Annette M. Matthews, MD

History: From sociable to sullen

Julie, a Hispanic/Native American, was adopted by a Caucasian couple when she was 6 weeks old. Before age 12, she had no psychiatric problems and was medically healthy though slightly overweight.

At age 12, Julie started having episodes of brooding depression, verbal and physical aggression, and impulsive suicidal behavior. She also began suffering intermittent migraines and having trouble falling asleep. She insisted on sleeping with her parents or with a nightlight in her room.

Once a sociable girl who enjoyed being in the middle school chorus and band, Julie suddenly became sullen and defiant. She dropped out of afterschool activities and stopped socializing with peers except for her best friend, Sheila, age 12, and Mark, age 13, an “almost boyfriend” who lived next door.

Julie also started arguing with her mother, often yelling and screaming when approached with minor requests. Sometimes, Julie hit and pushed her. A psychiatrist diagnosed the 12-year-old with major depressive disorder and prescribed fluoxetine, dosage unknown.

Soon after Julie’s symptoms surfaced, her adoptive father, a sales representative, was laid off. He found work in another state; the family left an ethnically diverse city for a predominantly Caucasian rural area. There, Julie completed middle school and her freshman year of high school, and lost contact with Sheila and Mark.

Midway through her freshman year, Julie tried to induce vomiting after eating so that she would lose weight and “fit in better with the other girls.” She stopped this at the end of the school year.

The following fall, 5 weeks into her sophomore year, she dropped out of high school and was ultimately enrolled in home school.

Treatment: 4 hospitalizations in 3 years

Between ages 12 and 15, Julie was hospitalized four times for outbursts of violence with impulsive self-harm. She “overdosed” on eight aceta-minophen/diphenhydramine tablets on one occasion and superficially cut her forearm on another. During these episodes, she said, she heard voices telling her to harm her mother and herself.

During this period, Julie was diagnosed as having schizophrenia, major depressive disorder, attention-deficit/hyperactivity disorder (ADHD), and oppositional defiant disorder (ODD). Numerous antidepressant and mood stabilizer regimens produced no lasting improvement, though her angry and violent episodes became less frequent.

poll here

The authors’ observations

Although Julie’s psychotic symptoms might suggest an evolving disorder such as schizophrenia, no clear pattern supports this diagnosis. Also:

• Onset at age 12 is unusual. Schizophrenia typically begins in late teens to early adulthood.
  
• Julie showed no premorbid personality problems—found in up to one-third of patients with chronic schizophrenia—and no premorbid adjustment difficulties resulting from negative symptoms, cognitive deficits, or poor social function.¹
  

Julie’s angry behaviors and refusal to stay in school suggest ODD, but this disorder generally presents without self-harm or other impulsive behaviors and occurs apart from psychosis or mood disorder episodes.¹ Her low mood, withdrawal from activities, and suicidal actions may suggest major depressive disorder with psychotic features, but this diagnosis does not explain the sudden dramatic transformation in her baseline personality.

Julie’s birth parents’ mental health history would offer crucial information, but this was not available.

Continued history: ‘I left my body’

Shortly after her 15th birthday, Julie broke down and told her parents that 3 years earlier, four boys had gang-raped her while she was “on a first date” with one of them at a school football game. She said one attacker held a knife to her throat, and they threatened to kill her friend Sheila if anyone was told. Julie said she felt so terrorized that “I left my body and watched what was happening.”

After the rape, Julie went home, showered, and went to bed. She said she felt “emotionally numb” for 2 months, during which she threw herself into schoolwork, stopped attending after-school events, and began arguing with her parents. She developed nightmares of the trauma and, eventually, auditory command hallucinations. When stressed, she has “out of body” feelings lasting several minutes.

The parents, though angry at Julie‘s attackers, did not seek legal counsel or report the rape to authorities because they felt too much time had passed. They sought support from a counselor, who referred their daughter to a male psychiatrist for medication management. Julie, now age 16, preferred to be treated by a woman, so her care was transferred to our clinic.

Based on clinical observations, Julie gets along well with her father. She complains that her mother is overprotective yet Julie cannot bear to be separated from her for even a couple hours. She resents her mother’s overinvolvement but relies on it for emotional regulation. Her mother has been treated for major depressive disorder, generalized anxiety disorder, and alcohol dependence. These were in sustained remission when Julie presented to us.

 

At presentation, we diagnosed Julie as having chronic posttraumatic stress disorder (PTSD), recurrent major depressive disorder, and eating disorder not otherwise specified. At 5 feet, 7 inches and 190 pounds, her body mass index is 30 kg/m², indicating clinical obesity. She has been taking duloxetine, 60 mg/d, extended release dextroamphetamine, 20 mg/d, aripiprazole, 20 mg/d, and amitriptyline, 10 mg/d nightly. She also has been taking sumatriptan, 100 mg as needed, for migraines.

poll here

The authors’ observations

After a life-threatening sexual assault, Julie suddenly became irritable and hostile. She could not keep relationships, yet she feared being alone. She impulsively hurt herself, experienced nightmares, and systematically avoided school activities. These behaviors suggest PTSD,¹ which is prevalent among sexual assault victims (Box 1). For 3 years, however, psychiatrists kept missing the diagnosis as Julie kept her shame a secret.

Julie tells us that she re-experiences trauma-related dysphoria when exposed to cues, such as the anniversary of the rape. She endorses avoidance symptoms, including feelings of estrangement from her family and friends. She shuns thoughts, feelings, places, and conversations associated with the trauma, which partly explains her refusal to stay in school. She reports arousal symptoms, including difficulty falling and staying asleep and fears of harm if left alone, even during the day. At night she has rituals for checking windows and doors to ensure they are locked.

Julie’s decision to hide her trauma was understandable given her age and developmental phase. For a teenager trying to separate from her parents and fit in at school, the humiliation was overwhelming. She lacked the cognitive tools to process and describe her experience. She was assaulted while on a date, normally a positive rite of passage. Further, as a young Hispanic/Native American, Julie feared disappointing her Caucasian parents by not fitting in at school.

When a previously well-adjusted teenager presents with sudden-onset behavioral problems, ask about past or recent trauma. Watch for contextual, developmental, and sociocultural factors that may prevent the youth from disclosing embarrassing events.

Also question the diagnosis if several adequate medication trials have failed. Check for comorbidities, lack of adherence, or other circumstances that can hamper response to treatment.

Box 1

Factors that may signal ptsd

American Psychiatric Association (APA) practice guidelines for treating PTSD list several factors to consider if you suspect this diagnosis:⁵

Impulsive and episodic aggression can result from an anticipatory bias that increases readiness for “fight, flight, or freeze.” For Julie, this turned previously comfortable interactions into dissonance and conflict.

Self-injurious and suicidal behaviors often occur when trauma creates stigma, shame, or guilt. Julie felt these emotions while trying to establish herself in a new community and school. Her obesity and ethnic background further set her apart from peers. She also left behind friends who provided emotional support outside the home and helped her differentiate from her mother.

Trauma during early adolescence can impair age-appropriate development, making it difficult to develop a stable self-image, consolidate and integrate the personality, and form relationships. At age 16, poor self-image and maladaptive coping strategies were an enduring pattern in Julie’s life.

Psychiatric comorbidities. Many patients with PTSD develop psychiatric comorbidities that exaggerate symptoms, making the disorder more difficult to detect and treat. Julie’s depression increased her avoidance tendencies and rein-forced her isolation. Difficulty concentrating—misdiagnosed as ADHD—deterred her from engaging in school. Dissociative symptoms related to PTSD impaired her reality testing, diminishing her ability to interact with others.

Treatment: Medication change

We continued extended-release dextroamphetamine, 20 mg/d, as Julie felt the medication helped her focus on her schoolwork. We also:

• weaned her off aripiprazole, which was not helping her symptoms
  
• stopped amitriptyline and duloxetine because of her history of impulsive overdose and to reduce side-effect risk from polypharmacy
  
• titrated fluoxetine to 40 mg/d to treat her ongoing chronic depression and added trazodone, 50 mg/d as needed, to help her sleep
  
• stopped sumatriptan, as the headaches remitted after Julie’s eyes were tested and eyeglasses prescribed.
  

Initially, we managed Julie’s medications while she received psychotherapy from her counselor, but she eventually shifted her entire care to us. We then began seeing her weekly for psychoeducation and supportive therapy.

 

poll here

The authors’ observations

Medication. APA treatment guidelines support using SSRIs to treat all three PTSD symptom clusters—re-experiencing, avoidance, and hyperarousal—as well as coexisting depression. Evidence also supports use of the tricyclics amitriptyline and imipramine and some monoamine oxidase inhibitors (MAOIs).^6-10 Dietary restrictions associated with MAOIs, however, can pose a problem for teenagers.

Benzodiazepines can decrease anxiety and improve sleep, but they can be addictive and their efficacy in treating PTSD has not been established. Alpha-2-adrenergic agonists such as prazosin and clonidine may decrease hyperarousal and trauma-related nightmares.^11,12

Obtain informed parental consent before starting a child or adolescent on an antidepressant. These medications contain a black-box warning that the drug may increase suicide risk in youths.

Psychotherapy. Varying levels of evidence support psychotherapy models in PTSD (Box 2). Julie can benefit from psychoeducation, supportive therapy, psychodynamic psychotherapy, and cautious re-exposure to trauma where possible.

Psychoeducation provided a safe starting point for Julie’s therapy, engaged her parents and select school counselors and teachers, and helped her understand PTSD’s effects. This allowed us to teach stress reduction and coping strategies.

Supportive techniques helped Julie contain painful affects. She could then network with community resources such as AlaTeen and a peer support group via a local Native American mental health program. This approach helped us gain Julie’s trust, and we anticipate more in-depth work with time.

Trauma re-exposure helps some patients but worsens others’ symptoms. For Julie, trauma re-exposure has been minimal because of the many other issues she was facing.

Developing a trusting relationship over time is crucial to successful trauma re-exposure. Re-exposure should be gradual to keep affective arousal moderate. This will minimize dissociation and affective flooding, which can frustrate treatment.

Cognitive-behavioral therapy (CBT) might help Julie understand the automatic thoughts of failure and defeat that flood her when she is stressed. CBT could help her master her feelings and lay a foundation for improved coping.

Psychodynamic psychotherapy may be started later to help Julie verbalize feelings and modulate how she expresses affect. This model could promote her development, improve her self-image, and treat her depression.

Box 2

Follow-up: Back to school

After 2 months under our care, Julie begins to show improvement. Because of her progress and the fact that her parents drive 45 minutes each way to get to our clinic, we reduce visit frequency from weekly to biweekly.

Julie now attends school 2 hours daily, is earning additional credits through home study, and plans to graduate early and attend community college. Her depression has lifted, and she continues to take fluoxetine, 40 mg/d and extended-release dextroamphetamine, 20 mg/d. She still struggles with social isolation, failure to reach age-appropriate developmental milestones, and a poor body image.

Related resources

• American Psychiatric Association. Practice guideline for treating acute stress disorder and posttraumatic stress disorder. www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
  
• National Center for Post-Traumatic Stress Disorder. Information on obtaining Impact of Events Scale and Davidson Trauma Scale. www.ncptsd.va.gov/publications/assessment/adult_self_report.html
  

Drug brand names

• Amitriptyline • Elavil
  
• Aripiprazole • Abilify
  
• Clonidine • Catapres
  
• Dextroamphetamine (extended-release) • Adderall XR
  
• Duloxetine • Cymbalta
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Phenelzine • Nardil
  
• Prazosin • Minipress
  
• Sumatriptan • Imitrex
  
• Trazodone • Desyrel
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

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

Acknowledgements

The authors thank Larry Schwartz, MD, for his help in preparing this article for publication.

History: From sociable to sullen

Julie, a Hispanic/Native American, was adopted by a Caucasian couple when she was 6 weeks old. Before age 12, she had no psychiatric problems and was medically healthy though slightly overweight.

At age 12, Julie started having episodes of brooding depression, verbal and physical aggression, and impulsive suicidal behavior. She also began suffering intermittent migraines and having trouble falling asleep. She insisted on sleeping with her parents or with a nightlight in her room.

Once a sociable girl who enjoyed being in the middle school chorus and band, Julie suddenly became sullen and defiant. She dropped out of afterschool activities and stopped socializing with peers except for her best friend, Sheila, age 12, and Mark, age 13, an “almost boyfriend” who lived next door.

Julie also started arguing with her mother, often yelling and screaming when approached with minor requests. Sometimes, Julie hit and pushed her. A psychiatrist diagnosed the 12-year-old with major depressive disorder and prescribed fluoxetine, dosage unknown.

Soon after Julie’s symptoms surfaced, her adoptive father, a sales representative, was laid off. He found work in another state; the family left an ethnically diverse city for a predominantly Caucasian rural area. There, Julie completed middle school and her freshman year of high school, and lost contact with Sheila and Mark.

Midway through her freshman year, Julie tried to induce vomiting after eating so that she would lose weight and “fit in better with the other girls.” She stopped this at the end of the school year.

The following fall, 5 weeks into her sophomore year, she dropped out of high school and was ultimately enrolled in home school.

Treatment: 4 hospitalizations in 3 years

Between ages 12 and 15, Julie was hospitalized four times for outbursts of violence with impulsive self-harm. She “overdosed” on eight aceta-minophen/diphenhydramine tablets on one occasion and superficially cut her forearm on another. During these episodes, she said, she heard voices telling her to harm her mother and herself.

During this period, Julie was diagnosed as having schizophrenia, major depressive disorder, attention-deficit/hyperactivity disorder (ADHD), and oppositional defiant disorder (ODD). Numerous antidepressant and mood stabilizer regimens produced no lasting improvement, though her angry and violent episodes became less frequent.

poll here

The authors’ observations

Although Julie’s psychotic symptoms might suggest an evolving disorder such as schizophrenia, no clear pattern supports this diagnosis. Also:

• Onset at age 12 is unusual. Schizophrenia typically begins in late teens to early adulthood.
  
• Julie showed no premorbid personality problems—found in up to one-third of patients with chronic schizophrenia—and no premorbid adjustment difficulties resulting from negative symptoms, cognitive deficits, or poor social function.¹
  

Julie’s angry behaviors and refusal to stay in school suggest ODD, but this disorder generally presents without self-harm or other impulsive behaviors and occurs apart from psychosis or mood disorder episodes.¹ Her low mood, withdrawal from activities, and suicidal actions may suggest major depressive disorder with psychotic features, but this diagnosis does not explain the sudden dramatic transformation in her baseline personality.

Julie’s birth parents’ mental health history would offer crucial information, but this was not available.

Continued history: ‘I left my body’

Shortly after her 15th birthday, Julie broke down and told her parents that 3 years earlier, four boys had gang-raped her while she was “on a first date” with one of them at a school football game. She said one attacker held a knife to her throat, and they threatened to kill her friend Sheila if anyone was told. Julie said she felt so terrorized that “I left my body and watched what was happening.”

After the rape, Julie went home, showered, and went to bed. She said she felt “emotionally numb” for 2 months, during which she threw herself into schoolwork, stopped attending after-school events, and began arguing with her parents. She developed nightmares of the trauma and, eventually, auditory command hallucinations. When stressed, she has “out of body” feelings lasting several minutes.

The parents, though angry at Julie‘s attackers, did not seek legal counsel or report the rape to authorities because they felt too much time had passed. They sought support from a counselor, who referred their daughter to a male psychiatrist for medication management. Julie, now age 16, preferred to be treated by a woman, so her care was transferred to our clinic.

Based on clinical observations, Julie gets along well with her father. She complains that her mother is overprotective yet Julie cannot bear to be separated from her for even a couple hours. She resents her mother’s overinvolvement but relies on it for emotional regulation. Her mother has been treated for major depressive disorder, generalized anxiety disorder, and alcohol dependence. These were in sustained remission when Julie presented to us.

 

At presentation, we diagnosed Julie as having chronic posttraumatic stress disorder (PTSD), recurrent major depressive disorder, and eating disorder not otherwise specified. At 5 feet, 7 inches and 190 pounds, her body mass index is 30 kg/m², indicating clinical obesity. She has been taking duloxetine, 60 mg/d, extended release dextroamphetamine, 20 mg/d, aripiprazole, 20 mg/d, and amitriptyline, 10 mg/d nightly. She also has been taking sumatriptan, 100 mg as needed, for migraines.

poll here

The authors’ observations

After a life-threatening sexual assault, Julie suddenly became irritable and hostile. She could not keep relationships, yet she feared being alone. She impulsively hurt herself, experienced nightmares, and systematically avoided school activities. These behaviors suggest PTSD,¹ which is prevalent among sexual assault victims (Box 1). For 3 years, however, psychiatrists kept missing the diagnosis as Julie kept her shame a secret.

Julie tells us that she re-experiences trauma-related dysphoria when exposed to cues, such as the anniversary of the rape. She endorses avoidance symptoms, including feelings of estrangement from her family and friends. She shuns thoughts, feelings, places, and conversations associated with the trauma, which partly explains her refusal to stay in school. She reports arousal symptoms, including difficulty falling and staying asleep and fears of harm if left alone, even during the day. At night she has rituals for checking windows and doors to ensure they are locked.

Julie’s decision to hide her trauma was understandable given her age and developmental phase. For a teenager trying to separate from her parents and fit in at school, the humiliation was overwhelming. She lacked the cognitive tools to process and describe her experience. She was assaulted while on a date, normally a positive rite of passage. Further, as a young Hispanic/Native American, Julie feared disappointing her Caucasian parents by not fitting in at school.

When a previously well-adjusted teenager presents with sudden-onset behavioral problems, ask about past or recent trauma. Watch for contextual, developmental, and sociocultural factors that may prevent the youth from disclosing embarrassing events.

Also question the diagnosis if several adequate medication trials have failed. Check for comorbidities, lack of adherence, or other circumstances that can hamper response to treatment.

Box 1

Factors that may signal ptsd

American Psychiatric Association (APA) practice guidelines for treating PTSD list several factors to consider if you suspect this diagnosis:⁵

Impulsive and episodic aggression can result from an anticipatory bias that increases readiness for “fight, flight, or freeze.” For Julie, this turned previously comfortable interactions into dissonance and conflict.

Self-injurious and suicidal behaviors often occur when trauma creates stigma, shame, or guilt. Julie felt these emotions while trying to establish herself in a new community and school. Her obesity and ethnic background further set her apart from peers. She also left behind friends who provided emotional support outside the home and helped her differentiate from her mother.

Trauma during early adolescence can impair age-appropriate development, making it difficult to develop a stable self-image, consolidate and integrate the personality, and form relationships. At age 16, poor self-image and maladaptive coping strategies were an enduring pattern in Julie’s life.

Psychiatric comorbidities. Many patients with PTSD develop psychiatric comorbidities that exaggerate symptoms, making the disorder more difficult to detect and treat. Julie’s depression increased her avoidance tendencies and rein-forced her isolation. Difficulty concentrating—misdiagnosed as ADHD—deterred her from engaging in school. Dissociative symptoms related to PTSD impaired her reality testing, diminishing her ability to interact with others.

Treatment: Medication change

We continued extended-release dextroamphetamine, 20 mg/d, as Julie felt the medication helped her focus on her schoolwork. We also:

• weaned her off aripiprazole, which was not helping her symptoms
  
• stopped amitriptyline and duloxetine because of her history of impulsive overdose and to reduce side-effect risk from polypharmacy
  
• titrated fluoxetine to 40 mg/d to treat her ongoing chronic depression and added trazodone, 50 mg/d as needed, to help her sleep
  
• stopped sumatriptan, as the headaches remitted after Julie’s eyes were tested and eyeglasses prescribed.
  

Initially, we managed Julie’s medications while she received psychotherapy from her counselor, but she eventually shifted her entire care to us. We then began seeing her weekly for psychoeducation and supportive therapy.

 

poll here

The authors’ observations

Medication. APA treatment guidelines support using SSRIs to treat all three PTSD symptom clusters—re-experiencing, avoidance, and hyperarousal—as well as coexisting depression. Evidence also supports use of the tricyclics amitriptyline and imipramine and some monoamine oxidase inhibitors (MAOIs).^6-10 Dietary restrictions associated with MAOIs, however, can pose a problem for teenagers.

Benzodiazepines can decrease anxiety and improve sleep, but they can be addictive and their efficacy in treating PTSD has not been established. Alpha-2-adrenergic agonists such as prazosin and clonidine may decrease hyperarousal and trauma-related nightmares.^11,12

Obtain informed parental consent before starting a child or adolescent on an antidepressant. These medications contain a black-box warning that the drug may increase suicide risk in youths.

Psychotherapy. Varying levels of evidence support psychotherapy models in PTSD (Box 2). Julie can benefit from psychoeducation, supportive therapy, psychodynamic psychotherapy, and cautious re-exposure to trauma where possible.

Psychoeducation provided a safe starting point for Julie’s therapy, engaged her parents and select school counselors and teachers, and helped her understand PTSD’s effects. This allowed us to teach stress reduction and coping strategies.

Supportive techniques helped Julie contain painful affects. She could then network with community resources such as AlaTeen and a peer support group via a local Native American mental health program. This approach helped us gain Julie’s trust, and we anticipate more in-depth work with time.

Trauma re-exposure helps some patients but worsens others’ symptoms. For Julie, trauma re-exposure has been minimal because of the many other issues she was facing.

Developing a trusting relationship over time is crucial to successful trauma re-exposure. Re-exposure should be gradual to keep affective arousal moderate. This will minimize dissociation and affective flooding, which can frustrate treatment.

Cognitive-behavioral therapy (CBT) might help Julie understand the automatic thoughts of failure and defeat that flood her when she is stressed. CBT could help her master her feelings and lay a foundation for improved coping.

Psychodynamic psychotherapy may be started later to help Julie verbalize feelings and modulate how she expresses affect. This model could promote her development, improve her self-image, and treat her depression.

Box 2

Follow-up: Back to school

After 2 months under our care, Julie begins to show improvement. Because of her progress and the fact that her parents drive 45 minutes each way to get to our clinic, we reduce visit frequency from weekly to biweekly.

Julie now attends school 2 hours daily, is earning additional credits through home study, and plans to graduate early and attend community college. Her depression has lifted, and she continues to take fluoxetine, 40 mg/d and extended-release dextroamphetamine, 20 mg/d. She still struggles with social isolation, failure to reach age-appropriate developmental milestones, and a poor body image.

Related resources

• American Psychiatric Association. Practice guideline for treating acute stress disorder and posttraumatic stress disorder. www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
  
• National Center for Post-Traumatic Stress Disorder. Information on obtaining Impact of Events Scale and Davidson Trauma Scale. www.ncptsd.va.gov/publications/assessment/adult_self_report.html
  

Drug brand names

• Amitriptyline • Elavil
  
• Aripiprazole • Abilify
  
• Clonidine • Catapres
  
• Dextroamphetamine (extended-release) • Adderall XR
  
• Duloxetine • Cymbalta
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Phenelzine • Nardil
  
• Prazosin • Minipress
  
• Sumatriptan • Imitrex
  
• Trazodone • Desyrel
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

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

Acknowledgements

The authors thank Larry Schwartz, MD, for his help in preparing this article for publication.

History: From sociable to sullen

Julie, a Hispanic/Native American, was adopted by a Caucasian couple when she was 6 weeks old. Before age 12, she had no psychiatric problems and was medically healthy though slightly overweight.

At age 12, Julie started having episodes of brooding depression, verbal and physical aggression, and impulsive suicidal behavior. She also began suffering intermittent migraines and having trouble falling asleep. She insisted on sleeping with her parents or with a nightlight in her room.

Once a sociable girl who enjoyed being in the middle school chorus and band, Julie suddenly became sullen and defiant. She dropped out of afterschool activities and stopped socializing with peers except for her best friend, Sheila, age 12, and Mark, age 13, an “almost boyfriend” who lived next door.

Julie also started arguing with her mother, often yelling and screaming when approached with minor requests. Sometimes, Julie hit and pushed her. A psychiatrist diagnosed the 12-year-old with major depressive disorder and prescribed fluoxetine, dosage unknown.

Soon after Julie’s symptoms surfaced, her adoptive father, a sales representative, was laid off. He found work in another state; the family left an ethnically diverse city for a predominantly Caucasian rural area. There, Julie completed middle school and her freshman year of high school, and lost contact with Sheila and Mark.

Midway through her freshman year, Julie tried to induce vomiting after eating so that she would lose weight and “fit in better with the other girls.” She stopped this at the end of the school year.

The following fall, 5 weeks into her sophomore year, she dropped out of high school and was ultimately enrolled in home school.

Treatment: 4 hospitalizations in 3 years

Between ages 12 and 15, Julie was hospitalized four times for outbursts of violence with impulsive self-harm. She “overdosed” on eight aceta-minophen/diphenhydramine tablets on one occasion and superficially cut her forearm on another. During these episodes, she said, she heard voices telling her to harm her mother and herself.

During this period, Julie was diagnosed as having schizophrenia, major depressive disorder, attention-deficit/hyperactivity disorder (ADHD), and oppositional defiant disorder (ODD). Numerous antidepressant and mood stabilizer regimens produced no lasting improvement, though her angry and violent episodes became less frequent.

poll here

The authors’ observations

Although Julie’s psychotic symptoms might suggest an evolving disorder such as schizophrenia, no clear pattern supports this diagnosis. Also:

• Onset at age 12 is unusual. Schizophrenia typically begins in late teens to early adulthood.
  
• Julie showed no premorbid personality problems—found in up to one-third of patients with chronic schizophrenia—and no premorbid adjustment difficulties resulting from negative symptoms, cognitive deficits, or poor social function.¹
  

Julie’s angry behaviors and refusal to stay in school suggest ODD, but this disorder generally presents without self-harm or other impulsive behaviors and occurs apart from psychosis or mood disorder episodes.¹ Her low mood, withdrawal from activities, and suicidal actions may suggest major depressive disorder with psychotic features, but this diagnosis does not explain the sudden dramatic transformation in her baseline personality.

Julie’s birth parents’ mental health history would offer crucial information, but this was not available.

Continued history: ‘I left my body’

Shortly after her 15th birthday, Julie broke down and told her parents that 3 years earlier, four boys had gang-raped her while she was “on a first date” with one of them at a school football game. She said one attacker held a knife to her throat, and they threatened to kill her friend Sheila if anyone was told. Julie said she felt so terrorized that “I left my body and watched what was happening.”

After the rape, Julie went home, showered, and went to bed. She said she felt “emotionally numb” for 2 months, during which she threw herself into schoolwork, stopped attending after-school events, and began arguing with her parents. She developed nightmares of the trauma and, eventually, auditory command hallucinations. When stressed, she has “out of body” feelings lasting several minutes.

The parents, though angry at Julie‘s attackers, did not seek legal counsel or report the rape to authorities because they felt too much time had passed. They sought support from a counselor, who referred their daughter to a male psychiatrist for medication management. Julie, now age 16, preferred to be treated by a woman, so her care was transferred to our clinic.

Based on clinical observations, Julie gets along well with her father. She complains that her mother is overprotective yet Julie cannot bear to be separated from her for even a couple hours. She resents her mother’s overinvolvement but relies on it for emotional regulation. Her mother has been treated for major depressive disorder, generalized anxiety disorder, and alcohol dependence. These were in sustained remission when Julie presented to us.

 

At presentation, we diagnosed Julie as having chronic posttraumatic stress disorder (PTSD), recurrent major depressive disorder, and eating disorder not otherwise specified. At 5 feet, 7 inches and 190 pounds, her body mass index is 30 kg/m², indicating clinical obesity. She has been taking duloxetine, 60 mg/d, extended release dextroamphetamine, 20 mg/d, aripiprazole, 20 mg/d, and amitriptyline, 10 mg/d nightly. She also has been taking sumatriptan, 100 mg as needed, for migraines.

poll here

The authors’ observations

After a life-threatening sexual assault, Julie suddenly became irritable and hostile. She could not keep relationships, yet she feared being alone. She impulsively hurt herself, experienced nightmares, and systematically avoided school activities. These behaviors suggest PTSD,¹ which is prevalent among sexual assault victims (Box 1). For 3 years, however, psychiatrists kept missing the diagnosis as Julie kept her shame a secret.

Julie tells us that she re-experiences trauma-related dysphoria when exposed to cues, such as the anniversary of the rape. She endorses avoidance symptoms, including feelings of estrangement from her family and friends. She shuns thoughts, feelings, places, and conversations associated with the trauma, which partly explains her refusal to stay in school. She reports arousal symptoms, including difficulty falling and staying asleep and fears of harm if left alone, even during the day. At night she has rituals for checking windows and doors to ensure they are locked.

Julie’s decision to hide her trauma was understandable given her age and developmental phase. For a teenager trying to separate from her parents and fit in at school, the humiliation was overwhelming. She lacked the cognitive tools to process and describe her experience. She was assaulted while on a date, normally a positive rite of passage. Further, as a young Hispanic/Native American, Julie feared disappointing her Caucasian parents by not fitting in at school.

When a previously well-adjusted teenager presents with sudden-onset behavioral problems, ask about past or recent trauma. Watch for contextual, developmental, and sociocultural factors that may prevent the youth from disclosing embarrassing events.

Also question the diagnosis if several adequate medication trials have failed. Check for comorbidities, lack of adherence, or other circumstances that can hamper response to treatment.

Box 1

Factors that may signal ptsd

American Psychiatric Association (APA) practice guidelines for treating PTSD list several factors to consider if you suspect this diagnosis:⁵

Impulsive and episodic aggression can result from an anticipatory bias that increases readiness for “fight, flight, or freeze.” For Julie, this turned previously comfortable interactions into dissonance and conflict.

Self-injurious and suicidal behaviors often occur when trauma creates stigma, shame, or guilt. Julie felt these emotions while trying to establish herself in a new community and school. Her obesity and ethnic background further set her apart from peers. She also left behind friends who provided emotional support outside the home and helped her differentiate from her mother.

Trauma during early adolescence can impair age-appropriate development, making it difficult to develop a stable self-image, consolidate and integrate the personality, and form relationships. At age 16, poor self-image and maladaptive coping strategies were an enduring pattern in Julie’s life.

Psychiatric comorbidities. Many patients with PTSD develop psychiatric comorbidities that exaggerate symptoms, making the disorder more difficult to detect and treat. Julie’s depression increased her avoidance tendencies and rein-forced her isolation. Difficulty concentrating—misdiagnosed as ADHD—deterred her from engaging in school. Dissociative symptoms related to PTSD impaired her reality testing, diminishing her ability to interact with others.

Treatment: Medication change

We continued extended-release dextroamphetamine, 20 mg/d, as Julie felt the medication helped her focus on her schoolwork. We also:

• weaned her off aripiprazole, which was not helping her symptoms
  
• stopped amitriptyline and duloxetine because of her history of impulsive overdose and to reduce side-effect risk from polypharmacy
  
• titrated fluoxetine to 40 mg/d to treat her ongoing chronic depression and added trazodone, 50 mg/d as needed, to help her sleep
  
• stopped sumatriptan, as the headaches remitted after Julie’s eyes were tested and eyeglasses prescribed.
  

Initially, we managed Julie’s medications while she received psychotherapy from her counselor, but she eventually shifted her entire care to us. We then began seeing her weekly for psychoeducation and supportive therapy.

 

poll here

The authors’ observations

Medication. APA treatment guidelines support using SSRIs to treat all three PTSD symptom clusters—re-experiencing, avoidance, and hyperarousal—as well as coexisting depression. Evidence also supports use of the tricyclics amitriptyline and imipramine and some monoamine oxidase inhibitors (MAOIs).^6-10 Dietary restrictions associated with MAOIs, however, can pose a problem for teenagers.

Benzodiazepines can decrease anxiety and improve sleep, but they can be addictive and their efficacy in treating PTSD has not been established. Alpha-2-adrenergic agonists such as prazosin and clonidine may decrease hyperarousal and trauma-related nightmares.^11,12

Obtain informed parental consent before starting a child or adolescent on an antidepressant. These medications contain a black-box warning that the drug may increase suicide risk in youths.

Psychotherapy. Varying levels of evidence support psychotherapy models in PTSD (Box 2). Julie can benefit from psychoeducation, supportive therapy, psychodynamic psychotherapy, and cautious re-exposure to trauma where possible.

Psychoeducation provided a safe starting point for Julie’s therapy, engaged her parents and select school counselors and teachers, and helped her understand PTSD’s effects. This allowed us to teach stress reduction and coping strategies.

Supportive techniques helped Julie contain painful affects. She could then network with community resources such as AlaTeen and a peer support group via a local Native American mental health program. This approach helped us gain Julie’s trust, and we anticipate more in-depth work with time.

Trauma re-exposure helps some patients but worsens others’ symptoms. For Julie, trauma re-exposure has been minimal because of the many other issues she was facing.

Developing a trusting relationship over time is crucial to successful trauma re-exposure. Re-exposure should be gradual to keep affective arousal moderate. This will minimize dissociation and affective flooding, which can frustrate treatment.

Cognitive-behavioral therapy (CBT) might help Julie understand the automatic thoughts of failure and defeat that flood her when she is stressed. CBT could help her master her feelings and lay a foundation for improved coping.

Psychodynamic psychotherapy may be started later to help Julie verbalize feelings and modulate how she expresses affect. This model could promote her development, improve her self-image, and treat her depression.

Box 2

Follow-up: Back to school

After 2 months under our care, Julie begins to show improvement. Because of her progress and the fact that her parents drive 45 minutes each way to get to our clinic, we reduce visit frequency from weekly to biweekly.

Julie now attends school 2 hours daily, is earning additional credits through home study, and plans to graduate early and attend community college. Her depression has lifted, and she continues to take fluoxetine, 40 mg/d and extended-release dextroamphetamine, 20 mg/d. She still struggles with social isolation, failure to reach age-appropriate developmental milestones, and a poor body image.

Related resources

• American Psychiatric Association. Practice guideline for treating acute stress disorder and posttraumatic stress disorder. www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
  
• National Center for Post-Traumatic Stress Disorder. Information on obtaining Impact of Events Scale and Davidson Trauma Scale. www.ncptsd.va.gov/publications/assessment/adult_self_report.html
  

Drug brand names

• Amitriptyline • Elavil
  
• Aripiprazole • Abilify
  
• Clonidine • Catapres
  
• Dextroamphetamine (extended-release) • Adderall XR
  
• Duloxetine • Cymbalta
  
• Fluoxetine • Prozac
  
• Imipramine • Tofranil
  
• Phenelzine • Nardil
  
• Prazosin • Minipress
  
• Sumatriptan • Imitrex
  
• Trazodone • Desyrel
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

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

Acknowledgements

The authors thank Larry Schwartz, MD, for his help in preparing this article for publication.

HISTORY: TIRED OF LIVING

Mr. F, age 43, presents to the emergency room with complications of type 2 diabetes mellitus: blurry vision, increased urination, fatigue, and polydipsia. Blood glucose is 676 mg/dL.

The patient flees during treatment—possibly to attempt suicide—but returns 36 hours later, noticeably disoriented. He is readmitted to the ER, where he tells staff he is considering suicide and plans to self-inject a lethal substance. The ER staff refers him to the psychiatry service.

Mr. F also complains of shortness of breath after minimal exertion, aching joints throughout his body, and intense pain in his right great toe. He has been sleeping 12 to 20 hours daily, yet has trouble sleeping at night. He persistently feels fatigued, hopeless, and helpless. He says his suicidal urges have become more intense over 2 months, but he fears he will lose his computer repair job if he is admitted. He also shows difficulties with short-term memory. We admit him for observation.

Mental status examination suggests that Mr. F is generally withdrawn. Eye contact is poor and he is quiet and evasive, possibly signaling paranoia. He spends most of his stay watching television. His thought process is linear, and he thinks constantly of suicide. During the Mini-Mental State Examination, he gives the incorrect date and county. He misses two other items on recall but gets them correct with prompts.

A mild intention tremor distorts his handwriting. He has trouble keeping his balance during the Romberg test, and his gait is mildly ataxic. Ophthalmology consult suggests that diabetic retinopathy and optic disc cupping secondary to glaucoma may be blurring his vision.

Mr. F is taking no medications but had previously used insulin twice a day, and his outpatient doctor insists he should go back on insulin. He smokes 1 pack of cigarettes per day, drinks alcohol moderately (one to two drinks/day), and does not abuse illicit drugs.

The authors’ observations

Mr. F’s depressed mood, hopelessness, concentration problems, psychomotor retardation, and suicidal thoughts suggest major depressive disorder. Depression or a delirium secondary to diabetes may account for his referential ideas.

FURTHER HISTORY: ONE SHOT AT SATISFACTION

Over the following week, Mr. F becomes more talkative as the psychiatry staff develops a therapeutic rapport. He tells his treatment team that he feels urges to self-inject liquids he finds in his hospital room, such as shower gel and beverages.

Mr. F tells us that approximately 2 years ago, he tried to kill himself by swallowing boric acid. After 6 weeks in intensive care, the poison’s physical effects resolved and he no longer appeared suicidal. The staff at that time prepared to discharge Mr. F when, while left alone in his room, he dislodged a wall-mounted sphygmomanometer, disassembled it, and broke open the mercury tube. He then injected about 3 mL of mercury into his intravenous port and swallowed another 3 mL.

A nurse who checked on Mr. F minutes after the incident did not notice the sphygmomanometer was missing. He showed the broken device to the nurse, saying, “Look what I did.” When the nurse asked why, he responded, “I was just sitting here alone and saw the thing on the wall. I thought to myself, I can do this.”

The hospital viewed the episode as another suicide attempt. Staff immediately began chelation therapy with dimercaprol, 10 mg/kg every 8 hours for 5 days, then 10 mg/kg every 12 hours for 2 weeks. Within 24 hours of ingesting mercury, Mr. F developed shortness of breath, tachycardia (104 BPM), a fever (101.8°F), and had GI complaints. Increased blood urea nitrogen, increased creatinine, and decreased urination suggested declining renal function. He developed a pruritic rash over his back and mild skin loss on his soles.

Mr. F’s mercury levels were 20.8 mg/dL (serum) and 216 mg/dL (urine) 36 hours after ingestation, and 24.8 mg/dL (serum) and 397 mg/dL (urine) after chelation. Serum mercury >5 mg/dL is usually symptomatic.

Approximately 72 hours after the incident, most pulmonary, renal, and dermal manifestations of mercury toxicity began to improve. Mr. F was discharged after 21 days. He was diagnosed with major depression and started on sertraline, 150 mg/d.

‘The best feeling.’ Two years later, Mr. F tells us he has attempted suicide at least six times. Diffuse metallic foreign bodies throughout his lung vasculature and a 9.6 mg/dL serum mercury reading confirm he has injected mercury. His painful toe is x-rayed to check for mercury deposits, but he ultimately is diagnosed with gout.

During our evaluation, Mr. F admits that “the calmest, best feeling I have ever had” was while injecting mercury, yet he fears the incident has caused permanent physical and mental damage. He describes his desire to self-inject liquids as “impulses” triggered by twice-daily subcutaneous insulin use. For this reason, he has stopped taking insulin against his doctor’s advice.

 

The authors’ observations

Mr. F’s mental status changes and serum mercury suggest mercury poisoning. He shows numerous heavy-metal poisoning symptoms (Box 1) as well as erethism, a malaise that can result from heavy-metal exposure.²

The patient insists that insulin shots bring on self-injection urges, but his impulsive and repetitive suicidal behavior, dysphoria, and transient paranoia suggest borderline personality disorder. His impulses may reflect a subtle, long-term personality change caused by mercury’s neurotoxic effects.¹ Or they could be akin to cutting behaviors shown by some patients with personality disorders, particularly borderline personality disorder.

We ruled out substance abuse disorder, as Mr. F’s mercury ingestion was not premeditated, he has no history of illicit drug use, and intravenous elemental mercury is not psychoactive.

Box 1

An ever-present threat. Mercury exists in many organic, inorganic, and elemental forms—all toxic.

Elemental mercury found in thermometers, lamps, and dental amalgams slowly ionizes in the blood stream before crossing the blood-brain barrier. Mercury and carbon form toxic “organic” compounds, including methylmercury (found in the environment), phenylmercury (used in some commercial products), and dimethylmercury (found in solid waste sites).

Because mercury’s half-life is 60 days, it dissipates slowly, can accumulate with chronic exposure, and stays in the blood stream long after high-dose exposure.³

Serum mercury >5 mg/dL can cause subtle, enduring neurotoxic effects, including tremor, dizziness, shortness of breath, blurry vision, decreased visual fields, depression, memory loss, and irritability.³ Serum mercury rarely exceeds 1.5 mg/dL without direct exposure.

Irritability, depressive symptoms, and renal manifestations emerge when urine mercury reaches 200 to 1,000 mg/dL. Renal, respiratory, and GI effects are seen at 1,000 to 2,000 mg/dL.

Means of exposure. Vapor inhalation is the most common means of elemental mercury exposure.³ Elemental mercury used in manufacturing vaporizes at room temperature.

Orally ingested elemental mercury is poorly absorbed from the GI tract, mostly passes unabsorbed, and is toxic only at high doses. Injected elemental mercury is poorly absorbed but can cause mechanical and immunologic effects. The psychiatric literature describes some 200 cases of mercury self-injection^4-8 but offers little information on cognitive effects or long-term follow-up.

Consider heavy-metal poisoning in the differential diagnosis of patients with depressive symptoms. Ask about risk factors for environmental mercury exposure, including use of folk medicines, some cosmetics, over-the-counter nasal sprays, ophthalmic solutions, skin-lightening creams, daily fish consumption (particularly tuna or swordfish), living in a house painted with latex paint, or continuous exposure at work (Box 2).

Also ask if the patient or a household member recently ingested mercury or handled a broken thermometer. Liquid mercury on clothing and in bodily fluids may cause secondary contamination, whereas mercury vapor cannot.

Order serum mercury testing if you suspect chronic exposure. Refer patients with serum mercury ≥ 1.5 mg/dL to their primary care physicians and to a poison control center for evaluation and possible chelation. Refer patients with acute mercury exposure symptoms to the ER.

Box 2

The authors’ observations

Antidepressants generally will not reduce depression, irritability, personality changes, or apathy secondary to mercury poisoning. We have found that a psychostimulant such as methylphenidate, starting at 10 mg bid and titrating to therapeutic effect, can help treat mercury-related apathy.

 

We did not give Mr. F a psychostimulant, however, fearing it would worsen his impulsive behavior and disordered sleep. Also, more effectively managing Mr. F’s diabetes should improve his depression.

DISCHARGE: CHELATION CHALLENGE

Mr. F’s suicidal thoughts continued intermittently. Chelation was tried again with succimer, 1,000 mg tid for 5 days and bid for 5 more days, but the agent caused severe nausea without significantly decreasing serum mercury. He declined outpatient chelation.

After 2 weeks, Mr. F denied suicidal thoughts and said he felt physically better. He was discharged on venlafaxine, 300 mg/d, for his depressive symptoms; and metformin, 1,000 mg/d, glipizide, 10 mg bid, and rosiglitazone, 4 mg/d, to control his blood glucose. We arranged for medication management at a community mental health center. Mr. F was also told to visit the hospital’s outpatient clinic for endocrine follow-up but has not returned for 18 months.

Related resources

• Agency for Toxic Substances and Disease Registry. Information about toxic substances in the environment and diseases they may cause. www.atsdr.cdc.gov.
  

Drug brand names

• Dimercaprol • BAL in Oil
  
• Glipizide • Glucotrol
  
• Metformin • Glucophage
  
• Methylphenidate • Ritalin, Concerta
  
• Rosiglitazone • Avandia
  
• Sertraline • Zoloft
  
• Succimer • Chemet
  
• Venlafaxine • Effexor
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from GlaxoSmithKline, Hoffman LaRoche, and AstraZeneca Pharmaceuticals. He is a speaker for Abbott Laboratories, AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., GlaxoSmithKline, and Janssen Pharmaceuticals.

HISTORY: TIRED OF LIVING

Mr. F, age 43, presents to the emergency room with complications of type 2 diabetes mellitus: blurry vision, increased urination, fatigue, and polydipsia. Blood glucose is 676 mg/dL.

The patient flees during treatment—possibly to attempt suicide—but returns 36 hours later, noticeably disoriented. He is readmitted to the ER, where he tells staff he is considering suicide and plans to self-inject a lethal substance. The ER staff refers him to the psychiatry service.

Mr. F also complains of shortness of breath after minimal exertion, aching joints throughout his body, and intense pain in his right great toe. He has been sleeping 12 to 20 hours daily, yet has trouble sleeping at night. He persistently feels fatigued, hopeless, and helpless. He says his suicidal urges have become more intense over 2 months, but he fears he will lose his computer repair job if he is admitted. He also shows difficulties with short-term memory. We admit him for observation.

Mental status examination suggests that Mr. F is generally withdrawn. Eye contact is poor and he is quiet and evasive, possibly signaling paranoia. He spends most of his stay watching television. His thought process is linear, and he thinks constantly of suicide. During the Mini-Mental State Examination, he gives the incorrect date and county. He misses two other items on recall but gets them correct with prompts.

A mild intention tremor distorts his handwriting. He has trouble keeping his balance during the Romberg test, and his gait is mildly ataxic. Ophthalmology consult suggests that diabetic retinopathy and optic disc cupping secondary to glaucoma may be blurring his vision.

Mr. F is taking no medications but had previously used insulin twice a day, and his outpatient doctor insists he should go back on insulin. He smokes 1 pack of cigarettes per day, drinks alcohol moderately (one to two drinks/day), and does not abuse illicit drugs.

The authors’ observations

Mr. F’s depressed mood, hopelessness, concentration problems, psychomotor retardation, and suicidal thoughts suggest major depressive disorder. Depression or a delirium secondary to diabetes may account for his referential ideas.

FURTHER HISTORY: ONE SHOT AT SATISFACTION

Over the following week, Mr. F becomes more talkative as the psychiatry staff develops a therapeutic rapport. He tells his treatment team that he feels urges to self-inject liquids he finds in his hospital room, such as shower gel and beverages.

Mr. F tells us that approximately 2 years ago, he tried to kill himself by swallowing boric acid. After 6 weeks in intensive care, the poison’s physical effects resolved and he no longer appeared suicidal. The staff at that time prepared to discharge Mr. F when, while left alone in his room, he dislodged a wall-mounted sphygmomanometer, disassembled it, and broke open the mercury tube. He then injected about 3 mL of mercury into his intravenous port and swallowed another 3 mL.

A nurse who checked on Mr. F minutes after the incident did not notice the sphygmomanometer was missing. He showed the broken device to the nurse, saying, “Look what I did.” When the nurse asked why, he responded, “I was just sitting here alone and saw the thing on the wall. I thought to myself, I can do this.”

The hospital viewed the episode as another suicide attempt. Staff immediately began chelation therapy with dimercaprol, 10 mg/kg every 8 hours for 5 days, then 10 mg/kg every 12 hours for 2 weeks. Within 24 hours of ingesting mercury, Mr. F developed shortness of breath, tachycardia (104 BPM), a fever (101.8°F), and had GI complaints. Increased blood urea nitrogen, increased creatinine, and decreased urination suggested declining renal function. He developed a pruritic rash over his back and mild skin loss on his soles.

Mr. F’s mercury levels were 20.8 mg/dL (serum) and 216 mg/dL (urine) 36 hours after ingestation, and 24.8 mg/dL (serum) and 397 mg/dL (urine) after chelation. Serum mercury >5 mg/dL is usually symptomatic.

Approximately 72 hours after the incident, most pulmonary, renal, and dermal manifestations of mercury toxicity began to improve. Mr. F was discharged after 21 days. He was diagnosed with major depression and started on sertraline, 150 mg/d.

‘The best feeling.’ Two years later, Mr. F tells us he has attempted suicide at least six times. Diffuse metallic foreign bodies throughout his lung vasculature and a 9.6 mg/dL serum mercury reading confirm he has injected mercury. His painful toe is x-rayed to check for mercury deposits, but he ultimately is diagnosed with gout.

During our evaluation, Mr. F admits that “the calmest, best feeling I have ever had” was while injecting mercury, yet he fears the incident has caused permanent physical and mental damage. He describes his desire to self-inject liquids as “impulses” triggered by twice-daily subcutaneous insulin use. For this reason, he has stopped taking insulin against his doctor’s advice.

 

The authors’ observations

Mr. F’s mental status changes and serum mercury suggest mercury poisoning. He shows numerous heavy-metal poisoning symptoms (Box 1) as well as erethism, a malaise that can result from heavy-metal exposure.²

The patient insists that insulin shots bring on self-injection urges, but his impulsive and repetitive suicidal behavior, dysphoria, and transient paranoia suggest borderline personality disorder. His impulses may reflect a subtle, long-term personality change caused by mercury’s neurotoxic effects.¹ Or they could be akin to cutting behaviors shown by some patients with personality disorders, particularly borderline personality disorder.

We ruled out substance abuse disorder, as Mr. F’s mercury ingestion was not premeditated, he has no history of illicit drug use, and intravenous elemental mercury is not psychoactive.

Box 1

An ever-present threat. Mercury exists in many organic, inorganic, and elemental forms—all toxic.

Elemental mercury found in thermometers, lamps, and dental amalgams slowly ionizes in the blood stream before crossing the blood-brain barrier. Mercury and carbon form toxic “organic” compounds, including methylmercury (found in the environment), phenylmercury (used in some commercial products), and dimethylmercury (found in solid waste sites).

Because mercury’s half-life is 60 days, it dissipates slowly, can accumulate with chronic exposure, and stays in the blood stream long after high-dose exposure.³

Serum mercury >5 mg/dL can cause subtle, enduring neurotoxic effects, including tremor, dizziness, shortness of breath, blurry vision, decreased visual fields, depression, memory loss, and irritability.³ Serum mercury rarely exceeds 1.5 mg/dL without direct exposure.

Irritability, depressive symptoms, and renal manifestations emerge when urine mercury reaches 200 to 1,000 mg/dL. Renal, respiratory, and GI effects are seen at 1,000 to 2,000 mg/dL.

Means of exposure. Vapor inhalation is the most common means of elemental mercury exposure.³ Elemental mercury used in manufacturing vaporizes at room temperature.

Orally ingested elemental mercury is poorly absorbed from the GI tract, mostly passes unabsorbed, and is toxic only at high doses. Injected elemental mercury is poorly absorbed but can cause mechanical and immunologic effects. The psychiatric literature describes some 200 cases of mercury self-injection^4-8 but offers little information on cognitive effects or long-term follow-up.

Consider heavy-metal poisoning in the differential diagnosis of patients with depressive symptoms. Ask about risk factors for environmental mercury exposure, including use of folk medicines, some cosmetics, over-the-counter nasal sprays, ophthalmic solutions, skin-lightening creams, daily fish consumption (particularly tuna or swordfish), living in a house painted with latex paint, or continuous exposure at work (Box 2).

Also ask if the patient or a household member recently ingested mercury or handled a broken thermometer. Liquid mercury on clothing and in bodily fluids may cause secondary contamination, whereas mercury vapor cannot.

Order serum mercury testing if you suspect chronic exposure. Refer patients with serum mercury ≥ 1.5 mg/dL to their primary care physicians and to a poison control center for evaluation and possible chelation. Refer patients with acute mercury exposure symptoms to the ER.

Box 2

The authors’ observations

Antidepressants generally will not reduce depression, irritability, personality changes, or apathy secondary to mercury poisoning. We have found that a psychostimulant such as methylphenidate, starting at 10 mg bid and titrating to therapeutic effect, can help treat mercury-related apathy.

 

We did not give Mr. F a psychostimulant, however, fearing it would worsen his impulsive behavior and disordered sleep. Also, more effectively managing Mr. F’s diabetes should improve his depression.

DISCHARGE: CHELATION CHALLENGE

Mr. F’s suicidal thoughts continued intermittently. Chelation was tried again with succimer, 1,000 mg tid for 5 days and bid for 5 more days, but the agent caused severe nausea without significantly decreasing serum mercury. He declined outpatient chelation.

After 2 weeks, Mr. F denied suicidal thoughts and said he felt physically better. He was discharged on venlafaxine, 300 mg/d, for his depressive symptoms; and metformin, 1,000 mg/d, glipizide, 10 mg bid, and rosiglitazone, 4 mg/d, to control his blood glucose. We arranged for medication management at a community mental health center. Mr. F was also told to visit the hospital’s outpatient clinic for endocrine follow-up but has not returned for 18 months.

Related resources

• Agency for Toxic Substances and Disease Registry. Information about toxic substances in the environment and diseases they may cause. www.atsdr.cdc.gov.
  

Drug brand names

• Dimercaprol • BAL in Oil
  
• Glipizide • Glucotrol
  
• Metformin • Glucophage
  
• Methylphenidate • Ritalin, Concerta
  
• Rosiglitazone • Avandia
  
• Sertraline • Zoloft
  
• Succimer • Chemet
  
• Venlafaxine • Effexor
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from GlaxoSmithKline, Hoffman LaRoche, and AstraZeneca Pharmaceuticals. He is a speaker for Abbott Laboratories, AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., GlaxoSmithKline, and Janssen Pharmaceuticals.

HISTORY: TIRED OF LIVING

Mr. F, age 43, presents to the emergency room with complications of type 2 diabetes mellitus: blurry vision, increased urination, fatigue, and polydipsia. Blood glucose is 676 mg/dL.

The patient flees during treatment—possibly to attempt suicide—but returns 36 hours later, noticeably disoriented. He is readmitted to the ER, where he tells staff he is considering suicide and plans to self-inject a lethal substance. The ER staff refers him to the psychiatry service.

Mr. F also complains of shortness of breath after minimal exertion, aching joints throughout his body, and intense pain in his right great toe. He has been sleeping 12 to 20 hours daily, yet has trouble sleeping at night. He persistently feels fatigued, hopeless, and helpless. He says his suicidal urges have become more intense over 2 months, but he fears he will lose his computer repair job if he is admitted. He also shows difficulties with short-term memory. We admit him for observation.

Mental status examination suggests that Mr. F is generally withdrawn. Eye contact is poor and he is quiet and evasive, possibly signaling paranoia. He spends most of his stay watching television. His thought process is linear, and he thinks constantly of suicide. During the Mini-Mental State Examination, he gives the incorrect date and county. He misses two other items on recall but gets them correct with prompts.

A mild intention tremor distorts his handwriting. He has trouble keeping his balance during the Romberg test, and his gait is mildly ataxic. Ophthalmology consult suggests that diabetic retinopathy and optic disc cupping secondary to glaucoma may be blurring his vision.

Mr. F is taking no medications but had previously used insulin twice a day, and his outpatient doctor insists he should go back on insulin. He smokes 1 pack of cigarettes per day, drinks alcohol moderately (one to two drinks/day), and does not abuse illicit drugs.

The authors’ observations

Mr. F’s depressed mood, hopelessness, concentration problems, psychomotor retardation, and suicidal thoughts suggest major depressive disorder. Depression or a delirium secondary to diabetes may account for his referential ideas.

FURTHER HISTORY: ONE SHOT AT SATISFACTION

Over the following week, Mr. F becomes more talkative as the psychiatry staff develops a therapeutic rapport. He tells his treatment team that he feels urges to self-inject liquids he finds in his hospital room, such as shower gel and beverages.

Mr. F tells us that approximately 2 years ago, he tried to kill himself by swallowing boric acid. After 6 weeks in intensive care, the poison’s physical effects resolved and he no longer appeared suicidal. The staff at that time prepared to discharge Mr. F when, while left alone in his room, he dislodged a wall-mounted sphygmomanometer, disassembled it, and broke open the mercury tube. He then injected about 3 mL of mercury into his intravenous port and swallowed another 3 mL.

A nurse who checked on Mr. F minutes after the incident did not notice the sphygmomanometer was missing. He showed the broken device to the nurse, saying, “Look what I did.” When the nurse asked why, he responded, “I was just sitting here alone and saw the thing on the wall. I thought to myself, I can do this.”

The hospital viewed the episode as another suicide attempt. Staff immediately began chelation therapy with dimercaprol, 10 mg/kg every 8 hours for 5 days, then 10 mg/kg every 12 hours for 2 weeks. Within 24 hours of ingesting mercury, Mr. F developed shortness of breath, tachycardia (104 BPM), a fever (101.8°F), and had GI complaints. Increased blood urea nitrogen, increased creatinine, and decreased urination suggested declining renal function. He developed a pruritic rash over his back and mild skin loss on his soles.

Mr. F’s mercury levels were 20.8 mg/dL (serum) and 216 mg/dL (urine) 36 hours after ingestation, and 24.8 mg/dL (serum) and 397 mg/dL (urine) after chelation. Serum mercury >5 mg/dL is usually symptomatic.

Approximately 72 hours after the incident, most pulmonary, renal, and dermal manifestations of mercury toxicity began to improve. Mr. F was discharged after 21 days. He was diagnosed with major depression and started on sertraline, 150 mg/d.

‘The best feeling.’ Two years later, Mr. F tells us he has attempted suicide at least six times. Diffuse metallic foreign bodies throughout his lung vasculature and a 9.6 mg/dL serum mercury reading confirm he has injected mercury. His painful toe is x-rayed to check for mercury deposits, but he ultimately is diagnosed with gout.

During our evaluation, Mr. F admits that “the calmest, best feeling I have ever had” was while injecting mercury, yet he fears the incident has caused permanent physical and mental damage. He describes his desire to self-inject liquids as “impulses” triggered by twice-daily subcutaneous insulin use. For this reason, he has stopped taking insulin against his doctor’s advice.

 

The authors’ observations

Mr. F’s mental status changes and serum mercury suggest mercury poisoning. He shows numerous heavy-metal poisoning symptoms (Box 1) as well as erethism, a malaise that can result from heavy-metal exposure.²

The patient insists that insulin shots bring on self-injection urges, but his impulsive and repetitive suicidal behavior, dysphoria, and transient paranoia suggest borderline personality disorder. His impulses may reflect a subtle, long-term personality change caused by mercury’s neurotoxic effects.¹ Or they could be akin to cutting behaviors shown by some patients with personality disorders, particularly borderline personality disorder.

We ruled out substance abuse disorder, as Mr. F’s mercury ingestion was not premeditated, he has no history of illicit drug use, and intravenous elemental mercury is not psychoactive.

Box 1

An ever-present threat. Mercury exists in many organic, inorganic, and elemental forms—all toxic.

Elemental mercury found in thermometers, lamps, and dental amalgams slowly ionizes in the blood stream before crossing the blood-brain barrier. Mercury and carbon form toxic “organic” compounds, including methylmercury (found in the environment), phenylmercury (used in some commercial products), and dimethylmercury (found in solid waste sites).

Because mercury’s half-life is 60 days, it dissipates slowly, can accumulate with chronic exposure, and stays in the blood stream long after high-dose exposure.³

Serum mercury >5 mg/dL can cause subtle, enduring neurotoxic effects, including tremor, dizziness, shortness of breath, blurry vision, decreased visual fields, depression, memory loss, and irritability.³ Serum mercury rarely exceeds 1.5 mg/dL without direct exposure.

Irritability, depressive symptoms, and renal manifestations emerge when urine mercury reaches 200 to 1,000 mg/dL. Renal, respiratory, and GI effects are seen at 1,000 to 2,000 mg/dL.

Means of exposure. Vapor inhalation is the most common means of elemental mercury exposure.³ Elemental mercury used in manufacturing vaporizes at room temperature.

Orally ingested elemental mercury is poorly absorbed from the GI tract, mostly passes unabsorbed, and is toxic only at high doses. Injected elemental mercury is poorly absorbed but can cause mechanical and immunologic effects. The psychiatric literature describes some 200 cases of mercury self-injection^4-8 but offers little information on cognitive effects or long-term follow-up.

Consider heavy-metal poisoning in the differential diagnosis of patients with depressive symptoms. Ask about risk factors for environmental mercury exposure, including use of folk medicines, some cosmetics, over-the-counter nasal sprays, ophthalmic solutions, skin-lightening creams, daily fish consumption (particularly tuna or swordfish), living in a house painted with latex paint, or continuous exposure at work (Box 2).

Also ask if the patient or a household member recently ingested mercury or handled a broken thermometer. Liquid mercury on clothing and in bodily fluids may cause secondary contamination, whereas mercury vapor cannot.

Order serum mercury testing if you suspect chronic exposure. Refer patients with serum mercury ≥ 1.5 mg/dL to their primary care physicians and to a poison control center for evaluation and possible chelation. Refer patients with acute mercury exposure symptoms to the ER.

Box 2

The authors’ observations

Antidepressants generally will not reduce depression, irritability, personality changes, or apathy secondary to mercury poisoning. We have found that a psychostimulant such as methylphenidate, starting at 10 mg bid and titrating to therapeutic effect, can help treat mercury-related apathy.

 

We did not give Mr. F a psychostimulant, however, fearing it would worsen his impulsive behavior and disordered sleep. Also, more effectively managing Mr. F’s diabetes should improve his depression.

DISCHARGE: CHELATION CHALLENGE

Mr. F’s suicidal thoughts continued intermittently. Chelation was tried again with succimer, 1,000 mg tid for 5 days and bid for 5 more days, but the agent caused severe nausea without significantly decreasing serum mercury. He declined outpatient chelation.

After 2 weeks, Mr. F denied suicidal thoughts and said he felt physically better. He was discharged on venlafaxine, 300 mg/d, for his depressive symptoms; and metformin, 1,000 mg/d, glipizide, 10 mg bid, and rosiglitazone, 4 mg/d, to control his blood glucose. We arranged for medication management at a community mental health center. Mr. F was also told to visit the hospital’s outpatient clinic for endocrine follow-up but has not returned for 18 months.

Related resources

• Agency for Toxic Substances and Disease Registry. Information about toxic substances in the environment and diseases they may cause. www.atsdr.cdc.gov.
  

Drug brand names

• Dimercaprol • BAL in Oil
  
• Glipizide • Glucotrol
  
• Metformin • Glucophage
  
• Methylphenidate • Ritalin, Concerta
  
• Rosiglitazone • Avandia
  
• Sertraline • Zoloft
  
• Succimer • Chemet
  
• Venlafaxine • Effexor
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from GlaxoSmithKline, Hoffman LaRoche, and AstraZeneca Pharmaceuticals. He is a speaker for Abbott Laboratories, AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., GlaxoSmithKline, and Janssen Pharmaceuticals.

History: A mite disturbing

Mrs. K, age 60, a social worker, saw mites on her arm 3 months ago while going through a client’s old belongings. Since then, she reports, she and her house have become infested with mites.

Despite using copious amounts of lotions, baths, sprays, and prescription creams, she sees increasingly visible “creatures” all over her body and in her stool. Three doctors found no physical evidence of infestation, however, and she became indignant after one told her the problem is “in her head.”

A veterinarian treated Mrs. K’s cat for mites. Days later, Mrs. K suspected that the cat had become reinfested at home and returned it to the veterinarian. He assured her the cat was fine, but she was afraid to bring it home. The cat has remained at the veterinarian’s office—to the doctor’s displeasure—for weeks.

Two weeks after Mrs. K first spotted the mites, her husband, age 82, started believing he is infested. Mr. K, who is retired, has battled depression and drinks about a half-gallon of liquor daily.

After 2 months, Mrs. K quit her job for fear she would infest her co-workers, then locked herself and her husband in their house and allowed no visitors. Day and night for nearly 3 weeks, Mrs. K repeatedly vacuumed the house, shampooed the carpets, and sprayed the walls and furniture with a homemade insecticide. She taped the windows closed to keep bugs out and covered all furniture and surface areas with plastic. A toxic stench of insecticide and shampoo permeated every room.

A neighbor told Mrs. K’s son that his parents were locked inside their house. He came over and knocked on their door, but was refused entry. He eventually got Mrs. K out by threatening to call the police, then brought her to the emergency room.

At presentation, Mrs. K’s right leg has scratches and scabs caused by frequent scratching at mites she saw there. Her hands are reddened and dry, suggesting chemical dermatitis caused by cleaning and repeated insecticide use. Ritual cleaning and spraying has kept her from eating or sleeping; she has lost 12 lbs over 3 weeks and looks pale and tired.

A recovered alcoholic, Mrs. K has been sober for 12 years. She has no other psychiatric, medical, or dermatologic history, and has few social contacts beyond her family and workplace acquaintances.

Blood chemistry, CBC, and urine drug test results are normal. Head MRI reveal no neurologic abnormalities. Her Mini-Mental State Examination (MMSE) score (29/30) indicates no cognitive impairment.

Mrs. K is hospitalized to separate her from her allegedly bug-infested household and husband. At intake, she is panicked over leaving her husband alone and distressed that no one except she and her husband can see the bugs infesting their house and covering her skin. She asks doctors to test a small piece of toilet paper, which she says contains a sample of the bugs. She also fears that she infested her son by letting him into her house.

poll here

The authors’ observations

Mrs. K’s presentation and clinical course suggest delusional parasitosis, a fixed false belief of a parasitic infestation that can cause significant social and occupational dysfunction and medical problems. One patient calls this disorder “bugaphobia.”

The disorder may start as a self-perceived invisible infestation and evolve into visual hallucinations of bugs. Patients usually believe their skin is infested; some believe their internal organs, gums, or skin and internal organs are infested.^1,2

Table 1

Medical conditions that may precede delusional parasitosis

Anemia (severe)
Cancer
CNS infections
Head injury
Hepatitis
Hypertension
Hypovitaminosis of vitamin B12, folate, or thiamine
Multiple sclerosis
Pulmonary disease
Renal disease
Rheumatologic disease
Sight or hearing loss
Source: Reference 6

Skin lesions can result, including physical trauma from picking at sites the patient believes is infested. Some patients have sustained ocular trauma from picking at their eyes, which they believed contained insects.² At least one patient, depressed after failing to kill the parasites, killed himself.¹ As with Mrs. K, profuse use of insecticides or topical sprays can cause chemical dermatitis. Many patients isolate themselves to avoid infesting others.³

Some patients misinterpret scabs, abrasions, or skin irritation secondary to pesticide use as signs of infestation. Delusional parasitosis can also develop after a real, one-time infestation, as may have happened with Mrs. K.

Convinced they are infested, patients consult multiple providers—including dermatologists, gastroenterologists, and ophthalmologists—in search of the “right” treatment. They undergo numerous tests or procedures and repeatedly apply prescription creams and lotions, leading to chemical dermatitis. Patients often try to prove they are infested by bringing skin, dirt, or toilet tissue samples to doctors—this is called the “matchbox sign” because patients generally bring these samples in small boxes.⁴ They also may repeatedly ask veterinarians to disinfest their pets.

 

Box

Patients, however, do not believe the disorder is psychiatric⁵ and resist seeing a psychiatrist. Often a primary care physician or dermatologist calls on a psychiatrist as a consultant,⁶ as happened here.

Delusional parasitosis is most often found in socially isolated women age >40 of average or higher intelligence. Persons in some cultures may be more susceptible than others to some types of parasitic delusions. For example, several persons in India who considered ear cleanliness crucial to attaining cultural and spiritual purity reported having ear infestation.⁷

Delusional parasitosis also is associated with:

• medical conditions (Table 1)⁶
  
• use of cocaine, amphetamines,⁸ corticosteroids,^3,9 or phenelzine¹⁰
  
• occipital-temporal cerebral infarction¹¹
  
• cognitive impairment related to dementia, depression, mental retardation, or schizophrenia/schizophreniform disorder.
  

Cognitive impairment secondary to a medical problem may foster the delusion, or the patient may misinterpret a physical symptom as evidence of internal infestation. For example, a patient with chronic stomach pain may think he has bugs in his gut.⁵

Mrs. K’s delusional parasitosis may be a primary psychiatric disorder (Box). She is medically healthy and does not use drugs or alcohol. Her MMSE score is essentially normal, and she exhibited no psychotic symptoms or loss of function before her first mite sighting.

Diagnosis. Delusional parasitosis is diagnosed as delusional disorder, somatic type, if symptoms persist >1 month. Thorough laboratory and neurologic evaluation is recommended to rule out medical causes (Table 2). Eliminate schizophrenia and schizophreniform disorder with a detailed patient history and cognitive testing.

Also check for a comorbid psychiatric disorder that may be perpetuating the delusion. Delusional parasitosis often co-occurs with axis I disorders including major depressive disorder, substance abuse, dementia, and mental retardation.

poll here

The authors’ observations

Mr. K’s “bugaphobia” most likely was a form of shared secondary delusion called folie-a-deux. Between 11% and 25% of persons with primary delusional parasitosis induce secondary delusional parasitosis in another person, usually a spouse or longtime friend.² About 50% of folie-a-deux disorders involve a married couple. Often both partners are socially isolated.⁴

poll here

Treatment: Between two worlds

Mrs. K was given risperidone, 2 mg/d, for delusions and anxiety, and escitalopram, 10 mg/d, preventatively for a suspected underlying depression.

As her symptoms began to clear across 2 to 3 days, Mrs. K realized most times that she was not infested, but on occasion still feared that she was. She continued to worry about her husband being alone in a mite-infested house. We reassured her that her husband would be OK and told her to let us know if the mites resurfaced on her skin.

The authors’ observations

Building rapport. When treating delusional parasitosis, be accepting and non-confrontational. These patients tend to switch doctors until they find someone who understands their problem. Developing rapport can promote treatment adherence and prevent or minimize relapse.

Table 2

5 steps to confirm ‘bugaphobia’

Rule out infestation with skin scrapings/biopsy Get a thorough alcohol and drug use history to rule out substance abuse/dependence (particularly stimulant use) Perform a complete physical examination Order a CBC, urinalysis, liver function tests, thyroid function test, vitamin B 12 , folate, iron studies, blood urea nitrogen, serum electrolytes, and glucose to screen for associated medicalconditions Order head CT or MRI to rule out infarction or mass

Source: Adapted from Driscoll MS, Rothe MJ, Grant-Kels JM, Hale MS. Delusions of parasitosis: a dermatologic, psychiatric, and pharmacologic approach. J Am Acad Dermatol 1993;29:1023-33.

Start by getting the patient to leave the environment that feeds the delusion. Tell the patient, for example, “The hospital may have experts on your disorder who can help you.” Hospitalize the patient if he or she cannot function independently or will not leave the offending environment. Wait 1 to 2 days before starting medication to see if symptoms remit spontaneously, which they frequently do.

 

⁴

Also communicate with other specialists to gauge medication history, confirm test findings, and rule out medical causes.

Pharmacotherapy. If symptoms do not resolve after 1 or 2 days of observation, look for a comorbid medical or mental disorder. Prescribe an atypical antipsychotic such as risperidone, 2 to 4 mg/d, or olanzapine, 2.5 mg/d, both of which have been effective against delusional parasitosis.^14,16 Keep dosages low to reduce risk of sedation, extrapyramidal symptoms (EPS), and tardive dyskinesia.

Suggesting a psychotropic to patients who are convinced their problem is not psychiatric can be difficult. Try saying:

• Some people are more sensitive than others to sensations on their skin or in their body. This medication will help you tolerate the sensations.”
  
• or, “This drug will help reduce the anxiety your problem is causing.”
  

If symptoms persist another 3 days, try a different atypical or a conventional neuroleptic. Watch for EPS or other neuroleptic-related side effects in patients age >65.

Pimozide has shown efficacy against delusional parasitosis in placebo-controlled trials,^17,18 but it can alter cardiac conduction, especially at higherthan-recommended dosages. Start pimozide at 1 mg/d and increase by 1 mg/week until clinical response is achieved. Most patients respond to dosages used to treat psychotic disorders (4 to 10 mg/d).¹⁹ Order a baseline and periodic ECG to monitor for QTc prolongation, and do an abnormal involuntary movement scale examination every 3 to 6 months to test for EPS.

Other treatments that have shown benefit in case reports include naloxone, 10 mg/d;²⁰ haloperidol, 10 mg/d; trifluoperazine, 15 mg/d; chlorpromazine, 150 to 300 mg/d; and electroconvulsive therapy.⁷

We have found that prognosis usually is poor after first- and second-line treatments have failed. Continue to search for a missed disorder, and add an antidepressant if an underlying depression is found or suspected.

Psychotherapy. Perform supportive and harm reduction psychotherapy immediately after diagnosis. Supportive, rapport-building approaches can get the patient to comfortably discuss the issues that led to the delusion and help him/her confront a relapse. Harm reduction can discourage patients from requesting unnecessary invasive tests, using medications and toxic insecticides, or other potentially harmful behaviors.

Cognitive-behavioral therapy may help some patients with refractory delusional parasitosis, if they have enough insight to continue treatment.

Follow-up: A bug-free future

Mrs. K was released from the hospital after 4 days, and her delusional symptoms were gone after another 3 days. We followed her for 6 months.

Upon discharge, Mrs. K and her cat moved in with her daughter’s family. Within a few weeks she was able to visit her workplace and explain what had happened. She stopped taking risperidone after 2 weeks because of excessive sedation. No depressive symptoms were present after 3 months; escitalopram was stopped.

Mrs. K’s husband continued to drink and confine himself to the house. Upon visiting him, she was horrified to find the furniture still covered with plastic and the windows taped shut. Mrs. K threatened to divorce him if he did not seek help. He eventually was treated and has been sober—and bug-free—for 15 months.

Related resources

• Bohart Museum of Entomology, University of California, Davis: Delusional parasitosis. http://delusion.ucdavis.edu.
  

Drug brand names

• Chlorpromazine • Thorazine
  
• Escitalopram • Lexapro
  
• Haloperidol • Haldol
  
• naloxone • Narcan
  
• Olanzapine • Zyprexa
  
• Pimozide • Orap
  
• Phenelzine • Nardil
  
• Risperidone • Risperdal
  
• Trifluoperazine • Stelazine
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from and is a speaker for AstraZeneca Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, and Hoffman LaRoche. He is also receives research/grant support from Schering-Plough Corp. and is a speaker for Abbott Laboratories and Janssen Pharmaceutica.

History: A mite disturbing

Mrs. K, age 60, a social worker, saw mites on her arm 3 months ago while going through a client’s old belongings. Since then, she reports, she and her house have become infested with mites.

Despite using copious amounts of lotions, baths, sprays, and prescription creams, she sees increasingly visible “creatures” all over her body and in her stool. Three doctors found no physical evidence of infestation, however, and she became indignant after one told her the problem is “in her head.”

A veterinarian treated Mrs. K’s cat for mites. Days later, Mrs. K suspected that the cat had become reinfested at home and returned it to the veterinarian. He assured her the cat was fine, but she was afraid to bring it home. The cat has remained at the veterinarian’s office—to the doctor’s displeasure—for weeks.

Two weeks after Mrs. K first spotted the mites, her husband, age 82, started believing he is infested. Mr. K, who is retired, has battled depression and drinks about a half-gallon of liquor daily.

After 2 months, Mrs. K quit her job for fear she would infest her co-workers, then locked herself and her husband in their house and allowed no visitors. Day and night for nearly 3 weeks, Mrs. K repeatedly vacuumed the house, shampooed the carpets, and sprayed the walls and furniture with a homemade insecticide. She taped the windows closed to keep bugs out and covered all furniture and surface areas with plastic. A toxic stench of insecticide and shampoo permeated every room.

A neighbor told Mrs. K’s son that his parents were locked inside their house. He came over and knocked on their door, but was refused entry. He eventually got Mrs. K out by threatening to call the police, then brought her to the emergency room.

At presentation, Mrs. K’s right leg has scratches and scabs caused by frequent scratching at mites she saw there. Her hands are reddened and dry, suggesting chemical dermatitis caused by cleaning and repeated insecticide use. Ritual cleaning and spraying has kept her from eating or sleeping; she has lost 12 lbs over 3 weeks and looks pale and tired.

A recovered alcoholic, Mrs. K has been sober for 12 years. She has no other psychiatric, medical, or dermatologic history, and has few social contacts beyond her family and workplace acquaintances.

Blood chemistry, CBC, and urine drug test results are normal. Head MRI reveal no neurologic abnormalities. Her Mini-Mental State Examination (MMSE) score (29/30) indicates no cognitive impairment.

Mrs. K is hospitalized to separate her from her allegedly bug-infested household and husband. At intake, she is panicked over leaving her husband alone and distressed that no one except she and her husband can see the bugs infesting their house and covering her skin. She asks doctors to test a small piece of toilet paper, which she says contains a sample of the bugs. She also fears that she infested her son by letting him into her house.

poll here

The authors’ observations

Mrs. K’s presentation and clinical course suggest delusional parasitosis, a fixed false belief of a parasitic infestation that can cause significant social and occupational dysfunction and medical problems. One patient calls this disorder “bugaphobia.”

The disorder may start as a self-perceived invisible infestation and evolve into visual hallucinations of bugs. Patients usually believe their skin is infested; some believe their internal organs, gums, or skin and internal organs are infested.^1,2

Table 1

Medical conditions that may precede delusional parasitosis

Anemia (severe)
Cancer
CNS infections
Head injury
Hepatitis
Hypertension
Hypovitaminosis of vitamin B12, folate, or thiamine
Multiple sclerosis
Pulmonary disease
Renal disease
Rheumatologic disease
Sight or hearing loss
Source: Reference 6

Skin lesions can result, including physical trauma from picking at sites the patient believes is infested. Some patients have sustained ocular trauma from picking at their eyes, which they believed contained insects.² At least one patient, depressed after failing to kill the parasites, killed himself.¹ As with Mrs. K, profuse use of insecticides or topical sprays can cause chemical dermatitis. Many patients isolate themselves to avoid infesting others.³

Some patients misinterpret scabs, abrasions, or skin irritation secondary to pesticide use as signs of infestation. Delusional parasitosis can also develop after a real, one-time infestation, as may have happened with Mrs. K.

Convinced they are infested, patients consult multiple providers—including dermatologists, gastroenterologists, and ophthalmologists—in search of the “right” treatment. They undergo numerous tests or procedures and repeatedly apply prescription creams and lotions, leading to chemical dermatitis. Patients often try to prove they are infested by bringing skin, dirt, or toilet tissue samples to doctors—this is called the “matchbox sign” because patients generally bring these samples in small boxes.⁴ They also may repeatedly ask veterinarians to disinfest their pets.

 

Box

Patients, however, do not believe the disorder is psychiatric⁵ and resist seeing a psychiatrist. Often a primary care physician or dermatologist calls on a psychiatrist as a consultant,⁶ as happened here.

Delusional parasitosis is most often found in socially isolated women age >40 of average or higher intelligence. Persons in some cultures may be more susceptible than others to some types of parasitic delusions. For example, several persons in India who considered ear cleanliness crucial to attaining cultural and spiritual purity reported having ear infestation.⁷

Delusional parasitosis also is associated with:

• medical conditions (Table 1)⁶
  
• use of cocaine, amphetamines,⁸ corticosteroids,^3,9 or phenelzine¹⁰
  
• occipital-temporal cerebral infarction¹¹
  
• cognitive impairment related to dementia, depression, mental retardation, or schizophrenia/schizophreniform disorder.
  

Cognitive impairment secondary to a medical problem may foster the delusion, or the patient may misinterpret a physical symptom as evidence of internal infestation. For example, a patient with chronic stomach pain may think he has bugs in his gut.⁵

Mrs. K’s delusional parasitosis may be a primary psychiatric disorder (Box). She is medically healthy and does not use drugs or alcohol. Her MMSE score is essentially normal, and she exhibited no psychotic symptoms or loss of function before her first mite sighting.

Diagnosis. Delusional parasitosis is diagnosed as delusional disorder, somatic type, if symptoms persist >1 month. Thorough laboratory and neurologic evaluation is recommended to rule out medical causes (Table 2). Eliminate schizophrenia and schizophreniform disorder with a detailed patient history and cognitive testing.

Also check for a comorbid psychiatric disorder that may be perpetuating the delusion. Delusional parasitosis often co-occurs with axis I disorders including major depressive disorder, substance abuse, dementia, and mental retardation.

poll here

The authors’ observations

Mr. K’s “bugaphobia” most likely was a form of shared secondary delusion called folie-a-deux. Between 11% and 25% of persons with primary delusional parasitosis induce secondary delusional parasitosis in another person, usually a spouse or longtime friend.² About 50% of folie-a-deux disorders involve a married couple. Often both partners are socially isolated.⁴

poll here

Treatment: Between two worlds

Mrs. K was given risperidone, 2 mg/d, for delusions and anxiety, and escitalopram, 10 mg/d, preventatively for a suspected underlying depression.

As her symptoms began to clear across 2 to 3 days, Mrs. K realized most times that she was not infested, but on occasion still feared that she was. She continued to worry about her husband being alone in a mite-infested house. We reassured her that her husband would be OK and told her to let us know if the mites resurfaced on her skin.

The authors’ observations

Building rapport. When treating delusional parasitosis, be accepting and non-confrontational. These patients tend to switch doctors until they find someone who understands their problem. Developing rapport can promote treatment adherence and prevent or minimize relapse.

Table 2

5 steps to confirm ‘bugaphobia’

Rule out infestation with skin scrapings/biopsy Get a thorough alcohol and drug use history to rule out substance abuse/dependence (particularly stimulant use) Perform a complete physical examination Order a CBC, urinalysis, liver function tests, thyroid function test, vitamin B 12 , folate, iron studies, blood urea nitrogen, serum electrolytes, and glucose to screen for associated medicalconditions Order head CT or MRI to rule out infarction or mass

Source: Adapted from Driscoll MS, Rothe MJ, Grant-Kels JM, Hale MS. Delusions of parasitosis: a dermatologic, psychiatric, and pharmacologic approach. J Am Acad Dermatol 1993;29:1023-33.

Start by getting the patient to leave the environment that feeds the delusion. Tell the patient, for example, “The hospital may have experts on your disorder who can help you.” Hospitalize the patient if he or she cannot function independently or will not leave the offending environment. Wait 1 to 2 days before starting medication to see if symptoms remit spontaneously, which they frequently do.

 

⁴

Also communicate with other specialists to gauge medication history, confirm test findings, and rule out medical causes.

Pharmacotherapy. If symptoms do not resolve after 1 or 2 days of observation, look for a comorbid medical or mental disorder. Prescribe an atypical antipsychotic such as risperidone, 2 to 4 mg/d, or olanzapine, 2.5 mg/d, both of which have been effective against delusional parasitosis.^14,16 Keep dosages low to reduce risk of sedation, extrapyramidal symptoms (EPS), and tardive dyskinesia.

Suggesting a psychotropic to patients who are convinced their problem is not psychiatric can be difficult. Try saying:

• Some people are more sensitive than others to sensations on their skin or in their body. This medication will help you tolerate the sensations.”
  
• or, “This drug will help reduce the anxiety your problem is causing.”
  

If symptoms persist another 3 days, try a different atypical or a conventional neuroleptic. Watch for EPS or other neuroleptic-related side effects in patients age >65.

Pimozide has shown efficacy against delusional parasitosis in placebo-controlled trials,^17,18 but it can alter cardiac conduction, especially at higherthan-recommended dosages. Start pimozide at 1 mg/d and increase by 1 mg/week until clinical response is achieved. Most patients respond to dosages used to treat psychotic disorders (4 to 10 mg/d).¹⁹ Order a baseline and periodic ECG to monitor for QTc prolongation, and do an abnormal involuntary movement scale examination every 3 to 6 months to test for EPS.

Other treatments that have shown benefit in case reports include naloxone, 10 mg/d;²⁰ haloperidol, 10 mg/d; trifluoperazine, 15 mg/d; chlorpromazine, 150 to 300 mg/d; and electroconvulsive therapy.⁷

We have found that prognosis usually is poor after first- and second-line treatments have failed. Continue to search for a missed disorder, and add an antidepressant if an underlying depression is found or suspected.

Psychotherapy. Perform supportive and harm reduction psychotherapy immediately after diagnosis. Supportive, rapport-building approaches can get the patient to comfortably discuss the issues that led to the delusion and help him/her confront a relapse. Harm reduction can discourage patients from requesting unnecessary invasive tests, using medications and toxic insecticides, or other potentially harmful behaviors.

Cognitive-behavioral therapy may help some patients with refractory delusional parasitosis, if they have enough insight to continue treatment.

Follow-up: A bug-free future

Mrs. K was released from the hospital after 4 days, and her delusional symptoms were gone after another 3 days. We followed her for 6 months.

Upon discharge, Mrs. K and her cat moved in with her daughter’s family. Within a few weeks she was able to visit her workplace and explain what had happened. She stopped taking risperidone after 2 weeks because of excessive sedation. No depressive symptoms were present after 3 months; escitalopram was stopped.

Mrs. K’s husband continued to drink and confine himself to the house. Upon visiting him, she was horrified to find the furniture still covered with plastic and the windows taped shut. Mrs. K threatened to divorce him if he did not seek help. He eventually was treated and has been sober—and bug-free—for 15 months.

Related resources

• Bohart Museum of Entomology, University of California, Davis: Delusional parasitosis. http://delusion.ucdavis.edu.
  

Drug brand names

• Chlorpromazine • Thorazine
  
• Escitalopram • Lexapro
  
• Haloperidol • Haldol
  
• naloxone • Narcan
  
• Olanzapine • Zyprexa
  
• Pimozide • Orap
  
• Phenelzine • Nardil
  
• Risperidone • Risperdal
  
• Trifluoperazine • Stelazine
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from and is a speaker for AstraZeneca Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, and Hoffman LaRoche. He is also receives research/grant support from Schering-Plough Corp. and is a speaker for Abbott Laboratories and Janssen Pharmaceutica.

History: A mite disturbing

Mrs. K, age 60, a social worker, saw mites on her arm 3 months ago while going through a client’s old belongings. Since then, she reports, she and her house have become infested with mites.

Despite using copious amounts of lotions, baths, sprays, and prescription creams, she sees increasingly visible “creatures” all over her body and in her stool. Three doctors found no physical evidence of infestation, however, and she became indignant after one told her the problem is “in her head.”

A veterinarian treated Mrs. K’s cat for mites. Days later, Mrs. K suspected that the cat had become reinfested at home and returned it to the veterinarian. He assured her the cat was fine, but she was afraid to bring it home. The cat has remained at the veterinarian’s office—to the doctor’s displeasure—for weeks.

Two weeks after Mrs. K first spotted the mites, her husband, age 82, started believing he is infested. Mr. K, who is retired, has battled depression and drinks about a half-gallon of liquor daily.

After 2 months, Mrs. K quit her job for fear she would infest her co-workers, then locked herself and her husband in their house and allowed no visitors. Day and night for nearly 3 weeks, Mrs. K repeatedly vacuumed the house, shampooed the carpets, and sprayed the walls and furniture with a homemade insecticide. She taped the windows closed to keep bugs out and covered all furniture and surface areas with plastic. A toxic stench of insecticide and shampoo permeated every room.

A neighbor told Mrs. K’s son that his parents were locked inside their house. He came over and knocked on their door, but was refused entry. He eventually got Mrs. K out by threatening to call the police, then brought her to the emergency room.

At presentation, Mrs. K’s right leg has scratches and scabs caused by frequent scratching at mites she saw there. Her hands are reddened and dry, suggesting chemical dermatitis caused by cleaning and repeated insecticide use. Ritual cleaning and spraying has kept her from eating or sleeping; she has lost 12 lbs over 3 weeks and looks pale and tired.

A recovered alcoholic, Mrs. K has been sober for 12 years. She has no other psychiatric, medical, or dermatologic history, and has few social contacts beyond her family and workplace acquaintances.

Blood chemistry, CBC, and urine drug test results are normal. Head MRI reveal no neurologic abnormalities. Her Mini-Mental State Examination (MMSE) score (29/30) indicates no cognitive impairment.

Mrs. K is hospitalized to separate her from her allegedly bug-infested household and husband. At intake, she is panicked over leaving her husband alone and distressed that no one except she and her husband can see the bugs infesting their house and covering her skin. She asks doctors to test a small piece of toilet paper, which she says contains a sample of the bugs. She also fears that she infested her son by letting him into her house.

poll here

The authors’ observations

Mrs. K’s presentation and clinical course suggest delusional parasitosis, a fixed false belief of a parasitic infestation that can cause significant social and occupational dysfunction and medical problems. One patient calls this disorder “bugaphobia.”

The disorder may start as a self-perceived invisible infestation and evolve into visual hallucinations of bugs. Patients usually believe their skin is infested; some believe their internal organs, gums, or skin and internal organs are infested.^1,2

Table 1

Medical conditions that may precede delusional parasitosis

Anemia (severe)
Cancer
CNS infections
Head injury
Hepatitis
Hypertension
Hypovitaminosis of vitamin B12, folate, or thiamine
Multiple sclerosis
Pulmonary disease
Renal disease
Rheumatologic disease
Sight or hearing loss
Source: Reference 6

Skin lesions can result, including physical trauma from picking at sites the patient believes is infested. Some patients have sustained ocular trauma from picking at their eyes, which they believed contained insects.² At least one patient, depressed after failing to kill the parasites, killed himself.¹ As with Mrs. K, profuse use of insecticides or topical sprays can cause chemical dermatitis. Many patients isolate themselves to avoid infesting others.³

Some patients misinterpret scabs, abrasions, or skin irritation secondary to pesticide use as signs of infestation. Delusional parasitosis can also develop after a real, one-time infestation, as may have happened with Mrs. K.

Convinced they are infested, patients consult multiple providers—including dermatologists, gastroenterologists, and ophthalmologists—in search of the “right” treatment. They undergo numerous tests or procedures and repeatedly apply prescription creams and lotions, leading to chemical dermatitis. Patients often try to prove they are infested by bringing skin, dirt, or toilet tissue samples to doctors—this is called the “matchbox sign” because patients generally bring these samples in small boxes.⁴ They also may repeatedly ask veterinarians to disinfest their pets.

 

Box

Patients, however, do not believe the disorder is psychiatric⁵ and resist seeing a psychiatrist. Often a primary care physician or dermatologist calls on a psychiatrist as a consultant,⁶ as happened here.

Delusional parasitosis is most often found in socially isolated women age >40 of average or higher intelligence. Persons in some cultures may be more susceptible than others to some types of parasitic delusions. For example, several persons in India who considered ear cleanliness crucial to attaining cultural and spiritual purity reported having ear infestation.⁷

Delusional parasitosis also is associated with:

• medical conditions (Table 1)⁶
  
• use of cocaine, amphetamines,⁸ corticosteroids,^3,9 or phenelzine¹⁰
  
• occipital-temporal cerebral infarction¹¹
  
• cognitive impairment related to dementia, depression, mental retardation, or schizophrenia/schizophreniform disorder.
  

Cognitive impairment secondary to a medical problem may foster the delusion, or the patient may misinterpret a physical symptom as evidence of internal infestation. For example, a patient with chronic stomach pain may think he has bugs in his gut.⁵

Mrs. K’s delusional parasitosis may be a primary psychiatric disorder (Box). She is medically healthy and does not use drugs or alcohol. Her MMSE score is essentially normal, and she exhibited no psychotic symptoms or loss of function before her first mite sighting.

Diagnosis. Delusional parasitosis is diagnosed as delusional disorder, somatic type, if symptoms persist >1 month. Thorough laboratory and neurologic evaluation is recommended to rule out medical causes (Table 2). Eliminate schizophrenia and schizophreniform disorder with a detailed patient history and cognitive testing.

Also check for a comorbid psychiatric disorder that may be perpetuating the delusion. Delusional parasitosis often co-occurs with axis I disorders including major depressive disorder, substance abuse, dementia, and mental retardation.

poll here

The authors’ observations

Mr. K’s “bugaphobia” most likely was a form of shared secondary delusion called folie-a-deux. Between 11% and 25% of persons with primary delusional parasitosis induce secondary delusional parasitosis in another person, usually a spouse or longtime friend.² About 50% of folie-a-deux disorders involve a married couple. Often both partners are socially isolated.⁴

poll here

Treatment: Between two worlds

Mrs. K was given risperidone, 2 mg/d, for delusions and anxiety, and escitalopram, 10 mg/d, preventatively for a suspected underlying depression.

As her symptoms began to clear across 2 to 3 days, Mrs. K realized most times that she was not infested, but on occasion still feared that she was. She continued to worry about her husband being alone in a mite-infested house. We reassured her that her husband would be OK and told her to let us know if the mites resurfaced on her skin.

The authors’ observations

Building rapport. When treating delusional parasitosis, be accepting and non-confrontational. These patients tend to switch doctors until they find someone who understands their problem. Developing rapport can promote treatment adherence and prevent or minimize relapse.

Table 2

5 steps to confirm ‘bugaphobia’

Rule out infestation with skin scrapings/biopsy Get a thorough alcohol and drug use history to rule out substance abuse/dependence (particularly stimulant use) Perform a complete physical examination Order a CBC, urinalysis, liver function tests, thyroid function test, vitamin B 12 , folate, iron studies, blood urea nitrogen, serum electrolytes, and glucose to screen for associated medicalconditions Order head CT or MRI to rule out infarction or mass

Source: Adapted from Driscoll MS, Rothe MJ, Grant-Kels JM, Hale MS. Delusions of parasitosis: a dermatologic, psychiatric, and pharmacologic approach. J Am Acad Dermatol 1993;29:1023-33.

Start by getting the patient to leave the environment that feeds the delusion. Tell the patient, for example, “The hospital may have experts on your disorder who can help you.” Hospitalize the patient if he or she cannot function independently or will not leave the offending environment. Wait 1 to 2 days before starting medication to see if symptoms remit spontaneously, which they frequently do.

 

⁴

Also communicate with other specialists to gauge medication history, confirm test findings, and rule out medical causes.

Pharmacotherapy. If symptoms do not resolve after 1 or 2 days of observation, look for a comorbid medical or mental disorder. Prescribe an atypical antipsychotic such as risperidone, 2 to 4 mg/d, or olanzapine, 2.5 mg/d, both of which have been effective against delusional parasitosis.^14,16 Keep dosages low to reduce risk of sedation, extrapyramidal symptoms (EPS), and tardive dyskinesia.

Suggesting a psychotropic to patients who are convinced their problem is not psychiatric can be difficult. Try saying:

• Some people are more sensitive than others to sensations on their skin or in their body. This medication will help you tolerate the sensations.”
  
• or, “This drug will help reduce the anxiety your problem is causing.”
  

If symptoms persist another 3 days, try a different atypical or a conventional neuroleptic. Watch for EPS or other neuroleptic-related side effects in patients age >65.

Pimozide has shown efficacy against delusional parasitosis in placebo-controlled trials,^17,18 but it can alter cardiac conduction, especially at higherthan-recommended dosages. Start pimozide at 1 mg/d and increase by 1 mg/week until clinical response is achieved. Most patients respond to dosages used to treat psychotic disorders (4 to 10 mg/d).¹⁹ Order a baseline and periodic ECG to monitor for QTc prolongation, and do an abnormal involuntary movement scale examination every 3 to 6 months to test for EPS.

Other treatments that have shown benefit in case reports include naloxone, 10 mg/d;²⁰ haloperidol, 10 mg/d; trifluoperazine, 15 mg/d; chlorpromazine, 150 to 300 mg/d; and electroconvulsive therapy.⁷

We have found that prognosis usually is poor after first- and second-line treatments have failed. Continue to search for a missed disorder, and add an antidepressant if an underlying depression is found or suspected.

Psychotherapy. Perform supportive and harm reduction psychotherapy immediately after diagnosis. Supportive, rapport-building approaches can get the patient to comfortably discuss the issues that led to the delusion and help him/her confront a relapse. Harm reduction can discourage patients from requesting unnecessary invasive tests, using medications and toxic insecticides, or other potentially harmful behaviors.

Cognitive-behavioral therapy may help some patients with refractory delusional parasitosis, if they have enough insight to continue treatment.

Follow-up: A bug-free future

Mrs. K was released from the hospital after 4 days, and her delusional symptoms were gone after another 3 days. We followed her for 6 months.

Upon discharge, Mrs. K and her cat moved in with her daughter’s family. Within a few weeks she was able to visit her workplace and explain what had happened. She stopped taking risperidone after 2 weeks because of excessive sedation. No depressive symptoms were present after 3 months; escitalopram was stopped.

Mrs. K’s husband continued to drink and confine himself to the house. Upon visiting him, she was horrified to find the furniture still covered with plastic and the windows taped shut. Mrs. K threatened to divorce him if he did not seek help. He eventually was treated and has been sober—and bug-free—for 15 months.

Related resources

• Bohart Museum of Entomology, University of California, Davis: Delusional parasitosis. http://delusion.ucdavis.edu.
  

Drug brand names

• Chlorpromazine • Thorazine
  
• Escitalopram • Lexapro
  
• Haloperidol • Haldol
  
• naloxone • Narcan
  
• Olanzapine • Zyprexa
  
• Pimozide • Orap
  
• Phenelzine • Nardil
  
• Risperidone • Risperdal
  
• Trifluoperazine • Stelazine
  

Disclosure

Dr. Matthews is an American Psychiatric Association Bristol-Myers Squibb Co. fellow in public and community psychiatry.

Dr. Hauser receives research/grant support from and is a speaker for AstraZeneca Pharmaceuticals, Eli Lilly and Co., GlaxoSmithKline, and Hoffman LaRoche. He is also receives research/grant support from Schering-Plough Corp. and is a speaker for Abbott Laboratories and Janssen Pharmaceutica.