly with minimal treatment
• about one-half of patients were diagnosed with a schizophrenia-spectrum disorder (mostly paranoid schizophrenia) at follow up
• the gap between the marijuana-induced episode and diagnosis of a schizophrenia-spectrum disorder was >1 year in 47% of cases.
• the first episode of schizophrenia in these patients occurred several years earlier than in schizophrenia patients without marijuana-induced psychosis.

Although these findings require replication, they challenge the belief that marijuana-induced psychosis is benign (Box 3).

Implications for treatment

Most psychiatric practitioners treat patients who have psychotic illness and use marijuana (Box 4). Compared with nonusers, these patients tend to have:

• earlier age of schizophrenia onset
• more psychotic symptoms
• worse prognosis because of poorer treatment adherence
• increased symptom severity and persistence
• higher relapse rates.¹⁹

Therefore, ask patients with psychotic disorders about their marijuana use, and treat both the marijuana use and the psychosis. Evidence to guide treatment is scarce, however. Nicotine, marijuana, and alcohol use are often intertwined. This suggests that treatments that target a variety of substances may be more efficient than targeted ones, even if the generic interventions are brief.²⁰

A study of marijuana users with early psychosis showed, for example, that marijuana-focused treatment was not more effective than psychoeducation, although both resulted in reduced use.²¹ In nonpsychotic individuals, giving 90 adult patients incentive vouchers to exchange for retail items each time they provided a marijuana-negative urine specimen resulted in increased abstinence rates over a 12-month period (Box 5).^22,23 Cognitive-behavioral therapy helped to sustain the vouchers’ positive effect on abstinence after the initial 14-week treatment.²³

Box 5

Treatment with first-generation antipsychotics does not appear to decrease substance use. Several studies suggest that clozapine decreases the use of nicotine, alcohol, or other substances among patients with schizophrenia,²⁴ though this does not necessarily apply to other second-generation antipsychotics (Box 6).

Box 6

Implications for prevention

Psychiatric practitioners can play an important role in making young people aware of the mental health risks of using marijuana. Marijuana use fluctuates population-wide, depending in part on public perception of its harmfulness. Its use may diminish, therefore, as information on its mental health hazards percolates into high schools and the community at large. We also have the duty to make policy makers and legislators aware of this information.²⁵

Related resources

• National Institute on Drug Abuse. https://www.drugabuse.gov/drugs-abuse/marijuana.
• Cannabis dependence. www.mentalhealth.com/dis/p20-sb03.html.
• Castle D, Murray R, eds. Marijuana and madness: psychiatry and neurobiology. Cambridge, UK: Cambridge University Press; 2004.
• Hall W, Pacula RL. Cannabis use and dependence: public health and public policy. Cambridge, UK: Cambridge University Press; 2003.

Drug brand names

• Clozapine • Clozaril

Disclosure

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

Evidence grows that marijuana use can cause acute psychosis, bring forward in time a first schizophrenia episode, and worsen the prognosis of patients with psychotic disorders.

Roger, age 16, had been smoking marijuana on and off for about 2 years. His parents knew but believed this was a stage and not dangerous; they had tried marijuana in their youth without harm. Roger’s smoking had increased to several joints daily since he started a relationship with an older girl, who shared and encouraged his habit.

His parents became worried when Roger began making unusual comments, saying that food did not taste “right” and he thought someone was poisoning him. They brought Roger for psychiatric consultation at the recommendation of their family physician.

History and examination revealed that Roger had experienced vague persecutory ideas for several weeks but no systematized delusions or hallucinations. I told Roger and his parents he probably had a drug-induced psychosis and that symptoms would likely disappear without recurrence if he stopped using marijuana. At 2-weeks’ follow-up, he described no more psychotic experiences and said he now realized the danger for him of smoking marijuana. A review 1 month later showed Roger was doing well, and I discharged him after reinforcing the importance of abstinence. But his case didn’t end there.

Box 1

Two years later, I received a request for information about Roger’s episode from an acute inpatient facility. Roger had been admitted after an incident at the local mall in which he screamed at people and accused bystanders of trying to harm him. Despite using marijuana only occasionally, his behavior had been deteriorating and was becoming increasingly bizarre. The attending psychiatrist believed Roger had schizophrenia.

Clinicians regularly deal with patients such as Roger who suffer from a psychotic disorder and use marijuana. This is hardly surprising because marijuana is the most widely used illicit drug. In 2006, 5% of 12th graders in the United States reported using marijuana daily during the previous month, and 42% had tried it at least once.¹

Is psychotic patients’ use of marijuana a coincidence? Self-medication? Or could cannabis cause psychotic illness? This debate elicits strong views among community and professional groups. To help you provide up-to-date advice to patients and families, this review:

• describes the growing body of evidence on the mental health consequences of marijuana use
• seeks to help you detect and deal with the effects of marijuana use in clinical practice.

Marijuana and psychosis

Although the neurobiologic association is unclear (Box 1),^2-4 up to 15% of users report psychotic phenomena after consuming marijuana.⁵ Naturalistic and experimental studies have confirmed that marijuana can induce short-lived psychotic experiences.

In two parallel trials, 22 healthy individuals⁶ and 13 stable, antipsychotic-treated schizophrenia patients⁷ were given 2.5 mg and 5 mg intravenously of delta-9-tetrahydrocannabinol (delta-9-THC)—the primary psychoactive constituent of marijuana. Both groups developed dose-related, transient, schizophrenia-like symptoms and altered perceptions:

• Healthy volunteers showed the full range of psychotic symptoms. One individual said, “I thought you were giving me THC through the blood pressure machine and the sheets.”²
• Schizophrenia patients tended to report increases in the symptoms of their specific conditions. Those with paranoid illnesses, for example, reported an escalation in persecutory ideas.

Transient psychotic phenomena are not equivalent to a psychotic illness, however. To meet diagnostic criteria for a psychotic disorder, symptoms must be persistent and impair psychosocial functioning.

Early reports. Anecdotal clinical reports that marijuana use could cause psychosis emerged in the 1960s but were largely ignored. Many clinicians assumed that psychotic individuals used marijuana to relieve troubling symptoms (self-medication).

A 15-year, longitudinal study examined the incidence of schizophrenia in >50,000 Swedish conscripts and concluded that marijuana use during adolescence increased the risk of schizophrenia.⁸ Skeptics questioned the validity of the diagnosis and the etiologic role of other drugs in this study and suggested that prodromal symptoms might have led to marijuana use, rather than marijuana triggering the psychosis.

Recent evidence. Better-designed studies have shown that marijuana use increases the risk of psychosis later in life.

Adolescents who used marijuana by age 15 were more likely to develop a schizophreniform disorder by age 26 than nonusers, according to data from 759 New Zealanders who took part in a prospective, longitudinal, general population study. Marijuana use by age 15 was associated with a higher risk than later use (by age 18).⁹

A 3-year, longitudinal, population-based study from the Netherlands found marijuana use associated with increased risk of psychosis in 4,045 previously psychosis-free individuals. More than 50% of psychosis diagnoses could be attributed to marijuana use.¹⁰

Data from the 21-year longitudinal Christchurch Health and Development Study in New Zealand showed elevated rates of psychotic symptoms in young people with cannabis dependence at ages 18 and 21. The associations remained even after adjustments were made for previous psychotic symptoms and other confounding factors.¹¹

Follow-up analysis of data from the Swedish military conscripts study⁸ showed that the use of other psychoactive drugs or prodromal cases in the cohort did not explain the association between self-reported marijuana use and hospital admissions for schizophrenia and other psychoses.¹²

Box 2

Box 3

Researchers in Israel cross-linked a cohort of 9,724 youths aged 16 to 17 screened by the Israeli Draft Board with a national registry of psychiatric hospital admissions for schizophrenia in the following 4 to 15 years. Self-reported drug abuse (mostly marijuana) was higher in adolescents who were later hospitalized for schizophrenia (12.4%) than in those not hospitalized (5.9%).¹³

Box 4

Summary. A review of these 5 studies concluded that evidence supports the hypothesis that marijuana use acts as a risk factor in schizophrenia onset.¹⁴ Although marijuana use is not a “necessary” causal factor in psychotic illness—most users do not develop the disorder, and many persons with schizophrenia do not use marijuana—strong evidence indicates that it is one of many factors that can cause a psychotic illness (Box 2).^9-14

Who is at risk?

Can marijuana cause psychosis in any person or specifically in those at increased risk of psychosis? If the latter, then marijuana—rather than causing new, unanticipated cases—might bring forward schizophrenia onset in individuals who would have developed it later. This explanation is consistent with data showing that persons born in more-recent cohorts seem to have an earlier age of schizophrenia onset.¹⁵

Vulnerability for psychosis. Evidence strongly suggests that marijuana-induced psychotic symptoms are more prevalent among vulnerable or psychosis-prone individuals.

• When given 2.5 mg of delta-9-THC, 80% of 13 patients with well-controlled schizophrenia experienced high Positive and Negative Syndrome Scale scores, compared with 35% of 22 healthy controls.²
• Unusual perceptions or thought influence were more common following marijuana use in all participants in a naturalistic experiment, but much more so in “at risk” individuals who had previously described isolated psychotic symptoms.¹⁶
• Adolescents and young adults ages 14 to 24 who used marijuana and displayed high “psychoticism” scores at baseline had more than twice the risk of a psychosis outcome 4 years later than did those without high scores.¹⁷

Schizophrenia onset. Marijuana users who suffer a drug-induced psychosis are at very high risk of developing a psychotic illness later on. A ≥3-year follow-up study¹⁸ of 535 patients who had not been treated for psychotic problems before being diagnosed with marijuana-induced psychotic symptoms found that:

• marijuana-induced psychotic episodes often remitted quickly with minimal treatment
• about one-half of patients were diagnosed with a schizophrenia-spectrum disorder (mostly paranoid schizophrenia) at follow up
• the gap between the marijuana-induced episode and diagnosis of a schizophrenia-spectrum disorder was >1 year in 47% of cases.
• the first episode of schizophrenia in these patients occurred several years earlier than in schizophrenia patients without marijuana-induced psychosis.

Although these findings require replication, they challenge the belief that marijuana-induced psychosis is benign (Box 3).

Implications for treatment

Most psychiatric practitioners treat patients who have psychotic illness and use marijuana (Box 4). Compared with nonusers, these patients tend to have:

• earlier age of schizophrenia onset
• more psychotic symptoms
• worse prognosis because of poorer treatment adherence
• increased symptom severity and persistence
• higher relapse rates.¹⁹

Therefore, ask patients with psychotic disorders about their marijuana use, and treat both the marijuana use and the psychosis. Evidence to guide treatment is scarce, however. Nicotine, marijuana, and alcohol use are often intertwined. This suggests that treatments that target a variety of substances may be more efficient than targeted ones, even if the generic interventions are brief.²⁰

A study of marijuana users with early psychosis showed, for example, that marijuana-focused treatment was not more effective than psychoeducation, although both resulted in reduced use.²¹ In nonpsychotic individuals, giving 90 adult patients incentive vouchers to exchange for retail items each time they provided a marijuana-negative urine specimen resulted in increased abstinence rates over a 12-month period (Box 5).^22,23 Cognitive-behavioral therapy helped to sustain the vouchers’ positive effect on abstinence after the initial 14-week treatment.²³

Box 5

Treatment with first-generation antipsychotics does not appear to decrease substance use. Several studies suggest that clozapine decreases the use of nicotine, alcohol, or other substances among patients with schizophrenia,²⁴ though this does not necessarily apply to other second-generation antipsychotics (Box 6).

Box 6

Implications for prevention

Psychiatric practitioners can play an important role in making young people aware of the mental health risks of using marijuana. Marijuana use fluctuates population-wide, depending in part on public perception of its harmfulness. Its use may diminish, therefore, as information on its mental health hazards percolates into high schools and the community at large. We also have the duty to make policy makers and legislators aware of this information.²⁵

Related resources

• National Institute on Drug Abuse. https://www.drugabuse.gov/drugs-abuse/marijuana.
• Cannabis dependence. www.mentalhealth.com/dis/p20-sb03.html.
• Castle D, Murray R, eds. Marijuana and madness: psychiatry and neurobiology. Cambridge, UK: Cambridge University Press; 2004.
• Hall W, Pacula RL. Cannabis use and dependence: public health and public policy. Cambridge, UK: Cambridge University Press; 2003.

Drug brand names

• Clozapine • Clozaril

Disclosure

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

Evidence grows that marijuana use can cause acute psychosis, bring forward in time a first schizophrenia episode, and worsen the prognosis of patients with psychotic disorders.

Roger, age 16, had been smoking marijuana on and off for about 2 years. His parents knew but believed this was a stage and not dangerous; they had tried marijuana in their youth without harm. Roger’s smoking had increased to several joints daily since he started a relationship with an older girl, who shared and encouraged his habit.

His parents became worried when Roger began making unusual comments, saying that food did not taste “right” and he thought someone was poisoning him. They brought Roger for psychiatric consultation at the recommendation of their family physician.

History and examination revealed that Roger had experienced vague persecutory ideas for several weeks but no systematized delusions or hallucinations. I told Roger and his parents he probably had a drug-induced psychosis and that symptoms would likely disappear without recurrence if he stopped using marijuana. At 2-weeks’ follow-up, he described no more psychotic experiences and said he now realized the danger for him of smoking marijuana. A review 1 month later showed Roger was doing well, and I discharged him after reinforcing the importance of abstinence. But his case didn’t end there.

Box 1

Two years later, I received a request for information about Roger’s episode from an acute inpatient facility. Roger had been admitted after an incident at the local mall in which he screamed at people and accused bystanders of trying to harm him. Despite using marijuana only occasionally, his behavior had been deteriorating and was becoming increasingly bizarre. The attending psychiatrist believed Roger had schizophrenia.

Clinicians regularly deal with patients such as Roger who suffer from a psychotic disorder and use marijuana. This is hardly surprising because marijuana is the most widely used illicit drug. In 2006, 5% of 12th graders in the United States reported using marijuana daily during the previous month, and 42% had tried it at least once.¹

Is psychotic patients’ use of marijuana a coincidence? Self-medication? Or could cannabis cause psychotic illness? This debate elicits strong views among community and professional groups. To help you provide up-to-date advice to patients and families, this review:

• describes the growing body of evidence on the mental health consequences of marijuana use
• seeks to help you detect and deal with the effects of marijuana use in clinical practice.

Marijuana and psychosis

Although the neurobiologic association is unclear (Box 1),^2-4 up to 15% of users report psychotic phenomena after consuming marijuana.⁵ Naturalistic and experimental studies have confirmed that marijuana can induce short-lived psychotic experiences.

In two parallel trials, 22 healthy individuals⁶ and 13 stable, antipsychotic-treated schizophrenia patients⁷ were given 2.5 mg and 5 mg intravenously of delta-9-tetrahydrocannabinol (delta-9-THC)—the primary psychoactive constituent of marijuana. Both groups developed dose-related, transient, schizophrenia-like symptoms and altered perceptions:

• Healthy volunteers showed the full range of psychotic symptoms. One individual said, “I thought you were giving me THC through the blood pressure machine and the sheets.”²
• Schizophrenia patients tended to report increases in the symptoms of their specific conditions. Those with paranoid illnesses, for example, reported an escalation in persecutory ideas.

Transient psychotic phenomena are not equivalent to a psychotic illness, however. To meet diagnostic criteria for a psychotic disorder, symptoms must be persistent and impair psychosocial functioning.

Early reports. Anecdotal clinical reports that marijuana use could cause psychosis emerged in the 1960s but were largely ignored. Many clinicians assumed that psychotic individuals used marijuana to relieve troubling symptoms (self-medication).

A 15-year, longitudinal study examined the incidence of schizophrenia in >50,000 Swedish conscripts and concluded that marijuana use during adolescence increased the risk of schizophrenia.⁸ Skeptics questioned the validity of the diagnosis and the etiologic role of other drugs in this study and suggested that prodromal symptoms might have led to marijuana use, rather than marijuana triggering the psychosis.

Recent evidence. Better-designed studies have shown that marijuana use increases the risk of psychosis later in life.

Adolescents who used marijuana by age 15 were more likely to develop a schizophreniform disorder by age 26 than nonusers, according to data from 759 New Zealanders who took part in a prospective, longitudinal, general population study. Marijuana use by age 15 was associated with a higher risk than later use (by age 18).⁹

A 3-year, longitudinal, population-based study from the Netherlands found marijuana use associated with increased risk of psychosis in 4,045 previously psychosis-free individuals. More than 50% of psychosis diagnoses could be attributed to marijuana use.¹⁰

Data from the 21-year longitudinal Christchurch Health and Development Study in New Zealand showed elevated rates of psychotic symptoms in young people with cannabis dependence at ages 18 and 21. The associations remained even after adjustments were made for previous psychotic symptoms and other confounding factors.¹¹

Follow-up analysis of data from the Swedish military conscripts study⁸ showed that the use of other psychoactive drugs or prodromal cases in the cohort did not explain the association between self-reported marijuana use and hospital admissions for schizophrenia and other psychoses.¹²

Box 2

Box 3

Researchers in Israel cross-linked a cohort of 9,724 youths aged 16 to 17 screened by the Israeli Draft Board with a national registry of psychiatric hospital admissions for schizophrenia in the following 4 to 15 years. Self-reported drug abuse (mostly marijuana) was higher in adolescents who were later hospitalized for schizophrenia (12.4%) than in those not hospitalized (5.9%).¹³

Box 4

Summary. A review of these 5 studies concluded that evidence supports the hypothesis that marijuana use acts as a risk factor in schizophrenia onset.¹⁴ Although marijuana use is not a “necessary” causal factor in psychotic illness—most users do not develop the disorder, and many persons with schizophrenia do not use marijuana—strong evidence indicates that it is one of many factors that can cause a psychotic illness (Box 2).^9-14

Who is at risk?

Can marijuana cause psychosis in any person or specifically in those at increased risk of psychosis? If the latter, then marijuana—rather than causing new, unanticipated cases—might bring forward schizophrenia onset in individuals who would have developed it later. This explanation is consistent with data showing that persons born in more-recent cohorts seem to have an earlier age of schizophrenia onset.¹⁵

Vulnerability for psychosis. Evidence strongly suggests that marijuana-induced psychotic symptoms are more prevalent among vulnerable or psychosis-prone individuals.

• When given 2.5 mg of delta-9-THC, 80% of 13 patients with well-controlled schizophrenia experienced high Positive and Negative Syndrome Scale scores, compared with 35% of 22 healthy controls.²
• Unusual perceptions or thought influence were more common following marijuana use in all participants in a naturalistic experiment, but much more so in “at risk” individuals who had previously described isolated psychotic symptoms.¹⁶
• Adolescents and young adults ages 14 to 24 who used marijuana and displayed high “psychoticism” scores at baseline had more than twice the risk of a psychosis outcome 4 years later than did those without high scores.¹⁷

Schizophrenia onset. Marijuana users who suffer a drug-induced psychosis are at very high risk of developing a psychotic illness later on. A ≥3-year follow-up study¹⁸ of 535 patients who had not been treated for psychotic problems before being diagnosed with marijuana-induced psychotic symptoms found that:

• marijuana-induced psychotic episodes often remitted quickly with minimal treatment
• about one-half of patients were diagnosed with a schizophrenia-spectrum disorder (mostly paranoid schizophrenia) at follow up
• the gap between the marijuana-induced episode and diagnosis of a schizophrenia-spectrum disorder was >1 year in 47% of cases.
• the first episode of schizophrenia in these patients occurred several years earlier than in schizophrenia patients without marijuana-induced psychosis.

Although these findings require replication, they challenge the belief that marijuana-induced psychosis is benign (Box 3).

Implications for treatment

Most psychiatric practitioners treat patients who have psychotic illness and use marijuana (Box 4). Compared with nonusers, these patients tend to have:

• earlier age of schizophrenia onset
• more psychotic symptoms
• worse prognosis because of poorer treatment adherence
• increased symptom severity and persistence
• higher relapse rates.¹⁹

Therefore, ask patients with psychotic disorders about their marijuana use, and treat both the marijuana use and the psychosis. Evidence to guide treatment is scarce, however. Nicotine, marijuana, and alcohol use are often intertwined. This suggests that treatments that target a variety of substances may be more efficient than targeted ones, even if the generic interventions are brief.²⁰

A study of marijuana users with early psychosis showed, for example, that marijuana-focused treatment was not more effective than psychoeducation, although both resulted in reduced use.²¹ In nonpsychotic individuals, giving 90 adult patients incentive vouchers to exchange for retail items each time they provided a marijuana-negative urine specimen resulted in increased abstinence rates over a 12-month period (Box 5).^22,23 Cognitive-behavioral therapy helped to sustain the vouchers’ positive effect on abstinence after the initial 14-week treatment.²³

Box 5

Treatment with first-generation antipsychotics does not appear to decrease substance use. Several studies suggest that clozapine decreases the use of nicotine, alcohol, or other substances among patients with schizophrenia,²⁴ though this does not necessarily apply to other second-generation antipsychotics (Box 6).

Box 6

Implications for prevention

Psychiatric practitioners can play an important role in making young people aware of the mental health risks of using marijuana. Marijuana use fluctuates population-wide, depending in part on public perception of its harmfulness. Its use may diminish, therefore, as information on its mental health hazards percolates into high schools and the community at large. We also have the duty to make policy makers and legislators aware of this information.²⁵

Related resources

• National Institute on Drug Abuse. https://www.drugabuse.gov/drugs-abuse/marijuana.
• Cannabis dependence. www.mentalhealth.com/dis/p20-sb03.html.
• Castle D, Murray R, eds. Marijuana and madness: psychiatry and neurobiology. Cambridge, UK: Cambridge University Press; 2004.
• Hall W, Pacula RL. Cannabis use and dependence: public health and public policy. Cambridge, UK: Cambridge University Press; 2003.

Drug brand names

• Clozapine • Clozaril

Disclosure

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

‘Immediately after the event I was a wreck. I vaguely remember talking to the family; I don’t know if I was much use to them. … That night I got drunk. It was the only way I could sleep. A sensitive colleague came and sat with me.”¹

Besides being targets of malpractice suits, psychiatrists also serve as resources for colleagues who are sued. Specific actions can help you and those you counsel deal with the stress of an adverse event before and during litigation. Remember that:

• anticipation is the best defense
• knowledge is power
• action counters passivity
• a supportive environment is essential.

ANTICIPATING LITIGATION

What is the risk? No nationwide reporting system tracks the incidence of medical malpractice claims, but industry experts suggest a claim is leveled against 7% of psychiatrists each year.² The risk is higher for other medical specialists: a recent survey by the American College of Obstetricians and Gynecologists found that 89% of practicing ObGyns had been sued at least once in their careers.³ Because a claim usually takes several years to resolve, a substantial number of physicians—including psychiatrists—are involved in litigation at any one time.

Successfully anticipating litigation begins with being familiar with your state’s statute of limitations—usually 2 to 3 years after discovery of the incident, with exceptions for children, the disabled, and designated special circumstances. If a plaintiff’s case is not filed within this time, a disputed outcome can never be the subject of a malpractice claim.

Adverse events. The severity of the outcome, the nature of your relationship with the patient, and the degree of your responsibility for an adverse event contribute to the intensity of your initial emotional response. If a mistake caused the event, your reaction may be even more severe.^4-6 Whatever the event’s specifics, you may ruminate about your role and degree of responsibility (Table 1).

Table 1

Nagging questions after a ‘bad’ patient outcome

Expect that your view of the circumstances will generate a complex array of feelings: shock, anxiety, depression, shame, guilt, self-blame, disbelief, self-doubt and inadequacy, anger, and even relief from not having to work with a difficult patient anymore.

Patient suicide. More than one-half of psychiatrists and up to one-third of psychiatric residents experience a patient suicide.^7-10 The Joint Commission on Accreditation of Healthcare Organizations reports that suicide is the most frequent sentinel event, representing 501 (13.1%) of the total 3,811 sentinel events reviewed since 1995.¹¹ Professional Risk Management Services, a major medical malpractice insurer of psychiatrists, reports that suicide and attempted suicide are the most frequently identifiable causes of liability payments (Figure).

Figure 1 Psychiatric claims by cause of loss in the United States, 1998 to 2005

Almost all lawsuits assert multiple allegations of negligence, and “cause of loss” represents the main allegation made in the claim or lawsuit. Thus, the category of “incorrect treatment” may be alleged in a lawsuit based on a patient suicide, but the main or chief allegation/complaint is stated as “incorrect treatment.” The most frequent identifiable cause of loss is suicide and attempted suicide.

* “Other” includes administrative issues, abandonment, premises liability, Tarasoff, third parties (such as parents), retained object, libel/slander, boundary violation, deleted duplicate file, Fen-phen, lack of informed consent, forensic issues, and miscellaneous.

Source: Prepared by Professional Risk Management Services, Inc. Reprinted with permission.

Psychiatrists’ feelings of distress after a patient suicide mirror the personal sense of failure and inadequacy most physicians feel when they are unable to prevent a patient’s death or serious injury. At the same time, we must:

• deal with the event’s medical complications, with relevant notifications and disclosures (Table 2)
• address the emotional pain of the injured patient or family
• participate in mandated reviews
• recognize and manage our emotional disruption (Table 3).

Table 2

Recommended medical steps, notifications,
and disclosures after an adverse event

Table 3

Managing your emotions before and during litigation

Self-evaluation. To cope with distress when a patient dies, you could attend the funeral. If the death was by suicide, consider consulting with a therapist about your reactions or review the case with your supervisor. You also might:

• make changes in your practice that alert you to problem patients
• introduce a more structured approach to patients with particular clinical conditions, using practice guidelines as a resource^12,13
• become more alert to patients who may benefit from consultation or referral.

Balance the time you devote to work and personal life. Schedule regular time for recreation and active sports, which can help you prepare for the prolonged stress that follows being sued. Engage a personal physician to monitor your physical and emotional health and to recommend appropriate referrals when indicated.

KNOWLEDGE IS POWER

What can I expect? A lawsuit generates a mixture of common emotions and exacerbates those felt at the time of the bad outcome: shock, outrage, anxiety, anguish, dread, depression, helplessness, hopelessness, feelings of being misunderstood, and the anger and vulnerability associated with a narcissistic injury. As one ObGyn stated, learning that a lawsuit was filed “just prolonged my misery.”¹⁴

Each of us reacts in our own way to a lawsuit—and differently to each lawsuit if we are sued more than once—because of:

• our personality traits and personal circumstances
• the specifics of each case
• our relationship with the patient
• the public nature of a lawsuit
• a range of other variables that makes each case unique.

Suddenly, we who perceive ourselves as caring, beneficent, well-meaning, and devoted to our patients are publicly accused of being careless and incompetent, of harming the patient by failing to meet our minimal obligations. Psychiatrists Richard Ferrell and Trevor Price¹⁵ capture the impact of these allegations:

"Here are the sense of assault and violation, the feelings of outrage and fear. Most painfully, here is the narcissistic injury, the astonishing wound to our understanding of ourselves as admirable, well-meaning people."

Litigation is a lengthy process with defined stages (Table 4). We have little control over a slow-paced process that involves an array of participants (lawyers, judges, jury, and experts) whose behavior is not predictable. This makes us feel dependent, vulnerable, and impotent.

Table 4

Stages of litigation: What happens in court

BE ACTIVE, NOT PASSIVE

What you can do. Contact your insurer and risk manager immediately. Inquire about the average length of litigation in your jurisdiction (might be 1 to 5 or more years, depending on locality, type of case, and severity of injury). Ask your lawyer to describe the steps in the process and your role as the case proceeds.

Take whatever steps are necessary to cover your clinical duties. If your initial emotional reaction is disruptive, obtain coverage or rearrange your schedule. Expect to change or limit your schedule before depositions and during trial to allow adequate time for preparation.

Accept the fact that you must play by rules far different from those of medical care. Litigation is time-consuming and frustrating. Delays and “continuances” are common in legal proceedings, so expect them. Consider adapting to your own situation strategies that other sued physicians have found useful in regaining control over their lives and work (Table 5).

Table 5

Regaining control: Managing your practice during litigation

GET NEEDED SUPPORT

Talking about the case. Sharing with responsible confidants your emotional reactions to being sued is healthy for you and others affected. Lawyers, however, may caution you not to “talk to anybody” about the case. They don’t want you to say anything that would suggest liability or jeopardize their defense of the case.

As psychiatrists, we know this is not good psychological advice. The support of others is a natural help during major life events that cause enormous stress and disruption.¹⁶ You can resolve this dilemma by accepting the discipline of talking about your feelings regarding the case without discussing the specifics of the case.

In addition to lawyers and claims representatives, you may talk with your spouse or another trusted person or colleague about your feelings. When other physicians or psychiatrists formally consult with you about their litigation experiences, you are protected by the confidentiality inherent in the doctor-patient relationship.

Trust issues. Trust lies at the core of psychotherapeutic work. After being sued, you may find it difficult to re-establish trusting and comfortable relationships with patients, especially those who are seriously ill.

Well-trained, competent physicians who keep current with standards of care and have good relationships with patients do not expect to be sued. Psychiatrists often feel unrealistically immune to litigation because we believe our training helps us understand our own psychology and relationships with others. A charge of negligence exposes our vulnerabilities and leaves us feeling hurt and betrayed. As one psychiatrist ruefully observed, “I lost my innocence.”¹⁴

Countertransference feelings may emerge. Most physicians acknowledge that after being sued their relationships with patients change^17,18—a particularly distressing outcome for psychiatrists. We may feel uncomfortable and threatened when we need to “stretch the patient-doctor relationship in a paternalistic direction,” such as when a psychotic patient needs involuntary commitment.¹⁵

Feelings that you must change the way you practice and chronic anxiety about your work are barriers to good practice. You may contemplate changing practice circumstances or retiring early. Personal therapy may help if you remain uneasy or cannot resolve life choices that overshadow your work with patients.

Medical or psychiatric care. Be alert to the point at which you or others involved in litigation need a referral for medical or psychiatric consultation. Sued physicians, their families, or colleagues often experience diagnosable psychiatric conditions or other behavioral problems, such as:

• major depression
• adjustment disorders
• posttraumatic stress disorder
• worsening of a previously diagnosed psychiatric illness
• physical symptoms that require diagnosis and treatment
• alcohol and drug misuse or abuse
• anxiety and distress that interfere with work
• self-medication, especially for insomnia
• disturbances and dysfunctional behaviors that affect marital and family life.^19,20

SUPPORT YOUR COLLEAGUES

When consulting with other physicians, be aware of litigation factors that may influence treatment.

Become familiar with the climate of litigation in the jurisdiction where the case was filed, including the incidence and outcome of cases. For example, does an attempted suicide case usually result in settlement or—if it goes to trial—take 2 to 5 or more years to resolve? More than 70% of cases filed nationwide result in no payment (no settlement) for the plaintiff. If cases go to trial, physicians win 80% of the time.²¹

Recognize that the source of the physician’s distress may be the trauma associated with the initial bad outcome, rather than the malpractice suit itself. As the case progresses and facts emerge, you may play a large role in helping your physician patient correct previous distortions of the event. Certain periods—during trial, for example—might require more-frequent visits, medication, and expressions of support.

You may harbor a bias about the case, but withhold judgment until it is resolved.

Related resources

• American College of Obstetricians and Gynecologists. From exam room to court room: navigating litigation and coping with stress (CD-ROM) http://sales.acog.com/acb/stores/1/product1.cfm?SID=1&Product_ID=589).
• Charles SC, Frisch PR. Adverse events, stress and litigation: a physician’s guide. New York: Oxford University Press; 2005.
• Physician Litigation Stress Resource Center. www.physicianlitigationstress.org.

Disclosure

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

‘Immediately after the event I was a wreck. I vaguely remember talking to the family; I don’t know if I was much use to them. … That night I got drunk. It was the only way I could sleep. A sensitive colleague came and sat with me.”¹

Besides being targets of malpractice suits, psychiatrists also serve as resources for colleagues who are sued. Specific actions can help you and those you counsel deal with the stress of an adverse event before and during litigation. Remember that:

• anticipation is the best defense
• knowledge is power
• action counters passivity
• a supportive environment is essential.

ANTICIPATING LITIGATION

What is the risk? No nationwide reporting system tracks the incidence of medical malpractice claims, but industry experts suggest a claim is leveled against 7% of psychiatrists each year.² The risk is higher for other medical specialists: a recent survey by the American College of Obstetricians and Gynecologists found that 89% of practicing ObGyns had been sued at least once in their careers.³ Because a claim usually takes several years to resolve, a substantial number of physicians—including psychiatrists—are involved in litigation at any one time.

Successfully anticipating litigation begins with being familiar with your state’s statute of limitations—usually 2 to 3 years after discovery of the incident, with exceptions for children, the disabled, and designated special circumstances. If a plaintiff’s case is not filed within this time, a disputed outcome can never be the subject of a malpractice claim.

Adverse events. The severity of the outcome, the nature of your relationship with the patient, and the degree of your responsibility for an adverse event contribute to the intensity of your initial emotional response. If a mistake caused the event, your reaction may be even more severe.^4-6 Whatever the event’s specifics, you may ruminate about your role and degree of responsibility (Table 1).

Table 1

Nagging questions after a ‘bad’ patient outcome

Expect that your view of the circumstances will generate a complex array of feelings: shock, anxiety, depression, shame, guilt, self-blame, disbelief, self-doubt and inadequacy, anger, and even relief from not having to work with a difficult patient anymore.

Patient suicide. More than one-half of psychiatrists and up to one-third of psychiatric residents experience a patient suicide.^7-10 The Joint Commission on Accreditation of Healthcare Organizations reports that suicide is the most frequent sentinel event, representing 501 (13.1%) of the total 3,811 sentinel events reviewed since 1995.¹¹ Professional Risk Management Services, a major medical malpractice insurer of psychiatrists, reports that suicide and attempted suicide are the most frequently identifiable causes of liability payments (Figure).

Figure 1 Psychiatric claims by cause of loss in the United States, 1998 to 2005

Almost all lawsuits assert multiple allegations of negligence, and “cause of loss” represents the main allegation made in the claim or lawsuit. Thus, the category of “incorrect treatment” may be alleged in a lawsuit based on a patient suicide, but the main or chief allegation/complaint is stated as “incorrect treatment.” The most frequent identifiable cause of loss is suicide and attempted suicide.

* “Other” includes administrative issues, abandonment, premises liability, Tarasoff, third parties (such as parents), retained object, libel/slander, boundary violation, deleted duplicate file, Fen-phen, lack of informed consent, forensic issues, and miscellaneous.

Source: Prepared by Professional Risk Management Services, Inc. Reprinted with permission.

Psychiatrists’ feelings of distress after a patient suicide mirror the personal sense of failure and inadequacy most physicians feel when they are unable to prevent a patient’s death or serious injury. At the same time, we must:

• deal with the event’s medical complications, with relevant notifications and disclosures (Table 2)
• address the emotional pain of the injured patient or family
• participate in mandated reviews
• recognize and manage our emotional disruption (Table 3).

Table 2

Recommended medical steps, notifications,
and disclosures after an adverse event

Table 3

Managing your emotions before and during litigation

Self-evaluation. To cope with distress when a patient dies, you could attend the funeral. If the death was by suicide, consider consulting with a therapist about your reactions or review the case with your supervisor. You also might:

• make changes in your practice that alert you to problem patients
• introduce a more structured approach to patients with particular clinical conditions, using practice guidelines as a resource^12,13
• become more alert to patients who may benefit from consultation or referral.

Balance the time you devote to work and personal life. Schedule regular time for recreation and active sports, which can help you prepare for the prolonged stress that follows being sued. Engage a personal physician to monitor your physical and emotional health and to recommend appropriate referrals when indicated.

KNOWLEDGE IS POWER

What can I expect? A lawsuit generates a mixture of common emotions and exacerbates those felt at the time of the bad outcome: shock, outrage, anxiety, anguish, dread, depression, helplessness, hopelessness, feelings of being misunderstood, and the anger and vulnerability associated with a narcissistic injury. As one ObGyn stated, learning that a lawsuit was filed “just prolonged my misery.”¹⁴

Each of us reacts in our own way to a lawsuit—and differently to each lawsuit if we are sued more than once—because of:

• our personality traits and personal circumstances
• the specifics of each case
• our relationship with the patient
• the public nature of a lawsuit
• a range of other variables that makes each case unique.

Suddenly, we who perceive ourselves as caring, beneficent, well-meaning, and devoted to our patients are publicly accused of being careless and incompetent, of harming the patient by failing to meet our minimal obligations. Psychiatrists Richard Ferrell and Trevor Price¹⁵ capture the impact of these allegations:

"Here are the sense of assault and violation, the feelings of outrage and fear. Most painfully, here is the narcissistic injury, the astonishing wound to our understanding of ourselves as admirable, well-meaning people."

Litigation is a lengthy process with defined stages (Table 4). We have little control over a slow-paced process that involves an array of participants (lawyers, judges, jury, and experts) whose behavior is not predictable. This makes us feel dependent, vulnerable, and impotent.

Table 4

Stages of litigation: What happens in court

BE ACTIVE, NOT PASSIVE

What you can do. Contact your insurer and risk manager immediately. Inquire about the average length of litigation in your jurisdiction (might be 1 to 5 or more years, depending on locality, type of case, and severity of injury). Ask your lawyer to describe the steps in the process and your role as the case proceeds.

Take whatever steps are necessary to cover your clinical duties. If your initial emotional reaction is disruptive, obtain coverage or rearrange your schedule. Expect to change or limit your schedule before depositions and during trial to allow adequate time for preparation.

Accept the fact that you must play by rules far different from those of medical care. Litigation is time-consuming and frustrating. Delays and “continuances” are common in legal proceedings, so expect them. Consider adapting to your own situation strategies that other sued physicians have found useful in regaining control over their lives and work (Table 5).

Table 5

Regaining control: Managing your practice during litigation

GET NEEDED SUPPORT

Talking about the case. Sharing with responsible confidants your emotional reactions to being sued is healthy for you and others affected. Lawyers, however, may caution you not to “talk to anybody” about the case. They don’t want you to say anything that would suggest liability or jeopardize their defense of the case.

As psychiatrists, we know this is not good psychological advice. The support of others is a natural help during major life events that cause enormous stress and disruption.¹⁶ You can resolve this dilemma by accepting the discipline of talking about your feelings regarding the case without discussing the specifics of the case.

In addition to lawyers and claims representatives, you may talk with your spouse or another trusted person or colleague about your feelings. When other physicians or psychiatrists formally consult with you about their litigation experiences, you are protected by the confidentiality inherent in the doctor-patient relationship.

Trust issues. Trust lies at the core of psychotherapeutic work. After being sued, you may find it difficult to re-establish trusting and comfortable relationships with patients, especially those who are seriously ill.

Well-trained, competent physicians who keep current with standards of care and have good relationships with patients do not expect to be sued. Psychiatrists often feel unrealistically immune to litigation because we believe our training helps us understand our own psychology and relationships with others. A charge of negligence exposes our vulnerabilities and leaves us feeling hurt and betrayed. As one psychiatrist ruefully observed, “I lost my innocence.”¹⁴

Countertransference feelings may emerge. Most physicians acknowledge that after being sued their relationships with patients change^17,18—a particularly distressing outcome for psychiatrists. We may feel uncomfortable and threatened when we need to “stretch the patient-doctor relationship in a paternalistic direction,” such as when a psychotic patient needs involuntary commitment.¹⁵

Feelings that you must change the way you practice and chronic anxiety about your work are barriers to good practice. You may contemplate changing practice circumstances or retiring early. Personal therapy may help if you remain uneasy or cannot resolve life choices that overshadow your work with patients.

Medical or psychiatric care. Be alert to the point at which you or others involved in litigation need a referral for medical or psychiatric consultation. Sued physicians, their families, or colleagues often experience diagnosable psychiatric conditions or other behavioral problems, such as:

• major depression
• adjustment disorders
• posttraumatic stress disorder
• worsening of a previously diagnosed psychiatric illness
• physical symptoms that require diagnosis and treatment
• alcohol and drug misuse or abuse
• anxiety and distress that interfere with work
• self-medication, especially for insomnia
• disturbances and dysfunctional behaviors that affect marital and family life.^19,20

SUPPORT YOUR COLLEAGUES

When consulting with other physicians, be aware of litigation factors that may influence treatment.

Become familiar with the climate of litigation in the jurisdiction where the case was filed, including the incidence and outcome of cases. For example, does an attempted suicide case usually result in settlement or—if it goes to trial—take 2 to 5 or more years to resolve? More than 70% of cases filed nationwide result in no payment (no settlement) for the plaintiff. If cases go to trial, physicians win 80% of the time.²¹

Recognize that the source of the physician’s distress may be the trauma associated with the initial bad outcome, rather than the malpractice suit itself. As the case progresses and facts emerge, you may play a large role in helping your physician patient correct previous distortions of the event. Certain periods—during trial, for example—might require more-frequent visits, medication, and expressions of support.

You may harbor a bias about the case, but withhold judgment until it is resolved.

Related resources

• American College of Obstetricians and Gynecologists. From exam room to court room: navigating litigation and coping with stress (CD-ROM) http://sales.acog.com/acb/stores/1/product1.cfm?SID=1&Product_ID=589).
• Charles SC, Frisch PR. Adverse events, stress and litigation: a physician’s guide. New York: Oxford University Press; 2005.
• Physician Litigation Stress Resource Center. www.physicianlitigationstress.org.

Disclosure

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

‘Immediately after the event I was a wreck. I vaguely remember talking to the family; I don’t know if I was much use to them. … That night I got drunk. It was the only way I could sleep. A sensitive colleague came and sat with me.”¹

Besides being targets of malpractice suits, psychiatrists also serve as resources for colleagues who are sued. Specific actions can help you and those you counsel deal with the stress of an adverse event before and during litigation. Remember that:

• anticipation is the best defense
• knowledge is power
• action counters passivity
• a supportive environment is essential.

ANTICIPATING LITIGATION

What is the risk? No nationwide reporting system tracks the incidence of medical malpractice claims, but industry experts suggest a claim is leveled against 7% of psychiatrists each year.² The risk is higher for other medical specialists: a recent survey by the American College of Obstetricians and Gynecologists found that 89% of practicing ObGyns had been sued at least once in their careers.³ Because a claim usually takes several years to resolve, a substantial number of physicians—including psychiatrists—are involved in litigation at any one time.

Successfully anticipating litigation begins with being familiar with your state’s statute of limitations—usually 2 to 3 years after discovery of the incident, with exceptions for children, the disabled, and designated special circumstances. If a plaintiff’s case is not filed within this time, a disputed outcome can never be the subject of a malpractice claim.

Adverse events. The severity of the outcome, the nature of your relationship with the patient, and the degree of your responsibility for an adverse event contribute to the intensity of your initial emotional response. If a mistake caused the event, your reaction may be even more severe.^4-6 Whatever the event’s specifics, you may ruminate about your role and degree of responsibility (Table 1).

Table 1

Nagging questions after a ‘bad’ patient outcome

Expect that your view of the circumstances will generate a complex array of feelings: shock, anxiety, depression, shame, guilt, self-blame, disbelief, self-doubt and inadequacy, anger, and even relief from not having to work with a difficult patient anymore.

Patient suicide. More than one-half of psychiatrists and up to one-third of psychiatric residents experience a patient suicide.^7-10 The Joint Commission on Accreditation of Healthcare Organizations reports that suicide is the most frequent sentinel event, representing 501 (13.1%) of the total 3,811 sentinel events reviewed since 1995.¹¹ Professional Risk Management Services, a major medical malpractice insurer of psychiatrists, reports that suicide and attempted suicide are the most frequently identifiable causes of liability payments (Figure).

Figure 1 Psychiatric claims by cause of loss in the United States, 1998 to 2005

Almost all lawsuits assert multiple allegations of negligence, and “cause of loss” represents the main allegation made in the claim or lawsuit. Thus, the category of “incorrect treatment” may be alleged in a lawsuit based on a patient suicide, but the main or chief allegation/complaint is stated as “incorrect treatment.” The most frequent identifiable cause of loss is suicide and attempted suicide.

* “Other” includes administrative issues, abandonment, premises liability, Tarasoff, third parties (such as parents), retained object, libel/slander, boundary violation, deleted duplicate file, Fen-phen, lack of informed consent, forensic issues, and miscellaneous.

Source: Prepared by Professional Risk Management Services, Inc. Reprinted with permission.

Psychiatrists’ feelings of distress after a patient suicide mirror the personal sense of failure and inadequacy most physicians feel when they are unable to prevent a patient’s death or serious injury. At the same time, we must:

• deal with the event’s medical complications, with relevant notifications and disclosures (Table 2)
• address the emotional pain of the injured patient or family
• participate in mandated reviews
• recognize and manage our emotional disruption (Table 3).

Table 2

Recommended medical steps, notifications,
and disclosures after an adverse event

Table 3

Managing your emotions before and during litigation

Self-evaluation. To cope with distress when a patient dies, you could attend the funeral. If the death was by suicide, consider consulting with a therapist about your reactions or review the case with your supervisor. You also might:

• make changes in your practice that alert you to problem patients
• introduce a more structured approach to patients with particular clinical conditions, using practice guidelines as a resource^12,13
• become more alert to patients who may benefit from consultation or referral.

Balance the time you devote to work and personal life. Schedule regular time for recreation and active sports, which can help you prepare for the prolonged stress that follows being sued. Engage a personal physician to monitor your physical and emotional health and to recommend appropriate referrals when indicated.

KNOWLEDGE IS POWER

What can I expect? A lawsuit generates a mixture of common emotions and exacerbates those felt at the time of the bad outcome: shock, outrage, anxiety, anguish, dread, depression, helplessness, hopelessness, feelings of being misunderstood, and the anger and vulnerability associated with a narcissistic injury. As one ObGyn stated, learning that a lawsuit was filed “just prolonged my misery.”¹⁴

Each of us reacts in our own way to a lawsuit—and differently to each lawsuit if we are sued more than once—because of:

• our personality traits and personal circumstances
• the specifics of each case
• our relationship with the patient
• the public nature of a lawsuit
• a range of other variables that makes each case unique.

Suddenly, we who perceive ourselves as caring, beneficent, well-meaning, and devoted to our patients are publicly accused of being careless and incompetent, of harming the patient by failing to meet our minimal obligations. Psychiatrists Richard Ferrell and Trevor Price¹⁵ capture the impact of these allegations:

"Here are the sense of assault and violation, the feelings of outrage and fear. Most painfully, here is the narcissistic injury, the astonishing wound to our understanding of ourselves as admirable, well-meaning people."

Litigation is a lengthy process with defined stages (Table 4). We have little control over a slow-paced process that involves an array of participants (lawyers, judges, jury, and experts) whose behavior is not predictable. This makes us feel dependent, vulnerable, and impotent.

Table 4

Stages of litigation: What happens in court

BE ACTIVE, NOT PASSIVE

What you can do. Contact your insurer and risk manager immediately. Inquire about the average length of litigation in your jurisdiction (might be 1 to 5 or more years, depending on locality, type of case, and severity of injury). Ask your lawyer to describe the steps in the process and your role as the case proceeds.

Take whatever steps are necessary to cover your clinical duties. If your initial emotional reaction is disruptive, obtain coverage or rearrange your schedule. Expect to change or limit your schedule before depositions and during trial to allow adequate time for preparation.

Accept the fact that you must play by rules far different from those of medical care. Litigation is time-consuming and frustrating. Delays and “continuances” are common in legal proceedings, so expect them. Consider adapting to your own situation strategies that other sued physicians have found useful in regaining control over their lives and work (Table 5).

Table 5

Regaining control: Managing your practice during litigation

GET NEEDED SUPPORT

Talking about the case. Sharing with responsible confidants your emotional reactions to being sued is healthy for you and others affected. Lawyers, however, may caution you not to “talk to anybody” about the case. They don’t want you to say anything that would suggest liability or jeopardize their defense of the case.

As psychiatrists, we know this is not good psychological advice. The support of others is a natural help during major life events that cause enormous stress and disruption.¹⁶ You can resolve this dilemma by accepting the discipline of talking about your feelings regarding the case without discussing the specifics of the case.

In addition to lawyers and claims representatives, you may talk with your spouse or another trusted person or colleague about your feelings. When other physicians or psychiatrists formally consult with you about their litigation experiences, you are protected by the confidentiality inherent in the doctor-patient relationship.

Trust issues. Trust lies at the core of psychotherapeutic work. After being sued, you may find it difficult to re-establish trusting and comfortable relationships with patients, especially those who are seriously ill.

Well-trained, competent physicians who keep current with standards of care and have good relationships with patients do not expect to be sued. Psychiatrists often feel unrealistically immune to litigation because we believe our training helps us understand our own psychology and relationships with others. A charge of negligence exposes our vulnerabilities and leaves us feeling hurt and betrayed. As one psychiatrist ruefully observed, “I lost my innocence.”¹⁴

Countertransference feelings may emerge. Most physicians acknowledge that after being sued their relationships with patients change^17,18—a particularly distressing outcome for psychiatrists. We may feel uncomfortable and threatened when we need to “stretch the patient-doctor relationship in a paternalistic direction,” such as when a psychotic patient needs involuntary commitment.¹⁵

Feelings that you must change the way you practice and chronic anxiety about your work are barriers to good practice. You may contemplate changing practice circumstances or retiring early. Personal therapy may help if you remain uneasy or cannot resolve life choices that overshadow your work with patients.

Medical or psychiatric care. Be alert to the point at which you or others involved in litigation need a referral for medical or psychiatric consultation. Sued physicians, their families, or colleagues often experience diagnosable psychiatric conditions or other behavioral problems, such as:

• major depression
• adjustment disorders
• posttraumatic stress disorder
• worsening of a previously diagnosed psychiatric illness
• physical symptoms that require diagnosis and treatment
• alcohol and drug misuse or abuse
• anxiety and distress that interfere with work
• self-medication, especially for insomnia
• disturbances and dysfunctional behaviors that affect marital and family life.^19,20

SUPPORT YOUR COLLEAGUES

When consulting with other physicians, be aware of litigation factors that may influence treatment.

Become familiar with the climate of litigation in the jurisdiction where the case was filed, including the incidence and outcome of cases. For example, does an attempted suicide case usually result in settlement or—if it goes to trial—take 2 to 5 or more years to resolve? More than 70% of cases filed nationwide result in no payment (no settlement) for the plaintiff. If cases go to trial, physicians win 80% of the time.²¹

Recognize that the source of the physician’s distress may be the trauma associated with the initial bad outcome, rather than the malpractice suit itself. As the case progresses and facts emerge, you may play a large role in helping your physician patient correct previous distortions of the event. Certain periods—during trial, for example—might require more-frequent visits, medication, and expressions of support.

You may harbor a bias about the case, but withhold judgment until it is resolved.

Related resources

• American College of Obstetricians and Gynecologists. From exam room to court room: navigating litigation and coping with stress (CD-ROM) http://sales.acog.com/acb/stores/1/product1.cfm?SID=1&Product_ID=589).
• Charles SC, Frisch PR. Adverse events, stress and litigation: a physician’s guide. New York: Oxford University Press; 2005.
• Physician Litigation Stress Resource Center. www.physicianlitigationstress.org.

Disclosure

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

The serendipitous discovery of medications that can improve mood transformed depression treatment more than 50 years ago.¹ Most antidepressants produced since then could be called “me-too” medications because they all work by affecting the release of monoamines—serotonin, norepinephrine, and dopamine—which, in turn, modulate the activity of neurons that release glutamate.

Weeks may pass before antidepressants’ effect on monoamine-releasing neurons produces a therapeutic benefit, however, leaving many patients impaired or even suicidal. This delayed onset of action might be explained by antidepressants’ indirect blockade of glutamate. The route to more rapid results, therefore, might be to cut out the monoamine middlemen.

Glutamate clues

Glutamate, instead of monoamines, might offer a more direct means to affect mood and could be a new target for antidepressant treatment:²

• Positron-emission tomography of neuron function in depressed patients shows abnormal activity in neurons that release glutamate—so-called glutamate neurons.
• Approximately 60 % of neurons are glutamate neurons, the largest network of neurons in the brain.
• Increased glutamate activity is seen in depressed patients.
• Animal studies have shown that blocking the N-methyl-D-aspartate (NMDA) receptor—1 of 3 types of glutamate receptors—decreases depressive behavior.
• Chronic administration of antidepressant medication reduces the expression of NMDA receptors.

Rapid glutamate blockade

Prompted by evidence that glutamate may be involved in mood disorders, researchers at the National Institute of Mental Health designed a study to determine if blocking the NMDA receptor can produce a rapid antidepressant effect.³ They chose the agent ketamine for this study because of its potent affinity for the NMDA receptor.

Ketamine was developed in the 1960s as a general anaesthetic, and its use in the United States is limited almost exclusively to veterinary medicine. The drug’s propensity to induce perceptual disturbances limits its clinical use but enhances its illicit use.

Eighteen patients with treatment-resistant depression were enrolled in a randomized, placebo-controlled, double-blind, crossover study. After 2 weeks without medication, they received a single infusion of IV ketamine or placebo. One week later they received the alternate intervention. Changes in Hamilton Rating Scale for Depression scores were assessed after each infusion.

Figure Decrease in depressive symptoms with IV ketamine

* = P <0.05

Patients who received ketamine (blue) showed a marked reduction of depressive symptoms within 2 hours compared with those who received placebo (red).

Source: Reference 3Patients receiving ketamine showed a robust and sustained reduction in depressive symptoms compared with placebo within 110 minutes (Figure). “To our knowledge,” the authors wrote, “there has never been a report of any other drug or somatic treatment—such as sleep deprivation, thyrotropin-releasing hormone, antidepressant, dexamethasone, or electroconvulsive therapy—that results in such a dramatic rapid and prolonged response with a single administration.”

Seventy-one percent of patients responded to IV ketamine within 24 hours, which is comparable to reported response rates after 8 weeks with oral antidepressants such as bupropion (62%), selective serotonin reuptake inhibitors (63%), and venlafaxine (65%).^4,5

Caution and caveats

Despite these “dramatic” results, we must be cautious about extrapolating too much from this small study. Glutamate blockers such as ketamine can have serious adverse effects—including psychosis—and patients may not tolerate long-term interventions. Likewise, oral administration of memantine—another NMDA blocker—in a double-blind study did not effectively treat depression.⁶ Finally, subjects in the ketamine trial had chronic, treatment-resistant depression, and the results might not apply to other forms of depression.

The results suggest the possibility of a new option for depression treatment, however. Specifically, this option could expedite response and “jump-start” treatment through a novel mechanism so that persons with depression can get back on their feet more rapidly.

Drug brand names

• Bupropion • Wellbutrin
• Ketamine • Ketalar
• Memantine • Namenda
• Venlafaxine • Effexor

The serendipitous discovery of medications that can improve mood transformed depression treatment more than 50 years ago.¹ Most antidepressants produced since then could be called “me-too” medications because they all work by affecting the release of monoamines—serotonin, norepinephrine, and dopamine—which, in turn, modulate the activity of neurons that release glutamate.

Weeks may pass before antidepressants’ effect on monoamine-releasing neurons produces a therapeutic benefit, however, leaving many patients impaired or even suicidal. This delayed onset of action might be explained by antidepressants’ indirect blockade of glutamate. The route to more rapid results, therefore, might be to cut out the monoamine middlemen.

Glutamate clues

Glutamate, instead of monoamines, might offer a more direct means to affect mood and could be a new target for antidepressant treatment:²

• Positron-emission tomography of neuron function in depressed patients shows abnormal activity in neurons that release glutamate—so-called glutamate neurons.
• Approximately 60 % of neurons are glutamate neurons, the largest network of neurons in the brain.
• Increased glutamate activity is seen in depressed patients.
• Animal studies have shown that blocking the N-methyl-D-aspartate (NMDA) receptor—1 of 3 types of glutamate receptors—decreases depressive behavior.
• Chronic administration of antidepressant medication reduces the expression of NMDA receptors.

Rapid glutamate blockade

Prompted by evidence that glutamate may be involved in mood disorders, researchers at the National Institute of Mental Health designed a study to determine if blocking the NMDA receptor can produce a rapid antidepressant effect.³ They chose the agent ketamine for this study because of its potent affinity for the NMDA receptor.

Ketamine was developed in the 1960s as a general anaesthetic, and its use in the United States is limited almost exclusively to veterinary medicine. The drug’s propensity to induce perceptual disturbances limits its clinical use but enhances its illicit use.

Eighteen patients with treatment-resistant depression were enrolled in a randomized, placebo-controlled, double-blind, crossover study. After 2 weeks without medication, they received a single infusion of IV ketamine or placebo. One week later they received the alternate intervention. Changes in Hamilton Rating Scale for Depression scores were assessed after each infusion.

Figure Decrease in depressive symptoms with IV ketamine

* = P <0.05

Patients who received ketamine (blue) showed a marked reduction of depressive symptoms within 2 hours compared with those who received placebo (red).

Source: Reference 3Patients receiving ketamine showed a robust and sustained reduction in depressive symptoms compared with placebo within 110 minutes (Figure). “To our knowledge,” the authors wrote, “there has never been a report of any other drug or somatic treatment—such as sleep deprivation, thyrotropin-releasing hormone, antidepressant, dexamethasone, or electroconvulsive therapy—that results in such a dramatic rapid and prolonged response with a single administration.”

Seventy-one percent of patients responded to IV ketamine within 24 hours, which is comparable to reported response rates after 8 weeks with oral antidepressants such as bupropion (62%), selective serotonin reuptake inhibitors (63%), and venlafaxine (65%).^4,5

Caution and caveats

Despite these “dramatic” results, we must be cautious about extrapolating too much from this small study. Glutamate blockers such as ketamine can have serious adverse effects—including psychosis—and patients may not tolerate long-term interventions. Likewise, oral administration of memantine—another NMDA blocker—in a double-blind study did not effectively treat depression.⁶ Finally, subjects in the ketamine trial had chronic, treatment-resistant depression, and the results might not apply to other forms of depression.

The results suggest the possibility of a new option for depression treatment, however. Specifically, this option could expedite response and “jump-start” treatment through a novel mechanism so that persons with depression can get back on their feet more rapidly.

Drug brand names

• Bupropion • Wellbutrin
• Ketamine • Ketalar
• Memantine • Namenda
• Venlafaxine • Effexor

The serendipitous discovery of medications that can improve mood transformed depression treatment more than 50 years ago.¹ Most antidepressants produced since then could be called “me-too” medications because they all work by affecting the release of monoamines—serotonin, norepinephrine, and dopamine—which, in turn, modulate the activity of neurons that release glutamate.

Weeks may pass before antidepressants’ effect on monoamine-releasing neurons produces a therapeutic benefit, however, leaving many patients impaired or even suicidal. This delayed onset of action might be explained by antidepressants’ indirect blockade of glutamate. The route to more rapid results, therefore, might be to cut out the monoamine middlemen.

Glutamate clues

Glutamate, instead of monoamines, might offer a more direct means to affect mood and could be a new target for antidepressant treatment:²

• Positron-emission tomography of neuron function in depressed patients shows abnormal activity in neurons that release glutamate—so-called glutamate neurons.
• Approximately 60 % of neurons are glutamate neurons, the largest network of neurons in the brain.
• Increased glutamate activity is seen in depressed patients.
• Animal studies have shown that blocking the N-methyl-D-aspartate (NMDA) receptor—1 of 3 types of glutamate receptors—decreases depressive behavior.
• Chronic administration of antidepressant medication reduces the expression of NMDA receptors.

Rapid glutamate blockade

Prompted by evidence that glutamate may be involved in mood disorders, researchers at the National Institute of Mental Health designed a study to determine if blocking the NMDA receptor can produce a rapid antidepressant effect.³ They chose the agent ketamine for this study because of its potent affinity for the NMDA receptor.

Ketamine was developed in the 1960s as a general anaesthetic, and its use in the United States is limited almost exclusively to veterinary medicine. The drug’s propensity to induce perceptual disturbances limits its clinical use but enhances its illicit use.

Eighteen patients with treatment-resistant depression were enrolled in a randomized, placebo-controlled, double-blind, crossover study. After 2 weeks without medication, they received a single infusion of IV ketamine or placebo. One week later they received the alternate intervention. Changes in Hamilton Rating Scale for Depression scores were assessed after each infusion.

Figure Decrease in depressive symptoms with IV ketamine

* = P <0.05

Patients who received ketamine (blue) showed a marked reduction of depressive symptoms within 2 hours compared with those who received placebo (red).

Source: Reference 3Patients receiving ketamine showed a robust and sustained reduction in depressive symptoms compared with placebo within 110 minutes (Figure). “To our knowledge,” the authors wrote, “there has never been a report of any other drug or somatic treatment—such as sleep deprivation, thyrotropin-releasing hormone, antidepressant, dexamethasone, or electroconvulsive therapy—that results in such a dramatic rapid and prolonged response with a single administration.”

Seventy-one percent of patients responded to IV ketamine within 24 hours, which is comparable to reported response rates after 8 weeks with oral antidepressants such as bupropion (62%), selective serotonin reuptake inhibitors (63%), and venlafaxine (65%).^4,5

Caution and caveats

Despite these “dramatic” results, we must be cautious about extrapolating too much from this small study. Glutamate blockers such as ketamine can have serious adverse effects—including psychosis—and patients may not tolerate long-term interventions. Likewise, oral administration of memantine—another NMDA blocker—in a double-blind study did not effectively treat depression.⁶ Finally, subjects in the ketamine trial had chronic, treatment-resistant depression, and the results might not apply to other forms of depression.

The results suggest the possibility of a new option for depression treatment, however. Specifically, this option could expedite response and “jump-start” treatment through a novel mechanism so that persons with depression can get back on their feet more rapidly.

Drug brand names

• Bupropion • Wellbutrin
• Ketamine • Ketalar
• Memantine • Namenda
• Venlafaxine • Effexor

Whenever you feel you are doing more work than the patient and are more invested than he is, something has gone wrong in collaborative care.

With resistant or hostile patients, fight the urge to move quickly into clinical assessment and to prescribe what you think should be worked on and how. Instead, spend more time—especially when building the treatment alliance in the first 15 minutes (Box¹)—exploring their ideas on how, when, and where they feel they can achieve what is most important to them (Table 1²).

Resistant patients may have different agendas, but taking a pragmatic approach can merge their goals with yours.

Box

Table 1

How to merge the reluctant patient’s goals with clinical needs assessment

What does the patient want?

When a patient is difficult to engage, begin by listening for the most important concern that brought him to your office.

He may be depressed, anxious, or tired, but exploring why he decided to seek help now (“My wife said she would leave me if I didn’t get help”) reveals what is most important. The “treatment contract,” then, is helping this patient save his marriage.

Initial engagement

Collaborative treatment begins with a genuinely interested dialogue about what prompted the patient’s visit.

Therapist: “Thank you for choosing to work with me. How may I serve you? What is the most important thing you want me to help you with?”

Mr. L: “I didn’t choose you; they made me come.”

T: “I didn’t see anyone drag you in. What would happen if you had not come today?”

Mr. L: “I might lose my job. I came because my boss told me to.”

Focus on what the patient wants, not just what others have said he or she needs (treatment for substance abuse, angry outbursts, conflict at work). The patient may want to stay out of jail, keep his job or relationship, regain custody of his or her children, obtain housing, or get people to “leave me alone and quit locking me up against my will.” Although the patient’s problem may be obvious to us, he needs “discovery” work, not “recovery” work.

Why has the patient come now? What is his highest priority? Can we help him discover the link between his drinking or anger that affects his work performance?

Therapist: “So you want to get the boss off your back. You want people to leave you alone. You feel people treat you unfairly and want them to stop. But why did you come today and not last week or last month?”

Mr. L: “I came now because yesterday my boss said I could lose my job if I didn’t get some help.”

T: “So what you want most importantly is to keep your job, is that it?”

Mr. L: “Well yeah, but I don’t have a drinking problem or any problem with my temper. They’re just overreacting. It wasn’t as bad as they said.”

T: “OK, I am willing to work on helping you keep your job if that’s what is most important to you. Do you know what you are doing that makes them think you have a drinking or anger problem?

Mr. L: “All I did was come in late a couple of times and got into a little argument with a couple of people.”

T: “If we are going to help you keep your job, we could spend our time talking about how unfair your boss is and how she’s misjudging you. Or we could work to show her that she has you all wrong and that you are a productive worker who does not have a substance or anger problem.

“Let’s think together how we could gather the data that would prove you don’t have a substance problem. If all that data is squeaky clean, then I can write a very supportive letter to your boss and tell her all is well. If, however, we discover you do have a problem, I can still write a very supportive letter. But we’ll have to show her how you are taking care of any problems that interfere with your work performance.”

Reframe the presenting complaint

Few patients present fully ready to work on definitive behavioral health recovery. If patients at least attend sessions or talk with you, they must be motivated to do something. Otherwise, they would not show up.

Our task is help patients such as Mr. L get what they want, not what we think they should want. Eventually you will get to explore the patient’s substance use, impulse or parenting problems, mental health symptoms, or communication problems, but this discussion will be in the service of allying with his or her goals.

Rather than viewing patients as unmotivated or resistant, think of resistance as an interactional process. “If we are going to stop them from locking you up,” you might say, “let’s talk about what you are doing that makes you look like you are dangerous and out of control. And when you were not locked away, let’s think of how you kept ‘them’ off your back.”

Instead of interpreting resistance as pathology, view the behavior as an opportunity to understand and respond to the patient’s stage of readiness to change.

Stages of change

By being “difficult,” patients are often declaring that they are not invested in what you think the problem is or in working on that problem. Resistance thrives when we and the patient have not allied around a common goal and are at different stages of change. Think of the therapeutic alliance in the context of the widely-used and well-researched Transtheoretical Model’s stages of change:^3,4

Precontemplation. A person at this stage is not considering the possibility of change, although others are aware of a problem. He or she will seldom appear for treatment without coercion. The person could benefit from nonthreatening information to raise awareness of a possible “problem” and possibilities for change.

Contemplation. The person is ambivalent, undecided, vacillating about whether he has a “problem.” He wants to change, but this desire exists simultaneously with resistance to change. Motivational strategies can be useful, but aggressive or premature confrontation could provoke strong resistance and defensive behaviors. Many persons at this stage have indefinite plans to take action in the next 6 months or so.

Preparation takes the person from the contemplation stage to specific steps to solve the problem in the action stage. He or she develops increasing confidence in the decision to change and takes the first steps on the road to action. Most people at this stage plan to take action within 1 month and are making final adjustments before beginning to change.

Action. The person takes specific actions intended to bring about change. This busiest stage of change is characterized by overt modification of behavior and surroundings and requires the greatest time and energy. Support and encouragement are crucial to prevent drop-out and regression in readiness to change.

Maintenance. Goals at this stage are to sustain the changes accomplished by previous action and to prevent relapse. Maintaining new behaviors requires different skills than were needed to initiate change. Gains are consolidated. “Maintenance” is not a static stage; it can last 6 months or up to a lifetime. The patient learns new coping and problem-solving strategies, replaces problem behaviors with a healthier life style, and works through emotional triggers of relapse.

Relapse/recycling can happen but is not inevitable. When setbacks occur, help the patient avoid becoming stuck, discouraged, or demoralized, and help him learn from relapse before committing to a new action cycle. Conduct a comprehensive, multidimensional assessment to explore all reasons for relapse.

Termination is the ultimate goal: to exit the cycle of change without fear of relapse. Certain problems may be terminated or merely kept in remission through maintenance strategies.

Match strategies with stages

Discovery planning. Engaging patients in collaborative care starts with honoring their stages of change and working with them and their families on different tasks for each stage of change.^4-6 A patient such as Mr. L, for example—who is at an early stage of change and thinks he has an “unfair boss problem” (not an alcohol problem) or a “nagging wife problem” (not an anger or domestic violence problem)—needs a discovery, drop-out prevention plan.

The cause of the patient’s work or relationship problem may be obvious to you, but a patient in early stages of change resists that information and, if pressed, gets frustrated and leaves treatment. A “discovery” treatment plan embraces the patient’s views and could be focused, for example, on gathering data that would prove to the employer that there is not an alcohol problem.

If random breath alcohol testing, feedback from family, and review of past job losses all prove negative for alcohol problems, the patient would have data to support his or her view that he does not have an alcohol problem. If, however, this exploration reveals an alcohol problem, the patient “discovers” he has more of a problem than he thought. For this plan, the challenge is to keep Mr. L engaged long enough to discover the connection between his alcohol problems and his employment or marital problems.

Recovery planning. On the other hand, a person at the action stage who wants to avoid becoming depressed again or wishes to live a life of sobriety collaborates on a recovery, relapse prevention plan. This patient is committed to developing the knowledge and skills to prevent relapse and open to whatever will promote health and well-being.

The Transtheoretical Model’s 9 processes of change^3,4 inform which interventions might be most effective at various stages of change (Table 2). For example, a patient might be proud of the fact that “I can hold my liquor and drink everyone under the table.” Consciousness-raising—such as by explaining that his high alcohol tolerance is a danger signal, not a beneficial ability—can enhance his change process. Even if he is not ready to commit to definitive change, at least exploring whether he has a problem may move him from precontemplation to a contemplation stage of change. Table 3 shows how other processes of change can help motivate patients in later stages of change.^4,5

Table 2

Transtheoretical model’s 9 processes of change: What happens at each step

Strategies and interventions to motivate patients at each stage of change

• Scott D. Miller, PhD. Institute for the Study of Therapeutic Change, Chicago, IL. (773) 404-5130; www.talkingcure.com.
  
• Miller WR, Rollnick S, Moyers TB. Motivational interviewing: professional training videotape series. Albuquerque, NM: University of New Mexico, 1998. Six videotapes (about $130 total); (505) 768-0279 or 0100.
  
• Miller WR, consensus panel chair. Treatment improvement protocol. Enhancing motivation for change in substance abuse treatment. Rockville, MD; Center for Substance Abuse Treatment, 1999. DHHS Publication 99-3354. Available from the National Clearinghouse for Alcohol/Drug Information, Rockville, MD; (800) 729-6686.
  

Dr. Mee-Lee is a board-certified psychiatrist and is certified by examination of the American Society of Addiction Medicine (ASAM). He is based in Davis, CA, and is involved in full-time training and consulting. For information, visit www.DMLMD.com.

Whenever you feel you are doing more work than the patient and are more invested than he is, something has gone wrong in collaborative care.

With resistant or hostile patients, fight the urge to move quickly into clinical assessment and to prescribe what you think should be worked on and how. Instead, spend more time—especially when building the treatment alliance in the first 15 minutes (Box¹)—exploring their ideas on how, when, and where they feel they can achieve what is most important to them (Table 1²).

Resistant patients may have different agendas, but taking a pragmatic approach can merge their goals with yours.

Box

Table 1

How to merge the reluctant patient’s goals with clinical needs assessment

What does the patient want?

When a patient is difficult to engage, begin by listening for the most important concern that brought him to your office.

He may be depressed, anxious, or tired, but exploring why he decided to seek help now (“My wife said she would leave me if I didn’t get help”) reveals what is most important. The “treatment contract,” then, is helping this patient save his marriage.

Initial engagement

Collaborative treatment begins with a genuinely interested dialogue about what prompted the patient’s visit.

Therapist: “Thank you for choosing to work with me. How may I serve you? What is the most important thing you want me to help you with?”

Mr. L: “I didn’t choose you; they made me come.”

T: “I didn’t see anyone drag you in. What would happen if you had not come today?”

Mr. L: “I might lose my job. I came because my boss told me to.”

Focus on what the patient wants, not just what others have said he or she needs (treatment for substance abuse, angry outbursts, conflict at work). The patient may want to stay out of jail, keep his job or relationship, regain custody of his or her children, obtain housing, or get people to “leave me alone and quit locking me up against my will.” Although the patient’s problem may be obvious to us, he needs “discovery” work, not “recovery” work.

Why has the patient come now? What is his highest priority? Can we help him discover the link between his drinking or anger that affects his work performance?

Therapist: “So you want to get the boss off your back. You want people to leave you alone. You feel people treat you unfairly and want them to stop. But why did you come today and not last week or last month?”

Mr. L: “I came now because yesterday my boss said I could lose my job if I didn’t get some help.”

T: “So what you want most importantly is to keep your job, is that it?”

Mr. L: “Well yeah, but I don’t have a drinking problem or any problem with my temper. They’re just overreacting. It wasn’t as bad as they said.”

T: “OK, I am willing to work on helping you keep your job if that’s what is most important to you. Do you know what you are doing that makes them think you have a drinking or anger problem?

Mr. L: “All I did was come in late a couple of times and got into a little argument with a couple of people.”

T: “If we are going to help you keep your job, we could spend our time talking about how unfair your boss is and how she’s misjudging you. Or we could work to show her that she has you all wrong and that you are a productive worker who does not have a substance or anger problem.

“Let’s think together how we could gather the data that would prove you don’t have a substance problem. If all that data is squeaky clean, then I can write a very supportive letter to your boss and tell her all is well. If, however, we discover you do have a problem, I can still write a very supportive letter. But we’ll have to show her how you are taking care of any problems that interfere with your work performance.”

Reframe the presenting complaint

Few patients present fully ready to work on definitive behavioral health recovery. If patients at least attend sessions or talk with you, they must be motivated to do something. Otherwise, they would not show up.

Our task is help patients such as Mr. L get what they want, not what we think they should want. Eventually you will get to explore the patient’s substance use, impulse or parenting problems, mental health symptoms, or communication problems, but this discussion will be in the service of allying with his or her goals.

Rather than viewing patients as unmotivated or resistant, think of resistance as an interactional process. “If we are going to stop them from locking you up,” you might say, “let’s talk about what you are doing that makes you look like you are dangerous and out of control. And when you were not locked away, let’s think of how you kept ‘them’ off your back.”

Instead of interpreting resistance as pathology, view the behavior as an opportunity to understand and respond to the patient’s stage of readiness to change.

Stages of change

By being “difficult,” patients are often declaring that they are not invested in what you think the problem is or in working on that problem. Resistance thrives when we and the patient have not allied around a common goal and are at different stages of change. Think of the therapeutic alliance in the context of the widely-used and well-researched Transtheoretical Model’s stages of change:^3,4

Precontemplation. A person at this stage is not considering the possibility of change, although others are aware of a problem. He or she will seldom appear for treatment without coercion. The person could benefit from nonthreatening information to raise awareness of a possible “problem” and possibilities for change.

Contemplation. The person is ambivalent, undecided, vacillating about whether he has a “problem.” He wants to change, but this desire exists simultaneously with resistance to change. Motivational strategies can be useful, but aggressive or premature confrontation could provoke strong resistance and defensive behaviors. Many persons at this stage have indefinite plans to take action in the next 6 months or so.

Preparation takes the person from the contemplation stage to specific steps to solve the problem in the action stage. He or she develops increasing confidence in the decision to change and takes the first steps on the road to action. Most people at this stage plan to take action within 1 month and are making final adjustments before beginning to change.

Action. The person takes specific actions intended to bring about change. This busiest stage of change is characterized by overt modification of behavior and surroundings and requires the greatest time and energy. Support and encouragement are crucial to prevent drop-out and regression in readiness to change.

Maintenance. Goals at this stage are to sustain the changes accomplished by previous action and to prevent relapse. Maintaining new behaviors requires different skills than were needed to initiate change. Gains are consolidated. “Maintenance” is not a static stage; it can last 6 months or up to a lifetime. The patient learns new coping and problem-solving strategies, replaces problem behaviors with a healthier life style, and works through emotional triggers of relapse.

Relapse/recycling can happen but is not inevitable. When setbacks occur, help the patient avoid becoming stuck, discouraged, or demoralized, and help him learn from relapse before committing to a new action cycle. Conduct a comprehensive, multidimensional assessment to explore all reasons for relapse.

Termination is the ultimate goal: to exit the cycle of change without fear of relapse. Certain problems may be terminated or merely kept in remission through maintenance strategies.

Match strategies with stages

Discovery planning. Engaging patients in collaborative care starts with honoring their stages of change and working with them and their families on different tasks for each stage of change.^4-6 A patient such as Mr. L, for example—who is at an early stage of change and thinks he has an “unfair boss problem” (not an alcohol problem) or a “nagging wife problem” (not an anger or domestic violence problem)—needs a discovery, drop-out prevention plan.

The cause of the patient’s work or relationship problem may be obvious to you, but a patient in early stages of change resists that information and, if pressed, gets frustrated and leaves treatment. A “discovery” treatment plan embraces the patient’s views and could be focused, for example, on gathering data that would prove to the employer that there is not an alcohol problem.

If random breath alcohol testing, feedback from family, and review of past job losses all prove negative for alcohol problems, the patient would have data to support his or her view that he does not have an alcohol problem. If, however, this exploration reveals an alcohol problem, the patient “discovers” he has more of a problem than he thought. For this plan, the challenge is to keep Mr. L engaged long enough to discover the connection between his alcohol problems and his employment or marital problems.

Recovery planning. On the other hand, a person at the action stage who wants to avoid becoming depressed again or wishes to live a life of sobriety collaborates on a recovery, relapse prevention plan. This patient is committed to developing the knowledge and skills to prevent relapse and open to whatever will promote health and well-being.

The Transtheoretical Model’s 9 processes of change^3,4 inform which interventions might be most effective at various stages of change (Table 2). For example, a patient might be proud of the fact that “I can hold my liquor and drink everyone under the table.” Consciousness-raising—such as by explaining that his high alcohol tolerance is a danger signal, not a beneficial ability—can enhance his change process. Even if he is not ready to commit to definitive change, at least exploring whether he has a problem may move him from precontemplation to a contemplation stage of change. Table 3 shows how other processes of change can help motivate patients in later stages of change.^4,5

Table 2

Transtheoretical model’s 9 processes of change: What happens at each step

Strategies and interventions to motivate patients at each stage of change