Current Psychiatry

We would like to counter the suggestion to use benztropine or clonidine as a means to control clozapine-induced hypersalivation as suggested in “Reducing clozapine-induced hypersalivation” (Pearls, Current Psychiatry, October 2011, p. 77-78).

As stated in the article, clozapine is an antagonist for all known muscarinic receptors except M4—where it is an agonist—making it a potent anticholinergic medication with the potential to cause excessive saliva production.^1,2 Another proposed mechanism for clozapine-induced hypersalivation is its antagonist activity at α-1 receptors, thus the suggestion to use clonidine to combat this side effect. The use of benztropine, another medication with known anticholinergic activity, or clonidine, a medication that may cause additional hypotension, to treat clozapine-induced hypersalivation may cause further unwanted complications and may not be the best option to treat this troubling side effect.

We have had great success locally using medications such as atropine or ipratropium as first-line treatments for clozapine-induced hypersalivation in an effort to minimize additional systemic side effects, such as those seen with benztropine and clonidine. Atropine eye drops administered orally, starting with 1 drop and titrated up to 2 drops twice daily to adequate response, has been shown to be successful according to patient opinion in several case reports.3 Alternatively, intranasal ipratropium orally administered 1 to 2 sprays, up to 3 times daily has shown improvement in clozapine-induced hypersalivation according to patient report.³ Although controlled trials to support the use of topical treatment for clozapine-induced hypersalivation are necessary, attempting to minimize additional adverse effects warrants a trial of atropine or ipratropium before using systemically acting medications such as benztropine or clonidine.

Sarah Hutfilz, PharmD
PGY1 Pharmacy Practice Resident
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Instructor
University of North Carolina
Eshelman School of Pharmacy

Shauna Garris, PharmD, BCPP
Neurology/Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina
Eshelman School of Pharmacy

M. Lindsey Kennedy, PharmD, BCPS, BCPP
Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina School
of Medicine
University of North Carolina
Eshelman School of Pharmacy
Chapel Hill, NC

The authors respond

We thank Drs. Hutfilz, Garris, and Kennedy for their response and comments. We acknowledge that the medications we suggested have potentially harmful adverse effects; however, they are evidence-based. Atropine eye drops and ipratropium are interesting suggestions; if their use is based on evidence, they should have been included in the article.

We agree that further studies may show these topical approaches to be superior, but our recommendation, based on the best evidence available from the clinical studies, would be to use medications that have been studied while advocating for further study of medications with a theoretical superiority that is not yet proven.

Gurprit Lamba, MD
Geriatric Psychiatry Fellow
Partners HealthCare Geriatric Psychiatry Fellowship
Boston, MA

James M. Ellison, MD, MPH
Associate Professor of Psychiatry
Harvard Medical School
Boston, MA

We would like to counter the suggestion to use benztropine or clonidine as a means to control clozapine-induced hypersalivation as suggested in “Reducing clozapine-induced hypersalivation” (Pearls, Current Psychiatry, October 2011, p. 77-78).

As stated in the article, clozapine is an antagonist for all known muscarinic receptors except M4—where it is an agonist—making it a potent anticholinergic medication with the potential to cause excessive saliva production.^1,2 Another proposed mechanism for clozapine-induced hypersalivation is its antagonist activity at α-1 receptors, thus the suggestion to use clonidine to combat this side effect. The use of benztropine, another medication with known anticholinergic activity, or clonidine, a medication that may cause additional hypotension, to treat clozapine-induced hypersalivation may cause further unwanted complications and may not be the best option to treat this troubling side effect.

We have had great success locally using medications such as atropine or ipratropium as first-line treatments for clozapine-induced hypersalivation in an effort to minimize additional systemic side effects, such as those seen with benztropine and clonidine. Atropine eye drops administered orally, starting with 1 drop and titrated up to 2 drops twice daily to adequate response, has been shown to be successful according to patient opinion in several case reports.3 Alternatively, intranasal ipratropium orally administered 1 to 2 sprays, up to 3 times daily has shown improvement in clozapine-induced hypersalivation according to patient report.³ Although controlled trials to support the use of topical treatment for clozapine-induced hypersalivation are necessary, attempting to minimize additional adverse effects warrants a trial of atropine or ipratropium before using systemically acting medications such as benztropine or clonidine.

Sarah Hutfilz, PharmD
PGY1 Pharmacy Practice Resident
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Instructor
University of North Carolina
Eshelman School of Pharmacy

Shauna Garris, PharmD, BCPP
Neurology/Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina
Eshelman School of Pharmacy

M. Lindsey Kennedy, PharmD, BCPS, BCPP
Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina School
of Medicine
University of North Carolina
Eshelman School of Pharmacy
Chapel Hill, NC

The authors respond

We thank Drs. Hutfilz, Garris, and Kennedy for their response and comments. We acknowledge that the medications we suggested have potentially harmful adverse effects; however, they are evidence-based. Atropine eye drops and ipratropium are interesting suggestions; if their use is based on evidence, they should have been included in the article.

We agree that further studies may show these topical approaches to be superior, but our recommendation, based on the best evidence available from the clinical studies, would be to use medications that have been studied while advocating for further study of medications with a theoretical superiority that is not yet proven.

Gurprit Lamba, MD
Geriatric Psychiatry Fellow
Partners HealthCare Geriatric Psychiatry Fellowship
Boston, MA

James M. Ellison, MD, MPH
Associate Professor of Psychiatry
Harvard Medical School
Boston, MA

We would like to counter the suggestion to use benztropine or clonidine as a means to control clozapine-induced hypersalivation as suggested in “Reducing clozapine-induced hypersalivation” (Pearls, Current Psychiatry, October 2011, p. 77-78).

As stated in the article, clozapine is an antagonist for all known muscarinic receptors except M4—where it is an agonist—making it a potent anticholinergic medication with the potential to cause excessive saliva production.^1,2 Another proposed mechanism for clozapine-induced hypersalivation is its antagonist activity at α-1 receptors, thus the suggestion to use clonidine to combat this side effect. The use of benztropine, another medication with known anticholinergic activity, or clonidine, a medication that may cause additional hypotension, to treat clozapine-induced hypersalivation may cause further unwanted complications and may not be the best option to treat this troubling side effect.

We have had great success locally using medications such as atropine or ipratropium as first-line treatments for clozapine-induced hypersalivation in an effort to minimize additional systemic side effects, such as those seen with benztropine and clonidine. Atropine eye drops administered orally, starting with 1 drop and titrated up to 2 drops twice daily to adequate response, has been shown to be successful according to patient opinion in several case reports.3 Alternatively, intranasal ipratropium orally administered 1 to 2 sprays, up to 3 times daily has shown improvement in clozapine-induced hypersalivation according to patient report.³ Although controlled trials to support the use of topical treatment for clozapine-induced hypersalivation are necessary, attempting to minimize additional adverse effects warrants a trial of atropine or ipratropium before using systemically acting medications such as benztropine or clonidine.

Sarah Hutfilz, PharmD
PGY1 Pharmacy Practice Resident
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Instructor
University of North Carolina
Eshelman School of Pharmacy

Shauna Garris, PharmD, BCPP
Neurology/Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina
Eshelman School of Pharmacy

M. Lindsey Kennedy, PharmD, BCPS, BCPP
Psychiatry Clinical Specialist
Department of Pharmacy
University of North Carolina Hospitals and Clinics
Clinical Assistant Professor
University of North Carolina School
of Medicine
University of North Carolina
Eshelman School of Pharmacy
Chapel Hill, NC

The authors respond

We thank Drs. Hutfilz, Garris, and Kennedy for their response and comments. We acknowledge that the medications we suggested have potentially harmful adverse effects; however, they are evidence-based. Atropine eye drops and ipratropium are interesting suggestions; if their use is based on evidence, they should have been included in the article.

We agree that further studies may show these topical approaches to be superior, but our recommendation, based on the best evidence available from the clinical studies, would be to use medications that have been studied while advocating for further study of medications with a theoretical superiority that is not yet proven.

Gurprit Lamba, MD
Geriatric Psychiatry Fellow
Partners HealthCare Geriatric Psychiatry Fellowship
Boston, MA

James M. Ellison, MD, MPH
Associate Professor of Psychiatry
Harvard Medical School
Boston, MA

As an advanced practice nurse in psychiatry who is passionate about my work, I was re-motivated by Dr. Nasrallah’s editorial on the model psychiatrist (“The model psychiatrist: 7 domains of excellence,” From the Editor, Current Psychiatry, November 2011, p. 5-6). It was great to see that these traits are being encouraged and practiced. I appreciated the piece, as well as the support that it gives to all types of mental health practitioners, telling us that there are still psychiatrists striving for “greatness.”

Gretchen Moeller, MSN-BC
Linden Oaks at Edward Hospital
St. Charles, IL

As an advanced practice nurse in psychiatry who is passionate about my work, I was re-motivated by Dr. Nasrallah’s editorial on the model psychiatrist (“The model psychiatrist: 7 domains of excellence,” From the Editor, Current Psychiatry, November 2011, p. 5-6). It was great to see that these traits are being encouraged and practiced. I appreciated the piece, as well as the support that it gives to all types of mental health practitioners, telling us that there are still psychiatrists striving for “greatness.”

Gretchen Moeller, MSN-BC
Linden Oaks at Edward Hospital
St. Charles, IL

As an advanced practice nurse in psychiatry who is passionate about my work, I was re-motivated by Dr. Nasrallah’s editorial on the model psychiatrist (“The model psychiatrist: 7 domains of excellence,” From the Editor, Current Psychiatry, November 2011, p. 5-6). It was great to see that these traits are being encouraged and practiced. I appreciated the piece, as well as the support that it gives to all types of mental health practitioners, telling us that there are still psychiatrists striving for “greatness.”

Gretchen Moeller, MSN-BC
Linden Oaks at Edward Hospital
St. Charles, IL

Discuss this article at www.facebook.com/CurrentPsychiatry

Formerly called self-mutilation, self-injury, or self-harm, nonsuicidal self-injury (NSSI) is the deliberate and direct alteration or destruction of healthy body tissue without suicidal intent; these behaviors range from skin cutting or burning to eye enucleation or amputation of body parts. NSSI must be deliberate, as opposed to accidental or indirect behaviors—such as overdoses or ingesting harmful substances—that cause injury that is uncertain, ambiguous as to course, or invisible (the injuries do not disfigure observable body tissue).¹ NSSI acts are done without an intent to die, although persons who self-harm may have suicidal ideation and passive thoughts of dying.² Persons who repeatedly engage in NSSI and are demoralized over their inability to control it are at risk for suicide attempts.³

NSSI can be classified as nonpathological or pathological.⁴ Culturally sanctioned, nonpathological NSSI consists of body modification practices such as tattoos or piercing. Body modification practices may be a sublimation of pathological NSSI. For a description of nonpathological NSSI, see the Box.⁵ Pathological NSSI typically is a method of emotional regulation. Understanding why patients engage in pathological NSSI and how it is categorized can help guide assessment and treatment.

Box

Why people engage in NSSI

NSSI is best regarded as a pathological approach to emotional regulation and distress tolerance that provides rapid but temporary relief from disturbing thoughts, feelings, and emotions. For approximately 90% of patients, NSSI decreases symptoms, most commonly untenable anxiety (“It’s like popping a balloon”), depressed mood, racing thoughts, swirling emotions, anger, hallucinations, and flashbacks.^6,7 In some instances, NSSI generates desired feelings and self-stimulation during periods of dissociation, depersonalization, grief, insecurity, loneliness, extreme boredom, self-pity, and alienation.^8,9 NSSI also may signal distress to elicit a caring response from others or provide a means of escape from intolerable social situations.¹⁰Table 1 lists factors associated with NSSI.

Table 1

Factors associated with NSSI

The functional approach

One model of classifying NSSI focuses on the behavioral functions it serves.^11,12 In this model, the most common function of NSSI is removal or escape from an aversive affective or cognitive state (automatic positive reinforcement). Automatic negative reinforcement explains using NSSI to generate feelings—eg, by patients with anhedonia or numbness. NSSI also may be used as a signal of distress to gain attention, access helpful environmental resources (social positive reinforcement), or remove distressing interpersonal demands (social negative reinforcement).

The functional model is key to providing thorough clinical evaluations that should include understanding the antecedent and consequent thoughts, feelings, situations, triggers, and vulnerabilities related to NSSI acts.

The medical approach

A descriptive, phenomenological model of NSSI classification uses concepts and terminology with which most psychiatrists are familiar, takes into account patients who have comorbid psychiatric disorders, is based on atheoretical, descriptive observations, and fits into what might be regarded as a “medical model.” In this classification, NSSI usually is regarded as a symptom or associated feature of a specific psychiatric disorder, although it may occur in persons who do not meet diagnostic criteria of a mental illness—eg, “copycat” cutting in high school students.^13,14 NSSI may fall within 4 descriptive categories: major, stereotypic, compulsive, or impulsive. For psychiatric disorders associated with these types of pathological NSSI, see Table 2.

Major NSSI includes infrequent acts that destroy significant body tissue, such as eye enucleation and amputation of body parts. They are sudden, messy, and often bloody acts. Seventy-five percent occur during a psychotic state, mainly schizophrenia; of these, approximately one-half occur during a first psychotic episode.¹⁵ The reasons patients typically offer for such behavior often defy logical understanding—eg, to enhance general well-being—but most center on religion, such as a concrete interpretation of biblical texts about removing an offending eye or hand or becoming an eunuch,^16,17 or on sexuality, such as controlling troubling hypersexuality or fear of giving in to homosexual urges.¹⁸

Stereotypic NSSI acts, most commonly associated with severe and profound mental retardation, include repetitive head banging; eye gouging; biting lips, the tongue, cheeks, or fingers; and face or head slapping. The behaviors may be monotonously repetitive, have a rhythmic pattern, and be performed without shame or guilt in the presence of onlookers.

Compulsive NSSI encompasses repetitive behaviors such as severe skin scratching and nail biting, hair pulling (trichotillomania), and skin digging (delusional parasitosis).

Impulsive NSSI consists of acts such as skin cutting, burning, and carving; sticking pins or other objects under the skin or into the chest or abdomen; interfering with wound healing; and smashing hand or foot bones. These behaviors usually are episodic and occur more frequently in females. The average age of onset in patients who engage in impulsive NSSI is 12 to 14, although it may occur throughout the life cycle.

One or 2 isolated instances of impulsive NSSI do not have much prognostic importance unless they are serious enough to warrant an emergency department visit. The real danger is when the behavior becomes repetitive and “addictive.” The crossover from episodic to repetitive usually varies from 5 to 10 episodes.

Persons who engage in repetitive NSSI may use multiple methods, but skin cutting predominates. Such persons often develop a self-identity as a “cutter,” are preoccupied with their NSSI, may carve words into their skin, and may perform acts of self-harm with other self-injurers. Some may cut themselves hundreds or even thousands of times, creating scars that result in social morbidity. They often seek professional help avidly, but may become so demoralized over their inability to stop their NSSI that they are at risk for suicide.³ In some repetitive self-injurers, other impulsive behaviors such as bulimia or substance abuse may alternate or coexist with NSSI. This pattern often runs its course in 5 to 15 years and may end abruptly, especially in patients with borderline personality disorder.

Table 2

Psychiatric disorders associated with pathological NSSI

First-line treatment: Psychotherapy

Many studies have demonstrated the efficacy of psychotherapy as the primary treatment for NSSI.^19-21 Except for patients with Lesch-Nyhan syndrome or other rare neurologic syndromes, the biologic causes of NSSI, including the role of endogenous opioids, are unclear. No medications are FDA-approved for NSSI. Pharmacotherapy may help NSSI patients, but such treatment recommendations are based on clinical experience, and polypharmacy is common.²² Studies have not demonstrated specific benefits or consistent efficacy of pharmacotherapy for NSSI.²³

Major NSSI. Prevention is key to addressing major NSSI. Consider atypical antipsychotics for psychotic patients who are preoccupied with religion, the Bible, or sexuality, as well as those who dramatically and suddenly change their appearance by cutting off their hair, engaging in extreme body modification practices, or wearing bizarre clothes.²⁴ In my clinical experience, agitated patients who have committed major NSSI are at high risk for a second episode and should receive pharmacotherapy based on treatment guidelines and hospitalized until the agitation is controlled.

Stereotypic NSSI. Patients with this form of NSSI often cannot articulate what is bothering them. With input from caretakers, assess the likelihood that a patient is reacting to pain. Analgesics may be effective. Also check for infections such as otitis media. Selecting a medication can be challenging. Start with a moderate dose of a selective serotonin reuptake inhibitor (SSRI), then slowly add an atypical antipsychotic, followed by a mood stabilizer, then clonidine, and then a beta blocker; a trial of naltrexone also is an option.²³ Behavior therapy is the primary treatment.

Compulsive NSSI. Compulsive NSSI patients typically seek help from dermatologists or family physicians. Literature on psychiatric treatment is limited, but SSRIs, lithium, benzodiazepines, and atypical antipsychotics (for delusional parasitosis) may be effective. N-acetylcysteine, 600 mg twice a day, may relieve trichotillomania.²⁵ Treatment should include psychotherapy.

Impulsive NSSI. Patients who engage in episodic impulsive NSSI should receive pharmacotherapy for underlying psychiatric illnesses such as generalized anxiety disorder, posttraumatic stress disorder, or depression. Do not automatically diagnose borderline personality disorder. Patients whose NSSI behavior is uncontrollable initially should receive high doses of SSRIs that can be lowered when impulsivity decreases, atypical antipsychotics, and a mood stabilizer such as lamotrigine. Psychotherapy is vital, especially dialectical behavior therapy. Cognitive-behavioral and interpersonal therapies also are effective, as is psychodynamic therapy.^19-21

NSSI patients and their families may benefit from Web sites that provide information, advice, monitored blogs, and support groups (see Related Resources).

Related Resources

• Favazza A. Bodies under siege: self-mutilation, nonsuicidal self-injury, and body modification in culture and psychiatry. 3rd ed. Baltimore, MD: Johns Hopkins University Press; 2011.
• Nock MK. Understanding nonsuicidal self-injury: origins, assessment, and treatment. Washington, DC: American Psychological Association; 2009.
• Cornell University Family Life Development Center. About self-injury. www.crpsib.com/whatissi.asp.

Drug Brand Names

• Clonidine • Catapres, Kapvay
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Naltrexone • ReVia

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Formerly called self-mutilation, self-injury, or self-harm, nonsuicidal self-injury (NSSI) is the deliberate and direct alteration or destruction of healthy body tissue without suicidal intent; these behaviors range from skin cutting or burning to eye enucleation or amputation of body parts. NSSI must be deliberate, as opposed to accidental or indirect behaviors—such as overdoses or ingesting harmful substances—that cause injury that is uncertain, ambiguous as to course, or invisible (the injuries do not disfigure observable body tissue).¹ NSSI acts are done without an intent to die, although persons who self-harm may have suicidal ideation and passive thoughts of dying.² Persons who repeatedly engage in NSSI and are demoralized over their inability to control it are at risk for suicide attempts.³

NSSI can be classified as nonpathological or pathological.⁴ Culturally sanctioned, nonpathological NSSI consists of body modification practices such as tattoos or piercing. Body modification practices may be a sublimation of pathological NSSI. For a description of nonpathological NSSI, see the Box.⁵ Pathological NSSI typically is a method of emotional regulation. Understanding why patients engage in pathological NSSI and how it is categorized can help guide assessment and treatment.

Box

Why people engage in NSSI

NSSI is best regarded as a pathological approach to emotional regulation and distress tolerance that provides rapid but temporary relief from disturbing thoughts, feelings, and emotions. For approximately 90% of patients, NSSI decreases symptoms, most commonly untenable anxiety (“It’s like popping a balloon”), depressed mood, racing thoughts, swirling emotions, anger, hallucinations, and flashbacks.^6,7 In some instances, NSSI generates desired feelings and self-stimulation during periods of dissociation, depersonalization, grief, insecurity, loneliness, extreme boredom, self-pity, and alienation.^8,9 NSSI also may signal distress to elicit a caring response from others or provide a means of escape from intolerable social situations.¹⁰Table 1 lists factors associated with NSSI.

Table 1

Factors associated with NSSI

The functional approach

One model of classifying NSSI focuses on the behavioral functions it serves.^11,12 In this model, the most common function of NSSI is removal or escape from an aversive affective or cognitive state (automatic positive reinforcement). Automatic negative reinforcement explains using NSSI to generate feelings—eg, by patients with anhedonia or numbness. NSSI also may be used as a signal of distress to gain attention, access helpful environmental resources (social positive reinforcement), or remove distressing interpersonal demands (social negative reinforcement).

The functional model is key to providing thorough clinical evaluations that should include understanding the antecedent and consequent thoughts, feelings, situations, triggers, and vulnerabilities related to NSSI acts.

The medical approach

A descriptive, phenomenological model of NSSI classification uses concepts and terminology with which most psychiatrists are familiar, takes into account patients who have comorbid psychiatric disorders, is based on atheoretical, descriptive observations, and fits into what might be regarded as a “medical model.” In this classification, NSSI usually is regarded as a symptom or associated feature of a specific psychiatric disorder, although it may occur in persons who do not meet diagnostic criteria of a mental illness—eg, “copycat” cutting in high school students.^13,14 NSSI may fall within 4 descriptive categories: major, stereotypic, compulsive, or impulsive. For psychiatric disorders associated with these types of pathological NSSI, see Table 2.

Major NSSI includes infrequent acts that destroy significant body tissue, such as eye enucleation and amputation of body parts. They are sudden, messy, and often bloody acts. Seventy-five percent occur during a psychotic state, mainly schizophrenia; of these, approximately one-half occur during a first psychotic episode.¹⁵ The reasons patients typically offer for such behavior often defy logical understanding—eg, to enhance general well-being—but most center on religion, such as a concrete interpretation of biblical texts about removing an offending eye or hand or becoming an eunuch,^16,17 or on sexuality, such as controlling troubling hypersexuality or fear of giving in to homosexual urges.¹⁸

Stereotypic NSSI acts, most commonly associated with severe and profound mental retardation, include repetitive head banging; eye gouging; biting lips, the tongue, cheeks, or fingers; and face or head slapping. The behaviors may be monotonously repetitive, have a rhythmic pattern, and be performed without shame or guilt in the presence of onlookers.

Compulsive NSSI encompasses repetitive behaviors such as severe skin scratching and nail biting, hair pulling (trichotillomania), and skin digging (delusional parasitosis).

Impulsive NSSI consists of acts such as skin cutting, burning, and carving; sticking pins or other objects under the skin or into the chest or abdomen; interfering with wound healing; and smashing hand or foot bones. These behaviors usually are episodic and occur more frequently in females. The average age of onset in patients who engage in impulsive NSSI is 12 to 14, although it may occur throughout the life cycle.

One or 2 isolated instances of impulsive NSSI do not have much prognostic importance unless they are serious enough to warrant an emergency department visit. The real danger is when the behavior becomes repetitive and “addictive.” The crossover from episodic to repetitive usually varies from 5 to 10 episodes.

Persons who engage in repetitive NSSI may use multiple methods, but skin cutting predominates. Such persons often develop a self-identity as a “cutter,” are preoccupied with their NSSI, may carve words into their skin, and may perform acts of self-harm with other self-injurers. Some may cut themselves hundreds or even thousands of times, creating scars that result in social morbidity. They often seek professional help avidly, but may become so demoralized over their inability to stop their NSSI that they are at risk for suicide.³ In some repetitive self-injurers, other impulsive behaviors such as bulimia or substance abuse may alternate or coexist with NSSI. This pattern often runs its course in 5 to 15 years and may end abruptly, especially in patients with borderline personality disorder.

Table 2

Psychiatric disorders associated with pathological NSSI

First-line treatment: Psychotherapy

Many studies have demonstrated the efficacy of psychotherapy as the primary treatment for NSSI.^19-21 Except for patients with Lesch-Nyhan syndrome or other rare neurologic syndromes, the biologic causes of NSSI, including the role of endogenous opioids, are unclear. No medications are FDA-approved for NSSI. Pharmacotherapy may help NSSI patients, but such treatment recommendations are based on clinical experience, and polypharmacy is common.²² Studies have not demonstrated specific benefits or consistent efficacy of pharmacotherapy for NSSI.²³

Major NSSI. Prevention is key to addressing major NSSI. Consider atypical antipsychotics for psychotic patients who are preoccupied with religion, the Bible, or sexuality, as well as those who dramatically and suddenly change their appearance by cutting off their hair, engaging in extreme body modification practices, or wearing bizarre clothes.²⁴ In my clinical experience, agitated patients who have committed major NSSI are at high risk for a second episode and should receive pharmacotherapy based on treatment guidelines and hospitalized until the agitation is controlled.

Stereotypic NSSI. Patients with this form of NSSI often cannot articulate what is bothering them. With input from caretakers, assess the likelihood that a patient is reacting to pain. Analgesics may be effective. Also check for infections such as otitis media. Selecting a medication can be challenging. Start with a moderate dose of a selective serotonin reuptake inhibitor (SSRI), then slowly add an atypical antipsychotic, followed by a mood stabilizer, then clonidine, and then a beta blocker; a trial of naltrexone also is an option.²³ Behavior therapy is the primary treatment.

Compulsive NSSI. Compulsive NSSI patients typically seek help from dermatologists or family physicians. Literature on psychiatric treatment is limited, but SSRIs, lithium, benzodiazepines, and atypical antipsychotics (for delusional parasitosis) may be effective. N-acetylcysteine, 600 mg twice a day, may relieve trichotillomania.²⁵ Treatment should include psychotherapy.

Impulsive NSSI. Patients who engage in episodic impulsive NSSI should receive pharmacotherapy for underlying psychiatric illnesses such as generalized anxiety disorder, posttraumatic stress disorder, or depression. Do not automatically diagnose borderline personality disorder. Patients whose NSSI behavior is uncontrollable initially should receive high doses of SSRIs that can be lowered when impulsivity decreases, atypical antipsychotics, and a mood stabilizer such as lamotrigine. Psychotherapy is vital, especially dialectical behavior therapy. Cognitive-behavioral and interpersonal therapies also are effective, as is psychodynamic therapy.^19-21

NSSI patients and their families may benefit from Web sites that provide information, advice, monitored blogs, and support groups (see Related Resources).

Related Resources

• Favazza A. Bodies under siege: self-mutilation, nonsuicidal self-injury, and body modification in culture and psychiatry. 3rd ed. Baltimore, MD: Johns Hopkins University Press; 2011.
• Nock MK. Understanding nonsuicidal self-injury: origins, assessment, and treatment. Washington, DC: American Psychological Association; 2009.
• Cornell University Family Life Development Center. About self-injury. www.crpsib.com/whatissi.asp.

Drug Brand Names

• Clonidine • Catapres, Kapvay
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Naltrexone • ReVia

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Formerly called self-mutilation, self-injury, or self-harm, nonsuicidal self-injury (NSSI) is the deliberate and direct alteration or destruction of healthy body tissue without suicidal intent; these behaviors range from skin cutting or burning to eye enucleation or amputation of body parts. NSSI must be deliberate, as opposed to accidental or indirect behaviors—such as overdoses or ingesting harmful substances—that cause injury that is uncertain, ambiguous as to course, or invisible (the injuries do not disfigure observable body tissue).¹ NSSI acts are done without an intent to die, although persons who self-harm may have suicidal ideation and passive thoughts of dying.² Persons who repeatedly engage in NSSI and are demoralized over their inability to control it are at risk for suicide attempts.³

NSSI can be classified as nonpathological or pathological.⁴ Culturally sanctioned, nonpathological NSSI consists of body modification practices such as tattoos or piercing. Body modification practices may be a sublimation of pathological NSSI. For a description of nonpathological NSSI, see the Box.⁵ Pathological NSSI typically is a method of emotional regulation. Understanding why patients engage in pathological NSSI and how it is categorized can help guide assessment and treatment.

Box

Why people engage in NSSI

NSSI is best regarded as a pathological approach to emotional regulation and distress tolerance that provides rapid but temporary relief from disturbing thoughts, feelings, and emotions. For approximately 90% of patients, NSSI decreases symptoms, most commonly untenable anxiety (“It’s like popping a balloon”), depressed mood, racing thoughts, swirling emotions, anger, hallucinations, and flashbacks.^6,7 In some instances, NSSI generates desired feelings and self-stimulation during periods of dissociation, depersonalization, grief, insecurity, loneliness, extreme boredom, self-pity, and alienation.^8,9 NSSI also may signal distress to elicit a caring response from others or provide a means of escape from intolerable social situations.¹⁰Table 1 lists factors associated with NSSI.

Table 1

Factors associated with NSSI

The functional approach

One model of classifying NSSI focuses on the behavioral functions it serves.^11,12 In this model, the most common function of NSSI is removal or escape from an aversive affective or cognitive state (automatic positive reinforcement). Automatic negative reinforcement explains using NSSI to generate feelings—eg, by patients with anhedonia or numbness. NSSI also may be used as a signal of distress to gain attention, access helpful environmental resources (social positive reinforcement), or remove distressing interpersonal demands (social negative reinforcement).

The functional model is key to providing thorough clinical evaluations that should include understanding the antecedent and consequent thoughts, feelings, situations, triggers, and vulnerabilities related to NSSI acts.

The medical approach

A descriptive, phenomenological model of NSSI classification uses concepts and terminology with which most psychiatrists are familiar, takes into account patients who have comorbid psychiatric disorders, is based on atheoretical, descriptive observations, and fits into what might be regarded as a “medical model.” In this classification, NSSI usually is regarded as a symptom or associated feature of a specific psychiatric disorder, although it may occur in persons who do not meet diagnostic criteria of a mental illness—eg, “copycat” cutting in high school students.^13,14 NSSI may fall within 4 descriptive categories: major, stereotypic, compulsive, or impulsive. For psychiatric disorders associated with these types of pathological NSSI, see Table 2.

Major NSSI includes infrequent acts that destroy significant body tissue, such as eye enucleation and amputation of body parts. They are sudden, messy, and often bloody acts. Seventy-five percent occur during a psychotic state, mainly schizophrenia; of these, approximately one-half occur during a first psychotic episode.¹⁵ The reasons patients typically offer for such behavior often defy logical understanding—eg, to enhance general well-being—but most center on religion, such as a concrete interpretation of biblical texts about removing an offending eye or hand or becoming an eunuch,^16,17 or on sexuality, such as controlling troubling hypersexuality or fear of giving in to homosexual urges.¹⁸

Stereotypic NSSI acts, most commonly associated with severe and profound mental retardation, include repetitive head banging; eye gouging; biting lips, the tongue, cheeks, or fingers; and face or head slapping. The behaviors may be monotonously repetitive, have a rhythmic pattern, and be performed without shame or guilt in the presence of onlookers.

Compulsive NSSI encompasses repetitive behaviors such as severe skin scratching and nail biting, hair pulling (trichotillomania), and skin digging (delusional parasitosis).

Impulsive NSSI consists of acts such as skin cutting, burning, and carving; sticking pins or other objects under the skin or into the chest or abdomen; interfering with wound healing; and smashing hand or foot bones. These behaviors usually are episodic and occur more frequently in females. The average age of onset in patients who engage in impulsive NSSI is 12 to 14, although it may occur throughout the life cycle.

One or 2 isolated instances of impulsive NSSI do not have much prognostic importance unless they are serious enough to warrant an emergency department visit. The real danger is when the behavior becomes repetitive and “addictive.” The crossover from episodic to repetitive usually varies from 5 to 10 episodes.

Persons who engage in repetitive NSSI may use multiple methods, but skin cutting predominates. Such persons often develop a self-identity as a “cutter,” are preoccupied with their NSSI, may carve words into their skin, and may perform acts of self-harm with other self-injurers. Some may cut themselves hundreds or even thousands of times, creating scars that result in social morbidity. They often seek professional help avidly, but may become so demoralized over their inability to stop their NSSI that they are at risk for suicide.³ In some repetitive self-injurers, other impulsive behaviors such as bulimia or substance abuse may alternate or coexist with NSSI. This pattern often runs its course in 5 to 15 years and may end abruptly, especially in patients with borderline personality disorder.

Table 2

Psychiatric disorders associated with pathological NSSI

First-line treatment: Psychotherapy

Many studies have demonstrated the efficacy of psychotherapy as the primary treatment for NSSI.^19-21 Except for patients with Lesch-Nyhan syndrome or other rare neurologic syndromes, the biologic causes of NSSI, including the role of endogenous opioids, are unclear. No medications are FDA-approved for NSSI. Pharmacotherapy may help NSSI patients, but such treatment recommendations are based on clinical experience, and polypharmacy is common.²² Studies have not demonstrated specific benefits or consistent efficacy of pharmacotherapy for NSSI.²³

Major NSSI. Prevention is key to addressing major NSSI. Consider atypical antipsychotics for psychotic patients who are preoccupied with religion, the Bible, or sexuality, as well as those who dramatically and suddenly change their appearance by cutting off their hair, engaging in extreme body modification practices, or wearing bizarre clothes.²⁴ In my clinical experience, agitated patients who have committed major NSSI are at high risk for a second episode and should receive pharmacotherapy based on treatment guidelines and hospitalized until the agitation is controlled.

Stereotypic NSSI. Patients with this form of NSSI often cannot articulate what is bothering them. With input from caretakers, assess the likelihood that a patient is reacting to pain. Analgesics may be effective. Also check for infections such as otitis media. Selecting a medication can be challenging. Start with a moderate dose of a selective serotonin reuptake inhibitor (SSRI), then slowly add an atypical antipsychotic, followed by a mood stabilizer, then clonidine, and then a beta blocker; a trial of naltrexone also is an option.²³ Behavior therapy is the primary treatment.

Compulsive NSSI. Compulsive NSSI patients typically seek help from dermatologists or family physicians. Literature on psychiatric treatment is limited, but SSRIs, lithium, benzodiazepines, and atypical antipsychotics (for delusional parasitosis) may be effective. N-acetylcysteine, 600 mg twice a day, may relieve trichotillomania.²⁵ Treatment should include psychotherapy.

Impulsive NSSI. Patients who engage in episodic impulsive NSSI should receive pharmacotherapy for underlying psychiatric illnesses such as generalized anxiety disorder, posttraumatic stress disorder, or depression. Do not automatically diagnose borderline personality disorder. Patients whose NSSI behavior is uncontrollable initially should receive high doses of SSRIs that can be lowered when impulsivity decreases, atypical antipsychotics, and a mood stabilizer such as lamotrigine. Psychotherapy is vital, especially dialectical behavior therapy. Cognitive-behavioral and interpersonal therapies also are effective, as is psychodynamic therapy.^19-21

NSSI patients and their families may benefit from Web sites that provide information, advice, monitored blogs, and support groups (see Related Resources).

Related Resources

• Favazza A. Bodies under siege: self-mutilation, nonsuicidal self-injury, and body modification in culture and psychiatry. 3rd ed. Baltimore, MD: Johns Hopkins University Press; 2011.
• Nock MK. Understanding nonsuicidal self-injury: origins, assessment, and treatment. Washington, DC: American Psychological Association; 2009.
• Cornell University Family Life Development Center. About self-injury. www.crpsib.com/whatissi.asp.

Drug Brand Names

• Clonidine • Catapres, Kapvay
• Lamotrigine • Lamictal
• Lithium • Eskalith, Lithobid
• Naltrexone • ReVia

Disclosure

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

Not ’antipsychiatry’

Dr. Nasrallah misrepresents Drs. Jacques Lacan, Erich Fromm, Theodore Lidz, and others in his December 2011 editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53). They were not antipsychiatry, nor am I.

I am “anti” the sort of concrete biological reductionism espoused by Dr. Nasrallah. The psychiatrist nattily dressed in a white jacket and a neat suit and tie looks like a real doctor, but the so-called rigorous objective medical practice he does ignores a huge domain that psychiatry used to be concerned about. In effect, under the leadership of those such as Dr. Nasrallah, psychiatry has “lost its mind.” The disorders we treat are real disorders, but getting rid of the mental dimension and reducing all to “brain disorders” reduces our effectiveness in helping patients, is not humane, and flees from the truth. Psychiatry needs to re-find its mind.

Ronald Abramson, MD, DLFAPA
Associate Clinical Professor of Psychiatry
Tufts University School of Medicine
Boston, MA

Defending Dr. Szasz

Dr. Nasrallah’s editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53) on the antipsychiatry movement was an excellent historical overview. It also was right on target in its conclusion, namely, that antipsychiatry can help keep psychiatry honest and rigorous.

However, the portrayal of Dr. Thomas Szasz as an antipsychiatrist is not wholly correct. For decades, Dr. Szasz has severely criticized both psychiatry and the antipsychiatry movement. Like antipsychiatrists, he is critical of psychiatry, but unlike antipsychiatrists, Dr. Szasz steadfastly has defended the right of consenting individuals to engage in treatment, as long as their participation is voluntary. It is this libertarian streak, the idea that people are free to choose any treatment arrangement they desire—including psychiatry—that distinguishes Dr. Szasz from antipsychiatrists such as Drs. Theodore Lidz, R.D. Laing, and others.

Thomas Rosko, MD
Private Practice
Los Angeles, CA

Perpetrators of abuse

Dr. Nasrallah appears to be deliberately avoiding some of the real abuses perpetrated by modern-day psychiatry (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53), including deliberately misdiagnosing alcoholics and drug abusers as bipolar in order to give them mood stabilizers, often while they are actively abusing substances.

It seems unfathomable for a physician to document a history of depressive episodes, let alone manic episodes, in someone who has been either intoxicated or in early withdrawal constantly over the years, yet this is done routinely. The abuser is happy to play along, as long as the psychiatrist prescribes benzodiazepines along with valproic acid, lithium, or lamotrigine for the patient’s persistent panic attacks and chronic insomnia.

This psychiatric version of “when you have a hammer, everything is a nail” extends to the treatment of uncomplicated grief with antidepressants, additionally labeling oppositional defiant adolescents as bipolar to give them mood stabilizers, and, of course, treating large-portion junk food eaters for “bulimia,” placing them into eating disorder programs, and prescribing psychotropics.

Dr. Nasrallah’s examples of old abuses are a “straw man” argument and unfortunately divert attention from the legitimate concerns about “scientific” modern psychiatry.

Ronald Cann, MD
Private Practice
San Diego, CA

Dr. Nasrallah responds

I appreciate the letters from Drs. Abramson, Rosko, and Cann. I particularly liked their “healthy skepticism” about parts of my editorial about antipsychiatry.

My clinical training was heavily “mind-oriented” with intensive psychodynamic as well as behavioral psychotherapy (not cognitive-behavioral therapy), and my National Institute of Mental Health research training was heavily “brain oriented” with a neuroscience focus. I integrated both brain (hardware) and mind (software) in my work with each patient and it worked spectacularly well for both of us! George Engel, the father of the biopsychosocial model, was one of my residency supervisors at the University of Rochester, so I was “inoculated” by his mentorship against the hazards of biological reductionism, to which Dr. Abramson assumes I subscribe.

Dr. Thomas Szasz certainly was more of a libertarian than an antipsychiatrist and did a great injustice to patients with severe brain disorders, such as schizophrenia, by asserting that they are competent enough to choose or deny treatment, possibly because of the early state of neurobiology research 50 years ago when the neurotoxic effects of psychosis were still undiscovered. Unlike persons with healthy brains and prefrontal executive functions that enable sound decision-making, schizophrenia patients have anosognosia—the neurologic term for lack of insight and self-monitoring—severe cognitive deficits in processing information and decision-making, and reality distortion, and they lack the capacity to determine that they urgently need treatment. Witness the death of thousands of schizophrenia patients who were abruptly released from Italy’s asylums in the 1980s because they lacked the basic brain functions needed to survive. It was a tragic mistake to leave them to their own devices in the name of freedom, conceptualized by lay legislators who had no idea how impaired the brain is in many schizophrenia patients.

Finally, Dr. Szasz practiced long before research demonstrated that the longer psychosis went untreated, the worse the deterioration and functional outcome. Thus, his stance to let patients with psychosis refuse medications significantly harmed those patients, worsened their symptoms, and reduced their chance for remission.

Dr. Cann’s allegations of the “real abuses” of modern day psychiatry are to the best of my knowledge just that–allegations. I have never seen valid documentation of the large-scale abuses he cites, although an occasional deviation occurs in any profession. The practice guidelines for various psychiatric disorders never recommend what Dr. Cann claims is happening with diagnostic distortions and ulterior motives.

Psychiatry still is evolving as a medical discipline and there are comorbidities that confound the primary diagnosis—such as anxiety or heavy drinking in bipolar disorder—but research is actively seeking a biopsychosocial explanation. The Epidemiological Catchment Area study,¹ published 20 years ago before any of the current medications were introduced, is upheld as the best estimate of the prevalence of psychiatric disorders in the United States—approximately 25% lifetime risk, which means approximately 75 million children, adolescents, and adults have a diagnosable psychiatric disorder. Some of them receive good evidence-based treatments and some do not, but many more never receive any treatment and suffer in quiet desperation.

Henry A. Nasrallah, MD
Editor-in-Chief

Not ’antipsychiatry’

Dr. Nasrallah misrepresents Drs. Jacques Lacan, Erich Fromm, Theodore Lidz, and others in his December 2011 editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53). They were not antipsychiatry, nor am I.

I am “anti” the sort of concrete biological reductionism espoused by Dr. Nasrallah. The psychiatrist nattily dressed in a white jacket and a neat suit and tie looks like a real doctor, but the so-called rigorous objective medical practice he does ignores a huge domain that psychiatry used to be concerned about. In effect, under the leadership of those such as Dr. Nasrallah, psychiatry has “lost its mind.” The disorders we treat are real disorders, but getting rid of the mental dimension and reducing all to “brain disorders” reduces our effectiveness in helping patients, is not humane, and flees from the truth. Psychiatry needs to re-find its mind.

Ronald Abramson, MD, DLFAPA
Associate Clinical Professor of Psychiatry
Tufts University School of Medicine
Boston, MA

Defending Dr. Szasz

Dr. Nasrallah’s editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53) on the antipsychiatry movement was an excellent historical overview. It also was right on target in its conclusion, namely, that antipsychiatry can help keep psychiatry honest and rigorous.

However, the portrayal of Dr. Thomas Szasz as an antipsychiatrist is not wholly correct. For decades, Dr. Szasz has severely criticized both psychiatry and the antipsychiatry movement. Like antipsychiatrists, he is critical of psychiatry, but unlike antipsychiatrists, Dr. Szasz steadfastly has defended the right of consenting individuals to engage in treatment, as long as their participation is voluntary. It is this libertarian streak, the idea that people are free to choose any treatment arrangement they desire—including psychiatry—that distinguishes Dr. Szasz from antipsychiatrists such as Drs. Theodore Lidz, R.D. Laing, and others.

Thomas Rosko, MD
Private Practice
Los Angeles, CA

Perpetrators of abuse

Dr. Nasrallah appears to be deliberately avoiding some of the real abuses perpetrated by modern-day psychiatry (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53), including deliberately misdiagnosing alcoholics and drug abusers as bipolar in order to give them mood stabilizers, often while they are actively abusing substances.

It seems unfathomable for a physician to document a history of depressive episodes, let alone manic episodes, in someone who has been either intoxicated or in early withdrawal constantly over the years, yet this is done routinely. The abuser is happy to play along, as long as the psychiatrist prescribes benzodiazepines along with valproic acid, lithium, or lamotrigine for the patient’s persistent panic attacks and chronic insomnia.

This psychiatric version of “when you have a hammer, everything is a nail” extends to the treatment of uncomplicated grief with antidepressants, additionally labeling oppositional defiant adolescents as bipolar to give them mood stabilizers, and, of course, treating large-portion junk food eaters for “bulimia,” placing them into eating disorder programs, and prescribing psychotropics.

Dr. Nasrallah’s examples of old abuses are a “straw man” argument and unfortunately divert attention from the legitimate concerns about “scientific” modern psychiatry.

Ronald Cann, MD
Private Practice
San Diego, CA

Dr. Nasrallah responds

I appreciate the letters from Drs. Abramson, Rosko, and Cann. I particularly liked their “healthy skepticism” about parts of my editorial about antipsychiatry.

My clinical training was heavily “mind-oriented” with intensive psychodynamic as well as behavioral psychotherapy (not cognitive-behavioral therapy), and my National Institute of Mental Health research training was heavily “brain oriented” with a neuroscience focus. I integrated both brain (hardware) and mind (software) in my work with each patient and it worked spectacularly well for both of us! George Engel, the father of the biopsychosocial model, was one of my residency supervisors at the University of Rochester, so I was “inoculated” by his mentorship against the hazards of biological reductionism, to which Dr. Abramson assumes I subscribe.

Dr. Thomas Szasz certainly was more of a libertarian than an antipsychiatrist and did a great injustice to patients with severe brain disorders, such as schizophrenia, by asserting that they are competent enough to choose or deny treatment, possibly because of the early state of neurobiology research 50 years ago when the neurotoxic effects of psychosis were still undiscovered. Unlike persons with healthy brains and prefrontal executive functions that enable sound decision-making, schizophrenia patients have anosognosia—the neurologic term for lack of insight and self-monitoring—severe cognitive deficits in processing information and decision-making, and reality distortion, and they lack the capacity to determine that they urgently need treatment. Witness the death of thousands of schizophrenia patients who were abruptly released from Italy’s asylums in the 1980s because they lacked the basic brain functions needed to survive. It was a tragic mistake to leave them to their own devices in the name of freedom, conceptualized by lay legislators who had no idea how impaired the brain is in many schizophrenia patients.

Finally, Dr. Szasz practiced long before research demonstrated that the longer psychosis went untreated, the worse the deterioration and functional outcome. Thus, his stance to let patients with psychosis refuse medications significantly harmed those patients, worsened their symptoms, and reduced their chance for remission.

Dr. Cann’s allegations of the “real abuses” of modern day psychiatry are to the best of my knowledge just that–allegations. I have never seen valid documentation of the large-scale abuses he cites, although an occasional deviation occurs in any profession. The practice guidelines for various psychiatric disorders never recommend what Dr. Cann claims is happening with diagnostic distortions and ulterior motives.

Psychiatry still is evolving as a medical discipline and there are comorbidities that confound the primary diagnosis—such as anxiety or heavy drinking in bipolar disorder—but research is actively seeking a biopsychosocial explanation. The Epidemiological Catchment Area study,¹ published 20 years ago before any of the current medications were introduced, is upheld as the best estimate of the prevalence of psychiatric disorders in the United States—approximately 25% lifetime risk, which means approximately 75 million children, adolescents, and adults have a diagnosable psychiatric disorder. Some of them receive good evidence-based treatments and some do not, but many more never receive any treatment and suffer in quiet desperation.

Henry A. Nasrallah, MD
Editor-in-Chief

Not ’antipsychiatry’

Dr. Nasrallah misrepresents Drs. Jacques Lacan, Erich Fromm, Theodore Lidz, and others in his December 2011 editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53). They were not antipsychiatry, nor am I.

I am “anti” the sort of concrete biological reductionism espoused by Dr. Nasrallah. The psychiatrist nattily dressed in a white jacket and a neat suit and tie looks like a real doctor, but the so-called rigorous objective medical practice he does ignores a huge domain that psychiatry used to be concerned about. In effect, under the leadership of those such as Dr. Nasrallah, psychiatry has “lost its mind.” The disorders we treat are real disorders, but getting rid of the mental dimension and reducing all to “brain disorders” reduces our effectiveness in helping patients, is not humane, and flees from the truth. Psychiatry needs to re-find its mind.

Ronald Abramson, MD, DLFAPA
Associate Clinical Professor of Psychiatry
Tufts University School of Medicine
Boston, MA

Defending Dr. Szasz

Dr. Nasrallah’s editorial (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53) on the antipsychiatry movement was an excellent historical overview. It also was right on target in its conclusion, namely, that antipsychiatry can help keep psychiatry honest and rigorous.

However, the portrayal of Dr. Thomas Szasz as an antipsychiatrist is not wholly correct. For decades, Dr. Szasz has severely criticized both psychiatry and the antipsychiatry movement. Like antipsychiatrists, he is critical of psychiatry, but unlike antipsychiatrists, Dr. Szasz steadfastly has defended the right of consenting individuals to engage in treatment, as long as their participation is voluntary. It is this libertarian streak, the idea that people are free to choose any treatment arrangement they desire—including psychiatry—that distinguishes Dr. Szasz from antipsychiatrists such as Drs. Theodore Lidz, R.D. Laing, and others.

Thomas Rosko, MD
Private Practice
Los Angeles, CA

Perpetrators of abuse

Dr. Nasrallah appears to be deliberately avoiding some of the real abuses perpetrated by modern-day psychiatry (“The antipsychiatry movement: Who and why,” From the Editor, Current Psychiatry, December 2011, p. 4-6, 53), including deliberately misdiagnosing alcoholics and drug abusers as bipolar in order to give them mood stabilizers, often while they are actively abusing substances.

It seems unfathomable for a physician to document a history of depressive episodes, let alone manic episodes, in someone who has been either intoxicated or in early withdrawal constantly over the years, yet this is done routinely. The abuser is happy to play along, as long as the psychiatrist prescribes benzodiazepines along with valproic acid, lithium, or lamotrigine for the patient’s persistent panic attacks and chronic insomnia.

This psychiatric version of “when you have a hammer, everything is a nail” extends to the treatment of uncomplicated grief with antidepressants, additionally labeling oppositional defiant adolescents as bipolar to give them mood stabilizers, and, of course, treating large-portion junk food eaters for “bulimia,” placing them into eating disorder programs, and prescribing psychotropics.

Dr. Nasrallah’s examples of old abuses are a “straw man” argument and unfortunately divert attention from the legitimate concerns about “scientific” modern psychiatry.

Ronald Cann, MD
Private Practice
San Diego, CA

Dr. Nasrallah responds

I appreciate the letters from Drs. Abramson, Rosko, and Cann. I particularly liked their “healthy skepticism” about parts of my editorial about antipsychiatry.

My clinical training was heavily “mind-oriented” with intensive psychodynamic as well as behavioral psychotherapy (not cognitive-behavioral therapy), and my National Institute of Mental Health research training was heavily “brain oriented” with a neuroscience focus. I integrated both brain (hardware) and mind (software) in my work with each patient and it worked spectacularly well for both of us! George Engel, the father of the biopsychosocial model, was one of my residency supervisors at the University of Rochester, so I was “inoculated” by his mentorship against the hazards of biological reductionism, to which Dr. Abramson assumes I subscribe.

Dr. Thomas Szasz certainly was more of a libertarian than an antipsychiatrist and did a great injustice to patients with severe brain disorders, such as schizophrenia, by asserting that they are competent enough to choose or deny treatment, possibly because of the early state of neurobiology research 50 years ago when the neurotoxic effects of psychosis were still undiscovered. Unlike persons with healthy brains and prefrontal executive functions that enable sound decision-making, schizophrenia patients have anosognosia—the neurologic term for lack of insight and self-monitoring—severe cognitive deficits in processing information and decision-making, and reality distortion, and they lack the capacity to determine that they urgently need treatment. Witness the death of thousands of schizophrenia patients who were abruptly released from Italy’s asylums in the 1980s because they lacked the basic brain functions needed to survive. It was a tragic mistake to leave them to their own devices in the name of freedom, conceptualized by lay legislators who had no idea how impaired the brain is in many schizophrenia patients.

Finally, Dr. Szasz practiced long before research demonstrated that the longer psychosis went untreated, the worse the deterioration and functional outcome. Thus, his stance to let patients with psychosis refuse medications significantly harmed those patients, worsened their symptoms, and reduced their chance for remission.

Dr. Cann’s allegations of the “real abuses” of modern day psychiatry are to the best of my knowledge just that–allegations. I have never seen valid documentation of the large-scale abuses he cites, although an occasional deviation occurs in any profession. The practice guidelines for various psychiatric disorders never recommend what Dr. Cann claims is happening with diagnostic distortions and ulterior motives.

Psychiatry still is evolving as a medical discipline and there are comorbidities that confound the primary diagnosis—such as anxiety or heavy drinking in bipolar disorder—but research is actively seeking a biopsychosocial explanation. The Epidemiological Catchment Area study,¹ published 20 years ago before any of the current medications were introduced, is upheld as the best estimate of the prevalence of psychiatric disorders in the United States—approximately 25% lifetime risk, which means approximately 75 million children, adolescents, and adults have a diagnosable psychiatric disorder. Some of them receive good evidence-based treatments and some do not, but many more never receive any treatment and suffer in quiet desperation.

Henry A. Nasrallah, MD
Editor-in-Chief

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. B, age 32, was diagnosed with human immunodeficiency virus (HIV) approximately 10 years ago. His current HIV regimen is highly active antiretroviral therapy, which includes the protease inhibitor (PI) indinavir and the combination product lamivudine and zidovudine, 2 nucleoside reverse transcriptase inhibitors. He shows no symptoms and his viral load has been undetectable for 9 years.

Several months ago, Mr. B reported to his primary care physician feelings of depressed mood, anhedonia, significant weight loss, fatigue, and feelings of worthlessness. He was diagnosed with major depressive disorder and started venlafaxine, 150 mg/d. The depressive episode is now in remission and the only major side effect he experiences is lethargy. His physician decides to check Mr. B’s viral load, which is 1,100 copies/mL. This viral load value indicates a significant elevation from the baseline (<48 copies/mL), which although still low, is considered virologic failure.¹ To rule out a lab error the viral load test is replicated, but the result is the same.

Mr. B’s case may represent an interaction between his antidepressant and one of his antiviral drugs that is a P-glycoprotein substrate. This protein transports a variety of drug substrates across cell membranes and affects the distribution and elimination of many prescription and nonprescription medications. Whether a drug induces or inhibits P-glycoprotein can affect plasma and cellular concentrations of drugs and can lead to unexpected increases or decreases in plasma concentrations of the affected drug. Understanding P-glycoprotein’s role can help you choose effective psychotropics for patients such as Mr. B.

Change in drug effect

Because depression is common among patients with HIV, my colleagues and I evaluated the pharmacokinetic effects of indinavir on venlafaxine and venlafaxine on indinavir to determine if venlafaxine would be safe to use in a patient taking a PI because of potential cytochrome P450 (CYP450) drug interactions in both classes of medications.² Adding venlafaxine resulted in a 36% decrease in maximum concentrations for indinavir and a 28% decrease in area under the curve Figure.² Study participants were healthy individuals; however, we concluded that had we studied patients with HIV, indinavir efficacy could decrease, resulting in an increased viral load. After this study, the manufacturer of venlafaxine included a caution about this combination in the product labeling.³ Because the extended-release formulation includes the same compound, the same effect could be expected and was included in the most recent version of the extended-release venlafaxine prescribing information.⁴

What is interesting about the venlafaxine-indinavir interaction is that there was no change in either agent’s half-life and therefore no reason to assume this effect was a traditional CYP450 drug interaction. The investigators considered other types of drug interactions and focused on mechanisms that could be presystemic, ie, affecting the absorption and bioavailability of indinavir. This led investigators to believe that the mechanism involved a drug transport protein such as P-glycoprotein, which is present in gut lumen. Subsequent studies have shown in a cellular model that venlafaxine—but not desvenlafaxine—is an inducer of P-glycoprotein and breast cancer resistant protein (BCRP).^5,6 Researchers are conducting animal studies to attempt to duplicate the cellular models. However, it could be presumed that the study of venlafaxine and indinavir in healthy individuals already had demonstrated this effect.²

Figure: Indinavir area under the curve before and after steady state venlafaxine
Decrease in area under the curve (AUC) for indinavir when healthy individuals achieved steady state dosing of venlafaxine
Source: Reference 2

Cause and effect

P-glycoprotein transports drugs or other foreign compounds out of the cells (efflux) of the target tissue so they can be further metabolized by metabolic enzymes for elimination. These proteins are called efflux proteins. There are many efflux proteins in addition to P-glycoprotein; a common one is BCRP, which confers resistance to some anticancer drugs. In addition to the gut lumen and breast tissue, efflux proteins are present in most tissues throughout the body, including the blood-brain barrier.

If drug A inhibits an efflux protein, then drug B would be able to enter the target tissue with greater ease and not be “kicked out” because the efflux system would be disabled. This could result in higher-than-expected tissue concentrations of drug B. Pharmaceutical companies often perform P-glycoprotein inhibition studies before a drug is marketed and include this data in the prescribing information.

If, on the other hand, drug A induces an efflux protein, then drug B would be “kicked out” at a greater rate than normal because the efflux system would be working in overdrive. In this case, tissue concentrations of drug B would be lower than expected and could lead to therapeutic failure. Typically, pharmaceutical companies either do not conduct these induction studies, or if they are performed, they often are not described in prescribing information. This lack of efficacy has been well documented with chemotherapeutic failure caused by drug efflux by BCRP.⁷ It is likely that Mr. B’s viral load increased when venlafaxine was added to his regimen—the antidepressant induced P-glycoprotein, which reduced indinavir concentrations and subsequent therapeutic effect.

Clinicians should review specific medications they are considering using if the drugs have a narrow therapeutic index or if therapeutic failure from subtherapeutic or supratherapeutic doses would be considered problematic Table.⁸ Kim⁹ provides a comprehensive list of P-glycoprotein substrates, inhibitors, and inducers. However, keep in mind that the list of substrates, inhibitors, and inducers changes regularly as new research becomes available.

Table

Selected psychotropics that affect P-glycoprotein

Related Resources

• Linnet K, Ejsing TB. A review on the impact of P-glycoprotein on the penetration of drugs into the brain. Focus on psychotropic drugs. Eur Neuropsychopharmacol. 2008;18(3):157-169.
• Weiss J, Dormann SM, Martin-Facklam M, et al. Inhibition of P-glycoprotein by newer antidepressants. J Pharmacol Exp Ther. 2003;305(1):197-204.

Drug Brand Names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Desipramine • Norpramin
• Desvenlafaxine • Pristiq
• Disulfiram • Antabuse
• Doxepin • Adapin, Silenor
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Imipramine • Tofranil
• Indinavir • Crixivan
• Lamivudine and zidovudine • Combivir
• Nefazodone • Serzone
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Thioridazine • Melleril
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro
• Trifluoperazine • Stelazine
• Trimipramine • Surmontil
• Venlafaxine • Effexor

Disclosure

Dr. Levin receives grant/research support from Pfizer.

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. B, age 32, was diagnosed with human immunodeficiency virus (HIV) approximately 10 years ago. His current HIV regimen is highly active antiretroviral therapy, which includes the protease inhibitor (PI) indinavir and the combination product lamivudine and zidovudine, 2 nucleoside reverse transcriptase inhibitors. He shows no symptoms and his viral load has been undetectable for 9 years.

Several months ago, Mr. B reported to his primary care physician feelings of depressed mood, anhedonia, significant weight loss, fatigue, and feelings of worthlessness. He was diagnosed with major depressive disorder and started venlafaxine, 150 mg/d. The depressive episode is now in remission and the only major side effect he experiences is lethargy. His physician decides to check Mr. B’s viral load, which is 1,100 copies/mL. This viral load value indicates a significant elevation from the baseline (<48 copies/mL), which although still low, is considered virologic failure.¹ To rule out a lab error the viral load test is replicated, but the result is the same.

Mr. B’s case may represent an interaction between his antidepressant and one of his antiviral drugs that is a P-glycoprotein substrate. This protein transports a variety of drug substrates across cell membranes and affects the distribution and elimination of many prescription and nonprescription medications. Whether a drug induces or inhibits P-glycoprotein can affect plasma and cellular concentrations of drugs and can lead to unexpected increases or decreases in plasma concentrations of the affected drug. Understanding P-glycoprotein’s role can help you choose effective psychotropics for patients such as Mr. B.

Change in drug effect

Because depression is common among patients with HIV, my colleagues and I evaluated the pharmacokinetic effects of indinavir on venlafaxine and venlafaxine on indinavir to determine if venlafaxine would be safe to use in a patient taking a PI because of potential cytochrome P450 (CYP450) drug interactions in both classes of medications.² Adding venlafaxine resulted in a 36% decrease in maximum concentrations for indinavir and a 28% decrease in area under the curve Figure.² Study participants were healthy individuals; however, we concluded that had we studied patients with HIV, indinavir efficacy could decrease, resulting in an increased viral load. After this study, the manufacturer of venlafaxine included a caution about this combination in the product labeling.³ Because the extended-release formulation includes the same compound, the same effect could be expected and was included in the most recent version of the extended-release venlafaxine prescribing information.⁴

What is interesting about the venlafaxine-indinavir interaction is that there was no change in either agent’s half-life and therefore no reason to assume this effect was a traditional CYP450 drug interaction. The investigators considered other types of drug interactions and focused on mechanisms that could be presystemic, ie, affecting the absorption and bioavailability of indinavir. This led investigators to believe that the mechanism involved a drug transport protein such as P-glycoprotein, which is present in gut lumen. Subsequent studies have shown in a cellular model that venlafaxine—but not desvenlafaxine—is an inducer of P-glycoprotein and breast cancer resistant protein (BCRP).^5,6 Researchers are conducting animal studies to attempt to duplicate the cellular models. However, it could be presumed that the study of venlafaxine and indinavir in healthy individuals already had demonstrated this effect.²

Figure: Indinavir area under the curve before and after steady state venlafaxine
Decrease in area under the curve (AUC) for indinavir when healthy individuals achieved steady state dosing of venlafaxine
Source: Reference 2

Cause and effect

P-glycoprotein transports drugs or other foreign compounds out of the cells (efflux) of the target tissue so they can be further metabolized by metabolic enzymes for elimination. These proteins are called efflux proteins. There are many efflux proteins in addition to P-glycoprotein; a common one is BCRP, which confers resistance to some anticancer drugs. In addition to the gut lumen and breast tissue, efflux proteins are present in most tissues throughout the body, including the blood-brain barrier.

If drug A inhibits an efflux protein, then drug B would be able to enter the target tissue with greater ease and not be “kicked out” because the efflux system would be disabled. This could result in higher-than-expected tissue concentrations of drug B. Pharmaceutical companies often perform P-glycoprotein inhibition studies before a drug is marketed and include this data in the prescribing information.

If, on the other hand, drug A induces an efflux protein, then drug B would be “kicked out” at a greater rate than normal because the efflux system would be working in overdrive. In this case, tissue concentrations of drug B would be lower than expected and could lead to therapeutic failure. Typically, pharmaceutical companies either do not conduct these induction studies, or if they are performed, they often are not described in prescribing information. This lack of efficacy has been well documented with chemotherapeutic failure caused by drug efflux by BCRP.⁷ It is likely that Mr. B’s viral load increased when venlafaxine was added to his regimen—the antidepressant induced P-glycoprotein, which reduced indinavir concentrations and subsequent therapeutic effect.

Clinicians should review specific medications they are considering using if the drugs have a narrow therapeutic index or if therapeutic failure from subtherapeutic or supratherapeutic doses would be considered problematic Table.⁸ Kim⁹ provides a comprehensive list of P-glycoprotein substrates, inhibitors, and inducers. However, keep in mind that the list of substrates, inhibitors, and inducers changes regularly as new research becomes available.

Table

Selected psychotropics that affect P-glycoprotein

Related Resources

• Linnet K, Ejsing TB. A review on the impact of P-glycoprotein on the penetration of drugs into the brain. Focus on psychotropic drugs. Eur Neuropsychopharmacol. 2008;18(3):157-169.
• Weiss J, Dormann SM, Martin-Facklam M, et al. Inhibition of P-glycoprotein by newer antidepressants. J Pharmacol Exp Ther. 2003;305(1):197-204.

Drug Brand Names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Desipramine • Norpramin
• Desvenlafaxine • Pristiq
• Disulfiram • Antabuse
• Doxepin • Adapin, Silenor
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Imipramine • Tofranil
• Indinavir • Crixivan
• Lamivudine and zidovudine • Combivir
• Nefazodone • Serzone
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Thioridazine • Melleril
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro
• Trifluoperazine • Stelazine
• Trimipramine • Surmontil
• Venlafaxine • Effexor

Disclosure

Dr. Levin receives grant/research support from Pfizer.

Discuss this article at www.facebook.com/CurrentPsychiatry

Mr. B, age 32, was diagnosed with human immunodeficiency virus (HIV) approximately 10 years ago. His current HIV regimen is highly active antiretroviral therapy, which includes the protease inhibitor (PI) indinavir and the combination product lamivudine and zidovudine, 2 nucleoside reverse transcriptase inhibitors. He shows no symptoms and his viral load has been undetectable for 9 years.

Several months ago, Mr. B reported to his primary care physician feelings of depressed mood, anhedonia, significant weight loss, fatigue, and feelings of worthlessness. He was diagnosed with major depressive disorder and started venlafaxine, 150 mg/d. The depressive episode is now in remission and the only major side effect he experiences is lethargy. His physician decides to check Mr. B’s viral load, which is 1,100 copies/mL. This viral load value indicates a significant elevation from the baseline (<48 copies/mL), which although still low, is considered virologic failure.¹ To rule out a lab error the viral load test is replicated, but the result is the same.

Mr. B’s case may represent an interaction between his antidepressant and one of his antiviral drugs that is a P-glycoprotein substrate. This protein transports a variety of drug substrates across cell membranes and affects the distribution and elimination of many prescription and nonprescription medications. Whether a drug induces or inhibits P-glycoprotein can affect plasma and cellular concentrations of drugs and can lead to unexpected increases or decreases in plasma concentrations of the affected drug. Understanding P-glycoprotein’s role can help you choose effective psychotropics for patients such as Mr. B.

Change in drug effect

Because depression is common among patients with HIV, my colleagues and I evaluated the pharmacokinetic effects of indinavir on venlafaxine and venlafaxine on indinavir to determine if venlafaxine would be safe to use in a patient taking a PI because of potential cytochrome P450 (CYP450) drug interactions in both classes of medications.² Adding venlafaxine resulted in a 36% decrease in maximum concentrations for indinavir and a 28% decrease in area under the curve Figure.² Study participants were healthy individuals; however, we concluded that had we studied patients with HIV, indinavir efficacy could decrease, resulting in an increased viral load. After this study, the manufacturer of venlafaxine included a caution about this combination in the product labeling.³ Because the extended-release formulation includes the same compound, the same effect could be expected and was included in the most recent version of the extended-release venlafaxine prescribing information.⁴

What is interesting about the venlafaxine-indinavir interaction is that there was no change in either agent’s half-life and therefore no reason to assume this effect was a traditional CYP450 drug interaction. The investigators considered other types of drug interactions and focused on mechanisms that could be presystemic, ie, affecting the absorption and bioavailability of indinavir. This led investigators to believe that the mechanism involved a drug transport protein such as P-glycoprotein, which is present in gut lumen. Subsequent studies have shown in a cellular model that venlafaxine—but not desvenlafaxine—is an inducer of P-glycoprotein and breast cancer resistant protein (BCRP).^5,6 Researchers are conducting animal studies to attempt to duplicate the cellular models. However, it could be presumed that the study of venlafaxine and indinavir in healthy individuals already had demonstrated this effect.²

Figure: Indinavir area under the curve before and after steady state venlafaxine
Decrease in area under the curve (AUC) for indinavir when healthy individuals achieved steady state dosing of venlafaxine
Source: Reference 2

Cause and effect

P-glycoprotein transports drugs or other foreign compounds out of the cells (efflux) of the target tissue so they can be further metabolized by metabolic enzymes for elimination. These proteins are called efflux proteins. There are many efflux proteins in addition to P-glycoprotein; a common one is BCRP, which confers resistance to some anticancer drugs. In addition to the gut lumen and breast tissue, efflux proteins are present in most tissues throughout the body, including the blood-brain barrier.

If drug A inhibits an efflux protein, then drug B would be able to enter the target tissue with greater ease and not be “kicked out” because the efflux system would be disabled. This could result in higher-than-expected tissue concentrations of drug B. Pharmaceutical companies often perform P-glycoprotein inhibition studies before a drug is marketed and include this data in the prescribing information.

If, on the other hand, drug A induces an efflux protein, then drug B would be “kicked out” at a greater rate than normal because the efflux system would be working in overdrive. In this case, tissue concentrations of drug B would be lower than expected and could lead to therapeutic failure. Typically, pharmaceutical companies either do not conduct these induction studies, or if they are performed, they often are not described in prescribing information. This lack of efficacy has been well documented with chemotherapeutic failure caused by drug efflux by BCRP.⁷ It is likely that Mr. B’s viral load increased when venlafaxine was added to his regimen—the antidepressant induced P-glycoprotein, which reduced indinavir concentrations and subsequent therapeutic effect.

Clinicians should review specific medications they are considering using if the drugs have a narrow therapeutic index or if therapeutic failure from subtherapeutic or supratherapeutic doses would be considered problematic Table.⁸ Kim⁹ provides a comprehensive list of P-glycoprotein substrates, inhibitors, and inducers. However, keep in mind that the list of substrates, inhibitors, and inducers changes regularly as new research becomes available.

Table

Selected psychotropics that affect P-glycoprotein

Related Resources

• Linnet K, Ejsing TB. A review on the impact of P-glycoprotein on the penetration of drugs into the brain. Focus on psychotropic drugs. Eur Neuropsychopharmacol. 2008;18(3):157-169.
• Weiss J, Dormann SM, Martin-Facklam M, et al. Inhibition of P-glycoprotein by newer antidepressants. J Pharmacol Exp Ther. 2003;305(1):197-204.

Drug Brand Names

• Amitriptyline • Elavil
• Carbamazepine • Tegretol
• Chlorpromazine • Thorazine
• Citalopram • Celexa
• Desipramine • Norpramin
• Desvenlafaxine • Pristiq
• Disulfiram • Antabuse
• Doxepin • Adapin, Silenor
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Imipramine • Tofranil
• Indinavir • Crixivan
• Lamivudine and zidovudine • Combivir
• Nefazodone • Serzone
• Nortriptyline • Aventyl, Pamelor
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Thioridazine • Melleril
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro
• Trifluoperazine • Stelazine
• Trimipramine • Surmontil
• Venlafaxine • Effexor

Disclosure

Dr. Levin receives grant/research support from Pfizer.

Discuss this article at www.facebook.com/CurrentPsychiatry

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

In a survey of 115 college students taking medication for attention-deficit/hyperactivity disorder (ADHD), 31% reported having taken their drugs more frequently or at a higher dose than prescribed, or used someone else’s medication since beginning college.¹ Fifty-six percent reported being asked to give or sell their medication in the past 6 months; 26% of those solicited gave or sold their medication to a peer.¹ The 3 most frequently reported reasons for misusing ADHD medications centered on studying: to improve concentration, to lengthen study time, and to feel less restless while studying.¹

Although treating ADHD with first-line stimulants may reduce the incidence of substance use disorders,^2,3 monitor patients closely to ensure therapeutic drugs are not being misused or abused.

1. Use screening tools such as the CRAFFT test⁴ for adolescents and the 5-question RAFFT test for adults.⁵ Also, consider toxicology screenings.
2. Consider extended-release formulations, which can reduce recreational stimulant use because subjective likeability is more strongly influenced by the drug delivery rate than by plasma concentration.
3. Consider other medications/formulas such as a transdermal patch delivery of methylphenidate or prodrug formulations such as lisdexamfetamine, which is gut enzyme-dependent to hydrolyze into lysine and d-amphetamine. Also, consider nonstimulants such as atomoxetine, bupropion, or tricyclic antidepressants.
4. Rule out mood disorders, especially depression, which may be driving the urge to get “high.”
5. Involve family members or other forms of supervision, who may be able to better monitor medications.
6. Improve physician/patient communication because active physician involvement and better patient communication about treatment-related issues is better for all involved.
7. Provide triplicate prescriptions in person to avoid “prescriptions lost in the mail,” and keep a log of all prescriptions you dispense.

Disclosure

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

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

Discuss this article at www.facebook.com/CurrentPsychiatry

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

Discuss this article at www.facebook.com/CurrentPsychiatry

Every psychiatrist has experienced professional highs and lows. Whether helping a schizophrenia patient return to college, collaborating effectively with nursing staff, or achieving board certification, doctors—like everyone else—thrive on success. These accomplishments motivate us to help others and advance our careers.

However, psychiatrists also are vulnerable to ego insults associated with unavoidable negative and sometimes disastrous outcomes of their work. Doctors fail to "cure" every patient, may be “fired” by a patient, or may lose a patient to suicide.

Physicians spend so much time caring for their patients that they often neglect their own health. Self-care is not a core competency for trainees and many residency programs ignore this important issue. Negative outcomes can have profound effects on physicians, including shock; crying/grief/sadness; changed relationships with colleagues; disassociation from the event; crises of faith in education, training, and competency; shame and embarrassment; fear of reprisal; grandiosity; or a belief that the physician should have been all-knowing. Even when a patient commits suicide, the impact of this difficult and painful event on the clinician often is ignored.¹ Physician suicide rates have been reported to be higher than those of the general population.² Barriers to self-preserving treatment include:

Time constraints. Many doctors work up to 80 hours per week. Self-preservation does not become a priority for professionals until a lack of self-care interferes with their personal or professional life.

Limited resources. Physicians, like the general public, find it difficult to get appointments with primary care physicians and psychiatrists. Some doctors feel guilty about taking a slot from another patient or failing to see one of their own patients during that time. Simply finding a provider who is comfortable treating another doctor may be a challenge.

Stigma. It can be embarrassing for doctors to admit they are human, are vulnerable, and have health care needs. Fear of scrutiny for having an illness such as depression is so severe that surveyed psychiatrists said they would rather treat themselves than seek professional help.³

Psychiatrists who face sensitive emotional material on an hourly basis are susceptible to internalizing their work. For those who work with the vulnerable and victimized, meeting our own needs is fundamental to our ability to thrive. Regular practices that promote reflection are crucial to a psychiatrist’s compassion and self-preservation. Suggestions for appropriate self-care are described in the Table.

Table

Psychiatrists’ health: Guidelines for self-preservation

Discuss this article at www.facebook.com/CurrentPsychiatry