Cases That Test Your Skills

History: A secluded life

Mr. K, 31, immigrated to Brooklyn as a child with his family. At age 19, he was working as an auto mechanic in a relative’s garage when he had his first psychotic episode. He was hospitalized and diagnosed with paranoid schizophrenia, which was confirmed by his subsequent course of illness and a recent structured diagnostic interview.

Since becoming ill, Mr. K almost never leaves his house and socializes only with his mother and sister. Unable to work, he helps around the house and often cares for his nieces and nephews. He has no history of substance abuse and has been faithfully taking his medication since his last hospitalization 8 years ago.

Mr. K’s outpatient clinic chart reflects concern about persistent negative symptoms. He hardly speaks in session. Even when “stable,” his social and vocational functioning has been poor. Therapeutic dosages of oral haloperidol, haloperidol decanoate, and fluphenazine have not worked, and trials of risperidone and olanzapine—administered in therapeutic dosages for at least 3 months—were only slightly more effective. Attempts to treat his social withdrawal as a depressive symptom equivalent, with use of adjunctive selective serotonin reuptake inhibitors, also have been disappointing.

We eventually discovered that his so-called negative symptoms were in fact the manifestation of persistent positive symptoms (Table 1). His social withdrawal stemmed not from lack of motivation but from ideas of reference and constant paranoid fears. He believed that if he left the house, a street gang would kill him or his family. When he did venture outdoors, he thought that strangers were ridiculing or insulting him or intended to brutally attack him.

Mr. K spent much of his time at home reading, occasionally visiting the public library just long enough to check out a few books. Family members convinced him to attend church services, but he could not interact with other parishioners because he feared they would find out something was “wrong” with him.

How would you address Mr. K’s positive symptoms? Would you try another antipsychotic after lack of response to five other agents?

Drug treatment: A clinical trial

After a thorough evaluation, Mr. K entered a clinical trial during which he began taking another antipsy-chotic. But after 4 months at high therapeutic dosages, his positive symptoms showed no change from baseline.

We then recommended that Mr. K try clozapine. His persistent paranoid delusions and lack of response to other antipsychotics made him an ideal candidate for this agent. Because he was compliant, motivated, and had available family support, we were confident that he could surmount the vicissitudes of a clozapine trial.

Mr. K refused to try clozapine, however. After so many unsuccessful medication trials over the years, he said he felt some (albeit minor) benefits from his current study medication and wanted to stick with it.

What treatment options remain for Mr. K?

Dr. Weiden’s and Burkholder’s observations

Although the newer antipsychotics have greatly improved outcomes in schizophrenia over the past decade, many patients still battle persistent psychotic (positive) symptoms despite compliance with these medications.¹ While clozapine remains the treatment of choice for positive symptoms, some patients cannot—or will not—take it because of its burdensome side-effect profile.

It is well accepted that supportive psychotherapy can help a person with schizophrenia confront the secondary issues of loss, disability, and stigma. But psychotherapy is rarely considered as an adjunct therapy for treatment-resistant positive symptoms. Skepticism about the role of psychotherapy is understandable, because older studies that demonstrated psychoanalytic psychotherapy’s lack of effect on schizophrenia’s positive symptoms² have driven psychiatric medical education and practice for the past half-century. Other non-psychoanalytic therapeutic approaches had not been studied until recently, so most of us generalized from the disappointing results of the psychoanalytic psychotherapy research.

Still, there is a resurgence of interest in using cognitive-behavioral principles to treat core schizophrenia symptoms. Several randomized, controlled studies—almost all performed in the United Kingdom—have demonstrated that a cognitive-behavioral therapy (CBT) approach, modified for schizophrenia, is superior to more traditional supportive therapies in treating persistent positive and negative symptoms.^3-5 Until recently, CBT for schizophrenia has generated little interest or research on this side of the Atlantic.

Continued treatment: A new approach

At this point, we decided to address Mr. K’s paranoid symptoms with CBT-based psychotherapy. The patient, whom we’d been seeing twice monthly for medication management, agreed to weekly 45-minute CBT sessions across 3 months. A third-year resident who had treated Mr. K during the antipsychotic clinical trial administered the therapy as described in the literature.^4-6

During the first sessions, we found that some of Mr. K's fears of leaving the house stemmed from living in a poor inner-city neighborhood with a high rate of violent crime. A few sessions later, Mr. K was able to question some of his beliefs that assassins had targeted his family.

By the fourth week, the therapist discovered that Mr. K liked to read and viewed the local library as a reasonably safe place. Mr. K agreed to visit the library once a week and to record his experiences commuting to and from there.

After roughly 8 weeks of treatment, Mr. K was visiting the library twice a week, usually for 90 minutes at a time. He reported that he “had a good time,” but still suspected other library patrons were talking about him. Upon exploring these suspicions, we learned that Mr. K feared other library goers viewed him as “stupid” and that this fear was exacerbating some of his paranoid delusions.

Table 1

POSITIVE SYMPTOMS THATMAYAPPEARASNEGATIVE SYMPTOMS

Once Mr. K acknowledged that his mental illness was not outwardly recognizable, we could convince him that his fear of appearing “stupid” should not keep him housebound. He began to visit the library more frequently. Although he was still anxious, it no longer took him all day to summon the courage to leave home.

After about 10 weeks of treatment, Mr. K began going on bike rides twice a week. We were concerned that he was making too many changes at once, but he insisted he felt more “comfortable” and enjoyed the exercise.

Did cognitive-behavioral therapy contribute to Mr. K’s improvement? How did the therapist’s treatment differ from accepted protocols?

Dr. Weiden’s and Burkholder’s observations

You might be thinking, “This sounds no different from what I do in practice!” The patient was reassured and encouraged to go out and live his life despite having symptoms.

In practice, however, some techniques used in the CBT approach to psychosis are quite different; some techniques are not intuitive, and some contradict most standard teachings of supportive psychotherapy in this country.

The CBT approach used for Mr. K differed greatly from traditional “medical model” supportive psychotherapy. The therapist:

• rejected a “brain disorder” approach to describing his illness⁷
• used the stress-vulnerability model to explain positive symptoms
• viewed psychotic symptoms as normal reactions rather than pathologic response
• considered psychological factors behind specific psychotic symptoms (Table 2).⁸

The “brain disorder” explanation. The Kraepelinian model, which characterizes schizophrenia as a degenerative brain disorder, drives patient education. For example, one brochure for patients and their families refers to schizophrenia as “a brain disorder like Alzheimer’s disease.”

Such a comparison could devastate a young adult who is overwhelmed by symptoms and after being told he had a “brain disorder” that “interfered with his cognition.” While this corresponded with our knowledge of schizophrenia, he took this to mean he is “retarded” and “stupid.”

Table 2

UNDERSTANDING PSYCHOSIS WITHIN THE COGNITIVE-BEHAVIORAL MODEL

Telling the patient that he or she has schizophrenia– known in some clinical circles as “the S word”–is not necessary and may even be harmful in some cases. We’re not saying that giving a diagnosis of schizophrenia or using a medical model approach is wrong. However, patient education based on symptoms instead of diagnosis may be more conducive in some cases.

The stress-vulnerability model explains psychosis without having to use a diagnostic label. Mr. K’s previous understanding of schizophrenia dovetailed with his low self-esteem. His self-perceived stupidity also had discouraged him from confronting his paranoid anxieties.

Once he realized that unrelenting psychotic symptoms—not his IQ—held him back, we could form a treatment plan. We explained Mr. K’s paranoid symptoms with the stress-vulnerability model: His fears and suspicions worsened whenever he was under stress. This allowed us to sidestep the “brain disorder” model that demoralized him.

By no means, however, did we reject the notion that schizophrenia has a biologic basis. Even if “schizophrenia” is never mentioned, this diagnosis still guides treatment.

Viewing psychotic symptoms as normal reactions. The therapist extensively examined Mr. K’s safety concerns for himself and his family. The therapist acknowledged that these concerns were legitimate, as the patient lives in an inner-city neighborhood plagued by violent crime. Mr. K was then praised for his devotion to his family.

By applying normalization techniques,⁹ the therapist found fact-based aspects of the delusional beliefs. Normalizing Mr. K’s safety concerns made him feel validated. From there, we could map out a plan for him to periodically leave his home. We devised a routine that addressed his safety concerns: He went to the library only in daylight. He chose a subway route that was less convenient but made him feel more comfortable. Once at the library, he called home to make sure his family was safe, then sat at an open table so he could watch other library patrons come and go.

Once this routine was established, we could address the more idiosyncratic delusions that caused Mr. K considerable stress and anxiety. We asked him to explain the evidence behind his belief that trained assassins were targeting his family. He could not do so and eventually admitted that this thinking was misguided. His fears gradually shifted from specific threats targeted at him and his family to nonspecific fears of the randomness and unfairness of life.

Placing psychosis in psychological context. We tried to understand the psychology of his paranoid thoughts while viewing his symptoms as part of a neurobiologic disorder.

What initially looked like “garden variety” paranoid delusions had a psychological meaning to Mr. K. His dread of public humiliation was intertwined with his fear of assassination. Once understood, these two fears could be isolated and became easier to treat.¹⁰ We traced Mr. K’s fear for his family’s safety to his being the oldest male in a matriarchal household. Because his illness prevented him from assuming the role of breadwinner, all that was left was for him to guard his family from the imagined threat of assassination.

Caveats The CBT techniques outlined in the literature for schizophrenia vary greatly from those used in depression or anxiety disorders. In order for CBT to be effective in schizophrenia, the therapist must have considerable experience working with patients with schizophrenia and must receive specialized training and supervision in CBT techniques modified for persons with schizophrenia.

Further, Mr. K continued to take his antipsychotic medication during the 3-month CBT course. We are not suggesting that CBT be administered in lieu of drug therapy, nor can we claim that CBT will be consistently effective against positive symptoms. What’s more, this case does not take into consideration patients who are persistently psychotic because of suboptimal dosing, poor compliance, or substance abuse.

Follow-up: Continued progress

Mr. K continued to improve after the CBT sessions ended. He completed a summer art class despite recurrent paranoia and lingering fears of social interaction. As of this writing, he was considering taking another course.

Three months after his last session, Mr. K was still regularly visiting the library. He also began walking his niece to and from school each day. His paranoid ideation and ideas of reference appeared to be lessening in intensity. Last fall, he joined a gym. He also reported comfortably conversing with people other than immediate family members or mental health clinicians.

Related resources

• Grech E. A review of the current evidence for the use of psychological interventions in psychosis. Int J Psychosoc Rehab 2002;6:79-88.
• Jones C, Cormac I, et al. Cognitive behaviour therapy for schizophrenia. Cochrane Library Issue 4, 2001. Available at: http://www.mediscope.ch/cochrane-abstracts/ab000524.htm. Accessed Feb. 10, 2003.

Drug brand names

• Clozapine • Clozaril
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

Dr. Weiden reports that he receives research/grant support from, is a consultant to, and/or is a speaker for AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., Pfizer Inc., and Janssen Pharmaceutica.

Dr. Burkholder reports that she is a consultant and speaker for Pfizer Inc. and Eli Lilly and Co.

Acknowledgments

The authors wish to thank Catie Camille for her assistance in preparing this article, and Drs. Motaz El Rafae and Najma Khanani for the care they provided to Mr. K.

History: A secluded life

Mr. K, 31, immigrated to Brooklyn as a child with his family. At age 19, he was working as an auto mechanic in a relative’s garage when he had his first psychotic episode. He was hospitalized and diagnosed with paranoid schizophrenia, which was confirmed by his subsequent course of illness and a recent structured diagnostic interview.

Since becoming ill, Mr. K almost never leaves his house and socializes only with his mother and sister. Unable to work, he helps around the house and often cares for his nieces and nephews. He has no history of substance abuse and has been faithfully taking his medication since his last hospitalization 8 years ago.

Mr. K’s outpatient clinic chart reflects concern about persistent negative symptoms. He hardly speaks in session. Even when “stable,” his social and vocational functioning has been poor. Therapeutic dosages of oral haloperidol, haloperidol decanoate, and fluphenazine have not worked, and trials of risperidone and olanzapine—administered in therapeutic dosages for at least 3 months—were only slightly more effective. Attempts to treat his social withdrawal as a depressive symptom equivalent, with use of adjunctive selective serotonin reuptake inhibitors, also have been disappointing.

We eventually discovered that his so-called negative symptoms were in fact the manifestation of persistent positive symptoms (Table 1). His social withdrawal stemmed not from lack of motivation but from ideas of reference and constant paranoid fears. He believed that if he left the house, a street gang would kill him or his family. When he did venture outdoors, he thought that strangers were ridiculing or insulting him or intended to brutally attack him.

Mr. K spent much of his time at home reading, occasionally visiting the public library just long enough to check out a few books. Family members convinced him to attend church services, but he could not interact with other parishioners because he feared they would find out something was “wrong” with him.

How would you address Mr. K’s positive symptoms? Would you try another antipsychotic after lack of response to five other agents?

Drug treatment: A clinical trial

After a thorough evaluation, Mr. K entered a clinical trial during which he began taking another antipsy-chotic. But after 4 months at high therapeutic dosages, his positive symptoms showed no change from baseline.

We then recommended that Mr. K try clozapine. His persistent paranoid delusions and lack of response to other antipsychotics made him an ideal candidate for this agent. Because he was compliant, motivated, and had available family support, we were confident that he could surmount the vicissitudes of a clozapine trial.

Mr. K refused to try clozapine, however. After so many unsuccessful medication trials over the years, he said he felt some (albeit minor) benefits from his current study medication and wanted to stick with it.

What treatment options remain for Mr. K?

Dr. Weiden’s and Burkholder’s observations

Although the newer antipsychotics have greatly improved outcomes in schizophrenia over the past decade, many patients still battle persistent psychotic (positive) symptoms despite compliance with these medications.¹ While clozapine remains the treatment of choice for positive symptoms, some patients cannot—or will not—take it because of its burdensome side-effect profile.

It is well accepted that supportive psychotherapy can help a person with schizophrenia confront the secondary issues of loss, disability, and stigma. But psychotherapy is rarely considered as an adjunct therapy for treatment-resistant positive symptoms. Skepticism about the role of psychotherapy is understandable, because older studies that demonstrated psychoanalytic psychotherapy’s lack of effect on schizophrenia’s positive symptoms² have driven psychiatric medical education and practice for the past half-century. Other non-psychoanalytic therapeutic approaches had not been studied until recently, so most of us generalized from the disappointing results of the psychoanalytic psychotherapy research.

Still, there is a resurgence of interest in using cognitive-behavioral principles to treat core schizophrenia symptoms. Several randomized, controlled studies—almost all performed in the United Kingdom—have demonstrated that a cognitive-behavioral therapy (CBT) approach, modified for schizophrenia, is superior to more traditional supportive therapies in treating persistent positive and negative symptoms.^3-5 Until recently, CBT for schizophrenia has generated little interest or research on this side of the Atlantic.

Continued treatment: A new approach

At this point, we decided to address Mr. K’s paranoid symptoms with CBT-based psychotherapy. The patient, whom we’d been seeing twice monthly for medication management, agreed to weekly 45-minute CBT sessions across 3 months. A third-year resident who had treated Mr. K during the antipsychotic clinical trial administered the therapy as described in the literature.^4-6

During the first sessions, we found that some of Mr. K's fears of leaving the house stemmed from living in a poor inner-city neighborhood with a high rate of violent crime. A few sessions later, Mr. K was able to question some of his beliefs that assassins had targeted his family.

By the fourth week, the therapist discovered that Mr. K liked to read and viewed the local library as a reasonably safe place. Mr. K agreed to visit the library once a week and to record his experiences commuting to and from there.

After roughly 8 weeks of treatment, Mr. K was visiting the library twice a week, usually for 90 minutes at a time. He reported that he “had a good time,” but still suspected other library patrons were talking about him. Upon exploring these suspicions, we learned that Mr. K feared other library goers viewed him as “stupid” and that this fear was exacerbating some of his paranoid delusions.

Table 1

POSITIVE SYMPTOMS THATMAYAPPEARASNEGATIVE SYMPTOMS

Once Mr. K acknowledged that his mental illness was not outwardly recognizable, we could convince him that his fear of appearing “stupid” should not keep him housebound. He began to visit the library more frequently. Although he was still anxious, it no longer took him all day to summon the courage to leave home.

After about 10 weeks of treatment, Mr. K began going on bike rides twice a week. We were concerned that he was making too many changes at once, but he insisted he felt more “comfortable” and enjoyed the exercise.

Did cognitive-behavioral therapy contribute to Mr. K’s improvement? How did the therapist’s treatment differ from accepted protocols?

Dr. Weiden’s and Burkholder’s observations

You might be thinking, “This sounds no different from what I do in practice!” The patient was reassured and encouraged to go out and live his life despite having symptoms.

In practice, however, some techniques used in the CBT approach to psychosis are quite different; some techniques are not intuitive, and some contradict most standard teachings of supportive psychotherapy in this country.

The CBT approach used for Mr. K differed greatly from traditional “medical model” supportive psychotherapy. The therapist:

• rejected a “brain disorder” approach to describing his illness⁷
• used the stress-vulnerability model to explain positive symptoms
• viewed psychotic symptoms as normal reactions rather than pathologic response
• considered psychological factors behind specific psychotic symptoms (Table 2).⁸

The “brain disorder” explanation. The Kraepelinian model, which characterizes schizophrenia as a degenerative brain disorder, drives patient education. For example, one brochure for patients and their families refers to schizophrenia as “a brain disorder like Alzheimer’s disease.”

Such a comparison could devastate a young adult who is overwhelmed by symptoms and after being told he had a “brain disorder” that “interfered with his cognition.” While this corresponded with our knowledge of schizophrenia, he took this to mean he is “retarded” and “stupid.”

Table 2

UNDERSTANDING PSYCHOSIS WITHIN THE COGNITIVE-BEHAVIORAL MODEL

Telling the patient that he or she has schizophrenia– known in some clinical circles as “the S word”–is not necessary and may even be harmful in some cases. We’re not saying that giving a diagnosis of schizophrenia or using a medical model approach is wrong. However, patient education based on symptoms instead of diagnosis may be more conducive in some cases.

The stress-vulnerability model explains psychosis without having to use a diagnostic label. Mr. K’s previous understanding of schizophrenia dovetailed with his low self-esteem. His self-perceived stupidity also had discouraged him from confronting his paranoid anxieties.

Once he realized that unrelenting psychotic symptoms—not his IQ—held him back, we could form a treatment plan. We explained Mr. K’s paranoid symptoms with the stress-vulnerability model: His fears and suspicions worsened whenever he was under stress. This allowed us to sidestep the “brain disorder” model that demoralized him.

By no means, however, did we reject the notion that schizophrenia has a biologic basis. Even if “schizophrenia” is never mentioned, this diagnosis still guides treatment.

Viewing psychotic symptoms as normal reactions. The therapist extensively examined Mr. K’s safety concerns for himself and his family. The therapist acknowledged that these concerns were legitimate, as the patient lives in an inner-city neighborhood plagued by violent crime. Mr. K was then praised for his devotion to his family.

By applying normalization techniques,⁹ the therapist found fact-based aspects of the delusional beliefs. Normalizing Mr. K’s safety concerns made him feel validated. From there, we could map out a plan for him to periodically leave his home. We devised a routine that addressed his safety concerns: He went to the library only in daylight. He chose a subway route that was less convenient but made him feel more comfortable. Once at the library, he called home to make sure his family was safe, then sat at an open table so he could watch other library patrons come and go.

Once this routine was established, we could address the more idiosyncratic delusions that caused Mr. K considerable stress and anxiety. We asked him to explain the evidence behind his belief that trained assassins were targeting his family. He could not do so and eventually admitted that this thinking was misguided. His fears gradually shifted from specific threats targeted at him and his family to nonspecific fears of the randomness and unfairness of life.

Placing psychosis in psychological context. We tried to understand the psychology of his paranoid thoughts while viewing his symptoms as part of a neurobiologic disorder.

What initially looked like “garden variety” paranoid delusions had a psychological meaning to Mr. K. His dread of public humiliation was intertwined with his fear of assassination. Once understood, these two fears could be isolated and became easier to treat.¹⁰ We traced Mr. K’s fear for his family’s safety to his being the oldest male in a matriarchal household. Because his illness prevented him from assuming the role of breadwinner, all that was left was for him to guard his family from the imagined threat of assassination.

Caveats The CBT techniques outlined in the literature for schizophrenia vary greatly from those used in depression or anxiety disorders. In order for CBT to be effective in schizophrenia, the therapist must have considerable experience working with patients with schizophrenia and must receive specialized training and supervision in CBT techniques modified for persons with schizophrenia.

Further, Mr. K continued to take his antipsychotic medication during the 3-month CBT course. We are not suggesting that CBT be administered in lieu of drug therapy, nor can we claim that CBT will be consistently effective against positive symptoms. What’s more, this case does not take into consideration patients who are persistently psychotic because of suboptimal dosing, poor compliance, or substance abuse.

Follow-up: Continued progress

Mr. K continued to improve after the CBT sessions ended. He completed a summer art class despite recurrent paranoia and lingering fears of social interaction. As of this writing, he was considering taking another course.

Three months after his last session, Mr. K was still regularly visiting the library. He also began walking his niece to and from school each day. His paranoid ideation and ideas of reference appeared to be lessening in intensity. Last fall, he joined a gym. He also reported comfortably conversing with people other than immediate family members or mental health clinicians.

Related resources

• Grech E. A review of the current evidence for the use of psychological interventions in psychosis. Int J Psychosoc Rehab 2002;6:79-88.
• Jones C, Cormac I, et al. Cognitive behaviour therapy for schizophrenia. Cochrane Library Issue 4, 2001. Available at: http://www.mediscope.ch/cochrane-abstracts/ab000524.htm. Accessed Feb. 10, 2003.

Drug brand names

• Clozapine • Clozaril
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

Dr. Weiden reports that he receives research/grant support from, is a consultant to, and/or is a speaker for AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., Pfizer Inc., and Janssen Pharmaceutica.

Dr. Burkholder reports that she is a consultant and speaker for Pfizer Inc. and Eli Lilly and Co.

Acknowledgments

The authors wish to thank Catie Camille for her assistance in preparing this article, and Drs. Motaz El Rafae and Najma Khanani for the care they provided to Mr. K.

History: A secluded life

Mr. K, 31, immigrated to Brooklyn as a child with his family. At age 19, he was working as an auto mechanic in a relative’s garage when he had his first psychotic episode. He was hospitalized and diagnosed with paranoid schizophrenia, which was confirmed by his subsequent course of illness and a recent structured diagnostic interview.

Since becoming ill, Mr. K almost never leaves his house and socializes only with his mother and sister. Unable to work, he helps around the house and often cares for his nieces and nephews. He has no history of substance abuse and has been faithfully taking his medication since his last hospitalization 8 years ago.

Mr. K’s outpatient clinic chart reflects concern about persistent negative symptoms. He hardly speaks in session. Even when “stable,” his social and vocational functioning has been poor. Therapeutic dosages of oral haloperidol, haloperidol decanoate, and fluphenazine have not worked, and trials of risperidone and olanzapine—administered in therapeutic dosages for at least 3 months—were only slightly more effective. Attempts to treat his social withdrawal as a depressive symptom equivalent, with use of adjunctive selective serotonin reuptake inhibitors, also have been disappointing.

We eventually discovered that his so-called negative symptoms were in fact the manifestation of persistent positive symptoms (Table 1). His social withdrawal stemmed not from lack of motivation but from ideas of reference and constant paranoid fears. He believed that if he left the house, a street gang would kill him or his family. When he did venture outdoors, he thought that strangers were ridiculing or insulting him or intended to brutally attack him.

Mr. K spent much of his time at home reading, occasionally visiting the public library just long enough to check out a few books. Family members convinced him to attend church services, but he could not interact with other parishioners because he feared they would find out something was “wrong” with him.

How would you address Mr. K’s positive symptoms? Would you try another antipsychotic after lack of response to five other agents?

Drug treatment: A clinical trial

After a thorough evaluation, Mr. K entered a clinical trial during which he began taking another antipsy-chotic. But after 4 months at high therapeutic dosages, his positive symptoms showed no change from baseline.

We then recommended that Mr. K try clozapine. His persistent paranoid delusions and lack of response to other antipsychotics made him an ideal candidate for this agent. Because he was compliant, motivated, and had available family support, we were confident that he could surmount the vicissitudes of a clozapine trial.

Mr. K refused to try clozapine, however. After so many unsuccessful medication trials over the years, he said he felt some (albeit minor) benefits from his current study medication and wanted to stick with it.

What treatment options remain for Mr. K?

Dr. Weiden’s and Burkholder’s observations

Although the newer antipsychotics have greatly improved outcomes in schizophrenia over the past decade, many patients still battle persistent psychotic (positive) symptoms despite compliance with these medications.¹ While clozapine remains the treatment of choice for positive symptoms, some patients cannot—or will not—take it because of its burdensome side-effect profile.

It is well accepted that supportive psychotherapy can help a person with schizophrenia confront the secondary issues of loss, disability, and stigma. But psychotherapy is rarely considered as an adjunct therapy for treatment-resistant positive symptoms. Skepticism about the role of psychotherapy is understandable, because older studies that demonstrated psychoanalytic psychotherapy’s lack of effect on schizophrenia’s positive symptoms² have driven psychiatric medical education and practice for the past half-century. Other non-psychoanalytic therapeutic approaches had not been studied until recently, so most of us generalized from the disappointing results of the psychoanalytic psychotherapy research.

Still, there is a resurgence of interest in using cognitive-behavioral principles to treat core schizophrenia symptoms. Several randomized, controlled studies—almost all performed in the United Kingdom—have demonstrated that a cognitive-behavioral therapy (CBT) approach, modified for schizophrenia, is superior to more traditional supportive therapies in treating persistent positive and negative symptoms.^3-5 Until recently, CBT for schizophrenia has generated little interest or research on this side of the Atlantic.

Continued treatment: A new approach

At this point, we decided to address Mr. K’s paranoid symptoms with CBT-based psychotherapy. The patient, whom we’d been seeing twice monthly for medication management, agreed to weekly 45-minute CBT sessions across 3 months. A third-year resident who had treated Mr. K during the antipsychotic clinical trial administered the therapy as described in the literature.^4-6

During the first sessions, we found that some of Mr. K's fears of leaving the house stemmed from living in a poor inner-city neighborhood with a high rate of violent crime. A few sessions later, Mr. K was able to question some of his beliefs that assassins had targeted his family.

By the fourth week, the therapist discovered that Mr. K liked to read and viewed the local library as a reasonably safe place. Mr. K agreed to visit the library once a week and to record his experiences commuting to and from there.

After roughly 8 weeks of treatment, Mr. K was visiting the library twice a week, usually for 90 minutes at a time. He reported that he “had a good time,” but still suspected other library patrons were talking about him. Upon exploring these suspicions, we learned that Mr. K feared other library goers viewed him as “stupid” and that this fear was exacerbating some of his paranoid delusions.

Table 1

POSITIVE SYMPTOMS THATMAYAPPEARASNEGATIVE SYMPTOMS

Once Mr. K acknowledged that his mental illness was not outwardly recognizable, we could convince him that his fear of appearing “stupid” should not keep him housebound. He began to visit the library more frequently. Although he was still anxious, it no longer took him all day to summon the courage to leave home.

After about 10 weeks of treatment, Mr. K began going on bike rides twice a week. We were concerned that he was making too many changes at once, but he insisted he felt more “comfortable” and enjoyed the exercise.

Did cognitive-behavioral therapy contribute to Mr. K’s improvement? How did the therapist’s treatment differ from accepted protocols?

Dr. Weiden’s and Burkholder’s observations

You might be thinking, “This sounds no different from what I do in practice!” The patient was reassured and encouraged to go out and live his life despite having symptoms.

In practice, however, some techniques used in the CBT approach to psychosis are quite different; some techniques are not intuitive, and some contradict most standard teachings of supportive psychotherapy in this country.

The CBT approach used for Mr. K differed greatly from traditional “medical model” supportive psychotherapy. The therapist:

• rejected a “brain disorder” approach to describing his illness⁷
• used the stress-vulnerability model to explain positive symptoms
• viewed psychotic symptoms as normal reactions rather than pathologic response
• considered psychological factors behind specific psychotic symptoms (Table 2).⁸

The “brain disorder” explanation. The Kraepelinian model, which characterizes schizophrenia as a degenerative brain disorder, drives patient education. For example, one brochure for patients and their families refers to schizophrenia as “a brain disorder like Alzheimer’s disease.”

Such a comparison could devastate a young adult who is overwhelmed by symptoms and after being told he had a “brain disorder” that “interfered with his cognition.” While this corresponded with our knowledge of schizophrenia, he took this to mean he is “retarded” and “stupid.”

Table 2

UNDERSTANDING PSYCHOSIS WITHIN THE COGNITIVE-BEHAVIORAL MODEL

Telling the patient that he or she has schizophrenia– known in some clinical circles as “the S word”–is not necessary and may even be harmful in some cases. We’re not saying that giving a diagnosis of schizophrenia or using a medical model approach is wrong. However, patient education based on symptoms instead of diagnosis may be more conducive in some cases.

The stress-vulnerability model explains psychosis without having to use a diagnostic label. Mr. K’s previous understanding of schizophrenia dovetailed with his low self-esteem. His self-perceived stupidity also had discouraged him from confronting his paranoid anxieties.

Once he realized that unrelenting psychotic symptoms—not his IQ—held him back, we could form a treatment plan. We explained Mr. K’s paranoid symptoms with the stress-vulnerability model: His fears and suspicions worsened whenever he was under stress. This allowed us to sidestep the “brain disorder” model that demoralized him.

By no means, however, did we reject the notion that schizophrenia has a biologic basis. Even if “schizophrenia” is never mentioned, this diagnosis still guides treatment.

Viewing psychotic symptoms as normal reactions. The therapist extensively examined Mr. K’s safety concerns for himself and his family. The therapist acknowledged that these concerns were legitimate, as the patient lives in an inner-city neighborhood plagued by violent crime. Mr. K was then praised for his devotion to his family.

By applying normalization techniques,⁹ the therapist found fact-based aspects of the delusional beliefs. Normalizing Mr. K’s safety concerns made him feel validated. From there, we could map out a plan for him to periodically leave his home. We devised a routine that addressed his safety concerns: He went to the library only in daylight. He chose a subway route that was less convenient but made him feel more comfortable. Once at the library, he called home to make sure his family was safe, then sat at an open table so he could watch other library patrons come and go.

Once this routine was established, we could address the more idiosyncratic delusions that caused Mr. K considerable stress and anxiety. We asked him to explain the evidence behind his belief that trained assassins were targeting his family. He could not do so and eventually admitted that this thinking was misguided. His fears gradually shifted from specific threats targeted at him and his family to nonspecific fears of the randomness and unfairness of life.

Placing psychosis in psychological context. We tried to understand the psychology of his paranoid thoughts while viewing his symptoms as part of a neurobiologic disorder.

What initially looked like “garden variety” paranoid delusions had a psychological meaning to Mr. K. His dread of public humiliation was intertwined with his fear of assassination. Once understood, these two fears could be isolated and became easier to treat.¹⁰ We traced Mr. K’s fear for his family’s safety to his being the oldest male in a matriarchal household. Because his illness prevented him from assuming the role of breadwinner, all that was left was for him to guard his family from the imagined threat of assassination.

Caveats The CBT techniques outlined in the literature for schizophrenia vary greatly from those used in depression or anxiety disorders. In order for CBT to be effective in schizophrenia, the therapist must have considerable experience working with patients with schizophrenia and must receive specialized training and supervision in CBT techniques modified for persons with schizophrenia.

Further, Mr. K continued to take his antipsychotic medication during the 3-month CBT course. We are not suggesting that CBT be administered in lieu of drug therapy, nor can we claim that CBT will be consistently effective against positive symptoms. What’s more, this case does not take into consideration patients who are persistently psychotic because of suboptimal dosing, poor compliance, or substance abuse.

Follow-up: Continued progress

Mr. K continued to improve after the CBT sessions ended. He completed a summer art class despite recurrent paranoia and lingering fears of social interaction. As of this writing, he was considering taking another course.

Three months after his last session, Mr. K was still regularly visiting the library. He also began walking his niece to and from school each day. His paranoid ideation and ideas of reference appeared to be lessening in intensity. Last fall, he joined a gym. He also reported comfortably conversing with people other than immediate family members or mental health clinicians.

Related resources

• Grech E. A review of the current evidence for the use of psychological interventions in psychosis. Int J Psychosoc Rehab 2002;6:79-88.
• Jones C, Cormac I, et al. Cognitive behaviour therapy for schizophrenia. Cochrane Library Issue 4, 2001. Available at: http://www.mediscope.ch/cochrane-abstracts/ab000524.htm. Accessed Feb. 10, 2003.

Drug brand names

• Clozapine • Clozaril
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Risperidone • Risperdal

Disclosure

Dr. Weiden reports that he receives research/grant support from, is a consultant to, and/or is a speaker for AstraZeneca Pharmaceuticals, Bristol-Myers Squibb Co., Pfizer Inc., and Janssen Pharmaceutica.

Dr. Burkholder reports that she is a consultant and speaker for Pfizer Inc. and Eli Lilly and Co.

Acknowledgments

The authors wish to thank Catie Camille for her assistance in preparing this article, and Drs. Motaz El Rafae and Najma Khanani for the care they provided to Mr. K.

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resource

• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

Initial visit: Road rage or ‘roid’ rage?

Mr. A, 25, was arrested after police interrupted an altercation between him and a senior citizen at a stoplight. He had emerged from his car, walked over to the older driver in front of him, ripped open the car door, and pulled the man out of the car and onto the street. He was still yelling at the victim when a passing officer intervened.

Mr. A was charged with assault. After a plea bargain, he was sentenced to probation and fined. He had been seeing his probation officer every 2 weeks, but his parents were worried about his erratic and sometimes defiant behavior and insisted he see a psychiatrist. He reluctantly agreed to one consultation, largely because his parents threatened to withhold financial support if he failed to do so.

The first thing the psychiatrist noticed was Mr. A’s striking muscular appearance. He was approximately 5 feet, 7 inches tall, weighed at least 200 pounds, and had a 30-inch waist and less than 10% body fat.

Dr. Carter’s and Pope’s observations

Mr. A’s diagnosis should be suspected immediately upon his entering the office. Extensive anabolic steroid use produces body changes that can be diagnosed almost at a glance. It is virtually impossible to achieve a level of muscle mass comparable to what Mr. A exhibited without the use of anabolic steroids.¹

Remarkably, however, most people—including Mr. A’s parents, law enforcement personnel, and even some members of the treatment team—failed to diagnose Mr. A’s steroid use. He somehow convinced them that his extreme muscularity was the result of hard work, dedication, and scrupulous attention to diet. This suggests that steroid abuse cases involving serious violence—such as that of Mr. A—frequently go unreported and undiagnosed and are probably more common than we suspect.

Epidemiologic data suggest that clinicians should become familiar with the presentation of patients who are using anabolic steroids (Box).

Evaluation: ‘Stacking’ up

Mr. A at first vehemently denied that he had ever used anabolic steroids. After a more detailed conversation, during which the clinician demonstrated some knowledge of this area, Mr. A eventually conceded that he was taking a substantial weekly dose of the drugs at the time of the assault.

A subsequent clinical evaluation revealed that Mr. A had taken several ‘cycles’ (courses) of anabolic steroids over the last 2 to 3 years. Each cycle lasted 10 to 16 weeks and had been characterized by simultaneous use of two or more steroids, a practice known as ‘stacking.’

Mr. A started his first cycle with a modest ‘stack’ of drugs: testosterone cypionate, 200 mg twice a week, and stanozolol, 10 mg/d. Taken together, these dosages represented roughly 470 mg of testosterone equivalent per week—about 10 times the weekly secretion of testosterone in a normal male. He noticed no change in mood during this initial cycle.

With subsequent cycles, however, Mr. A became increasingly obsessed with his body image and used higher dosages. When the assault occurred, he was taking testosterone cypionate, 800 mg a week, nandrolone decanoate, 400 mg a week, and oxymetholone, 50 mg/d. With this regimen—the weekly equivalent of 1,550 mg of testosterone—Mr. A noticed prominent mood changes that met DSM-IV criteria for a manic episode. He experienced euphoria, dramatic irritability, limitless self-confidence, decreased need for sleep, distractibility, extreme recklessness (driving too fast, spending too freely), and some mildly paranoid ideation (without frank delusions). He admitted that he had twice assaulted his girlfriend and that he invariably became enraged at even the slightest annoyance when driving in traffic. He revealed that although the altercation with the older driver had led to his first arrest for ‘road rage,’ it was his third such incident.

The clinician warned Mr. A that continued steroid use could worsen his behavior—and lead to more serious trouble later on. Mr. A, however, said he was more afraid of losing muscle mass and becoming ‘small again.’ When the clinician mentioned that use of anabolic steroids without a prescription is illegal, Mr. A retorted that several of his friends had used the drugs without legal consequences.

Mr. A left the office showing no inclination to return for further treatment. The clinician could only offer to be available in the future.

Box

What medical sequelae await Mr. A if he continues to abuse steroids? How would you convince him to stay in treatment?

Dr. Carter’s and Pope’s observations

Mr. A’s path to mania has been well demonstrated in the literature. Hypomania or even frank manic syndromes, sometimes associated with violent behavior, are rare at weekly doses of 300 mg of testosterone equivalent. At weekly doses of >1,000 mg, psychiatric syndromes such as hypomania or mania may occur in almost one-half of cases.⁵

If he continues to abuse anabolic steroids, however, Mr. A could experience adverse physical reactions ranging from embarrassing acne and male-pattern baldness (Table 1) to rare and life-threatening hepatic effects such as cholestatic jaundice and peliosis hepatitis (blood-filled cysts in the liver).

Table 1

ANABOLIC STEROID ABUSE: COMMON PHYSICAL FINDINGS

The risk of atherosclerotic disease or prostate cancer later in life may also be greatly increased.

More common laboratory changes include:

• increased red blood cell count, hemoglobin and hematocrit
• elevated liver function readings (although these must not be confused with enzymes that originate from muscle tissue)
• and unfavorable changes in triglycerides, total cholesterol, and HDL:LDL cholesterol ratios (Table 2).

Other potential laboratory changes with steroid abuse include decreased luteinizing hormone and follicle-stimulating hormone due to feedback inhibition. Feedback inhibition will also reduce testosterone and estradiol levels with use of anabolic steroids other than testosterone esters. These levels, however, would both be elevated with use of testosterone esters alone.

In men, testicular atrophy and decreased sperm count are generally reversible manifestations of steroid abuse, whereas gynecomastia may be irreversible and require surgical intervention in advanced cases.^3,6 Women who use anabolic steroids (such as for body-building) are vulnerable to disrupted menstrual cycles, decreased breast size, and masculinizing effects including enlarged clitoris, hirsutism, and deepening of the voice.⁶

In adolescents, anabolic steroid use may cause premature closure of the epiphyses, leading to shortened stature.³

Unfortunately, warnings about these many adverse effects rarely deter anabolic steroid users such as Mr. A or persuade them to continue in treatment of any type. Most young anabolic steroid abusers report that they have never felt significant adverse effects from steroid use and know of no one who has experienced such effects. The dramatic muscle gains they have witnessed in themselves and in other users decisively outweigh what they perceive to be remote threats of adverse consequences.

Follow-up: Return to treatment

We didn’t hear from Mr. A until about 18 months later, when he unexpectedly requested a consultation.

Upon arrival, Mr. A exhibited major depression with prominent anhedonia, hypersomnia of 12 to 14 hours per night, loss of appetite, fatigue, prominent psychomotor retardation, feelings of guilt, difficulty concentrating, and suicidal thoughts (but without a frank plan). He also reported panic attacks that were randomly occurring each day, usually in public.

Mr. A conceded that he had experienced similar depressive episodes after stopping anabolic steroid use, but that they typically ran their course after 2 to 3 weeks. He said the present episode showed no sign of abating after nearly 2 months. He had attempted to ‘treat’ this episode by resuming anabolic steroid use, but he could not get an adequate supply from his dealer.

Mr. A’s total testosterone level, measured in the morning when it should be near its diurnal peak, was 127 ng/dl (normal range is 270 to 1,070 ng/dl). Physical examination revealed that his testicles had shrunk to the size of marbles (each approximately 5 mm in diameter). He was referred to an endocrinologist for evaluation and was simultaneously started on fluoxetine, 20 mg/d.

Table 2

LABORATORY ABNORMALITIES ASSOCIATED WITH ANABOLIC STEROID ABUSE

He returned 2 weeks later, exhibiting little improvement and wanting to resume steroids ‘because it was the only thing that really helped.’ Instead, he agreed to continue on fluoxetine and remain in follow-up. At 4 weeks, he noticed a decrease in panic attacks, return of normal mood, decreased anhedonia, and loss of suicidal ideation. He continued taking fluoxetine for another 3 months but then abruptly disappeared from treatment.

Mr. A resurfaced about 1 year later, revealing to the psychiatrist that he had taken yet another cycle of anabolic steroids, largely because he feared losing his muscle mass. His panic attacks had recurred almost immediately when he began tapering down from the peak of this cycle, and he agreed to resume taking fluoxetine.

A look at Mr. A’s extended history may provide clues to his persistent anabolic steroid abuse problem. He had displayed prominent symptoms of conduct disorder as a child. He had been truant from school, had occasionally run away from home, and had been involved in several misdemeanors. While in high school, he typically drank 10 to 12 beers over a weekend and had experimented with hallucinogenic mushrooms and 3,4-methylenedioxymethamphetamine (‘ecstasy’).

He started weightlifting while in high school and by age 17 was visiting the gym every day. He began college on a football scholarship but dropped out after 1 year. Starting in his early 20s, he competed in several bodybuilding contests.

Despite his impressive muscularity, Mr. A was anxious about his body appearance. He often would not take off his shirt—even when at the beach or a swimming pool—for fear that he would appear too small. He sometimes wore heavy sweatpants in the sweltering heat to conceal his legs. He also admitted spending as much as 2 hours a day examining himself in the mirror. ‘Sometimes when I get a bad (look at) myself, I will refuse to go out for the rest of the day,’ he said.

Mr. A has had a succession of girlfriends, but his rigid commitment to diet and exercise invariably ended these relationships.

At this point, would you first address Mr. A’s apparent substance use problem or the underlying body dysmorphic symptoms?

Dr. Carter’s and Pope’s observations

Two comorbidities noted here—substance abuse and body dysmorphic disorder—are common among anabolic steroid abusers. Addressing these problems, especially the body dysmorphic disorder, may sometimes help patients who are unwilling to address their steroid use directly. Body dysmorphic disorder may respond to selective serotonin reuptake inhibitors⁷ and cognitive-behavioral therapy.⁸

Anabolic steroids are not associated with immediate intoxicating effects, and ICD-10 categorizes them as substances not associated with dependence. After prolonged use at high doses, however, anabolic steroids are often associated with euphoria. Researchers also have found that some steroid abusers do meet DSM-IV criteria for substance dependence.⁶

Beyond the direct psychotropic effects of anabolic steroids, the depressive symptoms commonly seen during their withdrawal may perpetuate the dependence, as was the case with Mr. A. Most depressive symptoms that follow steroid cessation do not require drug therapy,³ but Mr. A developed severe and persistent depressive symptoms, complicated by panic disorder and body image concerns at a level diagnostic of body dysmorphic disorder. Such body image concerns often precipitate relapse into steroid use.

Conclusion: Another setback

As of this writing, Mr. A is again lost to follow-up. After taking fluoxetine and keeping monthly appointments for about 6 months, he failed to arrive for a visit and did not set another appointment. The patient may have once again stopped medication and embarked on yet another cycle of anabolic steroid use. If this is so, we can only hope that he returns to treatment before it is too late.

Related resources

• NIDA Research Report: Anabolic Steroid Abuse. http://www.nida.nih.gov/ResearchReports/Steroids/AnabolicSteroids.html
• Lukas SE. Steroids. Hillside, NJ: Enslow Publishers, 1994.

Drug brand names

• Fluoxetine • Prozac
• Nandrolone decanoate • Deca-Durabolin
• Oxymetholone • Anadrol
• Stanozolol • Winstrol

Disclosure

Dr. Carter reports that he receives research/grant support from or is a consultant to Eli Lilly and Co., Pfizer Inc., and Ortho-McNeil Pharmaceutical.

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

History: Noncompliance and ‘resignation’

Mr. V, 43, has a history of diabetes. He was admitted to the hospital with altered mental status as manifested by confusion, fluctuating sensorium, and disorientation. His altered mental status was most likely caused by septicemia secondary to osteomyelitis from a right plantar foot ulcer that had become necrotic, tracking through the foot bones into the tibia and fibula.

An emergent amputation was performed of the right tibia and fibula approximately 15 cm distal to the patella, with intent to close the wound within 24 to 48 hours; Mr. V also was started on IV antibiotics. The patient, however, refused the closure procedure, stating that he had not been properly informed before the amputation and would not consent to another procedure until he could speak with his elder brothers.

The surgical team noted that Mr. V had signed the consent form before the amputation. The surgeons also feared that not closing the wound promptly could lead to reinfection, further limb loss, or even death.

The hospital’s psychiatric consultation service was asked to determine the patient’s mental capacity. It should be noted that Mr. V emigrated to the United States from a Laotian refugee camp 12 years prior to admission. He speaks only Hmong, the language of the Hmong people indigenous to Southeast Asia.

Mr. V was diagnosed 12 years ago with insulin-dependent diabetes mellitus and has been hospitalized numerous times for foot ulcers. His chart indicates that he has repeatedly disregarded doctors’ orders and has not performed proper foot hygiene.

Previous physicians and caregivers, however, were even more frustrated with the apparent attitude of resignation with which Mr. V has approached his diabetes. He seems to believe that his medical condition is causing his problems and that he cannot prevent diabetic sequelae. He has no history of mental disorders and to our knowledge had never received a psychiatric evaluation.

Why has Mr. V. not complied with diabetes treatment? Is he unable to understand the gravity of his condition?

Dr. Krassner’s observations

Noncompliance is a recurring theme in the treatment of Hmong patients,^1-4 as is clinician frustration with their lack of compliance.^5,6 This suggests that cultural differences that could have contributed to Mr. V’s noncompliance need to be examined before determining his mental state.

Approaching a culturally sensitive case with an open mind and a respectful attitude will increase the chances of a positive outcome and provide a valuable learning experience for the clinician. You might proceed as follows:

Question your assumptions. Some clinicians assume that psychiatry applies universally to any patient, regardless of cultural background. However, the categories psychiatry imposes on illnesses may not adequately describe an illness as a patient of a different culture experiences it.^7-9

Find an interpreter—one who speaks the language and has a “lexicon for emotional experience” similar to the patient’s.¹⁰ In this case, we wanted an interpreter who not only spoke Hmong, but who understood the complexities of the animistic Hmong spirituality and could reconcile it with our empirically derived Western belief system.

Depending on a family member to translate can be problematic if that person cannot accurately explain the patient’s disorder, the need for treatment, or the implications of noncompliance. We found the ideal interpreter: a Hmong registered nurse. If you cannot find an interpreter of the same ethnicity as the patient, at least find one who speaks the same language.

Beware of misinterpretation. A patient from another culture who understands some English may not assign the same meaning to words or phrases that we do. For example, when a Hmong says yes, he or she means, “I am listening, and I respect what you’re saying.” In this way, “yes” can be mistaken for consent; noncompliance by Hmong patients can often be traced to this misinterpretation.¹¹

Define “capacity” and its implications. Capacity is always assessed in the context of the question, “capacity to do what?” The context must be explicitly identified, because life decisions require varying levels of capacity. For example, elderly patients with dementia often lack capacity to manage their finances, but have capacity to resolve end-of-life issues (e.g., hospice placement, do-not-resuscitate requests).

For Mr. V, the question was whether he had capacity to refuse the second surgery. To have capacity to consent to or refuse a procedure, a patient must understand the procedure, its risks and benefits, and the risks and benefits of refusing the procedure. The patient also must not be vulnerable to coercion (e.g., by a family member).

Clearly, Mr. V understood the procedure based on his notions of health, illness, life, death, family, social structure, and other concepts.^6,12,13 One might question whether a patient such as Mr. V is ever fully informed before giving consent. Even though he had signed a consent form for the amputation, the signature in his eyes did not qualify as consent. Further, having read through our hospital’s consent form, I defy anyone to translate its legal subtleties into Hmong.

Perhaps even more important, the Hmong adhere to a strict social hierarchy: males are held in higher esteem than females, the elderly higher than the young.^6,11,14 Therefore, Mr. V’s desire to ask his brothers for advice before consenting to surgery makes sense within his cultural norms and was not a stalling tactic as the surgeons believed.

Try to understand the patient’s concept of illness. We found Mr. V to have capacity within the confines of his medical understanding. He knew the operation was major surgery, and he wanted to consult with his elder brothers—all eight of them (most of whom live in Minneapolis)—prior to consenting. Conversely, the surgeons could think only within the confines of their cultural and clinical understanding. They wanted to perform the procedure expediently to avoid additional diabetic sequelae.

We discussed these concerns with the patient and surgeons and struck a compromise: the surgeons agreed to defer surgery for 10 days, as long as Mr. V indemnified them against complications secondary to the delay. After that, the surgery would be performed regardless of whether Mr. V had consulted his brothers. Mr. V also agreed to continue IV antibiotic therapy. This compliance is not paradoxical: the Hmong often accept antibiotics because of their relatively rapid efficacy.⁶

For clinicians wishing to understand the Hmong and their view of illness, Anne Fadiman’s The Spirit Catches You and You Fall Down is an excellent resource.⁶ Kleinman’s seminal work on treating patients from other cultures also emphasizes the importance of eliciting the patient’s understanding in order to diagnose and negotiate treatment.¹⁵ Several good textbooks address transcultural patient care; curiously, most are nursing rather than physician texts (see “Related resources,”).

Treatment: Recovery’s rocky road

Closure was delayed for 8 days, during which no complications arose. Mr. V tolerated the antibiotics well. He contracted a low-grade fever at times, but septicemia did not re-emerge.

We continued to follow the patient, who on several occasions became delirious. He was neither violent nor agitated, so he was not treated with neuroleptics, which can cause delirium in Hmong patients.^3,4

The patient contacted his brothers and consented to closure surgery, after which he recuperated well for 3 days. On day four, however, he developed respiratory failure. He was resuscitated, intubated, and transferred to the intensive care unit. He was extubated and returned to the floor 24 hours later, at which time he appeared despondent. He exhibited depressed mood, blunted affect, anorexia, anhedonia, and minimal interaction with family or physicians.

Could a different approach to treatment have produced a more favorable response? Also, would you address Mr. V’s depression and, if so, how?

Dr. Krassner’s observations

One might argue that being culturally sensitive and exposing Mr. V to the risks of infection and respiratory distress was a poor medical judgment. This argument takes into account only the biological aspect of Mr. V’s illness, however. Viewed from a biopsychosocial perspective, Mr. V’s course, even with its vicissitudes, was not a “failure” in any sense. He consented to the procedure on his own terms. We identified roadblocks to treatment and unearthed cultural resources (in our case, the patient’s brothers) that could enhance or even replace traditional psychiatric treatments.

To treat Mr. V’s depression, we first assessed the symptoms. We then tried to understand how he experienced his illness within the context of his culture.⁸ Mr. V’s symptoms certainly implied depression, but in many Asian cultures, patients with depression often present with somatic complaints.¹

Also, how were we to know that these symptoms were not due to what Asian cultures refer to as loss of vital energy—or qi—because his sadness and frustration compressed on his heart?¹ In order to treat Mr. V’s depression, we must instead call it qi. Only then can we diagnose and treat the patient in a way that makes sense to him or her.¹⁵

Even arriving at a differential diagnosis is complicated. For example, if Mr. V were Chinese, we would have to include (in addition to our own narrowly defined depression and dysthymia): mên, depressed or troubled; fan-tsao, anxious or troubled; kan-huo, angry; and hsin-ching pu-hao, generalized, nonspecific emotional upset or bad spirits.¹⁵

Further treatment: From grave to grateful

Mr. V was started on sertraline, 50 mg/d, for symptoms of depression. He tolerated the agent well (no GI upset or other side effects). After only 1 week, he had a brighter affect and was more conversant. He expressed thanks for all we had done for him.

The remainder of his recovery was incident-free, and he was discharged 6 days later on sertraline, with psychiatric follow-up arranged with the county mental health services’ Southeast Asian Team.

Related resources

• Giger JN, Davidhizar RE. Transcultural nursing: assessment & intervention (3rd ed). St. Louis: Mosby, 1999.
• Leininger M, McFarland M. Transcultural nursing: concepts, theories, research & practice (2nd ed). New York: McGraw-Hill, 1995.
• Spector RE. Cultural diversity in health & illness (5th ed). Upper Saddle River, NJ: Prentice Hall Health, 2000.

Author affiliations

David Krassner, MD, third-year resident in psychiatry, department of psychiatry, University of California at San Francisco-Fresno Residency Training Program, Fresno, CA.

Drug brand names

• Sertraline • Zoloft

History: Noncompliance and ‘resignation’

Mr. V, 43, has a history of diabetes. He was admitted to the hospital with altered mental status as manifested by confusion, fluctuating sensorium, and disorientation. His altered mental status was most likely caused by septicemia secondary to osteomyelitis from a right plantar foot ulcer that had become necrotic, tracking through the foot bones into the tibia and fibula.

An emergent amputation was performed of the right tibia and fibula approximately 15 cm distal to the patella, with intent to close the wound within 24 to 48 hours; Mr. V also was started on IV antibiotics. The patient, however, refused the closure procedure, stating that he had not been properly informed before the amputation and would not consent to another procedure until he could speak with his elder brothers.

The surgical team noted that Mr. V had signed the consent form before the amputation. The surgeons also feared that not closing the wound promptly could lead to reinfection, further limb loss, or even death.

The hospital’s psychiatric consultation service was asked to determine the patient’s mental capacity. It should be noted that Mr. V emigrated to the United States from a Laotian refugee camp 12 years prior to admission. He speaks only Hmong, the language of the Hmong people indigenous to Southeast Asia.

Mr. V was diagnosed 12 years ago with insulin-dependent diabetes mellitus and has been hospitalized numerous times for foot ulcers. His chart indicates that he has repeatedly disregarded doctors’ orders and has not performed proper foot hygiene.

Previous physicians and caregivers, however, were even more frustrated with the apparent attitude of resignation with which Mr. V has approached his diabetes. He seems to believe that his medical condition is causing his problems and that he cannot prevent diabetic sequelae. He has no history of mental disorders and to our knowledge had never received a psychiatric evaluation.

Why has Mr. V. not complied with diabetes treatment? Is he unable to understand the gravity of his condition?

Dr. Krassner’s observations

Noncompliance is a recurring theme in the treatment of Hmong patients,^1-4 as is clinician frustration with their lack of compliance.^5,6 This suggests that cultural differences that could have contributed to Mr. V’s noncompliance need to be examined before determining his mental state.

Approaching a culturally sensitive case with an open mind and a respectful attitude will increase the chances of a positive outcome and provide a valuable learning experience for the clinician. You might proceed as follows:

Question your assumptions. Some clinicians assume that psychiatry applies universally to any patient, regardless of cultural background. However, the categories psychiatry imposes on illnesses may not adequately describe an illness as a patient of a different culture experiences it.^7-9

Find an interpreter—one who speaks the language and has a “lexicon for emotional experience” similar to the patient’s.¹⁰ In this case, we wanted an interpreter who not only spoke Hmong, but who understood the complexities of the animistic Hmong spirituality and could reconcile it with our empirically derived Western belief system.

Depending on a family member to translate can be problematic if that person cannot accurately explain the patient’s disorder, the need for treatment, or the implications of noncompliance. We found the ideal interpreter: a Hmong registered nurse. If you cannot find an interpreter of the same ethnicity as the patient, at least find one who speaks the same language.

Beware of misinterpretation. A patient from another culture who understands some English may not assign the same meaning to words or phrases that we do. For example, when a Hmong says yes, he or she means, “I am listening, and I respect what you’re saying.” In this way, “yes” can be mistaken for consent; noncompliance by Hmong patients can often be traced to this misinterpretation.¹¹

Define “capacity” and its implications. Capacity is always assessed in the context of the question, “capacity to do what?” The context must be explicitly identified, because life decisions require varying levels of capacity. For example, elderly patients with dementia often lack capacity to manage their finances, but have capacity to resolve end-of-life issues (e.g., hospice placement, do-not-resuscitate requests).

For Mr. V, the question was whether he had capacity to refuse the second surgery. To have capacity to consent to or refuse a procedure, a patient must understand the procedure, its risks and benefits, and the risks and benefits of refusing the procedure. The patient also must not be vulnerable to coercion (e.g., by a family member).

Clearly, Mr. V understood the procedure based on his notions of health, illness, life, death, family, social structure, and other concepts.^6,12,13 One might question whether a patient such as Mr. V is ever fully informed before giving consent. Even though he had signed a consent form for the amputation, the signature in his eyes did not qualify as consent. Further, having read through our hospital’s consent form, I defy anyone to translate its legal subtleties into Hmong.

Perhaps even more important, the Hmong adhere to a strict social hierarchy: males are held in higher esteem than females, the elderly higher than the young.^6,11,14 Therefore, Mr. V’s desire to ask his brothers for advice before consenting to surgery makes sense within his cultural norms and was not a stalling tactic as the surgeons believed.

Try to understand the patient’s concept of illness. We found Mr. V to have capacity within the confines of his medical understanding. He knew the operation was major surgery, and he wanted to consult with his elder brothers—all eight of them (most of whom live in Minneapolis)—prior to consenting. Conversely, the surgeons could think only within the confines of their cultural and clinical understanding. They wanted to perform the procedure expediently to avoid additional diabetic sequelae.

We discussed these concerns with the patient and surgeons and struck a compromise: the surgeons agreed to defer surgery for 10 days, as long as Mr. V indemnified them against complications secondary to the delay. After that, the surgery would be performed regardless of whether Mr. V had consulted his brothers. Mr. V also agreed to continue IV antibiotic therapy. This compliance is not paradoxical: the Hmong often accept antibiotics because of their relatively rapid efficacy.⁶

For clinicians wishing to understand the Hmong and their view of illness, Anne Fadiman’s The Spirit Catches You and You Fall Down is an excellent resource.⁶ Kleinman’s seminal work on treating patients from other cultures also emphasizes the importance of eliciting the patient’s understanding in order to diagnose and negotiate treatment.¹⁵ Several good textbooks address transcultural patient care; curiously, most are nursing rather than physician texts (see “Related resources,”).

Treatment: Recovery’s rocky road

Closure was delayed for 8 days, during which no complications arose. Mr. V tolerated the antibiotics well. He contracted a low-grade fever at times, but septicemia did not re-emerge.

We continued to follow the patient, who on several occasions became delirious. He was neither violent nor agitated, so he was not treated with neuroleptics, which can cause delirium in Hmong patients.^3,4

The patient contacted his brothers and consented to closure surgery, after which he recuperated well for 3 days. On day four, however, he developed respiratory failure. He was resuscitated, intubated, and transferred to the intensive care unit. He was extubated and returned to the floor 24 hours later, at which time he appeared despondent. He exhibited depressed mood, blunted affect, anorexia, anhedonia, and minimal interaction with family or physicians.

Could a different approach to treatment have produced a more favorable response? Also, would you address Mr. V’s depression and, if so, how?

Dr. Krassner’s observations

One might argue that being culturally sensitive and exposing Mr. V to the risks of infection and respiratory distress was a poor medical judgment. This argument takes into account only the biological aspect of Mr. V’s illness, however. Viewed from a biopsychosocial perspective, Mr. V’s course, even with its vicissitudes, was not a “failure” in any sense. He consented to the procedure on his own terms. We identified roadblocks to treatment and unearthed cultural resources (in our case, the patient’s brothers) that could enhance or even replace traditional psychiatric treatments.

To treat Mr. V’s depression, we first assessed the symptoms. We then tried to understand how he experienced his illness within the context of his culture.⁸ Mr. V’s symptoms certainly implied depression, but in many Asian cultures, patients with depression often present with somatic complaints.¹

Also, how were we to know that these symptoms were not due to what Asian cultures refer to as loss of vital energy—or qi—because his sadness and frustration compressed on his heart?¹ In order to treat Mr. V’s depression, we must instead call it qi. Only then can we diagnose and treat the patient in a way that makes sense to him or her.¹⁵

Even arriving at a differential diagnosis is complicated. For example, if Mr. V were Chinese, we would have to include (in addition to our own narrowly defined depression and dysthymia): mên, depressed or troubled; fan-tsao, anxious or troubled; kan-huo, angry; and hsin-ching pu-hao, generalized, nonspecific emotional upset or bad spirits.¹⁵

Further treatment: From grave to grateful

Mr. V was started on sertraline, 50 mg/d, for symptoms of depression. He tolerated the agent well (no GI upset or other side effects). After only 1 week, he had a brighter affect and was more conversant. He expressed thanks for all we had done for him.

The remainder of his recovery was incident-free, and he was discharged 6 days later on sertraline, with psychiatric follow-up arranged with the county mental health services’ Southeast Asian Team.

Related resources

• Giger JN, Davidhizar RE. Transcultural nursing: assessment & intervention (3rd ed). St. Louis: Mosby, 1999.
• Leininger M, McFarland M. Transcultural nursing: concepts, theories, research & practice (2nd ed). New York: McGraw-Hill, 1995.
• Spector RE. Cultural diversity in health & illness (5th ed). Upper Saddle River, NJ: Prentice Hall Health, 2000.

Author affiliations

David Krassner, MD, third-year resident in psychiatry, department of psychiatry, University of California at San Francisco-Fresno Residency Training Program, Fresno, CA.

Drug brand names

• Sertraline • Zoloft

History: Noncompliance and ‘resignation’

Mr. V, 43, has a history of diabetes. He was admitted to the hospital with altered mental status as manifested by confusion, fluctuating sensorium, and disorientation. His altered mental status was most likely caused by septicemia secondary to osteomyelitis from a right plantar foot ulcer that had become necrotic, tracking through the foot bones into the tibia and fibula.

An emergent amputation was performed of the right tibia and fibula approximately 15 cm distal to the patella, with intent to close the wound within 24 to 48 hours; Mr. V also was started on IV antibiotics. The patient, however, refused the closure procedure, stating that he had not been properly informed before the amputation and would not consent to another procedure until he could speak with his elder brothers.

The surgical team noted that Mr. V had signed the consent form before the amputation. The surgeons also feared that not closing the wound promptly could lead to reinfection, further limb loss, or even death.

The hospital’s psychiatric consultation service was asked to determine the patient’s mental capacity. It should be noted that Mr. V emigrated to the United States from a Laotian refugee camp 12 years prior to admission. He speaks only Hmong, the language of the Hmong people indigenous to Southeast Asia.

Mr. V was diagnosed 12 years ago with insulin-dependent diabetes mellitus and has been hospitalized numerous times for foot ulcers. His chart indicates that he has repeatedly disregarded doctors’ orders and has not performed proper foot hygiene.

Previous physicians and caregivers, however, were even more frustrated with the apparent attitude of resignation with which Mr. V has approached his diabetes. He seems to believe that his medical condition is causing his problems and that he cannot prevent diabetic sequelae. He has no history of mental disorders and to our knowledge had never received a psychiatric evaluation.

Why has Mr. V. not complied with diabetes treatment? Is he unable to understand the gravity of his condition?

Dr. Krassner’s observations

Noncompliance is a recurring theme in the treatment of Hmong patients,^1-4 as is clinician frustration with their lack of compliance.^5,6 This suggests that cultural differences that could have contributed to Mr. V’s noncompliance need to be examined before determining his mental state.

Approaching a culturally sensitive case with an open mind and a respectful attitude will increase the chances of a positive outcome and provide a valuable learning experience for the clinician. You might proceed as follows:

Question your assumptions. Some clinicians assume that psychiatry applies universally to any patient, regardless of cultural background. However, the categories psychiatry imposes on illnesses may not adequately describe an illness as a patient of a different culture experiences it.^7-9

Find an interpreter—one who speaks the language and has a “lexicon for emotional experience” similar to the patient’s.¹⁰ In this case, we wanted an interpreter who not only spoke Hmong, but who understood the complexities of the animistic Hmong spirituality and could reconcile it with our empirically derived Western belief system.

Depending on a family member to translate can be problematic if that person cannot accurately explain the patient’s disorder, the need for treatment, or the implications of noncompliance. We found the ideal interpreter: a Hmong registered nurse. If you cannot find an interpreter of the same ethnicity as the patient, at least find one who speaks the same language.

Beware of misinterpretation. A patient from another culture who understands some English may not assign the same meaning to words or phrases that we do. For example, when a Hmong says yes, he or she means, “I am listening, and I respect what you’re saying.” In this way, “yes” can be mistaken for consent; noncompliance by Hmong patients can often be traced to this misinterpretation.¹¹

Define “capacity” and its implications. Capacity is always assessed in the context of the question, “capacity to do what?” The context must be explicitly identified, because life decisions require varying levels of capacity. For example, elderly patients with dementia often lack capacity to manage their finances, but have capacity to resolve end-of-life issues (e.g., hospice placement, do-not-resuscitate requests).

For Mr. V, the question was whether he had capacity to refuse the second surgery. To have capacity to consent to or refuse a procedure, a patient must understand the procedure, its risks and benefits, and the risks and benefits of refusing the procedure. The patient also must not be vulnerable to coercion (e.g., by a family member).

Clearly, Mr. V understood the procedure based on his notions of health, illness, life, death, family, social structure, and other concepts.^6,12,13 One might question whether a patient such as Mr. V is ever fully informed before giving consent. Even though he had signed a consent form for the amputation, the signature in his eyes did not qualify as consent. Further, having read through our hospital’s consent form, I defy anyone to translate its legal subtleties into Hmong.

Perhaps even more important, the Hmong adhere to a strict social hierarchy: males are held in higher esteem than females, the elderly higher than the young.^6,11,14 Therefore, Mr. V’s desire to ask his brothers for advice before consenting to surgery makes sense within his cultural norms and was not a stalling tactic as the surgeons believed.

Try to understand the patient’s concept of illness. We found Mr. V to have capacity within the confines of his medical understanding. He knew the operation was major surgery, and he wanted to consult with his elder brothers—all eight of them (most of whom live in Minneapolis)—prior to consenting. Conversely, the surgeons could think only within the confines of their cultural and clinical understanding. They wanted to perform the procedure expediently to avoid additional diabetic sequelae.

We discussed these concerns with the patient and surgeons and struck a compromise: the surgeons agreed to defer surgery for 10 days, as long as Mr. V indemnified them against complications secondary to the delay. After that, the surgery would be performed regardless of whether Mr. V had consulted his brothers. Mr. V also agreed to continue IV antibiotic therapy. This compliance is not paradoxical: the Hmong often accept antibiotics because of their relatively rapid efficacy.⁶

For clinicians wishing to understand the Hmong and their view of illness, Anne Fadiman’s The Spirit Catches You and You Fall Down is an excellent resource.⁶ Kleinman’s seminal work on treating patients from other cultures also emphasizes the importance of eliciting the patient’s understanding in order to diagnose and negotiate treatment.¹⁵ Several good textbooks address transcultural patient care; curiously, most are nursing rather than physician texts (see “Related resources,”).

Treatment: Recovery’s rocky road

Closure was delayed for 8 days, during which no complications arose. Mr. V tolerated the antibiotics well. He contracted a low-grade fever at times, but septicemia did not re-emerge.

We continued to follow the patient, who on several occasions became delirious. He was neither violent nor agitated, so he was not treated with neuroleptics, which can cause delirium in Hmong patients.^3,4

The patient contacted his brothers and consented to closure surgery, after which he recuperated well for 3 days. On day four, however, he developed respiratory failure. He was resuscitated, intubated, and transferred to the intensive care unit. He was extubated and returned to the floor 24 hours later, at which time he appeared despondent. He exhibited depressed mood, blunted affect, anorexia, anhedonia, and minimal interaction with family or physicians.

Could a different approach to treatment have produced a more favorable response? Also, would you address Mr. V’s depression and, if so, how?

Dr. Krassner’s observations

One might argue that being culturally sensitive and exposing Mr. V to the risks of infection and respiratory distress was a poor medical judgment. This argument takes into account only the biological aspect of Mr. V’s illness, however. Viewed from a biopsychosocial perspective, Mr. V’s course, even with its vicissitudes, was not a “failure” in any sense. He consented to the procedure on his own terms. We identified roadblocks to treatment and unearthed cultural resources (in our case, the patient’s brothers) that could enhance or even replace traditional psychiatric treatments.

To treat Mr. V’s depression, we first assessed the symptoms. We then tried to understand how he experienced his illness within the context of his culture.⁸ Mr. V’s symptoms certainly implied depression, but in many Asian cultures, patients with depression often present with somatic complaints.¹

Also, how were we to know that these symptoms were not due to what Asian cultures refer to as loss of vital energy—or qi—because his sadness and frustration compressed on his heart?¹ In order to treat Mr. V’s depression, we must instead call it qi. Only then can we diagnose and treat the patient in a way that makes sense to him or her.¹⁵

Even arriving at a differential diagnosis is complicated. For example, if Mr. V were Chinese, we would have to include (in addition to our own narrowly defined depression and dysthymia): mên, depressed or troubled; fan-tsao, anxious or troubled; kan-huo, angry; and hsin-ching pu-hao, generalized, nonspecific emotional upset or bad spirits.¹⁵

Further treatment: From grave to grateful

Mr. V was started on sertraline, 50 mg/d, for symptoms of depression. He tolerated the agent well (no GI upset or other side effects). After only 1 week, he had a brighter affect and was more conversant. He expressed thanks for all we had done for him.

The remainder of his recovery was incident-free, and he was discharged 6 days later on sertraline, with psychiatric follow-up arranged with the county mental health services’ Southeast Asian Team.

Related resources

• Giger JN, Davidhizar RE. Transcultural nursing: assessment & intervention (3rd ed). St. Louis: Mosby, 1999.
• Leininger M, McFarland M. Transcultural nursing: concepts, theories, research & practice (2nd ed). New York: McGraw-Hill, 1995.
• Spector RE. Cultural diversity in health & illness (5th ed). Upper Saddle River, NJ: Prentice Hall Health, 2000.

Author affiliations

David Krassner, MD, third-year resident in psychiatry, department of psychiatry, University of California at San Francisco-Fresno Residency Training Program, Fresno, CA.

Drug brand names

• Sertraline • Zoloft

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

History: A turn for the worse

Mr. P, 22, presented as intelligent and well-oriented. He was serving a 1-year prison term after pleading guilty to a charge of distribution of dangerous material.

Mr. P had no history of psychiatric treatment or hospitalizations, drug addiction, paranoia, hallucinations, or suicide or homicide attempts. In fact, before his arrest in 1999, he had always been viewed as a model youth.

Born in a small Midwestern town, Mr. P’s childhood and early adolescence were unremarkable. He was popular, always on the honor roll, and exhibited no serious behavioral problems. He and his best friend had been inseparable since the third grade. Both played school soccer and were in the marching band. As Boy Scouts they hiked, canoed, swam, and did good deeds together.

Mr. P’s life changed 7 years ago, when he and his friend, then both 16, rode to the local mall in a late-model Thunderbird. Mr. P’s friend, a newly licensed driver, sped at 50 mph in a 35-mph zone, on a curving, gravel-covered back road in foggy weather. The youth lost control of the car, which spun around and smashed into a tree on the passenger’s side. The driver emerged unharmed, but the impact rendered Mr. P tetraplegic. An incomplete C6 spinal cord transection allowed some movement in the arms and wrist, but no lower extremity function. Sensation was intact, except for orgasmic anesthesia.

After the accident, their friendship ended. The youth did not respond to Mr. P’s phone calls or letters. A year later, Mr. P sued his former friend for driving to endanger, but the defendant, under 18, was too young to be held legally responsible under state law.

Mr. P missed months of school, but with tutoring, summer sessions, and an indomitable will he graduated from high school on time and with honors. He won a scholarship to college, where he studied computer sciences.

Those familiar with Mr. P were impressed—and inspired—by his courage, but his inward suffering was well concealed. Activities he once enjoyed were now out of reach. Unable to even get in and out of bed independently, he had no social life. Despite his hard work and intelligence, he was a bored quadriplegic teenager with time on his hands.

Mr. P turned to the Internet, where he ultimately began communicating with members of a chat room for students of a middle school 1,000-plus miles away. The younger students with whom he dialogued could not see he was wheelchair-bound. Freed from the identity of a physically disabled person, he could “try on” other identities. He assumed the identity of an eighth-grader, and kept a data bank on students with whom he had online contact at the school: their names, addresses, interests, pets, etc. Before long, he was spending 8 hours a day online.¹

Eventually, Mr. P. blew his cover. Some of the youths picked up on his online slip-ups and challenged him, demanding that he reveal his identity.

Infuriated, Mr. P. identified himself by the name of one of their classmates. (That classmate was harassed at school, a result Mr. P said he later regretted). He then told the youths, “If you don’t believe me, I’ll blow you up.”

What started as a source of restoration for Mr. P suddenly left him feeling discredited and rejected. The more he went online, the more disrespected he felt.

On Oct. 19, 1999, Mr. P posted two photos on the chat room: the school in the cross hairs of a rifle scope and the principal bleeding through simulated bullet holes in the head and chest. He invoked the horror of the recent Columbine High School massacre with the words: “Remembering those two heroes in Columbine, ’99: R.I.P. Eric Harris and Dylan Klebold.” Beneath a “hit list” of 24 eighth-graders and three of their teachers, he wrote: “Some of you lucky individuals will go home with more bullet holes in your body than you came with.”

Mr. P also directed the students to Web sites featuring graphic photos of child pornography and sex abuse. One state attorney general remarked that the pictures were among the most graphic he had ever seen.

Before the students arrived for school the next morning, police with bomb-sniffing dogs patrolled the hallways and inspected classrooms. Teachers searched student’s books and backpacks for suspicious items. Parents of youths on Mr. P’s “hit list” were in panic, too scared to let their offspring leave their houses, let alone go to school.

If Mr. P’s goal was to invoke terror within the middle school’s community, he had done just that. Just 6 months after the Columbine tragedy, the threat of another school massacre had hit home. The terrorist was a quadriplegic several states away, but as far as anyone in town knew, a potential killer lurked among them.

Would you consider the patient a terrorist? Can a pattern of escalation be discerned in Mr. P’s case?

Dr. Sperber’s observations

Terrorism is defined as the use of violence or threats to intimidate or arouse anxiety to further some objective. The objectives, which terrorists feel cannot be accomplished in conventional ways, may be political, religious, ethno-nationalistic, or psychosocial (as was Mr. P’s objective).

Mr. P’s emotional state evolved from feelings of powerlessness and disrespect, to mortification, to shame rage and a thirst for vengeance that ultimately drove him to a terroristic act. It is hypothesized that these emotions are also the precipitating factors in all of terrorism’s guises (Table).

Powerlessness. Feelings of impotence constitute one of the most important factors that give rise to terrorism. As Hoffman writes, “All terrorism involves the quest for power—power to dominate and coerce, to intimidate and control … Terrorism is designed to create power where there is none, or to consolidate power where there is very little.”²

Table

ESCALATION TO TERRORISM

Kaufman notes that those who feel powerless identify with the aggressor. “Terrorism is essentially a strategy of the powerless. Groups who have felt decidedly powerless and humiliated for decades have reversed roles. The tormented now become tormentors.”³

The crippling auto accident rendered Mr. P physically powerless. This was compounded by the psychic impotence that began when his once-inseparable friend abandoned him.

Disrespect. We all need to bond with other humans. Those who feel disrespected, rejected, abandoned, or marginalized may use violence to reconnect.

“The need to belong is of central importance,” Post writes. “Alone, alienated, on the margins of society, seeking to belong, to find acceptance, to find others who feel the same way…for such individuals what a wonderful feeling it is to find that one is not alone, to find likeminded individuals … to be accepted at last.”⁴

Through their disrespect, the students in the chat room made Mr. P feel discredited and marginalized. That intense pain also reopened the psychic wound of having lost his best friend.

Mortification. Disrespect, coupled with the powerlessness of being unable to alter the humiliation, produces the most dysphoric of all human emotions—mortification.

Mortification, from the Latin mortis (death) and facere (to make), makes one literally feel like dying. Such feelings often result in suicide, although murder or homicide accompanied by suicide may also occur.

At the time of his arrest in 1999, Mr. P told police, “I’d like to slit my ex-friend’s throat.”¹ When questioned about his statement, he replied, “It was just a figure of speech. I would never do such a thing.”

Shame rage. Shame is a difficult emotion to dispel. When overwhelmed by guilt, one can place blame: “It’s not my fault—he did it.” The ashamed, however, are unable to project or externalize their shame, which only intensifies the dysphoria, increasing the angry affect and further mortifying the victim.

Vengeance. At a certain level of intensity, the urge to end shame rage curdles it into the yearning for “sweet” revenge. The desire to “get even” and “right wrongs,” however, only adds to the disrespect and disempowerment, fueling retaliative flames and increasing the victim’s likelihood of committing a terrorist act.

What is Mr. P’s diagnosis? What treatment goals would you set for this patient?

Dr. Sperber’s observations

Psychopathologists seek to find a mental disorder or personality type common to all terrorists. Antisocial, narcissistic, and borderline personality disorders are the most frequently identified. “Terrorism is characterized by what I call paradoxical narcissism,” Pies writes. “Terrorists—particularly those with a radical or fundamentalist religious bent—appoint themselves as judge, jury and (quite literally) executioner of those they despise.⁵

Regarding antisocial personality disorder, Cooper states that political terrorists might more accurately be described as “psychopathic or sociopathic personalities for whom political terrorism provides a vehicle for impulses that would otherwise find another outlet.”⁶

A study of the psychodynamic factors leading to terrorism may be more fruitful than the ongoing search for a personality type or cognitive style common to all terrorists. Those who fit the mold of a terrorist perceive some inequity or injustice that they seek to rectify and may or may not have a personality disorder. Mr. P, in fact, was diagnosed with a personality disorder.

The correlation between age and terorrism also cannot be ignored. Many young people embark on the challenges of adulthood with confidence, enthusiasm, and idealism, but some, like Mr. P, encounter marginalization, disrespect, and powerlessness. In exploring the relationship of terrorism to age and group process, Levine reports:

“If, at this critical juncture [from adolescence to adulthood, youths] are exposed to ministrations and solicitations of individuals and groups who seemingly offer ‘antidotes’ to their melancholic miasma, they may be particularly susceptible to these initiations.” Once at-risk youths join a group, he writes, “they see a way out, either ideologically or psychologically, and start to feel considerably better about themselves and their circumstances.”⁷

This was the case with Mr. P when he started visiting the middle school chat room: “In real life, I was isolated from my friends and stayed at home most of the time. The very thing I was missing in my social life was discovered on the Internet. I found these friends, and it made me feel good to be part of the community again … Even though these friends were 1,500 miles away and I had never seen them, I felt a strong connection and involvement with them … However, when they started to disbelieve me, I threatened to kill them all.”

The host-vector model, a paradigm commonly used to analyze infectious diseases, also may help explain why some people respond in terroristic fashion while others who experience the same injustices do not. People who feel secure are less likely to be infected by the viruses of disrespect and disempowerment and can more easily halt their escalation to violence.

At the time of Mr. P’s cybercrime, his “resistance” to deprecation was low, since he had still not overcome an earlier “infection,” i.e., the crippling accident and his ex-friend’s subsequent abandonment.

Although it is hazardous to draw parallels between a single clinical case and global terrorism, certain generalizations appear self-evident. A recent Harvard symposium that addressed hostility toward the United States, especially in the Arab and Muslim world, touched upon how perceived powerlessness can fuel terrorism. Symposium participants referred to Frantz Fanon’s concept of the “cleansing valve of violence.” “Even random violence against a perceived oppressor is seen as a redemptive act … a way for peerless people to feel power, to feel they can gain their self-respect.”⁸

Violence, however, has no cleansing value. It only disempowers the perpetrator, leads to more violence, and in the end imperils human survival. As we have seen with Mr. P, one person’s evolution from victim to terrorist threw an entire town of 10,000 people into a panic.

How would you treat Mr. P?

Treatment: Restoring self-respect

Biweekly psychiatric treatment sessions, lasting from 15 minutes to an hour, were conducted in the prison infirmary during Mr. P’s incarceration.

The long-term treatment goals—empowering the patient mentally and spiritually, and restoring his self-respect—began with empathy. In the first 2 months, I tried to get from Mr. P some sense of what it feels like to be a quadriplegic. He provided verbal and written responses to my questions. In one of these responses—a letter titled “What It’s Like To Be Me”—Mr. P described at length the daunting daily difficulties behind such simple tasks as getting dressed, opening containers (with his mouth because of right-hand paralysis), and sitting up and shifting positions in bed.

Role-playing was another crucial therapeutic tool. By playing the role of his former friend, Mr. P gradually realized that his friend’s “indifference” to his plight was a way of distancing himself from overwhelming guilt over the injury he had caused. In this way, Mr. P could experience his ex-friend’s guilt and forgive him.

In the final months of therapy, we used the insights derived from treatment to write this report, to which he contributed. He felt remorseful about his crime, but at the same time found his collaboration on this article empowering. He was gratified that the tragedy of his quadriplegia and the ensuing terror incident could be used to educate physicians and other patients. Psychotropic medications were never prescribed. Mr. P was paroled after serving 6 months of his 1-year sentence. He is back at college, and his outlook on life has improved greatly.

Dr. Sperber’s observations

By understanding the pattern of escalation to terrorism, psychiatrists can help break the cycle of violence in some patients. Empathic compassion, introduced at any step in the cycle of terrorism, can disrupt the patient’s pattern of escalation. In Mr. P’s case, a treatment plan that emphasized empowerment offered transformative potential.

Related resources

• Mannix M, Locy T, Clark K, et al. Internet crime: the Web’s dark side. US News World Rep Aug. 28, 2000:36.
• States of Mind. Washington, DC: Woodrow Wilson Center Press, 1998:65-85.
• Juergensmeyer. Terror in the Mind of God: The Global Rise of Religious Violence. Berkeley: University of California Press, 2000.

Author affiliations

Michael A. Sperber, MD, psychiatric consultant, Middlesex (MA) Sheriff’s

Department, Billerica, MA.

Disclosure

The views expressed in this article are not necessarily those of the Middlesex (MA) sheriff or the sheriff’s department

Case history: A sudden GI problem

Ms. M, 32, was transferred to our university medical center’s psychiatric ward for assessment and treatment of persistent vomiting. She had been in good health until 5 months previously, when she was hospitalized with dehydration after a weeklong bout with acute nausea and vomiting. An ultrasonogram of the abdomen and pelvis and oral cholecystography were normal.

Ms. M’s diagnosis at that time was gastroenteritis. She received IV rehydration and was released after 5 days, with results of thyroid stimulating hormone (TSH) tests pending. TSH results received 1 week post-hospitalization were 50 mU/ml. (A normal reading is

Symptoms re-emerged 3 weeks later, and the patient was hospitalized again for persistent fatigue, nausea, vomiting, and dehydration. Additional lab test results were normal. The patient was discharged tolerating a regular diet following 2 days of IV rehydration and an increase in antiemetic chemotherapy.

The patient’s emesis continued despite treatment, and she was losing weight. A general surgeon examined Ms. M 3 months after she became ill. He recommended no further work-up, citing the absence of abdominal pain or stool changes and an unclear etiology.

Three weeks later, Ms. M was referred to a dermatologist for evaluation of pigmentation changes of her lips and gums. Hyperpigmentation of the oral mucosa had developed over several weeks. A dermatologic evaluation indicated hypervitaminosis, although vitamin supplementation was denied.

Severe continuous vomiting resulting in dehydration precipitated the third hospitalization in 4 months. Ms. M continued to lose weight, dropping 25 lbs since illness onset. Diagnostic studies, including a head CT, urine drug screen, electrolyte assessment, and thyroid function tests were normal. Again no specific etiology was identified, and a psychologist was consulted. Results of the Minnesota Multiphasic Personality Inventory test demonstrated a strong tendency toward somatization. Significant depression also was noted, and Ms. M was diagnosed with dysthymia.

Ms. M’s clinical status improved slightly after 3 more days of IV rehydration. She was discharged tolerating a regular diet, and the treatment plan included psychological counseling. Three days later, the patient was admitted to a hospital psychiatric ward with continuous vomiting. She was noted to be confused, lethargic, and hysterical.

At this point, would you suspect anorexia nervosa or bulimia? If not, how else would you explain Ms. M’s persistent vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

Psychogenic vomiting is a form of chronic emesis where the etiology is unrelated to a primary anatomic or physiologic defect. It differs from anorexia nervosa or bulimorexia because it lacks the characteristic features of body image distortion, abnormal fear of weight gain, or self-induced vomiting.¹ Symptoms include absence of nausea, insignificant weight loss, occurrence usually after meals, and limited control over emesis.²

Out of 24 patients with psychogenic vomiting examined by Rosenthal, 18 received psychological evaluation and testing.³ The illness was found to be chronic but not debilitating in these patients. Most were without major psychiatric diagnoses or personality disorders, although stressful life events were temporally related with acute exacerbations of vomiting.

Muraoka, in a study of 59 patients admitted with psychogenic vomiting, concluded that most subjects had previous structural or functional GI problems and a history of emesis.⁴

Ms. M did not exhibit body image distortion, nor was she causing herself to vomit or attempting to lose weight. Instead, there appeared to be no medical reason for her symptoms. It was therefore assumed she had psychogenic vomiting.

Patient history: A ‘death-bed’ promise

According to the social history obtained by the hospital’s psychiatric team. Ms. M is a married mother of three who works part-time. She denied using alcohol or other substances and had recently stopped smoking with the aid of hypnosis. She did not follow a special diet, took no medications, and was quite active when healthy. Her father had been treated for hyperthyroidism; otherwise her medical, psychiatric, and family history were noncontributory.

The patient described her relationship with her husband and her children as good, without significant interpersonal conflicts. The psychiatric team, however, viewed her husband as domineering and her as dependent upon him to make decisions.

The patient reported the death of a friend from complications of anorexia nervosa 6 months before the onset of her current symptoms. Ms. M had made a “death-bed promise” to care for her friend’s elderly mother. A contract was written, and Ms. M was remunerated for providing companionship and housekeeping. Before her symptoms developed, the patient’s time commitment to this task increased to the point that she felt “she was neglecting her own family.” Upon becoming ill, however, she willingly terminated this agreement.

About 1 week before the onset of vomiting, Ms. M, who was approximately 60 lbs overweight at the onset of symptoms, received a subliminal message tape from her father pertaining to weight loss. She had listened to the tape for several days and wondered if this could have bearing on her current symptoms, since the tape represented the only change in her routine before the vomiting started.

The attending psychiatrist surmised that the escalating demands of the patient’s elderly ward created a psychological conflict between caring for her family and for her deceased friend's mother. Although the recurrent hospitalizations added to her stress, the vomiting relieved her internal conflict by rendering her unable to care for anyone, including herself.

Because physical examination findings, blood chemistries and counts, and imaging studies did not indicate a physical disorder, Ms. M's diagnosis now was psychogenic vomiting and eating disorder not otherwise specified (NOS).

How would you treat this apparent case of psychogenic vomiting? To what extent can psychological factors contribute to excessive vomiting or other gastrointestinal distress?

Dr. Wiseman’s and Dr. Dunlop’s observations

Clarke described the use of emesis to communicate psychological distress in three cases of female Asian immigrants with psychogenic vomiting.⁵ In each patient the onset of emesis was related to a psychological stressor, and each patient felt she gained a benefit from the chronic vomiting.

In one case, a young woman with unexplained vomiting for 3 weeks was admitted to a psychiatric hospital. During several interviews the patient revealed that she was angry with her parents because she had been relocated against her wishes and required to perform traditional domestic duties. She also felt frightened that her hostile thoughts may have caused her father to have a heart attack. A psychiatric social worker intervened with the patient and her family to address the woman’s desire to be independent. The vomiting stopped without recurrence. Continued vomiting would have changed the family’s expectations and demands, as the patient would have assumed the role of the chronically ill family member.

Of the patients with persistent psychogenic vomiting reviewed by Rosenthal, most had adjustment disorders, poor assertiveness skills, or lack of limit-setting abilities.³ In this psychological setting, vomiting can best be understood as a mechanism for decreasing anxiety and unconscious conflict. Many patients reported difficulty expressing anger, and vomiting eliminated the negative emotion.³

Further evaluaton: Another diagnosis

During her fourth hospitalization, this time at our medical center, Ms. M was treated with amitriptyline, 50 mg at bedtime, but this was discontinued when she developed orthostatic hypotension. Following 2 weeks of psychiatric inpatient treatment without improvement, Ms. M was transferred to a tertiary medical center's psychiatric service for further evaluation.

The examination revealed a mildly dehydrated, ill-appearing woman with sallow skin, hyperpigmentation of the oral mucosa, and minimal enlargement of the thyroid gland. Her blood pressure was 88/62 mm Hg, and her pulse was 112/min supine with orthostatic changes. Her weight had decreased from 195 to 144 lbs across 5 months. Serum sodium was 134 mmol/L (135-145); potassium, 5.7 mmol/L (3.5-5.5); chloride, 100 mmol/L (95-105); bicarbonate, 22 mmol/L (22-27); urea, 7 mg/dl (5-20); creatinine, 1.0 mg/dl (0.5-1.5); glucose, 117 mg/dl (70-110); and calcium, 9.6 mg/dl (8.5-10.5). Ms. M’s complete blood count was normal.

A mental status exam revealed a cooperative but anxious and ill woman without delusions or distorted body image. Ms. M did exhibit a depressed mood and diminished concentration. Her affect was sad, but she denied hopelessness or worthlessness and did not meet DSM-IV criteria for major depression or personality disorder. Results of the modified Mini Mental State Examination were normal.

As we accumulated and carefully reviewed the patient’s medical records, a constellation of signs and symptoms became apparent. These included fatigue, nausea, vomiting, hypotension, hyponatremia, hyperkalemia, weight loss, hyperpigmentation, and the report of subtle episodic psychiatric changes. The index of suspicion for a primary pathophysiologic process was raised. Hypothalamic-pituitary-adrenal axis pathology, specifically adrenal insufficiency, was considered.

An abnormal plasma cortisol level obtained at 8 AM was

A diagnosis of adrenocortical insufficiency, probably caused by autoimmune adrenalitis, was made. In addition, a thyroid function test showed TSH 22.5 IU/ml (0.13-4.6), T4 6.3 mg/dl (4.5-12.0), and T3 176 mg/dl (90-245). Consistent with primary hypothyroidism and adrenal insufficiency, Schmidt’s syndrome—an autoimmune disease of the adrenal and thyroid glands that is a subtype of Addison’s disease—was established.

Ms. M was transferred to a medical ward, where endocrinologists prescribed hydrocortisone, 30 mg in divided daily doses; fludrocortisone acetate, 0.05 mg as a single daily dose; and levothyroxine, 0.1 mg/d. She responded clinically and was discharged after 2 days. A 6-month follow-up found the patient symptom-free with body weight exceeding premorbid levels.

How was the diagnosis of Addison’s disease missed in this patient? What symptoms mask adrenal insufficiency to the point that it mimics psychogenic vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

As this case demonstrates, physiologic vomiting may be misclassified as a conversion disorder because symbolic meaning is given to the emesis, psychological gain is inferred from the symptoms, and clinicians cannot find the true cause of the vomiting. (See Box for DSM-IV guidelines for diagnosing conversion disorder.)

Several case reports describe various psychiatric manifestations of Addison’s disease as components of presenting symptoms of anorexia nervosa, self-mutilation, bereavement, and schizophrenia.^6-9 Often specialists from several disciplines see patients with chronic adrenal insufficiency before an accurate diagnosis is established.¹⁰ The presentation is so diverse and insidious that when unexplained emesis is a symptom, psychogenic vomiting may mistakenly be considered the etiology.

In our patient’s case, the correct diagnosis was initially obscured for two reasons:

• First, the lack of definitive medical results led to multiple diagnoses. Ms. M was diagnosed with conversion disorder, eating disorder NOS, hypervitaminosis, and hypothyroidism, when only one disorder—Schmidt’s syndrome—was present.
  
• Second, conversion disorder was mistaken for the etiology when significant physical signs and symptoms and laboratory abnormalities—including weight loss, severe debilitation, dehydration, hyperpigmentation, hyponatremia, and hyperkalemia—were present.
  

Box

• Margulies P. Addison’s disease: The facts you need to know. National Adrenal Diseases Foundation. http://www.medhelp.org/nadf/nadf3.htm.
  
• Family Practice notebook.com: Psychogenic vomiting. http://www.fpnotebook.com/GI191.htm
  
• National Institute of Diabetes & Digestive & Kidney Diseases: Addison’s disease. http://www.niddk.nih.gov/health/endo/pubs/addison/addison.htm
  

• Fludrocortisone acetate • Florineff
  

William J. Wiseman, MD, Psychiatrist, Stress Center, St. Vincent Hospital, Indianapolis, IN

Stephen Dunlop, MD, Director of Behavioral Care, Saint Francis Hospital Center, Indianapolis, IN

Disclosure

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

Case history: A sudden GI problem

Ms. M, 32, was transferred to our university medical center’s psychiatric ward for assessment and treatment of persistent vomiting. She had been in good health until 5 months previously, when she was hospitalized with dehydration after a weeklong bout with acute nausea and vomiting. An ultrasonogram of the abdomen and pelvis and oral cholecystography were normal.

Ms. M’s diagnosis at that time was gastroenteritis. She received IV rehydration and was released after 5 days, with results of thyroid stimulating hormone (TSH) tests pending. TSH results received 1 week post-hospitalization were 50 mU/ml. (A normal reading is

Symptoms re-emerged 3 weeks later, and the patient was hospitalized again for persistent fatigue, nausea, vomiting, and dehydration. Additional lab test results were normal. The patient was discharged tolerating a regular diet following 2 days of IV rehydration and an increase in antiemetic chemotherapy.

The patient’s emesis continued despite treatment, and she was losing weight. A general surgeon examined Ms. M 3 months after she became ill. He recommended no further work-up, citing the absence of abdominal pain or stool changes and an unclear etiology.

Three weeks later, Ms. M was referred to a dermatologist for evaluation of pigmentation changes of her lips and gums. Hyperpigmentation of the oral mucosa had developed over several weeks. A dermatologic evaluation indicated hypervitaminosis, although vitamin supplementation was denied.

Severe continuous vomiting resulting in dehydration precipitated the third hospitalization in 4 months. Ms. M continued to lose weight, dropping 25 lbs since illness onset. Diagnostic studies, including a head CT, urine drug screen, electrolyte assessment, and thyroid function tests were normal. Again no specific etiology was identified, and a psychologist was consulted. Results of the Minnesota Multiphasic Personality Inventory test demonstrated a strong tendency toward somatization. Significant depression also was noted, and Ms. M was diagnosed with dysthymia.

Ms. M’s clinical status improved slightly after 3 more days of IV rehydration. She was discharged tolerating a regular diet, and the treatment plan included psychological counseling. Three days later, the patient was admitted to a hospital psychiatric ward with continuous vomiting. She was noted to be confused, lethargic, and hysterical.

At this point, would you suspect anorexia nervosa or bulimia? If not, how else would you explain Ms. M’s persistent vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

Psychogenic vomiting is a form of chronic emesis where the etiology is unrelated to a primary anatomic or physiologic defect. It differs from anorexia nervosa or bulimorexia because it lacks the characteristic features of body image distortion, abnormal fear of weight gain, or self-induced vomiting.¹ Symptoms include absence of nausea, insignificant weight loss, occurrence usually after meals, and limited control over emesis.²

Out of 24 patients with psychogenic vomiting examined by Rosenthal, 18 received psychological evaluation and testing.³ The illness was found to be chronic but not debilitating in these patients. Most were without major psychiatric diagnoses or personality disorders, although stressful life events were temporally related with acute exacerbations of vomiting.

Muraoka, in a study of 59 patients admitted with psychogenic vomiting, concluded that most subjects had previous structural or functional GI problems and a history of emesis.⁴

Ms. M did not exhibit body image distortion, nor was she causing herself to vomit or attempting to lose weight. Instead, there appeared to be no medical reason for her symptoms. It was therefore assumed she had psychogenic vomiting.

Patient history: A ‘death-bed’ promise

According to the social history obtained by the hospital’s psychiatric team. Ms. M is a married mother of three who works part-time. She denied using alcohol or other substances and had recently stopped smoking with the aid of hypnosis. She did not follow a special diet, took no medications, and was quite active when healthy. Her father had been treated for hyperthyroidism; otherwise her medical, psychiatric, and family history were noncontributory.

The patient described her relationship with her husband and her children as good, without significant interpersonal conflicts. The psychiatric team, however, viewed her husband as domineering and her as dependent upon him to make decisions.

The patient reported the death of a friend from complications of anorexia nervosa 6 months before the onset of her current symptoms. Ms. M had made a “death-bed promise” to care for her friend’s elderly mother. A contract was written, and Ms. M was remunerated for providing companionship and housekeeping. Before her symptoms developed, the patient’s time commitment to this task increased to the point that she felt “she was neglecting her own family.” Upon becoming ill, however, she willingly terminated this agreement.

About 1 week before the onset of vomiting, Ms. M, who was approximately 60 lbs overweight at the onset of symptoms, received a subliminal message tape from her father pertaining to weight loss. She had listened to the tape for several days and wondered if this could have bearing on her current symptoms, since the tape represented the only change in her routine before the vomiting started.

The attending psychiatrist surmised that the escalating demands of the patient’s elderly ward created a psychological conflict between caring for her family and for her deceased friend's mother. Although the recurrent hospitalizations added to her stress, the vomiting relieved her internal conflict by rendering her unable to care for anyone, including herself.

Because physical examination findings, blood chemistries and counts, and imaging studies did not indicate a physical disorder, Ms. M's diagnosis now was psychogenic vomiting and eating disorder not otherwise specified (NOS).

How would you treat this apparent case of psychogenic vomiting? To what extent can psychological factors contribute to excessive vomiting or other gastrointestinal distress?

Dr. Wiseman’s and Dr. Dunlop’s observations

Clarke described the use of emesis to communicate psychological distress in three cases of female Asian immigrants with psychogenic vomiting.⁵ In each patient the onset of emesis was related to a psychological stressor, and each patient felt she gained a benefit from the chronic vomiting.

In one case, a young woman with unexplained vomiting for 3 weeks was admitted to a psychiatric hospital. During several interviews the patient revealed that she was angry with her parents because she had been relocated against her wishes and required to perform traditional domestic duties. She also felt frightened that her hostile thoughts may have caused her father to have a heart attack. A psychiatric social worker intervened with the patient and her family to address the woman’s desire to be independent. The vomiting stopped without recurrence. Continued vomiting would have changed the family’s expectations and demands, as the patient would have assumed the role of the chronically ill family member.

Of the patients with persistent psychogenic vomiting reviewed by Rosenthal, most had adjustment disorders, poor assertiveness skills, or lack of limit-setting abilities.³ In this psychological setting, vomiting can best be understood as a mechanism for decreasing anxiety and unconscious conflict. Many patients reported difficulty expressing anger, and vomiting eliminated the negative emotion.³

Further evaluaton: Another diagnosis

During her fourth hospitalization, this time at our medical center, Ms. M was treated with amitriptyline, 50 mg at bedtime, but this was discontinued when she developed orthostatic hypotension. Following 2 weeks of psychiatric inpatient treatment without improvement, Ms. M was transferred to a tertiary medical center's psychiatric service for further evaluation.

The examination revealed a mildly dehydrated, ill-appearing woman with sallow skin, hyperpigmentation of the oral mucosa, and minimal enlargement of the thyroid gland. Her blood pressure was 88/62 mm Hg, and her pulse was 112/min supine with orthostatic changes. Her weight had decreased from 195 to 144 lbs across 5 months. Serum sodium was 134 mmol/L (135-145); potassium, 5.7 mmol/L (3.5-5.5); chloride, 100 mmol/L (95-105); bicarbonate, 22 mmol/L (22-27); urea, 7 mg/dl (5-20); creatinine, 1.0 mg/dl (0.5-1.5); glucose, 117 mg/dl (70-110); and calcium, 9.6 mg/dl (8.5-10.5). Ms. M’s complete blood count was normal.

A mental status exam revealed a cooperative but anxious and ill woman without delusions or distorted body image. Ms. M did exhibit a depressed mood and diminished concentration. Her affect was sad, but she denied hopelessness or worthlessness and did not meet DSM-IV criteria for major depression or personality disorder. Results of the modified Mini Mental State Examination were normal.

As we accumulated and carefully reviewed the patient’s medical records, a constellation of signs and symptoms became apparent. These included fatigue, nausea, vomiting, hypotension, hyponatremia, hyperkalemia, weight loss, hyperpigmentation, and the report of subtle episodic psychiatric changes. The index of suspicion for a primary pathophysiologic process was raised. Hypothalamic-pituitary-adrenal axis pathology, specifically adrenal insufficiency, was considered.

An abnormal plasma cortisol level obtained at 8 AM was

A diagnosis of adrenocortical insufficiency, probably caused by autoimmune adrenalitis, was made. In addition, a thyroid function test showed TSH 22.5 IU/ml (0.13-4.6), T4 6.3 mg/dl (4.5-12.0), and T3 176 mg/dl (90-245). Consistent with primary hypothyroidism and adrenal insufficiency, Schmidt’s syndrome—an autoimmune disease of the adrenal and thyroid glands that is a subtype of Addison’s disease—was established.

Ms. M was transferred to a medical ward, where endocrinologists prescribed hydrocortisone, 30 mg in divided daily doses; fludrocortisone acetate, 0.05 mg as a single daily dose; and levothyroxine, 0.1 mg/d. She responded clinically and was discharged after 2 days. A 6-month follow-up found the patient symptom-free with body weight exceeding premorbid levels.

How was the diagnosis of Addison’s disease missed in this patient? What symptoms mask adrenal insufficiency to the point that it mimics psychogenic vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

As this case demonstrates, physiologic vomiting may be misclassified as a conversion disorder because symbolic meaning is given to the emesis, psychological gain is inferred from the symptoms, and clinicians cannot find the true cause of the vomiting. (See Box for DSM-IV guidelines for diagnosing conversion disorder.)

Several case reports describe various psychiatric manifestations of Addison’s disease as components of presenting symptoms of anorexia nervosa, self-mutilation, bereavement, and schizophrenia.^6-9 Often specialists from several disciplines see patients with chronic adrenal insufficiency before an accurate diagnosis is established.¹⁰ The presentation is so diverse and insidious that when unexplained emesis is a symptom, psychogenic vomiting may mistakenly be considered the etiology.

In our patient’s case, the correct diagnosis was initially obscured for two reasons:

• First, the lack of definitive medical results led to multiple diagnoses. Ms. M was diagnosed with conversion disorder, eating disorder NOS, hypervitaminosis, and hypothyroidism, when only one disorder—Schmidt’s syndrome—was present.
  
• Second, conversion disorder was mistaken for the etiology when significant physical signs and symptoms and laboratory abnormalities—including weight loss, severe debilitation, dehydration, hyperpigmentation, hyponatremia, and hyperkalemia—were present.
  

Box

• Margulies P. Addison’s disease: The facts you need to know. National Adrenal Diseases Foundation. http://www.medhelp.org/nadf/nadf3.htm.
  
• Family Practice notebook.com: Psychogenic vomiting. http://www.fpnotebook.com/GI191.htm
  
• National Institute of Diabetes & Digestive & Kidney Diseases: Addison’s disease. http://www.niddk.nih.gov/health/endo/pubs/addison/addison.htm
  

• Fludrocortisone acetate • Florineff
  

William J. Wiseman, MD, Psychiatrist, Stress Center, St. Vincent Hospital, Indianapolis, IN

Stephen Dunlop, MD, Director of Behavioral Care, Saint Francis Hospital Center, Indianapolis, IN

Disclosure

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

Case history: A sudden GI problem

Ms. M, 32, was transferred to our university medical center’s psychiatric ward for assessment and treatment of persistent vomiting. She had been in good health until 5 months previously, when she was hospitalized with dehydration after a weeklong bout with acute nausea and vomiting. An ultrasonogram of the abdomen and pelvis and oral cholecystography were normal.

Ms. M’s diagnosis at that time was gastroenteritis. She received IV rehydration and was released after 5 days, with results of thyroid stimulating hormone (TSH) tests pending. TSH results received 1 week post-hospitalization were 50 mU/ml. (A normal reading is

Symptoms re-emerged 3 weeks later, and the patient was hospitalized again for persistent fatigue, nausea, vomiting, and dehydration. Additional lab test results were normal. The patient was discharged tolerating a regular diet following 2 days of IV rehydration and an increase in antiemetic chemotherapy.

The patient’s emesis continued despite treatment, and she was losing weight. A general surgeon examined Ms. M 3 months after she became ill. He recommended no further work-up, citing the absence of abdominal pain or stool changes and an unclear etiology.

Three weeks later, Ms. M was referred to a dermatologist for evaluation of pigmentation changes of her lips and gums. Hyperpigmentation of the oral mucosa had developed over several weeks. A dermatologic evaluation indicated hypervitaminosis, although vitamin supplementation was denied.

Severe continuous vomiting resulting in dehydration precipitated the third hospitalization in 4 months. Ms. M continued to lose weight, dropping 25 lbs since illness onset. Diagnostic studies, including a head CT, urine drug screen, electrolyte assessment, and thyroid function tests were normal. Again no specific etiology was identified, and a psychologist was consulted. Results of the Minnesota Multiphasic Personality Inventory test demonstrated a strong tendency toward somatization. Significant depression also was noted, and Ms. M was diagnosed with dysthymia.

Ms. M’s clinical status improved slightly after 3 more days of IV rehydration. She was discharged tolerating a regular diet, and the treatment plan included psychological counseling. Three days later, the patient was admitted to a hospital psychiatric ward with continuous vomiting. She was noted to be confused, lethargic, and hysterical.

At this point, would you suspect anorexia nervosa or bulimia? If not, how else would you explain Ms. M’s persistent vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

Psychogenic vomiting is a form of chronic emesis where the etiology is unrelated to a primary anatomic or physiologic defect. It differs from anorexia nervosa or bulimorexia because it lacks the characteristic features of body image distortion, abnormal fear of weight gain, or self-induced vomiting.¹ Symptoms include absence of nausea, insignificant weight loss, occurrence usually after meals, and limited control over emesis.²

Out of 24 patients with psychogenic vomiting examined by Rosenthal, 18 received psychological evaluation and testing.³ The illness was found to be chronic but not debilitating in these patients. Most were without major psychiatric diagnoses or personality disorders, although stressful life events were temporally related with acute exacerbations of vomiting.

Muraoka, in a study of 59 patients admitted with psychogenic vomiting, concluded that most subjects had previous structural or functional GI problems and a history of emesis.⁴

Ms. M did not exhibit body image distortion, nor was she causing herself to vomit or attempting to lose weight. Instead, there appeared to be no medical reason for her symptoms. It was therefore assumed she had psychogenic vomiting.

Patient history: A ‘death-bed’ promise

According to the social history obtained by the hospital’s psychiatric team. Ms. M is a married mother of three who works part-time. She denied using alcohol or other substances and had recently stopped smoking with the aid of hypnosis. She did not follow a special diet, took no medications, and was quite active when healthy. Her father had been treated for hyperthyroidism; otherwise her medical, psychiatric, and family history were noncontributory.

The patient described her relationship with her husband and her children as good, without significant interpersonal conflicts. The psychiatric team, however, viewed her husband as domineering and her as dependent upon him to make decisions.

The patient reported the death of a friend from complications of anorexia nervosa 6 months before the onset of her current symptoms. Ms. M had made a “death-bed promise” to care for her friend’s elderly mother. A contract was written, and Ms. M was remunerated for providing companionship and housekeeping. Before her symptoms developed, the patient’s time commitment to this task increased to the point that she felt “she was neglecting her own family.” Upon becoming ill, however, she willingly terminated this agreement.

About 1 week before the onset of vomiting, Ms. M, who was approximately 60 lbs overweight at the onset of symptoms, received a subliminal message tape from her father pertaining to weight loss. She had listened to the tape for several days and wondered if this could have bearing on her current symptoms, since the tape represented the only change in her routine before the vomiting started.

The attending psychiatrist surmised that the escalating demands of the patient’s elderly ward created a psychological conflict between caring for her family and for her deceased friend's mother. Although the recurrent hospitalizations added to her stress, the vomiting relieved her internal conflict by rendering her unable to care for anyone, including herself.

Because physical examination findings, blood chemistries and counts, and imaging studies did not indicate a physical disorder, Ms. M's diagnosis now was psychogenic vomiting and eating disorder not otherwise specified (NOS).

How would you treat this apparent case of psychogenic vomiting? To what extent can psychological factors contribute to excessive vomiting or other gastrointestinal distress?

Dr. Wiseman’s and Dr. Dunlop’s observations

Clarke described the use of emesis to communicate psychological distress in three cases of female Asian immigrants with psychogenic vomiting.⁵ In each patient the onset of emesis was related to a psychological stressor, and each patient felt she gained a benefit from the chronic vomiting.

In one case, a young woman with unexplained vomiting for 3 weeks was admitted to a psychiatric hospital. During several interviews the patient revealed that she was angry with her parents because she had been relocated against her wishes and required to perform traditional domestic duties. She also felt frightened that her hostile thoughts may have caused her father to have a heart attack. A psychiatric social worker intervened with the patient and her family to address the woman’s desire to be independent. The vomiting stopped without recurrence. Continued vomiting would have changed the family’s expectations and demands, as the patient would have assumed the role of the chronically ill family member.

Of the patients with persistent psychogenic vomiting reviewed by Rosenthal, most had adjustment disorders, poor assertiveness skills, or lack of limit-setting abilities.³ In this psychological setting, vomiting can best be understood as a mechanism for decreasing anxiety and unconscious conflict. Many patients reported difficulty expressing anger, and vomiting eliminated the negative emotion.³

Further evaluaton: Another diagnosis

During her fourth hospitalization, this time at our medical center, Ms. M was treated with amitriptyline, 50 mg at bedtime, but this was discontinued when she developed orthostatic hypotension. Following 2 weeks of psychiatric inpatient treatment without improvement, Ms. M was transferred to a tertiary medical center's psychiatric service for further evaluation.

The examination revealed a mildly dehydrated, ill-appearing woman with sallow skin, hyperpigmentation of the oral mucosa, and minimal enlargement of the thyroid gland. Her blood pressure was 88/62 mm Hg, and her pulse was 112/min supine with orthostatic changes. Her weight had decreased from 195 to 144 lbs across 5 months. Serum sodium was 134 mmol/L (135-145); potassium, 5.7 mmol/L (3.5-5.5); chloride, 100 mmol/L (95-105); bicarbonate, 22 mmol/L (22-27); urea, 7 mg/dl (5-20); creatinine, 1.0 mg/dl (0.5-1.5); glucose, 117 mg/dl (70-110); and calcium, 9.6 mg/dl (8.5-10.5). Ms. M’s complete blood count was normal.

A mental status exam revealed a cooperative but anxious and ill woman without delusions or distorted body image. Ms. M did exhibit a depressed mood and diminished concentration. Her affect was sad, but she denied hopelessness or worthlessness and did not meet DSM-IV criteria for major depression or personality disorder. Results of the modified Mini Mental State Examination were normal.

As we accumulated and carefully reviewed the patient’s medical records, a constellation of signs and symptoms became apparent. These included fatigue, nausea, vomiting, hypotension, hyponatremia, hyperkalemia, weight loss, hyperpigmentation, and the report of subtle episodic psychiatric changes. The index of suspicion for a primary pathophysiologic process was raised. Hypothalamic-pituitary-adrenal axis pathology, specifically adrenal insufficiency, was considered.

An abnormal plasma cortisol level obtained at 8 AM was

A diagnosis of adrenocortical insufficiency, probably caused by autoimmune adrenalitis, was made. In addition, a thyroid function test showed TSH 22.5 IU/ml (0.13-4.6), T4 6.3 mg/dl (4.5-12.0), and T3 176 mg/dl (90-245). Consistent with primary hypothyroidism and adrenal insufficiency, Schmidt’s syndrome—an autoimmune disease of the adrenal and thyroid glands that is a subtype of Addison’s disease—was established.

Ms. M was transferred to a medical ward, where endocrinologists prescribed hydrocortisone, 30 mg in divided daily doses; fludrocortisone acetate, 0.05 mg as a single daily dose; and levothyroxine, 0.1 mg/d. She responded clinically and was discharged after 2 days. A 6-month follow-up found the patient symptom-free with body weight exceeding premorbid levels.

How was the diagnosis of Addison’s disease missed in this patient? What symptoms mask adrenal insufficiency to the point that it mimics psychogenic vomiting?

Dr. Wiseman’s and Dr. Dunlop’s observations

As this case demonstrates, physiologic vomiting may be misclassified as a conversion disorder because symbolic meaning is given to the emesis, psychological gain is inferred from the symptoms, and clinicians cannot find the true cause of the vomiting. (See Box for DSM-IV guidelines for diagnosing conversion disorder.)

Several case reports describe various psychiatric manifestations of Addison’s disease as components of presenting symptoms of anorexia nervosa, self-mutilation, bereavement, and schizophrenia.^6-9 Often specialists from several disciplines see patients with chronic adrenal insufficiency before an accurate diagnosis is established.¹⁰ The presentation is so diverse and insidious that when unexplained emesis is a symptom, psychogenic vomiting may mistakenly be considered the etiology.

In our patient’s case, the correct diagnosis was initially obscured for two reasons:

• First, the lack of definitive medical results led to multiple diagnoses. Ms. M was diagnosed with conversion disorder, eating disorder NOS, hypervitaminosis, and hypothyroidism, when only one disorder—Schmidt’s syndrome—was present.
  
• Second, conversion disorder was mistaken for the etiology when significant physical signs and symptoms and laboratory abnormalities—including weight loss, severe debilitation, dehydration, hyperpigmentation, hyponatremia, and hyperkalemia—were present.
  

Box

• Margulies P. Addison’s disease: The facts you need to know. National Adrenal Diseases Foundation. http://www.medhelp.org/nadf/nadf3.htm.
  
• Family Practice notebook.com: Psychogenic vomiting. http://www.fpnotebook.com/GI191.htm
  
• National Institute of Diabetes & Digestive & Kidney Diseases: Addison’s disease. http://www.niddk.nih.gov/health/endo/pubs/addison/addison.htm
  

• Fludrocortisone acetate • Florineff
  

William J. Wiseman, MD, Psychiatrist, Stress Center, St. Vincent Hospital, Indianapolis, IN

Stephen Dunlop, MD, Director of Behavioral Care, Saint Francis Hospital Center, Indianapolis, IN

Disclosure

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

History: A long, losing battle

Mr. X, 41, has had schizophrenia, paranoid type, since age 24. Unable to work, keep house, or even groom himself, he has lived his entire life with his mother, his principal advocate and caretaker. He has been hospitalized 11 times for persecutory delusions, most recently 2 years ago at our medical center..

Numerous antipsychotics, including risperidone, haloperidol, quetiapine, clozapine, and thiothixene, did not work. He has responded best to olanzapine, but some mild paranoid symptoms and significant negative symptoms (alogia, anhedonia, amotivation, hypersomnia, restricted affect) persist.

He gained 30 pounds within 6 months after starting olanzapine. He was keeping his weight at 230 pounds and his body mass index (BMI) at 31.3. (A normal BMI is <25; a BMI >30 is considered obese.)

The patient was maintained on olanzapine 20 mg/d, but higher dosages caused oversedation. At the hospital, he would sleep through breakfast, get up late in the morning, then lie around until bedtime.

As an outpatient, he had no social contact outside the home. While hospitalized, Mr. X attended a therapy group on his ward, but never participated in the discussion. His speech was profoundly deficient; he never volunteered information and never responded to questions with anything more than a barely audible “yes” or “ no ”

How would you help Mr. X? Would you augment the olanzapine therapy or consider another antipsychotic, even one that failed the first time? Which negative symptom would you address first?

Drs. Yu’s and Maguire’s observations

Compared with the older antipsychotic agents, specifically haloperidol and thiothixene in this case, the newer antipsychotics (clozapine, risperidone, olanzapine, quetiapine, and ziprasidone) have demonstrated the ability to comprehensively treat schizophrenia.^1-4 But these novel agents sometimes fail to remedy the negative symptoms. Thus, as is the case with Mr. X, many patients with schizophrenia whose positive symptoms are controlled realize little or no improvement in quality of life.

Olanzapine and risperidone have more effectively reduced the negative symptoms of schizophrenia than have the older antipsychotics,^1-4 but—as we see with Mr. X—their record in treating negative symptoms is far from perfect. Additionally, sedation secondary to the antipsychotic may worsen the negative symptoms.

What’s more, the newer agents are associated with potential weight gain.^5-7 Mr. X’s weight will need to be addressed, but with much caution. Many agents prescribed for weight loss, notably amphetamines, are avoided in psychotic patients because of the potential for abuse and worsening psychosis.⁸

Augmentation with modafinil, a wakefulness-promoting agent, is being considered for Mr. X. Although modafinil’s efficacy against obesity has not specifically been tested, studies have shown that this agent, which has actions similar to those of sympathomimetic agents, offers a lower abuse potential. Gold and Balster found that the medication was 250 times less potent than amphetamine and 15 times less potent than ephedrine in producing cocaine-like discriminative stimulus effects in rats.⁹ Single oral doses of modafinil did not cause elation or euphoria in healthy volunteers or those with substance abuse disorders.^10,11 And compared with amphetamines, modafinil has a limited side-effect profile, with weak peripheral sympathomimetic activity and minimal effects on hemodynamics.¹²

Though it is best to minimize both the number of medications and the dosage for each patient, augmentation is still needed in some cases.^13-15

Treatment augmentation: An agent is added

Mr. X’s olanzapine was increased to 30 mg/d. Modafinil, 100 mg/d, was then added to reduce the sedation associated with the higher olanzapine dosage.

Within a week, Mr. X’s negative symptoms had begun to improve. He started to speak more often and more clearly; his previously monotone voice exhibited a small degree of intonation and inflection. His fatigue decreased, and he was able to stay awake through breakfast and throughout the day.

That first week, he exhibited a brightened affect and more energy. He began to socialize to some extent with other patients in the hospital therapy group and was less isolated than before.

This slight but sudden improvement encouraged us. While he still showed slight paranoid ideations, he looked forward to a safe discharge and returning home to his family.

At this point, would you increase the dosage of either modafinil or olanzapine, or stay the course and monitor the patient’s improvement?

Drs. Yu’s and Maguire’s observations

Modafinil is a novel compound indicated for narcolepsy treatment. Though its precise mechanism is unknown, modafinil is neither a direct- nor indirect-acting dopamine receptor agonist and is inactive in several in vivo preclinical models capable of detecting enhanced dopaminergic activity.¹⁶ Therefore, the agent’s pharmacologic profile may be favorable for off-label use in treating negative symptoms of schizophrenia. Modafinil also has been shown to be effective as an augmentation therapy in depression, especially with treating fatigue symptoms.¹⁷

Continued treatment: Improving symptoms

After 1 month, we increased Mr. X’s modafinil dosage to 200 mg/d and olanzapine to 40 mg/d. Both were well tolerated. No extrapyramidal symptoms were noted.

Over the next 4 months, his negative symptoms improved to the point where he had some concept of self-image. He was more alert, less isolated, and better groomed.

Once too sleepy to even eat breakfast, Mr. X began to participate in an exercise program, performing aerobic exercise including regular use of a treadmill, at a local gymnasium 3 days a week. This may have contributed to his loss of 20 pounds across 4 months. Over the next 6 months, the patient maintained his weight at 210 pounds, with a resultant BMI of 28.5. (He has lost slightly more weight since then.)

His socialization skills, while still far from mainstream levels, also improved. His mother began taking him to support group meetings at the local office of the National Alliance for the Mentally Ill (NAMI). There, he interacted with persons with schizophrenia and other psychiatric disorders.

During this time, his psychiatric condition remained stable, and his paranoia showed a mild improvement. Whereas Mr. X once required hospitalization every 6 months to 2 years, he has now been an outpatient for more than 2 years.

The modafinil dosage was titrated to 400 mg/d to further improve his negative symptoms and prevent antipsychotic-associated sedation. Mr. X has noted a continued increase in his alertness. He is still exercising, remains well groomed, and has begun taking vacations with his family. His mother, an active NAMI member, has continued to be his advocate and encourage his improvement.

Overall, we estimate that Mr. X is now functioning at about 65% of normal human capacity. When we began olanzapine with modafinil augmentation 2 years ago, he was functioning at barely one-half that level.

In your view, what should be the next step toward reintegration for Mr. X?

Drs. Yu’s and Maguire’s observations

The olanzapine/modafinil regimen brought about great improvement, but pharmacologic therapy only goes so far. As of this writing, Mr. X has never held a job or lived independently. Also, socialization beyond the family and NAMI support group meetings remains nonexistent.

Behavioral strategies may be just as important as medication treatment for patients with schizophrenia. We would consider behavioral therapy for Mr. X, employing token economies and social skills training to increase social abilities, self-sufficiency, practical skills, and interpersonal communication—skills that may further improve his negative symptoms and lessen the chance of relapse. Social skills training through the use of videotapes, role playing in therapy, and homework assignments to practice specific skills may allow Mr. X to improve his maladaptive behaviors.

Educating the patient and his family would help them understand what to expect in the course of his illness and can enhance treatment. NAMI is one useful referral source. NAMI and similar organizations offer emotional and practical advice about obtaining care in today’s complex health care delivery system.

A case manager also plays an invaluable role, ensuring that efforts are coordinated and that the patient keeps appointments and complies with treatment plans. The case manager may make home visits and even accompany the patient to work. The program’s success depends on the educational background, training, and qualifications of the case manager, which are variable.

Other behavioral strategies that could help Mr. X and other patients with schizophrenia include:

• Group therapy, which focuses on real-life plans, problems, and relationships. Group therapy effectively reduces social isolation, increases cohesiveness, and improves reality testing. Groups led in a supportive rather than interpretative manner appear to be most helpful in schizophrenia.
• Cognitive-behavioral therapy, which has been used in schizophrenia to improve cognitive distortions, reduce distractibility, and correct errors in judgment.
• Individual psychotherapy, which has been shown to effectively complement pharmacologic treatment.¹⁸

As patients’ symptoms improve, we as psychiatrists can help by encouraging them to gradually reintegrate into society, often by offering resources such as NAMI or referrals to appropriate rehabilitation programs.

We plan to continue Mr. X’s olanzapine/modafinil regimen to keep positive and negative symptoms at bay while improving his chances at reintegration. Careful monitoring of medications during reintegration is key to preventing relapse. We will continue to see Mr. X once a month.

Related resources

• National Alliance for the Mentally Ill. www.nami.org
• The Center for Reintegration. www.reintegration.com
• National Alliance for Research on Schizophrenia and Depression. www.mhsource.com/narsad/ or www.narsad.org

Drug brand names

• Clozapine • Clozaril
• Ephedrine • Rynatuss
• Haloperidol • Haldol
• Modafinil • Provigil
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Ziprasidone • Geodon

Author affiliations

Benjamin P. Yu, MD

Resident physician

Gerald A. Maguire, MD

Assistant dean for continuing medical education, Director of residency training,

Associate clinical professor

Department of psychiatry and human behavior

University of California-Irvine Medical Center

Disclosure

Dr. Yu reports that he serves on the speaker’s bureau of Cephalon Inc.

Dr. Maguire reports that he receives research/grant support from, serves as a consultant to, and is on the speaker’s bureau of Eli Lilly & Co.

History: A long, losing battle