Current Psychiatry

The night started like any other for Dr. Z. Kids in bed (too late) by 10:30, dog out by 11, fell asleep reading journal by 11:15. Sirens jolt her out of a solid stage 4. Her eyes widen, pulse quickens, mouth dries as she follows the glow of the TV into the living room. On TV, fire frames shots of tearful faces, body bags, and firefighters in protective suits. She catches the announcer’s voice: “…explosion at City Power and Light nuclear facility at 3:10 AM today. Fifty-five are known dead, and thousands are being told to evacuate. The blast’s cause is unknown, but terrorism is suspected.”

As her numbness slowly ebbs, Dr. Z’s questions rise insistently. How can I help the survivors? My patients? My children? What if the media call me? How could I have been better prepared for this?

Disaster shakes us to our human and biological core. More than any other clinical encounter, it reminds us that psychiatrists share the vulnerabilities of those we seek to help. Yet it also reminds us that even simple concepts and interventions can mobilize the healing process.

Are you ready to provide emergency psychiatric care following a disaster in your community—be it a nuclear accident, tornado, airplane crash, or terrorist act? Here is evidence—some counterintuitive—that can help you prepare.

Table 1

‘Psychological first aid’ for disaster survivors

Disaster’s psychobiology

Human reactions to disaster are often conceptualized as the mammalian survival response: flight, fight, and fright (freezing). In most cases, these reactions are adaptive and dissipate after safety is restored. Posttraumatic stress disorder (PTSD) develops in about 5% of natural disaster victims and 33% of mass shooting victims.¹

Responses that do go awry appear to be associated with abnormally low cortisol and persistent adrenergic activation, leading to sensitization of the fear response.² Reminders of trauma or persistent stressors—such as pain, problems with finances or housing, or bereavement—may exacerbate sensitization. On the other hand, preclinical studies suggest that social support^3,4 and active coping⁵ mitigate physiologic stress responses, confirming numerous clinical observations that associate lack of social support and avoidant coping with eventual PTSD development.

Three basics. Just as our emergency medicine colleagues must often revert to life-support basics, we must remind ourselves of biology’s three basics for psychic resilience:

• safety (including—as much as possible—protection from reminders of trauma and ongoing stress)
• meaningful social connection
• re-establishing a sense of efficacy to overcome helplessness (Table 1).

Like the stress response, these protective factors seem hard-wired into our biological make-up. They form the foundation for all phases of disaster psychiatry interventions, from planning to immediate interventions through longterm follow-up.

Disaster planning

As a mental health professional, plan to operate within established disaster plans and agencies, not only for the sake of efficiency but also because structure and support are paramount in disaster situations. Check with the American Psychiatric Association’s local branch to determine if a disaster mental health plan exists. If not, explore how to work directly with local American Red Cross chapters and hospitals, which recruit personnel for the Disaster Medical Assistance Teams mobilized by the public health service.

Table 2

Normal reactions to disaster for adults and children

Immediate disaster mental health plans vary in detail according to local needs and resources but should at least address:

• providing on-site interventions
• disseminating information about responses to trauma
• identifying and publicizing local mental health resources.

Immediate interventions

Immediately following a disaster, psychiatrists are frequently asked to assist with on-site crisis and medical interventions, evaluate survivors with unusual or intense reactions, and provide public education about psychological reactions to disaster.

On-site response. All responders, regardless of discipline, should provide disaster survivors with “psychological first aid,” which is directed at reestablishing safety, connection, and efficacy. Basic crisis intervention principles are useful when support and reassurance are not enough.⁶

For example, relaxation exercises can reduce anxiety and improve sleep. Use focused, structured relaxation tools—such as progressive muscle relaxation and breathing training—as unstructured exercises can exacerbate dissociation and re-experiencing. Grounding techniques, by which survivors learn to focus all senses on immediate surroundings, often alleviate dissociation and flashbacks.

Care for children. Because children’s reactions to disaster greatly depend on their caregivers’ responses (social referencing), focus acute interventions for children on:

• re-connecting them with their families
• reducing caregivers’ distress
• educating caregivers about providing age appropriate information and support (see Related resources).

Medical care. As physicians, psychiatrists may be called upon to intervene medically. Although it is generally advisable to stay within our usual practice, medical personnel may be in short supply. Fortunately, Good Samaritan laws exist in every state, and the potential for a successful malpractice suit against a physician responding in a disaster is almost zero, unless the physician’s performance is grossly negligent (such as moving the neck of a patient with obvious head or neck injuries).⁷

Principles regarding informed consent and right to refuse treatment—along with the usual exceptions—apply during disasters.

Evaluating survivors in shelters and hospitals requires knowing the normal and abnormal responses to disaster, being able to differentially diagnose changes in mental status, and understanding risk factors for trauma’s psychiatric sequelae. Aside from PTSD, trauma’s long-term effects include other anxiety disorders, depression, substance abuse, and eating disorders. In addition to the usual components of a psychiatric evaluation, assessments must address event-related factors such as proximity to the disaster, loss of significant others or property, physical injuries, immediate needs, and social support.⁸

Normal stress reactions. Frequently described as “a normal response to an abnormal situation,” the normal stress reaction is multidimensional and depends on the person’s developmental level (Table 2). About 10% to 25% of survivors experience intense affect and dissociation, whereas a similar number may appear unusually calm.

Interventions beyond the“first aid” described above are not usually needed unless individuals:

• are a danger to themselves or others
• are psychotic
• have no social supports
• cannot perform tasks necessary for self-care and to begin the recovery process.

Always re-assess when there is any question about a survivor’s immediate reaction to trauma.

In DSM-IV-TR’s trauma-related diagnoses, the symptom clusters often do not capture many disaster survivors’ subjective experience: the shattering of fundamental beliefs regarding themselves (invulnerability), the world (predictability, safety), and others (trust, benevolence).⁹ By empathizing with these responses, you can help survivors feel less isolated and estranged.

Differential diagnosis. Survivors’ mental status changes may be manifestations of the stress response, but they also may represent:

• exacerbations of pre-existing psychiatric or general medical conditions
• hypoxemia, hypovolemia, or CNS trauma from physical injury
• responses to medications used for resuscitation or pain control, such as atropine, epinephrine, lidocaine, or morphine.

Effects of bioterrorism agents must also be considered. For example, organophosphorus compounds such as the nerve agents sarin and soman can cause impaired concentration, depression, and anxiety. Anthrax can cause rapidly progressing meningitis.¹⁰ Delirium must be differentiated from dissociation; patients with dissociation can be re-oriented, and changes will resolve with time rather than fluctuate.¹¹

Psychopathology risk factors. Multiple studies have addressed risk factors for post-disaster psychiatric sequelae (usually PTSD). In general, risk increases with repeated trauma exposure (including TV viewing), prior trauma, lack of social support, injury, pre-existing psychiatric problems, traumatic bereavement (having witnessed the violent death of a loved one), avoidant coping, and having strong negative beliefs about the meanings of normal stress reactions such as tearfulness, anxiety, and insomnia.

Because a recent meta-analysis supports these observations,¹² follow-up evaluation for signs of PTSD is recommended for:

• survivors with one or more of the risk factors discussed above
• vulnerable groups such as rescue workers, children, and dependent individuals
• survivors whose symptoms persist after 2 months.¹³

Decompensation immediately after a disaster seems to be the exception for psychiatric patients, despite their longer-term vulnerability. One psychiatrist who in 1989 survived Hurricane Hugo—the most intense storm to strike the Mid-Atlantic region in 100 years—noted that demand for inpatient psychiatric services did not increase in the storm’s aftermath. The only patient calls she received were inquiries about her own physical safety.¹⁴

Caregivers and rescue workers—including psychi-atrists—are also disaster survivors, and you need to tend to your needs for safety and support. Consult frequently with colleagues within and outside the disaster area, as much for support as for information and guidance.¹⁵ Remember also that rescue workers are occasionally targets for victims’ rage at their circumstances. Anticipating and explaining this displacement reduces its toxicity.

Using medications

Uses psychotropics judiciously in the first 48 hours of trauma. Medication effects may interfere with neurologic assessment of the injured, and monitoring and follow-up may not be possible.

However, drug therapy should start quickly when survivors are acutely psychotic or their behavior endangers themselves, others, or the milieu. Medications usually include a fast-acting benzodiazepine and/or an antipsychotic, as described in guidelines for managing agitation.¹⁶ Always provide structure and supervision for medicated patients.

No guidelines exist for using medications to manage distressing—but less-severe—acute stress-related symptoms. Some experts advocate using adrenergic antagonists such as clonidine, guanfacine, and beta blockers to reduce excessive arousal. These drugs have not been adequately studied in this setting, however, and may harm those with cardiovascular instability from preexisting conditions or injuries.

Table 3

Psychoeducation: Simple messages for workers and trauma survivors

Short-term (<1 week) benzodiazepine use for panic symptoms and severe insomnia is acceptable, but longer-term use may increase PTSD risk.¹⁷ A selective serotonin reuptake inhibitor may help individuals with pre-existing PTSD or depression, if you can arrange follow-up.

In the aftermath

‘Debriefing.’ Critical incident stress debriefing (CISD) is a structured, one-session group intervention in which survivors’ experiences and emotional reactions are discussed and education and follow-up recommendations are provided. Developed by Mitchell in 1983,¹⁸ CISD was widely used until systematic evaluations revealed that it did not alleviate psychological distress or prevent PTSD.¹⁹

Table 4

How to interact with news media during and after a disaster

Thus, although survivor meetings may provide information, education, screening, and support, avoid detailed discussions of events and emotions. Any meetings should be conducted by mental health clinicians and should not be mandatory. Reserve the term “debriefing” for operational reviews by rescue personnel.²⁰

Public education. Educate survivors, rescue workers, health care providers, teachers, and relief agency workers. Provide concise, simple messages as suggested in Table 3. News media provide our most effective means of reaching out to survivors, which is why having a pre-existing relationship is so important. Some guidelines for working with the media are presented in Table 4.

Outreach. Numerous educational resources are available for survivors and their caregivers (see Related resources). Other potentially useful outreach tools include:

• meetings with teachers’ organizations
• continuing medical education activities for primary care providers
• telephone hot lines.

Legal and ethical issues

Disaster scenes are chaotic and informal, and professionals must be flexible, often providing general support and information rather than specific clinical interventions. However, it is important in each encounter to decide whether a patient-physician relationship has begun.

As a general rule, a physician-patient relationship is established whenever diagnosis or treatment is discussed. Once that happens, briefly document:

• signs and symptoms
• working diagnosis
• suicide or violence potential
• treatment and/or follow-up plans.

Confidentiality may be difficult to preserve in chaotic situations involving workers from many agencies. Even in disasters, however, you must obtain permission before sharing information unless the individual’s situation is emergent.

Table 5

Keys to effective disaster psychiatry

Long-term interventions

Longer-term disaster interventions include continued outreach and education and needed follow-up services. Existing structures may provide effective follow-up, but additional resources are often needed.

Federal programs. Following a presidentialdeclared disaster, the Federal Emergency Management Agency (FEMA) provides funding for crisis counseling. Programs are typically funded for 9 to 15 months and administered through the emergency services and disaster relief branch of the Substance Abuse and Mental Health Services Administration (SAMHSA) and community mental health organizations. Examples include Project Heartland following the 1995 Oklahoma City federal building bombing and Project COPE following California’s 1989 Loma Prieta earthquake.

Cognitive-behavioral therapy. For adult survivors with acute stress disorder, specific cognitive-behavioral therapy (CBT) provided by trained therapists may prevent PTSD and other trauma sequelae, such as depression.²¹ CBT interventions may begin as early as 2 weeks after trauma and focus sequentially on anxiety management, cognitive restructuring, imaginal exposure followed by in vivo exposure, and relapse prevention.

Three controlled trials found 6-month PTSD rates of 14% to 20% among acute stress disorder patients treated with CBT, compared with 58% to 67% with supportive counseling.^22-24 Although studies of interventions immediately following trauma are lacking, trauma-focused CBT is also recommended for children.²⁵ Evidence-based treatments for PTSD are discussed in detail elsewhere.²⁶

Not unprepared after all

With some reflection, Dr. Z realized she had the tools to help her community. Her feelings of helplessness receded as she envisioned how she could help survivors understand their experiences, re-create a sense of safety, restore important connections to loved ones, and begin to rebuild their lives (Table 5).

Related resources

For clinicians

• Young BH, Ford JD, Ruzek JI, et al. Disaster mental health: a guidebook for clinicians and administrators. Washington, DC: National Center for Post-Traumatic Stress Disorder, 1998. http://ncptsd.org/publications/disaster/index.html
• Hillman JL. Crisis intervention and trauma: new approaches to evidence-based practice. New York: Kluwer Academic/Plenum Publishers, 2002.
• Office of the Surgeon General Web site on medical aspects of nuclear, biological, and chemical warfare. http://www.nbc-med.org

For survivors and clinicians

• National Center for Post-Traumatic Stress Disorder. Disaster mental health: Dealing with the aftereffects of terrorism. http://www.ncptsd.org/terrorism/index.html
• Substance Abuse and Mental Health Services Administration. Emergency mental health and traumatic stress. http://www.mentalhealth.org/cmhs/EmergencyServices/default.asp
• American Academy of Child and Adolescent Psychiatry. Talking to children about terrorism and war. http://www.aacap.org/publications/factsFam/87.htm

Drug brand names

• Clonidine • Catapres
• Guanfacine • Tenex

Disclosure

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

The night started like any other for Dr. Z. Kids in bed (too late) by 10:30, dog out by 11, fell asleep reading journal by 11:15. Sirens jolt her out of a solid stage 4. Her eyes widen, pulse quickens, mouth dries as she follows the glow of the TV into the living room. On TV, fire frames shots of tearful faces, body bags, and firefighters in protective suits. She catches the announcer’s voice: “…explosion at City Power and Light nuclear facility at 3:10 AM today. Fifty-five are known dead, and thousands are being told to evacuate. The blast’s cause is unknown, but terrorism is suspected.”

As her numbness slowly ebbs, Dr. Z’s questions rise insistently. How can I help the survivors? My patients? My children? What if the media call me? How could I have been better prepared for this?

Disaster shakes us to our human and biological core. More than any other clinical encounter, it reminds us that psychiatrists share the vulnerabilities of those we seek to help. Yet it also reminds us that even simple concepts and interventions can mobilize the healing process.

Are you ready to provide emergency psychiatric care following a disaster in your community—be it a nuclear accident, tornado, airplane crash, or terrorist act? Here is evidence—some counterintuitive—that can help you prepare.

Table 1

‘Psychological first aid’ for disaster survivors

Disaster’s psychobiology

Human reactions to disaster are often conceptualized as the mammalian survival response: flight, fight, and fright (freezing). In most cases, these reactions are adaptive and dissipate after safety is restored. Posttraumatic stress disorder (PTSD) develops in about 5% of natural disaster victims and 33% of mass shooting victims.¹

Responses that do go awry appear to be associated with abnormally low cortisol and persistent adrenergic activation, leading to sensitization of the fear response.² Reminders of trauma or persistent stressors—such as pain, problems with finances or housing, or bereavement—may exacerbate sensitization. On the other hand, preclinical studies suggest that social support^3,4 and active coping⁵ mitigate physiologic stress responses, confirming numerous clinical observations that associate lack of social support and avoidant coping with eventual PTSD development.

Three basics. Just as our emergency medicine colleagues must often revert to life-support basics, we must remind ourselves of biology’s three basics for psychic resilience:

• safety (including—as much as possible—protection from reminders of trauma and ongoing stress)
• meaningful social connection
• re-establishing a sense of efficacy to overcome helplessness (Table 1).

Like the stress response, these protective factors seem hard-wired into our biological make-up. They form the foundation for all phases of disaster psychiatry interventions, from planning to immediate interventions through longterm follow-up.

Disaster planning

As a mental health professional, plan to operate within established disaster plans and agencies, not only for the sake of efficiency but also because structure and support are paramount in disaster situations. Check with the American Psychiatric Association’s local branch to determine if a disaster mental health plan exists. If not, explore how to work directly with local American Red Cross chapters and hospitals, which recruit personnel for the Disaster Medical Assistance Teams mobilized by the public health service.

Table 2

Normal reactions to disaster for adults and children

Immediate disaster mental health plans vary in detail according to local needs and resources but should at least address:

• providing on-site interventions
• disseminating information about responses to trauma
• identifying and publicizing local mental health resources.

Immediate interventions

Immediately following a disaster, psychiatrists are frequently asked to assist with on-site crisis and medical interventions, evaluate survivors with unusual or intense reactions, and provide public education about psychological reactions to disaster.

On-site response. All responders, regardless of discipline, should provide disaster survivors with “psychological first aid,” which is directed at reestablishing safety, connection, and efficacy. Basic crisis intervention principles are useful when support and reassurance are not enough.⁶

For example, relaxation exercises can reduce anxiety and improve sleep. Use focused, structured relaxation tools—such as progressive muscle relaxation and breathing training—as unstructured exercises can exacerbate dissociation and re-experiencing. Grounding techniques, by which survivors learn to focus all senses on immediate surroundings, often alleviate dissociation and flashbacks.

Care for children. Because children’s reactions to disaster greatly depend on their caregivers’ responses (social referencing), focus acute interventions for children on:

• re-connecting them with their families
• reducing caregivers’ distress
• educating caregivers about providing age appropriate information and support (see Related resources).

Medical care. As physicians, psychiatrists may be called upon to intervene medically. Although it is generally advisable to stay within our usual practice, medical personnel may be in short supply. Fortunately, Good Samaritan laws exist in every state, and the potential for a successful malpractice suit against a physician responding in a disaster is almost zero, unless the physician’s performance is grossly negligent (such as moving the neck of a patient with obvious head or neck injuries).⁷

Principles regarding informed consent and right to refuse treatment—along with the usual exceptions—apply during disasters.

Evaluating survivors in shelters and hospitals requires knowing the normal and abnormal responses to disaster, being able to differentially diagnose changes in mental status, and understanding risk factors for trauma’s psychiatric sequelae. Aside from PTSD, trauma’s long-term effects include other anxiety disorders, depression, substance abuse, and eating disorders. In addition to the usual components of a psychiatric evaluation, assessments must address event-related factors such as proximity to the disaster, loss of significant others or property, physical injuries, immediate needs, and social support.⁸

Normal stress reactions. Frequently described as “a normal response to an abnormal situation,” the normal stress reaction is multidimensional and depends on the person’s developmental level (Table 2). About 10% to 25% of survivors experience intense affect and dissociation, whereas a similar number may appear unusually calm.

Interventions beyond the“first aid” described above are not usually needed unless individuals:

• are a danger to themselves or others
• are psychotic
• have no social supports
• cannot perform tasks necessary for self-care and to begin the recovery process.

Always re-assess when there is any question about a survivor’s immediate reaction to trauma.

In DSM-IV-TR’s trauma-related diagnoses, the symptom clusters often do not capture many disaster survivors’ subjective experience: the shattering of fundamental beliefs regarding themselves (invulnerability), the world (predictability, safety), and others (trust, benevolence).⁹ By empathizing with these responses, you can help survivors feel less isolated and estranged.

Differential diagnosis. Survivors’ mental status changes may be manifestations of the stress response, but they also may represent:

• exacerbations of pre-existing psychiatric or general medical conditions
• hypoxemia, hypovolemia, or CNS trauma from physical injury
• responses to medications used for resuscitation or pain control, such as atropine, epinephrine, lidocaine, or morphine.

Effects of bioterrorism agents must also be considered. For example, organophosphorus compounds such as the nerve agents sarin and soman can cause impaired concentration, depression, and anxiety. Anthrax can cause rapidly progressing meningitis.¹⁰ Delirium must be differentiated from dissociation; patients with dissociation can be re-oriented, and changes will resolve with time rather than fluctuate.¹¹

Psychopathology risk factors. Multiple studies have addressed risk factors for post-disaster psychiatric sequelae (usually PTSD). In general, risk increases with repeated trauma exposure (including TV viewing), prior trauma, lack of social support, injury, pre-existing psychiatric problems, traumatic bereavement (having witnessed the violent death of a loved one), avoidant coping, and having strong negative beliefs about the meanings of normal stress reactions such as tearfulness, anxiety, and insomnia.

Because a recent meta-analysis supports these observations,¹² follow-up evaluation for signs of PTSD is recommended for:

• survivors with one or more of the risk factors discussed above
• vulnerable groups such as rescue workers, children, and dependent individuals
• survivors whose symptoms persist after 2 months.¹³

Decompensation immediately after a disaster seems to be the exception for psychiatric patients, despite their longer-term vulnerability. One psychiatrist who in 1989 survived Hurricane Hugo—the most intense storm to strike the Mid-Atlantic region in 100 years—noted that demand for inpatient psychiatric services did not increase in the storm’s aftermath. The only patient calls she received were inquiries about her own physical safety.¹⁴

Caregivers and rescue workers—including psychi-atrists—are also disaster survivors, and you need to tend to your needs for safety and support. Consult frequently with colleagues within and outside the disaster area, as much for support as for information and guidance.¹⁵ Remember also that rescue workers are occasionally targets for victims’ rage at their circumstances. Anticipating and explaining this displacement reduces its toxicity.

Using medications

Uses psychotropics judiciously in the first 48 hours of trauma. Medication effects may interfere with neurologic assessment of the injured, and monitoring and follow-up may not be possible.

However, drug therapy should start quickly when survivors are acutely psychotic or their behavior endangers themselves, others, or the milieu. Medications usually include a fast-acting benzodiazepine and/or an antipsychotic, as described in guidelines for managing agitation.¹⁶ Always provide structure and supervision for medicated patients.

No guidelines exist for using medications to manage distressing—but less-severe—acute stress-related symptoms. Some experts advocate using adrenergic antagonists such as clonidine, guanfacine, and beta blockers to reduce excessive arousal. These drugs have not been adequately studied in this setting, however, and may harm those with cardiovascular instability from preexisting conditions or injuries.

Table 3

Psychoeducation: Simple messages for workers and trauma survivors

Short-term (<1 week) benzodiazepine use for panic symptoms and severe insomnia is acceptable, but longer-term use may increase PTSD risk.¹⁷ A selective serotonin reuptake inhibitor may help individuals with pre-existing PTSD or depression, if you can arrange follow-up.

In the aftermath

‘Debriefing.’ Critical incident stress debriefing (CISD) is a structured, one-session group intervention in which survivors’ experiences and emotional reactions are discussed and education and follow-up recommendations are provided. Developed by Mitchell in 1983,¹⁸ CISD was widely used until systematic evaluations revealed that it did not alleviate psychological distress or prevent PTSD.¹⁹

Table 4

How to interact with news media during and after a disaster

Thus, although survivor meetings may provide information, education, screening, and support, avoid detailed discussions of events and emotions. Any meetings should be conducted by mental health clinicians and should not be mandatory. Reserve the term “debriefing” for operational reviews by rescue personnel.²⁰

Public education. Educate survivors, rescue workers, health care providers, teachers, and relief agency workers. Provide concise, simple messages as suggested in Table 3. News media provide our most effective means of reaching out to survivors, which is why having a pre-existing relationship is so important. Some guidelines for working with the media are presented in Table 4.

Outreach. Numerous educational resources are available for survivors and their caregivers (see Related resources). Other potentially useful outreach tools include:

• meetings with teachers’ organizations
• continuing medical education activities for primary care providers
• telephone hot lines.

Legal and ethical issues

Disaster scenes are chaotic and informal, and professionals must be flexible, often providing general support and information rather than specific clinical interventions. However, it is important in each encounter to decide whether a patient-physician relationship has begun.

As a general rule, a physician-patient relationship is established whenever diagnosis or treatment is discussed. Once that happens, briefly document:

• signs and symptoms
• working diagnosis
• suicide or violence potential
• treatment and/or follow-up plans.

Confidentiality may be difficult to preserve in chaotic situations involving workers from many agencies. Even in disasters, however, you must obtain permission before sharing information unless the individual’s situation is emergent.

Table 5

Keys to effective disaster psychiatry

Long-term interventions

Longer-term disaster interventions include continued outreach and education and needed follow-up services. Existing structures may provide effective follow-up, but additional resources are often needed.

Federal programs. Following a presidentialdeclared disaster, the Federal Emergency Management Agency (FEMA) provides funding for crisis counseling. Programs are typically funded for 9 to 15 months and administered through the emergency services and disaster relief branch of the Substance Abuse and Mental Health Services Administration (SAMHSA) and community mental health organizations. Examples include Project Heartland following the 1995 Oklahoma City federal building bombing and Project COPE following California’s 1989 Loma Prieta earthquake.

Cognitive-behavioral therapy. For adult survivors with acute stress disorder, specific cognitive-behavioral therapy (CBT) provided by trained therapists may prevent PTSD and other trauma sequelae, such as depression.²¹ CBT interventions may begin as early as 2 weeks after trauma and focus sequentially on anxiety management, cognitive restructuring, imaginal exposure followed by in vivo exposure, and relapse prevention.

Three controlled trials found 6-month PTSD rates of 14% to 20% among acute stress disorder patients treated with CBT, compared with 58% to 67% with supportive counseling.^22-24 Although studies of interventions immediately following trauma are lacking, trauma-focused CBT is also recommended for children.²⁵ Evidence-based treatments for PTSD are discussed in detail elsewhere.²⁶

Not unprepared after all

With some reflection, Dr. Z realized she had the tools to help her community. Her feelings of helplessness receded as she envisioned how she could help survivors understand their experiences, re-create a sense of safety, restore important connections to loved ones, and begin to rebuild their lives (Table 5).

Related resources

For clinicians

• Young BH, Ford JD, Ruzek JI, et al. Disaster mental health: a guidebook for clinicians and administrators. Washington, DC: National Center for Post-Traumatic Stress Disorder, 1998. http://ncptsd.org/publications/disaster/index.html
• Hillman JL. Crisis intervention and trauma: new approaches to evidence-based practice. New York: Kluwer Academic/Plenum Publishers, 2002.
• Office of the Surgeon General Web site on medical aspects of nuclear, biological, and chemical warfare. http://www.nbc-med.org

For survivors and clinicians

• National Center for Post-Traumatic Stress Disorder. Disaster mental health: Dealing with the aftereffects of terrorism. http://www.ncptsd.org/terrorism/index.html
• Substance Abuse and Mental Health Services Administration. Emergency mental health and traumatic stress. http://www.mentalhealth.org/cmhs/EmergencyServices/default.asp
• American Academy of Child and Adolescent Psychiatry. Talking to children about terrorism and war. http://www.aacap.org/publications/factsFam/87.htm

Drug brand names

• Clonidine • Catapres
• Guanfacine • Tenex

Disclosure

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

The night started like any other for Dr. Z. Kids in bed (too late) by 10:30, dog out by 11, fell asleep reading journal by 11:15. Sirens jolt her out of a solid stage 4. Her eyes widen, pulse quickens, mouth dries as she follows the glow of the TV into the living room. On TV, fire frames shots of tearful faces, body bags, and firefighters in protective suits. She catches the announcer’s voice: “…explosion at City Power and Light nuclear facility at 3:10 AM today. Fifty-five are known dead, and thousands are being told to evacuate. The blast’s cause is unknown, but terrorism is suspected.”

As her numbness slowly ebbs, Dr. Z’s questions rise insistently. How can I help the survivors? My patients? My children? What if the media call me? How could I have been better prepared for this?

Disaster shakes us to our human and biological core. More than any other clinical encounter, it reminds us that psychiatrists share the vulnerabilities of those we seek to help. Yet it also reminds us that even simple concepts and interventions can mobilize the healing process.

Are you ready to provide emergency psychiatric care following a disaster in your community—be it a nuclear accident, tornado, airplane crash, or terrorist act? Here is evidence—some counterintuitive—that can help you prepare.

Table 1

‘Psychological first aid’ for disaster survivors

Disaster’s psychobiology

Human reactions to disaster are often conceptualized as the mammalian survival response: flight, fight, and fright (freezing). In most cases, these reactions are adaptive and dissipate after safety is restored. Posttraumatic stress disorder (PTSD) develops in about 5% of natural disaster victims and 33% of mass shooting victims.¹

Responses that do go awry appear to be associated with abnormally low cortisol and persistent adrenergic activation, leading to sensitization of the fear response.² Reminders of trauma or persistent stressors—such as pain, problems with finances or housing, or bereavement—may exacerbate sensitization. On the other hand, preclinical studies suggest that social support^3,4 and active coping⁵ mitigate physiologic stress responses, confirming numerous clinical observations that associate lack of social support and avoidant coping with eventual PTSD development.

Three basics. Just as our emergency medicine colleagues must often revert to life-support basics, we must remind ourselves of biology’s three basics for psychic resilience:

• safety (including—as much as possible—protection from reminders of trauma and ongoing stress)
• meaningful social connection
• re-establishing a sense of efficacy to overcome helplessness (Table 1).

Like the stress response, these protective factors seem hard-wired into our biological make-up. They form the foundation for all phases of disaster psychiatry interventions, from planning to immediate interventions through longterm follow-up.

Disaster planning

As a mental health professional, plan to operate within established disaster plans and agencies, not only for the sake of efficiency but also because structure and support are paramount in disaster situations. Check with the American Psychiatric Association’s local branch to determine if a disaster mental health plan exists. If not, explore how to work directly with local American Red Cross chapters and hospitals, which recruit personnel for the Disaster Medical Assistance Teams mobilized by the public health service.

Table 2

Normal reactions to disaster for adults and children

Immediate disaster mental health plans vary in detail according to local needs and resources but should at least address:

• providing on-site interventions
• disseminating information about responses to trauma
• identifying and publicizing local mental health resources.

Immediate interventions

Immediately following a disaster, psychiatrists are frequently asked to assist with on-site crisis and medical interventions, evaluate survivors with unusual or intense reactions, and provide public education about psychological reactions to disaster.

On-site response. All responders, regardless of discipline, should provide disaster survivors with “psychological first aid,” which is directed at reestablishing safety, connection, and efficacy. Basic crisis intervention principles are useful when support and reassurance are not enough.⁶

For example, relaxation exercises can reduce anxiety and improve sleep. Use focused, structured relaxation tools—such as progressive muscle relaxation and breathing training—as unstructured exercises can exacerbate dissociation and re-experiencing. Grounding techniques, by which survivors learn to focus all senses on immediate surroundings, often alleviate dissociation and flashbacks.

Care for children. Because children’s reactions to disaster greatly depend on their caregivers’ responses (social referencing), focus acute interventions for children on:

• re-connecting them with their families
• reducing caregivers’ distress
• educating caregivers about providing age appropriate information and support (see Related resources).

Medical care. As physicians, psychiatrists may be called upon to intervene medically. Although it is generally advisable to stay within our usual practice, medical personnel may be in short supply. Fortunately, Good Samaritan laws exist in every state, and the potential for a successful malpractice suit against a physician responding in a disaster is almost zero, unless the physician’s performance is grossly negligent (such as moving the neck of a patient with obvious head or neck injuries).⁷

Principles regarding informed consent and right to refuse treatment—along with the usual exceptions—apply during disasters.

Evaluating survivors in shelters and hospitals requires knowing the normal and abnormal responses to disaster, being able to differentially diagnose changes in mental status, and understanding risk factors for trauma’s psychiatric sequelae. Aside from PTSD, trauma’s long-term effects include other anxiety disorders, depression, substance abuse, and eating disorders. In addition to the usual components of a psychiatric evaluation, assessments must address event-related factors such as proximity to the disaster, loss of significant others or property, physical injuries, immediate needs, and social support.⁸

Normal stress reactions. Frequently described as “a normal response to an abnormal situation,” the normal stress reaction is multidimensional and depends on the person’s developmental level (Table 2). About 10% to 25% of survivors experience intense affect and dissociation, whereas a similar number may appear unusually calm.

Interventions beyond the“first aid” described above are not usually needed unless individuals:

• are a danger to themselves or others
• are psychotic
• have no social supports
• cannot perform tasks necessary for self-care and to begin the recovery process.

Always re-assess when there is any question about a survivor’s immediate reaction to trauma.

In DSM-IV-TR’s trauma-related diagnoses, the symptom clusters often do not capture many disaster survivors’ subjective experience: the shattering of fundamental beliefs regarding themselves (invulnerability), the world (predictability, safety), and others (trust, benevolence).⁹ By empathizing with these responses, you can help survivors feel less isolated and estranged.

Differential diagnosis. Survivors’ mental status changes may be manifestations of the stress response, but they also may represent:

• exacerbations of pre-existing psychiatric or general medical conditions
• hypoxemia, hypovolemia, or CNS trauma from physical injury
• responses to medications used for resuscitation or pain control, such as atropine, epinephrine, lidocaine, or morphine.

Effects of bioterrorism agents must also be considered. For example, organophosphorus compounds such as the nerve agents sarin and soman can cause impaired concentration, depression, and anxiety. Anthrax can cause rapidly progressing meningitis.¹⁰ Delirium must be differentiated from dissociation; patients with dissociation can be re-oriented, and changes will resolve with time rather than fluctuate.¹¹

Psychopathology risk factors. Multiple studies have addressed risk factors for post-disaster psychiatric sequelae (usually PTSD). In general, risk increases with repeated trauma exposure (including TV viewing), prior trauma, lack of social support, injury, pre-existing psychiatric problems, traumatic bereavement (having witnessed the violent death of a loved one), avoidant coping, and having strong negative beliefs about the meanings of normal stress reactions such as tearfulness, anxiety, and insomnia.

Because a recent meta-analysis supports these observations,¹² follow-up evaluation for signs of PTSD is recommended for:

• survivors with one or more of the risk factors discussed above
• vulnerable groups such as rescue workers, children, and dependent individuals
• survivors whose symptoms persist after 2 months.¹³

Decompensation immediately after a disaster seems to be the exception for psychiatric patients, despite their longer-term vulnerability. One psychiatrist who in 1989 survived Hurricane Hugo—the most intense storm to strike the Mid-Atlantic region in 100 years—noted that demand for inpatient psychiatric services did not increase in the storm’s aftermath. The only patient calls she received were inquiries about her own physical safety.¹⁴

Caregivers and rescue workers—including psychi-atrists—are also disaster survivors, and you need to tend to your needs for safety and support. Consult frequently with colleagues within and outside the disaster area, as much for support as for information and guidance.¹⁵ Remember also that rescue workers are occasionally targets for victims’ rage at their circumstances. Anticipating and explaining this displacement reduces its toxicity.

Using medications

Uses psychotropics judiciously in the first 48 hours of trauma. Medication effects may interfere with neurologic assessment of the injured, and monitoring and follow-up may not be possible.

However, drug therapy should start quickly when survivors are acutely psychotic or their behavior endangers themselves, others, or the milieu. Medications usually include a fast-acting benzodiazepine and/or an antipsychotic, as described in guidelines for managing agitation.¹⁶ Always provide structure and supervision for medicated patients.

No guidelines exist for using medications to manage distressing—but less-severe—acute stress-related symptoms. Some experts advocate using adrenergic antagonists such as clonidine, guanfacine, and beta blockers to reduce excessive arousal. These drugs have not been adequately studied in this setting, however, and may harm those with cardiovascular instability from preexisting conditions or injuries.

Table 3

Psychoeducation: Simple messages for workers and trauma survivors

Short-term (<1 week) benzodiazepine use for panic symptoms and severe insomnia is acceptable, but longer-term use may increase PTSD risk.¹⁷ A selective serotonin reuptake inhibitor may help individuals with pre-existing PTSD or depression, if you can arrange follow-up.

In the aftermath

‘Debriefing.’ Critical incident stress debriefing (CISD) is a structured, one-session group intervention in which survivors’ experiences and emotional reactions are discussed and education and follow-up recommendations are provided. Developed by Mitchell in 1983,¹⁸ CISD was widely used until systematic evaluations revealed that it did not alleviate psychological distress or prevent PTSD.¹⁹

Table 4

How to interact with news media during and after a disaster

Thus, although survivor meetings may provide information, education, screening, and support, avoid detailed discussions of events and emotions. Any meetings should be conducted by mental health clinicians and should not be mandatory. Reserve the term “debriefing” for operational reviews by rescue personnel.²⁰

Public education. Educate survivors, rescue workers, health care providers, teachers, and relief agency workers. Provide concise, simple messages as suggested in Table 3. News media provide our most effective means of reaching out to survivors, which is why having a pre-existing relationship is so important. Some guidelines for working with the media are presented in Table 4.

Outreach. Numerous educational resources are available for survivors and their caregivers (see Related resources). Other potentially useful outreach tools include:

• meetings with teachers’ organizations
• continuing medical education activities for primary care providers
• telephone hot lines.

Legal and ethical issues

Disaster scenes are chaotic and informal, and professionals must be flexible, often providing general support and information rather than specific clinical interventions. However, it is important in each encounter to decide whether a patient-physician relationship has begun.

As a general rule, a physician-patient relationship is established whenever diagnosis or treatment is discussed. Once that happens, briefly document:

• signs and symptoms
• working diagnosis
• suicide or violence potential
• treatment and/or follow-up plans.

Confidentiality may be difficult to preserve in chaotic situations involving workers from many agencies. Even in disasters, however, you must obtain permission before sharing information unless the individual’s situation is emergent.

Table 5

Keys to effective disaster psychiatry

Long-term interventions

Longer-term disaster interventions include continued outreach and education and needed follow-up services. Existing structures may provide effective follow-up, but additional resources are often needed.

Federal programs. Following a presidentialdeclared disaster, the Federal Emergency Management Agency (FEMA) provides funding for crisis counseling. Programs are typically funded for 9 to 15 months and administered through the emergency services and disaster relief branch of the Substance Abuse and Mental Health Services Administration (SAMHSA) and community mental health organizations. Examples include Project Heartland following the 1995 Oklahoma City federal building bombing and Project COPE following California’s 1989 Loma Prieta earthquake.

Cognitive-behavioral therapy. For adult survivors with acute stress disorder, specific cognitive-behavioral therapy (CBT) provided by trained therapists may prevent PTSD and other trauma sequelae, such as depression.²¹ CBT interventions may begin as early as 2 weeks after trauma and focus sequentially on anxiety management, cognitive restructuring, imaginal exposure followed by in vivo exposure, and relapse prevention.

Three controlled trials found 6-month PTSD rates of 14% to 20% among acute stress disorder patients treated with CBT, compared with 58% to 67% with supportive counseling.^22-24 Although studies of interventions immediately following trauma are lacking, trauma-focused CBT is also recommended for children.²⁵ Evidence-based treatments for PTSD are discussed in detail elsewhere.²⁶

Not unprepared after all

With some reflection, Dr. Z realized she had the tools to help her community. Her feelings of helplessness receded as she envisioned how she could help survivors understand their experiences, re-create a sense of safety, restore important connections to loved ones, and begin to rebuild their lives (Table 5).

Related resources

For clinicians

• Young BH, Ford JD, Ruzek JI, et al. Disaster mental health: a guidebook for clinicians and administrators. Washington, DC: National Center for Post-Traumatic Stress Disorder, 1998. http://ncptsd.org/publications/disaster/index.html
• Hillman JL. Crisis intervention and trauma: new approaches to evidence-based practice. New York: Kluwer Academic/Plenum Publishers, 2002.
• Office of the Surgeon General Web site on medical aspects of nuclear, biological, and chemical warfare. http://www.nbc-med.org

For survivors and clinicians

• National Center for Post-Traumatic Stress Disorder. Disaster mental health: Dealing with the aftereffects of terrorism. http://www.ncptsd.org/terrorism/index.html
• Substance Abuse and Mental Health Services Administration. Emergency mental health and traumatic stress. http://www.mentalhealth.org/cmhs/EmergencyServices/default.asp
• American Academy of Child and Adolescent Psychiatry. Talking to children about terrorism and war. http://www.aacap.org/publications/factsFam/87.htm

Drug brand names

• Clonidine • Catapres
• Guanfacine • Tenex

Disclosure

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

History: Bald at age 9

Ms. D, age 41, began compulsively pulling out and eating her hair at age 8. When she didn’t get her way at home or was nervous about school, she would sit for hours, pulling and eating a strand or two at a time, ultimately ingesting a clump of hair.

By age 9, Ms. D was bald. In grade school, she often wore hats and scarves to class to avoid teasing from other children about her baldness. In high school, she kept to herself and frequently wore wigs.

Ms. D stops pulling for brief periods and her hair grows out, but she invariably resumes pulling when psychosocial stressors mount. Many of life’s normal anxieties—job interviews, work-related stress, social rejection—trigger episodes.

When she is bald, Ms. D pulls and eats hair off her wig. Over the years, she has spent thousands of dollars on custom-made wigs that mask her baldness while feeding her habit.

Ms. D’s episodes are increasingly interfering with her life. She has been steadily employed as an office assistant, but does not socialize with coworkers. She has not dated in years, and during an exacerbation leaves home only to go to work. She also pulls her eyelashes and eyebrows and picks her nails and cuticles.

Ms. D first presented in 1994 after seeing a television segment I did on trichotillomania. At intake, she was wearing a wig and exhibited anxious mood. She also has Crohn’s disease; a gastroenterologist monitors her closely.

Ms. D reports compulsive counting and checking but denies other similar behaviors. No immediate family members have exhibited obsessive-compulsive or hair-pulling behaviors. Her father abused alcohol and a sister has a stuttering problem, although Ms. D denies that these have affected her psychologically.

Ms. D’s hair-pulling behavior suggests:

• a pica disorder
• an impulse control disorder
• or an obsessive-compulsive disorder?

Box

Dr. Lundt’s observations

Trichotillomania, defined as compulsive pulling of hair, usually begins in childhood or adolescence. Scalp hair is most commonly pulled, but some patients also pull their eyelashes, pubic hair, and other body hair. Some, especially children, have reportedly pulled their pets’ hair.

Mansueto et al estimate that trichotillomania afflicts approximately 1.5% of males and 3.5% of females.¹ These estimates, however, do not include persons with the disorder who are too embarrassed to seek treatment.

DSM-IV-TR classifies trichotillomania as an impulse control disorder (Box). Although comorbid anxiety and depressive disorders are common, Ms. D did not meet criteria for any other psychiatric disorder.

Trichotillomania often is episodic. Months or years of abstinence is common after periods of exacerbation, usually caused by stress (Figure).

Many clinicians mistakenly consider trichotillomania a benign disorder with few consequences beyond alopecia.² Some patients, however, progress into trichophagia—ingestion of pulled hair. Trichophagia is a form of pica disorder, typically defined as persistent eating of non-nutritive substances. Patients often harbor tremendous shame over their hair-eating behavior and resist psychiatric or medical treatment.²

The undigested hair can form sometimes massive clumps called trichobezoars, which are most common among children and the developmentally disabled.⁴ Persons with trichophagia face a 37.5% risk of forming a trichobezoar.⁵ The mass can cause abdominal pain, nausea, vomiting, and weight loss; complications include GI obstruction, ulceration, perforation, and peritonitis.⁶ An untreated trichobezoar can be fatal,⁷ although such deaths are rare among patients being treated for trichotillomania.

Patients with trichotillomania often respond to medications used to treat obsessive-compulsive disorder, such as clomipramine. Some clinicians believe this agent is more effective than selective serotonin reuptake inhibitors (SSRIs) but more difficult to tolerate. For Ms. D, I started with both.

Treatment: ‘I Don’t need medication’

Initial treatments—including fluoxetine, 20 mg/d for 6 months; hypnotherapy; and clomipramine, 25 mg/d—were unsuccessful. Ms. D was only marginally compliant, believing that she did not need medication.

I referred Ms. D to an out-of-state residential behavioral program specializing in trichotillomania, but she refused to go even as her hair-pulling intensified. Clomipramine was gradually increased to 75 mg nightly, briefly decreasing her pulling, then to 100 mg nightly when symptoms re-emerged. Clomipramine blood levels were monitored with each dosage change to guard against CNS and cardiac toxicity and other side effects (GI complaints, dizziness, cardiac arrhythmias, somnolence).

After watching for seasonal patterns, I found that Ms. D’s hair-pulling worsened during the winter, although no seasonal change in mood was detected. Phototherapy produced initial success, but Ms. D continued to pull her eyelashes.

Eight weeks later, however, Ms. D’s symptoms escalated. Clomipramine was increased to 150 mg nightly, resulting in blood levels of 99 ng/mL for clomipramine and 204 ng/mL for the metabolite N-desmethylclomipramine—both within the therapeutic range. As she continued pulling, I added buspirone, 10 mg/d.

At this point, would you:

• continue clomipramine and increase the dosage?
• discontinue clomipramine and start another psychotropic?
• or maintain clomipramine at the same dosage and add another psychotropic?

Dr. Lundt’s observations

Drug treatment of trichotillomania has not been studied extensively or long-term, and no consensus exists. Psychoanalysis, cognitive-behavioral therapy (CBT), and hypnotherapy are usually administered with psychotropics.⁸ Patients often respond to treatment at first, then reach a plateau and resume pulling their hair.⁹

Numerous psychotropics are used off-label to treat trichotillomania. Several agents have been shown in clinical trials and case reports to reduce hair pulling/eating behaviors (Table), but these findings are limited by small sample size, lack of control groups, and lack of a standard symptom rating scale.

Figure Trichotillomania: Excessive grooming, habit, or vicious circle?

When clomipramine did not work initally, I explored serotonergic combination strategies.

Table

Medications shown to benefit patients with trichotillomania

Further treatment: Relapse, resection

Ms. D was lost to follow-up for 1 year. She returned in 1996, just after undergoing a laparotomy for removal of a trichobezoar large enough to fill two 2-inch-by-6-inch bags. She also had been treated for pneumonia and a pulmonary embolus.

Riddled with shame and embarrassment, Ms. D had stopped pulling for 10 months, during which time she was off medication. Her pulling behaviors re-emerged, however, and clomipramine was restarted and titrated to 250 mg nightly.

One year later, a second trichobezoar was resected. Her clomipramine/N-desmethylclomipramine level reached 1,535 ng/mL, although an ECG reading was normal. Subsequent clomipramine/N-desmethylclomipramine blood levels were within the therapeutic range. Fluvoxamine, 25 mg/d titrated across 6 weeks to 150 mg/d, was added.

Again, Ms. D stopped taking her medications and was lost to follow-up. Her gastroenterologist began managing her care and started sertraline, dosage unknown, to address her depressed mood. A third trichobezoar was removed.

When Ms. D returned to my practice, I resumed CBT and increased sertraline over 1 month from 100 to 300 mg/d. Adding olanzapine, 2.5 mg/d, diminished her anxiety and markedly decreased her hair pulling.

Months later, her hair-pulling/eating behaviors again intensified, resulting in a small-bowel obstruction and a fourth trichobezoar removal. Olanzapine was increased to 5 mg nightly without significant benefit and with sedating effects.

Clomipramine, 125 mg/d, was reintroduced and her symptoms improved dramatically. On a regimen of sertraline, clomipramine and olanzapine, Ms. D remained stable for 2 years.

Last year, however, a fifth trichobezoar measuring 20 x 15 cm was removed. Subsequent trials of methylphenidate, titrated to 72 mg every morning, and tramadol, titrated to 100 mg/d, were unsuccessful.

After 10 years of medication and psychotherapy with three different providers, Ms. D’s hair-pulling/eating behaviors persist. She is taking ziprasidone, 120 mg bid, and naltrexone, 100 mg bid, to help her impulse control, as well as sertraline, 300 mg/d, and clomipramine, 125 mg/d. Another trichobezoar removal—her sixth in 8 years—is scheduled.

What strategies exist for minimizing Ms. D’s hair-pulling behavior and keeping her in therapy?

Dr. Lundt’s observations

Trichotillomania’s waxing and waning course—and its destructive effects on a patient’s self-esteem—pose a clinical challenge. The disorder’s severity can range from cosmetically annoying to life-threatening, as in Ms. D’s case. Patients embarrassed by their behavior often prematurely leave treatment, desperate to cut off all social contact—including medical appointments.

It is crucial to maintain a nonjudgmental, inviting demeanor to alleviate the patient’s fears and facilitate a return to treatment. Support groups, especially online, can help decrease patients’ isolation and provide a reliable information network (see Related resources).

I have had excellent results with other trichotillomania patients—especially children and adolescents. Simply naming their condition and demystifying the problem can be therapeutic. Many patients have responded to SSRIs combined with CBT.

Not long ago, trichotillomania patients were met with ignorance and disbelief within the medical community as the disorder was poorly understood. We need to break this cycle of shame and continue investigating treatment strategies.

Related resources

• StopPulling.com, an interactive behavioral program for persons with trichotillomania. www.stoppulling.com.
• Penzel F. The hair pulling problem: a complete guide to trichotillomania. New York: Oxford University Press, 2003.
• Keuthen NJ, Stein DJ, Christenson GA. Help for hair pullers: understanding and coping with trichotillomania. Oakland, CA: New Harbinger Publications, 2001.

Drug brand names

• Amitriptyline • Elavil
• Buspirone • BuSpar
• Clomipramine • Anafranil
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Methylphenidate • Concerta, Ritalin
• Naltrexone • ReVia
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tramadol • Ultram
• Ziprasidone • Geodon

Disclosure

Dr. Lundt receives research grants from and/or is a speaker for Eli Lilly and Co., Pfizer Inc., GlaxoSmithKline, and Bristol-Myers Squibb Co.

History: Bald at age 9

Ms. D, age 41, began compulsively pulling out and eating her hair at age 8. When she didn’t get her way at home or was nervous about school, she would sit for hours, pulling and eating a strand or two at a time, ultimately ingesting a clump of hair.

By age 9, Ms. D was bald. In grade school, she often wore hats and scarves to class to avoid teasing from other children about her baldness. In high school, she kept to herself and frequently wore wigs.

Ms. D stops pulling for brief periods and her hair grows out, but she invariably resumes pulling when psychosocial stressors mount. Many of life’s normal anxieties—job interviews, work-related stress, social rejection—trigger episodes.

When she is bald, Ms. D pulls and eats hair off her wig. Over the years, she has spent thousands of dollars on custom-made wigs that mask her baldness while feeding her habit.

Ms. D’s episodes are increasingly interfering with her life. She has been steadily employed as an office assistant, but does not socialize with coworkers. She has not dated in years, and during an exacerbation leaves home only to go to work. She also pulls her eyelashes and eyebrows and picks her nails and cuticles.

Ms. D first presented in 1994 after seeing a television segment I did on trichotillomania. At intake, she was wearing a wig and exhibited anxious mood. She also has Crohn’s disease; a gastroenterologist monitors her closely.

Ms. D reports compulsive counting and checking but denies other similar behaviors. No immediate family members have exhibited obsessive-compulsive or hair-pulling behaviors. Her father abused alcohol and a sister has a stuttering problem, although Ms. D denies that these have affected her psychologically.

Ms. D’s hair-pulling behavior suggests:

• a pica disorder
• an impulse control disorder
• or an obsessive-compulsive disorder?

Box

Dr. Lundt’s observations

Trichotillomania, defined as compulsive pulling of hair, usually begins in childhood or adolescence. Scalp hair is most commonly pulled, but some patients also pull their eyelashes, pubic hair, and other body hair. Some, especially children, have reportedly pulled their pets’ hair.

Mansueto et al estimate that trichotillomania afflicts approximately 1.5% of males and 3.5% of females.¹ These estimates, however, do not include persons with the disorder who are too embarrassed to seek treatment.

DSM-IV-TR classifies trichotillomania as an impulse control disorder (Box). Although comorbid anxiety and depressive disorders are common, Ms. D did not meet criteria for any other psychiatric disorder.

Trichotillomania often is episodic. Months or years of abstinence is common after periods of exacerbation, usually caused by stress (Figure).

Many clinicians mistakenly consider trichotillomania a benign disorder with few consequences beyond alopecia.² Some patients, however, progress into trichophagia—ingestion of pulled hair. Trichophagia is a form of pica disorder, typically defined as persistent eating of non-nutritive substances. Patients often harbor tremendous shame over their hair-eating behavior and resist psychiatric or medical treatment.²

The undigested hair can form sometimes massive clumps called trichobezoars, which are most common among children and the developmentally disabled.⁴ Persons with trichophagia face a 37.5% risk of forming a trichobezoar.⁵ The mass can cause abdominal pain, nausea, vomiting, and weight loss; complications include GI obstruction, ulceration, perforation, and peritonitis.⁶ An untreated trichobezoar can be fatal,⁷ although such deaths are rare among patients being treated for trichotillomania.

Patients with trichotillomania often respond to medications used to treat obsessive-compulsive disorder, such as clomipramine. Some clinicians believe this agent is more effective than selective serotonin reuptake inhibitors (SSRIs) but more difficult to tolerate. For Ms. D, I started with both.

Treatment: ‘I Don’t need medication’

Initial treatments—including fluoxetine, 20 mg/d for 6 months; hypnotherapy; and clomipramine, 25 mg/d—were unsuccessful. Ms. D was only marginally compliant, believing that she did not need medication.

I referred Ms. D to an out-of-state residential behavioral program specializing in trichotillomania, but she refused to go even as her hair-pulling intensified. Clomipramine was gradually increased to 75 mg nightly, briefly decreasing her pulling, then to 100 mg nightly when symptoms re-emerged. Clomipramine blood levels were monitored with each dosage change to guard against CNS and cardiac toxicity and other side effects (GI complaints, dizziness, cardiac arrhythmias, somnolence).

After watching for seasonal patterns, I found that Ms. D’s hair-pulling worsened during the winter, although no seasonal change in mood was detected. Phototherapy produced initial success, but Ms. D continued to pull her eyelashes.

Eight weeks later, however, Ms. D’s symptoms escalated. Clomipramine was increased to 150 mg nightly, resulting in blood levels of 99 ng/mL for clomipramine and 204 ng/mL for the metabolite N-desmethylclomipramine—both within the therapeutic range. As she continued pulling, I added buspirone, 10 mg/d.

At this point, would you:

• continue clomipramine and increase the dosage?
• discontinue clomipramine and start another psychotropic?
• or maintain clomipramine at the same dosage and add another psychotropic?

Dr. Lundt’s observations

Drug treatment of trichotillomania has not been studied extensively or long-term, and no consensus exists. Psychoanalysis, cognitive-behavioral therapy (CBT), and hypnotherapy are usually administered with psychotropics.⁸ Patients often respond to treatment at first, then reach a plateau and resume pulling their hair.⁹

Numerous psychotropics are used off-label to treat trichotillomania. Several agents have been shown in clinical trials and case reports to reduce hair pulling/eating behaviors (Table), but these findings are limited by small sample size, lack of control groups, and lack of a standard symptom rating scale.

Figure Trichotillomania: Excessive grooming, habit, or vicious circle?

When clomipramine did not work initally, I explored serotonergic combination strategies.

Table

Medications shown to benefit patients with trichotillomania

Further treatment: Relapse, resection

Ms. D was lost to follow-up for 1 year. She returned in 1996, just after undergoing a laparotomy for removal of a trichobezoar large enough to fill two 2-inch-by-6-inch bags. She also had been treated for pneumonia and a pulmonary embolus.

Riddled with shame and embarrassment, Ms. D had stopped pulling for 10 months, during which time she was off medication. Her pulling behaviors re-emerged, however, and clomipramine was restarted and titrated to 250 mg nightly.

One year later, a second trichobezoar was resected. Her clomipramine/N-desmethylclomipramine level reached 1,535 ng/mL, although an ECG reading was normal. Subsequent clomipramine/N-desmethylclomipramine blood levels were within the therapeutic range. Fluvoxamine, 25 mg/d titrated across 6 weeks to 150 mg/d, was added.

Again, Ms. D stopped taking her medications and was lost to follow-up. Her gastroenterologist began managing her care and started sertraline, dosage unknown, to address her depressed mood. A third trichobezoar was removed.

When Ms. D returned to my practice, I resumed CBT and increased sertraline over 1 month from 100 to 300 mg/d. Adding olanzapine, 2.5 mg/d, diminished her anxiety and markedly decreased her hair pulling.

Months later, her hair-pulling/eating behaviors again intensified, resulting in a small-bowel obstruction and a fourth trichobezoar removal. Olanzapine was increased to 5 mg nightly without significant benefit and with sedating effects.

Clomipramine, 125 mg/d, was reintroduced and her symptoms improved dramatically. On a regimen of sertraline, clomipramine and olanzapine, Ms. D remained stable for 2 years.

Last year, however, a fifth trichobezoar measuring 20 x 15 cm was removed. Subsequent trials of methylphenidate, titrated to 72 mg every morning, and tramadol, titrated to 100 mg/d, were unsuccessful.

After 10 years of medication and psychotherapy with three different providers, Ms. D’s hair-pulling/eating behaviors persist. She is taking ziprasidone, 120 mg bid, and naltrexone, 100 mg bid, to help her impulse control, as well as sertraline, 300 mg/d, and clomipramine, 125 mg/d. Another trichobezoar removal—her sixth in 8 years—is scheduled.

What strategies exist for minimizing Ms. D’s hair-pulling behavior and keeping her in therapy?

Dr. Lundt’s observations

Trichotillomania’s waxing and waning course—and its destructive effects on a patient’s self-esteem—pose a clinical challenge. The disorder’s severity can range from cosmetically annoying to life-threatening, as in Ms. D’s case. Patients embarrassed by their behavior often prematurely leave treatment, desperate to cut off all social contact—including medical appointments.

It is crucial to maintain a nonjudgmental, inviting demeanor to alleviate the patient’s fears and facilitate a return to treatment. Support groups, especially online, can help decrease patients’ isolation and provide a reliable information network (see Related resources).

I have had excellent results with other trichotillomania patients—especially children and adolescents. Simply naming their condition and demystifying the problem can be therapeutic. Many patients have responded to SSRIs combined with CBT.

Not long ago, trichotillomania patients were met with ignorance and disbelief within the medical community as the disorder was poorly understood. We need to break this cycle of shame and continue investigating treatment strategies.

Related resources

• StopPulling.com, an interactive behavioral program for persons with trichotillomania. www.stoppulling.com.
• Penzel F. The hair pulling problem: a complete guide to trichotillomania. New York: Oxford University Press, 2003.
• Keuthen NJ, Stein DJ, Christenson GA. Help for hair pullers: understanding and coping with trichotillomania. Oakland, CA: New Harbinger Publications, 2001.

Drug brand names

• Amitriptyline • Elavil
• Buspirone • BuSpar
• Clomipramine • Anafranil
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Methylphenidate • Concerta, Ritalin
• Naltrexone • ReVia
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tramadol • Ultram
• Ziprasidone • Geodon

Disclosure

Dr. Lundt receives research grants from and/or is a speaker for Eli Lilly and Co., Pfizer Inc., GlaxoSmithKline, and Bristol-Myers Squibb Co.

History: Bald at age 9

Ms. D, age 41, began compulsively pulling out and eating her hair at age 8. When she didn’t get her way at home or was nervous about school, she would sit for hours, pulling and eating a strand or two at a time, ultimately ingesting a clump of hair.

By age 9, Ms. D was bald. In grade school, she often wore hats and scarves to class to avoid teasing from other children about her baldness. In high school, she kept to herself and frequently wore wigs.

Ms. D stops pulling for brief periods and her hair grows out, but she invariably resumes pulling when psychosocial stressors mount. Many of life’s normal anxieties—job interviews, work-related stress, social rejection—trigger episodes.

When she is bald, Ms. D pulls and eats hair off her wig. Over the years, she has spent thousands of dollars on custom-made wigs that mask her baldness while feeding her habit.

Ms. D’s episodes are increasingly interfering with her life. She has been steadily employed as an office assistant, but does not socialize with coworkers. She has not dated in years, and during an exacerbation leaves home only to go to work. She also pulls her eyelashes and eyebrows and picks her nails and cuticles.

Ms. D first presented in 1994 after seeing a television segment I did on trichotillomania. At intake, she was wearing a wig and exhibited anxious mood. She also has Crohn’s disease; a gastroenterologist monitors her closely.

Ms. D reports compulsive counting and checking but denies other similar behaviors. No immediate family members have exhibited obsessive-compulsive or hair-pulling behaviors. Her father abused alcohol and a sister has a stuttering problem, although Ms. D denies that these have affected her psychologically.

Ms. D’s hair-pulling behavior suggests:

• a pica disorder
• an impulse control disorder
• or an obsessive-compulsive disorder?

Box

Dr. Lundt’s observations

Trichotillomania, defined as compulsive pulling of hair, usually begins in childhood or adolescence. Scalp hair is most commonly pulled, but some patients also pull their eyelashes, pubic hair, and other body hair. Some, especially children, have reportedly pulled their pets’ hair.

Mansueto et al estimate that trichotillomania afflicts approximately 1.5% of males and 3.5% of females.¹ These estimates, however, do not include persons with the disorder who are too embarrassed to seek treatment.

DSM-IV-TR classifies trichotillomania as an impulse control disorder (Box). Although comorbid anxiety and depressive disorders are common, Ms. D did not meet criteria for any other psychiatric disorder.

Trichotillomania often is episodic. Months or years of abstinence is common after periods of exacerbation, usually caused by stress (Figure).

Many clinicians mistakenly consider trichotillomania a benign disorder with few consequences beyond alopecia.² Some patients, however, progress into trichophagia—ingestion of pulled hair. Trichophagia is a form of pica disorder, typically defined as persistent eating of non-nutritive substances. Patients often harbor tremendous shame over their hair-eating behavior and resist psychiatric or medical treatment.²

The undigested hair can form sometimes massive clumps called trichobezoars, which are most common among children and the developmentally disabled.⁴ Persons with trichophagia face a 37.5% risk of forming a trichobezoar.⁵ The mass can cause abdominal pain, nausea, vomiting, and weight loss; complications include GI obstruction, ulceration, perforation, and peritonitis.⁶ An untreated trichobezoar can be fatal,⁷ although such deaths are rare among patients being treated for trichotillomania.

Patients with trichotillomania often respond to medications used to treat obsessive-compulsive disorder, such as clomipramine. Some clinicians believe this agent is more effective than selective serotonin reuptake inhibitors (SSRIs) but more difficult to tolerate. For Ms. D, I started with both.

Treatment: ‘I Don’t need medication’

Initial treatments—including fluoxetine, 20 mg/d for 6 months; hypnotherapy; and clomipramine, 25 mg/d—were unsuccessful. Ms. D was only marginally compliant, believing that she did not need medication.

I referred Ms. D to an out-of-state residential behavioral program specializing in trichotillomania, but she refused to go even as her hair-pulling intensified. Clomipramine was gradually increased to 75 mg nightly, briefly decreasing her pulling, then to 100 mg nightly when symptoms re-emerged. Clomipramine blood levels were monitored with each dosage change to guard against CNS and cardiac toxicity and other side effects (GI complaints, dizziness, cardiac arrhythmias, somnolence).

After watching for seasonal patterns, I found that Ms. D’s hair-pulling worsened during the winter, although no seasonal change in mood was detected. Phototherapy produced initial success, but Ms. D continued to pull her eyelashes.

Eight weeks later, however, Ms. D’s symptoms escalated. Clomipramine was increased to 150 mg nightly, resulting in blood levels of 99 ng/mL for clomipramine and 204 ng/mL for the metabolite N-desmethylclomipramine—both within the therapeutic range. As she continued pulling, I added buspirone, 10 mg/d.

At this point, would you:

• continue clomipramine and increase the dosage?
• discontinue clomipramine and start another psychotropic?
• or maintain clomipramine at the same dosage and add another psychotropic?

Dr. Lundt’s observations

Drug treatment of trichotillomania has not been studied extensively or long-term, and no consensus exists. Psychoanalysis, cognitive-behavioral therapy (CBT), and hypnotherapy are usually administered with psychotropics.⁸ Patients often respond to treatment at first, then reach a plateau and resume pulling their hair.⁹

Numerous psychotropics are used off-label to treat trichotillomania. Several agents have been shown in clinical trials and case reports to reduce hair pulling/eating behaviors (Table), but these findings are limited by small sample size, lack of control groups, and lack of a standard symptom rating scale.

Figure Trichotillomania: Excessive grooming, habit, or vicious circle?

When clomipramine did not work initally, I explored serotonergic combination strategies.

Table

Medications shown to benefit patients with trichotillomania

Further treatment: Relapse, resection

Ms. D was lost to follow-up for 1 year. She returned in 1996, just after undergoing a laparotomy for removal of a trichobezoar large enough to fill two 2-inch-by-6-inch bags. She also had been treated for pneumonia and a pulmonary embolus.

Riddled with shame and embarrassment, Ms. D had stopped pulling for 10 months, during which time she was off medication. Her pulling behaviors re-emerged, however, and clomipramine was restarted and titrated to 250 mg nightly.

One year later, a second trichobezoar was resected. Her clomipramine/N-desmethylclomipramine level reached 1,535 ng/mL, although an ECG reading was normal. Subsequent clomipramine/N-desmethylclomipramine blood levels were within the therapeutic range. Fluvoxamine, 25 mg/d titrated across 6 weeks to 150 mg/d, was added.

Again, Ms. D stopped taking her medications and was lost to follow-up. Her gastroenterologist began managing her care and started sertraline, dosage unknown, to address her depressed mood. A third trichobezoar was removed.

When Ms. D returned to my practice, I resumed CBT and increased sertraline over 1 month from 100 to 300 mg/d. Adding olanzapine, 2.5 mg/d, diminished her anxiety and markedly decreased her hair pulling.

Months later, her hair-pulling/eating behaviors again intensified, resulting in a small-bowel obstruction and a fourth trichobezoar removal. Olanzapine was increased to 5 mg nightly without significant benefit and with sedating effects.

Clomipramine, 125 mg/d, was reintroduced and her symptoms improved dramatically. On a regimen of sertraline, clomipramine and olanzapine, Ms. D remained stable for 2 years.

Last year, however, a fifth trichobezoar measuring 20 x 15 cm was removed. Subsequent trials of methylphenidate, titrated to 72 mg every morning, and tramadol, titrated to 100 mg/d, were unsuccessful.

After 10 years of medication and psychotherapy with three different providers, Ms. D’s hair-pulling/eating behaviors persist. She is taking ziprasidone, 120 mg bid, and naltrexone, 100 mg bid, to help her impulse control, as well as sertraline, 300 mg/d, and clomipramine, 125 mg/d. Another trichobezoar removal—her sixth in 8 years—is scheduled.

What strategies exist for minimizing Ms. D’s hair-pulling behavior and keeping her in therapy?

Dr. Lundt’s observations

Trichotillomania’s waxing and waning course—and its destructive effects on a patient’s self-esteem—pose a clinical challenge. The disorder’s severity can range from cosmetically annoying to life-threatening, as in Ms. D’s case. Patients embarrassed by their behavior often prematurely leave treatment, desperate to cut off all social contact—including medical appointments.

It is crucial to maintain a nonjudgmental, inviting demeanor to alleviate the patient’s fears and facilitate a return to treatment. Support groups, especially online, can help decrease patients’ isolation and provide a reliable information network (see Related resources).

I have had excellent results with other trichotillomania patients—especially children and adolescents. Simply naming their condition and demystifying the problem can be therapeutic. Many patients have responded to SSRIs combined with CBT.

Not long ago, trichotillomania patients were met with ignorance and disbelief within the medical community as the disorder was poorly understood. We need to break this cycle of shame and continue investigating treatment strategies.

Related resources

• StopPulling.com, an interactive behavioral program for persons with trichotillomania. www.stoppulling.com.
• Penzel F. The hair pulling problem: a complete guide to trichotillomania. New York: Oxford University Press, 2003.
• Keuthen NJ, Stein DJ, Christenson GA. Help for hair pullers: understanding and coping with trichotillomania. Oakland, CA: New Harbinger Publications, 2001.

Drug brand names

• Amitriptyline • Elavil
• Buspirone • BuSpar
• Clomipramine • Anafranil
• Fluoxetine • Prozac
• Fluvoxamine • Luvox
• Haloperidol • Haldol
• Lithium • Eskalith, others
• Methylphenidate • Concerta, Ritalin
• Naltrexone • ReVia
• Olanzapine • Zyprexa
• Paroxetine • Paxil
• Pimozide • Orap
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Sertraline • Zoloft
• Tramadol • Ultram
• Ziprasidone • Geodon

Disclosure

Dr. Lundt receives research grants from and/or is a speaker for Eli Lilly and Co., Pfizer Inc., GlaxoSmithKline, and Bristol-Myers Squibb Co.

Mr. M, a world-class athlete, collapsed suddenly in an alley. He was rushed to a hospital emergency room, where he nearly died of internal bleeding from a grapefruit-sized abdominal lymphoma. He was hospitalized and placed on chemotherapy.

Increasing doses of opiates hardly reduced his pain, and he became extremely anxious. Staff described him as “climbing the walls.” He lay in bed writhing, and his parents feared he was becoming a “drug addict.”

Anxiety about his life-threatening illness was clearly compounding his pain, so his attending physician ordered a psychiatric evaluation. When I interviewed the patient, I felt that hypnosis could help.

Hypnosis—as a state of highly focused attention—can help us treat patients’ anxiety, phobias, pain, posttraumatic stress disorder (PTSD), and dissociative disorders. With training, an experienced psychiatrist can quickly start using hypnosis as an adjunct to other therapies.

This article describes how hypnosis helped Mr. M and a young woman traumatized by a criminal assault. Based on my experience and the literature, I discuss what hypnosis is, what training is required, how to measure hypnotizability, and the value of hypnosis in helping patients control their anxiety, posttraumatic, and dissociative states.

Case continued: ‘Surfing’ in Hawaii

When I met Mr. M in the hospital, I acknowledged his distress and the reasons for it, saying “You don’t really want to be here, do you?”

“How many years of medical training did it take you to figure that out?” he replied.

“Well then,” I said, “let’s go somewhere else. Where would you like to be right now?”

He responded, “I’ve never surfed.”

“Good,” I replied, “let’s go to Hawaii.” In hypnosis, I had him picture himself surfing. He continued to groan, but the pattern changed. “What happened?” I asked. “I fell off the surfboard,” he replied. “OK, get back on, and do it right,” I told him.

He learned to practice self-hypnosis, which markedly reduced his anxiety and pain. Two days later he was off pain medications and joking with the nurses in the hall. The attending physician noted in the patient’s record: “Patient off pain meds. Tumor must be regressing.”

What is hypnosis?

Mr. M’s response, though unusually strong, underscores the fact that hypnosis can rapidly produce analgesia and anxiolysis in the medical setting. Hypnosis—often called “believed-in imagination”—is characterized by an ability to sustain a state of attentive, receptive, intense focal concentration with diminished peripheral awareness. The hypnotized person is awake and alert, not asleep. Hypnosis’ three main components are absorption, dissociation, and suggestibility.

Biological basis. The hypnotic state has no brain “signature” per se, but brain imaging portrays hypnosis as a state of alertness with altered anterior cingulate gyrus activation, which helps to focus attention.^1-3 Hypnotized persons can demonstrably alter blood flow in brain regions involved in perceptual processing in response to suggestions of altered perception, whether somatosensory, visual, or olfactory.^4,5 Thus, patients report not only reduced pain but changes in how they experience pain with hypnotic analgesia.

The brain’s dopamine neurotransmitter system—especially in the frontal lobes—also may be involved in hypnosis, as highly hypnotizable persons have elevated levels of dopamine metabolites in their cerebrospinal fluid.⁶

Hypnotic trance. The trance experience is often best explained to patients as similar to being absorbed in a good novel. One loses awareness of one’s surroundings and enters the imagined world. When the novel is finished, the reader requires a moment of reorientation to the surrounding world.

A trance is a state of sustained, attentive-receptive concentration in response to a signal from within or from someone else. The signal activates this shift of awareness and permits more-intensive concentration in a designated direction.

All hypnosis is self-hypnosis. Much of its clinical value is that it can be self-induced throughout the day and whenever symptoms emerge. During the first weeks, patients can be encouraged to practice every 1 or 2 hours.

Applying hypnosis to practice. A well-trained clinician can learn to use hypnosis in classes offered by the two professional hypnosis societies or the American Psychiatric Association (Box 1) Because hypnosis is not something “done to” a patient but rather a capacity to be measured, tapped, and utilized, psychiatrists can integrate hypnosis into clinical practice after some initial training, with ongoing learning and supervision.

Who can be hypnotized?

Not everyone is equally hypnotizable, and hypnotizability is a stable and measurable trait. Approximately one-quarter of adults cannot respond to hypnotic instructions, whereas 10% are extremely hypnotizable.⁷

Brief, clinically useful tests of hypnotic responsiveness have been developed, such as the Hypnotic Induction Profile (HIP).⁸ The clinician usually can induce the trance experience and systematically measure the patient’s response within 5 minutes. A HIP score of 5 indicates usable hypnotizability.

The HIP test includes instructions to produce a sense of lightness in the left arm and hand, with tests of response to this instruction. Response is characterized by dissociation, hand elevation after it is lowered, involuntariness, response to the cutoff signal, and altered sensation.

Turning hypnotic induction into a test of hypnotic capacity transforms the initial encounter by:

• removing pressure on the clinician to successfully hypnotize the subject
• reducing patients’ experiences of complying with the clinician’s wishes, rather than exploring and discovering their own hypnotic capacity.

Placing the hypnotic experience in the context of a test also makes it consonant with other medical examinations and procedures.⁸

Once a patient’s hypnotizability is determined, structured measurement is no longer necessary. The test-retest correlation for hypnotizability scores is 0.7 over 25 years, which is more consistent than IQ testing.⁷ Subsequent inductions usually can be generated by the patient or signaled by the clinician, and only seconds are required for the shift into trance.

Box 1

Reducing anxiety

Anxiety can be understood as a vaguely defined but immobilizing sense of distress. Lack of clarity about the discomfort’s source enhances the patient’s sense of helplessness and avoidance. One therapeutic challenge is to convert anxiety into fear—to give it a focus so that something can be done about it.

Box 2

Anxiety sets up a negative feedback cycle between psychological preoccupation and somatic discomfort, a “snowball effect” in which subjective anxiety and somatic tension reinforce each other. Hypnosis can help reduce anxiety and induce relaxation,⁹ and its dissociative component can help separate anxiety’s psychological and somatic components.

Hypnosis is as effective at reducing anxiety as 1 mg of alprazolam, at least in a study of college students.¹⁰ Student volunteers with high and low hypnotizability were given alprazolam, 1 mg, and a hypnotic suggestion based on their reactions to the drug. Four days later, when students received hypnosis only and hypnosis plus alprazolam:

• combination therapy reduced anxiety more effectively than did hypnosis or alprazolam alone, as measured by the Profile of Mood States tension-anxiety scale
• improvement was comparable with hypnosis or alprazolam alone
• highly hypnotizable students showed significantly greater relaxation than did those with low hypnotizability in all three treatment groups
• EEG data showed similar frontal and occipital changes in the alprazolam and hypnotic suggestion groups.

In randomized trials, simple self-hypnosis training has reduced pain and anxiety during medical procedures, reducing procedure time by an average 17 minutes and resulting in fewer complications.¹¹

A typical hypnotic instruction for managing anxiety is provided in Box 2. This approach teaches patients how to deal with stressors that complicate their anxiety and to control their somatic response. Hypnosis expands patients’ repertoire of responses and enables them to feel less helpless.

Confronting phobias

Phobic symptoms of fear and avoidance or exposure with distress respond especially well to brief hypnosis interventions. Although behavior modification and antidepressants also can treat phobias successfully, one or two hypnosis sessions often can reduce or cure phobic symptoms.

For example, one can help patients with airplane phobia prepare for flight by going into a hypnotic state and learning three concepts:

• Think of the airplane as an extension of the body, such as a bicycle.
• Float with the plane.
• Think about the difference between probability and possibility.

The hypnotic state—with its focused attention and physical relaxation—can amplify this cognitive restructuring technique. Phobic patients can feel more in control of their somatic reactions and, by extrapolation, the flying experience itself. In one study, 52% of patients taught this self-hypnosis exercise remained improved or cured at least 7 years later.¹²

Treating traumatic reactions

Evidence is growing that trauma elicits dissociation. Thus, hypnosis could help us understand and treat traumatic reactions, including patients with acute and posttraumatic stress disorder (PTSD) and dissociative disorders.

The hypnotic state’s controlled dissociation can be used to model the uncontrolled dissociation represented by posttraumatic phenomena such as flashbacks, numbing, and amnesia.¹³ This view is supported by evidence that PTSD is associated with high hypnotizability.^14,15

Acute stress disorder—as introduced in DSM-IV¹⁶—is characterized by prominent dissociative symptoms, with intrusion, avoidance, and hyperarousal. These diagnostic criteria recognize that acute dissociation is a common and predictable reaction to trauma.

Hypnosis involving grief work, exploration of trauma-related transference issues, and emotional expression are effective psychotherapies for persons exposed to trauma. Becoming familiar with hypnotic states can teach patients to recognize, understand, and control their dissociative states.

Evidence suggests that hypnosis’ intense concentration may reverse the dissociative mind fragmentation caused by trauma.¹⁷ Traumatic memories may seem less overwhelming and intrusive once patients discover they can:

• exert greater control over memory access and retrieval
• work through and assimilate disturbing thoughts.

The controlled experience of hypnotic abreaction (reliving traumatic and other memories with strong emotion) provides boundaries for psychotherapeutic grief work.^18,19 Instead of telling patients not to ruminate over a traumatic event, the clinician instructs the patient how to think about the experience.

The inferred message is that the patient can work on other things—such as relationships and daily living problems—after this therapeutic work is done.

Patients are slowly separated from the victim role. The goal is to help them restructure their memories, both cognitively and emotionally. They bear the memories’ impact, yet come to see the information differently.⁷ Traumatic input becomes more bearable when linked to a cognitively restructured recognition of an adaptive response.^,20 For example, patients may acknowledge what they did during a traumatic event that was self-protective or helped others.

PTSD. Hypnosis shares common elements with other cognitive and behavioral treatments for PTSD, including exposure to traumatic memories for cognitive and emotional processing. Few studies have examined using hypnosis to treat PTSD, but evidence suggests it is at least as effective as other cognitive-behavioral treatments.^20,21

Patients can be taught to view PTSD’s intrusive memories and bodily symptoms as re-experiencing painful memories. The memories often intrude less frequently after patients find a controlled method—such as self-hypnosis—to access and work them through.²²

Box 3

Self-blame. Many trauma victims would rather feel guilty than helpless. They blame themselves inappropriately for events over which they had no control, rather than accept their helplessness. They misuse hindsight about the trauma to assume the events were predictable and therefore avoidable. They imagine they can replay the events and change the outcome.

Such an approach to trauma can be profoundly demoralizing, leaving victims burdened by needless guilt and shame. Helping them face and bear the feelings associated with traumatic events can free them from efforts to “undo” or take responsibility for the trauma and accept what happened.

Split-screen technique. Using hypnosis with a “split-screen” technique can help patients restructure the memory of trauma. The left screen symbolizes the trauma in condensed form. The right screen helps patients focus on how they tried to master the situation. This grief work allows patients to acknowledge, bear, and put into perspective the humiliation of the experience and their loss of invulnerability, health, or loved ones (Box 3).¹⁸

Dissociation. Dissociating during a threatening situation may enable a person to put aside some awareness of the danger and take self-protective action. Persistent dissociation, however, may make it too easy to avoid working through the traumatic experiences later on.^22-24

Dissociation makes subsequent exposure to reminders of the trauma more similar to a reexperiencing rather than a controlled remembering of it. This can trigger physiologic stress reactions and lead to or worsen PTSD.^25-27

Dissociative disorders can be understood as chronic and severe PTSDs.²⁸ Many individuals with dissociative disorders have histories of sexual and physical abuse.^29-31 Clearly, traumatic experiences sensitize survivors to subsequent trauma through conditioned activation of fear circuitry involving the amygdala, hippocampus, and frontal lobes.³²

Hypnosis can be especially helpful—both for diagnosis and therapy.³³ It can assist the controlled recovery of memories, while allowing some images to remain dissociated from cognition until the patient is ready to deal with them. The patient can turn memories on and off by entering and exiting the hypnotic state and thereby recover and reprocess memories at a tolerable pace.

Related resources

• Society for Clinical and Experimental Hypnosis. http://ijceh.educ.wsu.edu
• American Society of Clinical Hypnosis. www.asch.net
• American Psychological Association, Division 30. Society of Psychological Hypnosis. http://www.apa.org/about/division/div30.html

Mr. M, a world-class athlete, collapsed suddenly in an alley. He was rushed to a hospital emergency room, where he nearly died of internal bleeding from a grapefruit-sized abdominal lymphoma. He was hospitalized and placed on chemotherapy.

Increasing doses of opiates hardly reduced his pain, and he became extremely anxious. Staff described him as “climbing the walls.” He lay in bed writhing, and his parents feared he was becoming a “drug addict.”

Anxiety about his life-threatening illness was clearly compounding his pain, so his attending physician ordered a psychiatric evaluation. When I interviewed the patient, I felt that hypnosis could help.

Hypnosis—as a state of highly focused attention—can help us treat patients’ anxiety, phobias, pain, posttraumatic stress disorder (PTSD), and dissociative disorders. With training, an experienced psychiatrist can quickly start using hypnosis as an adjunct to other therapies.

This article describes how hypnosis helped Mr. M and a young woman traumatized by a criminal assault. Based on my experience and the literature, I discuss what hypnosis is, what training is required, how to measure hypnotizability, and the value of hypnosis in helping patients control their anxiety, posttraumatic, and dissociative states.

Case continued: ‘Surfing’ in Hawaii

When I met Mr. M in the hospital, I acknowledged his distress and the reasons for it, saying “You don’t really want to be here, do you?”

“How many years of medical training did it take you to figure that out?” he replied.

“Well then,” I said, “let’s go somewhere else. Where would you like to be right now?”

He responded, “I’ve never surfed.”

“Good,” I replied, “let’s go to Hawaii.” In hypnosis, I had him picture himself surfing. He continued to groan, but the pattern changed. “What happened?” I asked. “I fell off the surfboard,” he replied. “OK, get back on, and do it right,” I told him.

He learned to practice self-hypnosis, which markedly reduced his anxiety and pain. Two days later he was off pain medications and joking with the nurses in the hall. The attending physician noted in the patient’s record: “Patient off pain meds. Tumor must be regressing.”

What is hypnosis?

Mr. M’s response, though unusually strong, underscores the fact that hypnosis can rapidly produce analgesia and anxiolysis in the medical setting. Hypnosis—often called “believed-in imagination”—is characterized by an ability to sustain a state of attentive, receptive, intense focal concentration with diminished peripheral awareness. The hypnotized person is awake and alert, not asleep. Hypnosis’ three main components are absorption, dissociation, and suggestibility.

Biological basis. The hypnotic state has no brain “signature” per se, but brain imaging portrays hypnosis as a state of alertness with altered anterior cingulate gyrus activation, which helps to focus attention.^1-3 Hypnotized persons can demonstrably alter blood flow in brain regions involved in perceptual processing in response to suggestions of altered perception, whether somatosensory, visual, or olfactory.^4,5 Thus, patients report not only reduced pain but changes in how they experience pain with hypnotic analgesia.

The brain’s dopamine neurotransmitter system—especially in the frontal lobes—also may be involved in hypnosis, as highly hypnotizable persons have elevated levels of dopamine metabolites in their cerebrospinal fluid.⁶

Hypnotic trance. The trance experience is often best explained to patients as similar to being absorbed in a good novel. One loses awareness of one’s surroundings and enters the imagined world. When the novel is finished, the reader requires a moment of reorientation to the surrounding world.

A trance is a state of sustained, attentive-receptive concentration in response to a signal from within or from someone else. The signal activates this shift of awareness and permits more-intensive concentration in a designated direction.

All hypnosis is self-hypnosis. Much of its clinical value is that it can be self-induced throughout the day and whenever symptoms emerge. During the first weeks, patients can be encouraged to practice every 1 or 2 hours.

Applying hypnosis to practice. A well-trained clinician can learn to use hypnosis in classes offered by the two professional hypnosis societies or the American Psychiatric Association (Box 1) Because hypnosis is not something “done to” a patient but rather a capacity to be measured, tapped, and utilized, psychiatrists can integrate hypnosis into clinical practice after some initial training, with ongoing learning and supervision.

Who can be hypnotized?

Not everyone is equally hypnotizable, and hypnotizability is a stable and measurable trait. Approximately one-quarter of adults cannot respond to hypnotic instructions, whereas 10% are extremely hypnotizable.⁷

Brief, clinically useful tests of hypnotic responsiveness have been developed, such as the Hypnotic Induction Profile (HIP).⁸ The clinician usually can induce the trance experience and systematically measure the patient’s response within 5 minutes. A HIP score of 5 indicates usable hypnotizability.

The HIP test includes instructions to produce a sense of lightness in the left arm and hand, with tests of response to this instruction. Response is characterized by dissociation, hand elevation after it is lowered, involuntariness, response to the cutoff signal, and altered sensation.

Turning hypnotic induction into a test of hypnotic capacity transforms the initial encounter by:

• removing pressure on the clinician to successfully hypnotize the subject
• reducing patients’ experiences of complying with the clinician’s wishes, rather than exploring and discovering their own hypnotic capacity.

Placing the hypnotic experience in the context of a test also makes it consonant with other medical examinations and procedures.⁸

Once a patient’s hypnotizability is determined, structured measurement is no longer necessary. The test-retest correlation for hypnotizability scores is 0.7 over 25 years, which is more consistent than IQ testing.⁷ Subsequent inductions usually can be generated by the patient or signaled by the clinician, and only seconds are required for the shift into trance.

Box 1

Reducing anxiety

Anxiety can be understood as a vaguely defined but immobilizing sense of distress. Lack of clarity about the discomfort’s source enhances the patient’s sense of helplessness and avoidance. One therapeutic challenge is to convert anxiety into fear—to give it a focus so that something can be done about it.

Box 2

Anxiety sets up a negative feedback cycle between psychological preoccupation and somatic discomfort, a “snowball effect” in which subjective anxiety and somatic tension reinforce each other. Hypnosis can help reduce anxiety and induce relaxation,⁹ and its dissociative component can help separate anxiety’s psychological and somatic components.

Hypnosis is as effective at reducing anxiety as 1 mg of alprazolam, at least in a study of college students.¹⁰ Student volunteers with high and low hypnotizability were given alprazolam, 1 mg, and a hypnotic suggestion based on their reactions to the drug. Four days later, when students received hypnosis only and hypnosis plus alprazolam:

• combination therapy reduced anxiety more effectively than did hypnosis or alprazolam alone, as measured by the Profile of Mood States tension-anxiety scale
• improvement was comparable with hypnosis or alprazolam alone
• highly hypnotizable students showed significantly greater relaxation than did those with low hypnotizability in all three treatment groups
• EEG data showed similar frontal and occipital changes in the alprazolam and hypnotic suggestion groups.

In randomized trials, simple self-hypnosis training has reduced pain and anxiety during medical procedures, reducing procedure time by an average 17 minutes and resulting in fewer complications.¹¹

A typical hypnotic instruction for managing anxiety is provided in Box 2. This approach teaches patients how to deal with stressors that complicate their anxiety and to control their somatic response. Hypnosis expands patients’ repertoire of responses and enables them to feel less helpless.

Confronting phobias

Phobic symptoms of fear and avoidance or exposure with distress respond especially well to brief hypnosis interventions. Although behavior modification and antidepressants also can treat phobias successfully, one or two hypnosis sessions often can reduce or cure phobic symptoms.

For example, one can help patients with airplane phobia prepare for flight by going into a hypnotic state and learning three concepts:

• Think of the airplane as an extension of the body, such as a bicycle.
• Float with the plane.
• Think about the difference between probability and possibility.

The hypnotic state—with its focused attention and physical relaxation—can amplify this cognitive restructuring technique. Phobic patients can feel more in control of their somatic reactions and, by extrapolation, the flying experience itself. In one study, 52% of patients taught this self-hypnosis exercise remained improved or cured at least 7 years later.¹²

Treating traumatic reactions

Evidence is growing that trauma elicits dissociation. Thus, hypnosis could help us understand and treat traumatic reactions, including patients with acute and posttraumatic stress disorder (PTSD) and dissociative disorders.

The hypnotic state’s controlled dissociation can be used to model the uncontrolled dissociation represented by posttraumatic phenomena such as flashbacks, numbing, and amnesia.¹³ This view is supported by evidence that PTSD is associated with high hypnotizability.^14,15

Acute stress disorder—as introduced in DSM-IV¹⁶—is characterized by prominent dissociative symptoms, with intrusion, avoidance, and hyperarousal. These diagnostic criteria recognize that acute dissociation is a common and predictable reaction to trauma.

Hypnosis involving grief work, exploration of trauma-related transference issues, and emotional expression are effective psychotherapies for persons exposed to trauma. Becoming familiar with hypnotic states can teach patients to recognize, understand, and control their dissociative states.

Evidence suggests that hypnosis’ intense concentration may reverse the dissociative mind fragmentation caused by trauma.¹⁷ Traumatic memories may seem less overwhelming and intrusive once patients discover they can:

• exert greater control over memory access and retrieval
• work through and assimilate disturbing thoughts.

The controlled experience of hypnotic abreaction (reliving traumatic and other memories with strong emotion) provides boundaries for psychotherapeutic grief work.^18,19 Instead of telling patients not to ruminate over a traumatic event, the clinician instructs the patient how to think about the experience.

The inferred message is that the patient can work on other things—such as relationships and daily living problems—after this therapeutic work is done.

Patients are slowly separated from the victim role. The goal is to help them restructure their memories, both cognitively and emotionally. They bear the memories’ impact, yet come to see the information differently.⁷ Traumatic input becomes more bearable when linked to a cognitively restructured recognition of an adaptive response.^,20 For example, patients may acknowledge what they did during a traumatic event that was self-protective or helped others.

PTSD. Hypnosis shares common elements with other cognitive and behavioral treatments for PTSD, including exposure to traumatic memories for cognitive and emotional processing. Few studies have examined using hypnosis to treat PTSD, but evidence suggests it is at least as effective as other cognitive-behavioral treatments.^20,21

Patients can be taught to view PTSD’s intrusive memories and bodily symptoms as re-experiencing painful memories. The memories often intrude less frequently after patients find a controlled method—such as self-hypnosis—to access and work them through.²²

Box 3

Self-blame. Many trauma victims would rather feel guilty than helpless. They blame themselves inappropriately for events over which they had no control, rather than accept their helplessness. They misuse hindsight about the trauma to assume the events were predictable and therefore avoidable. They imagine they can replay the events and change the outcome.

Such an approach to trauma can be profoundly demoralizing, leaving victims burdened by needless guilt and shame. Helping them face and bear the feelings associated with traumatic events can free them from efforts to “undo” or take responsibility for the trauma and accept what happened.

Split-screen technique. Using hypnosis with a “split-screen” technique can help patients restructure the memory of trauma. The left screen symbolizes the trauma in condensed form. The right screen helps patients focus on how they tried to master the situation. This grief work allows patients to acknowledge, bear, and put into perspective the humiliation of the experience and their loss of invulnerability, health, or loved ones (Box 3).¹⁸

Dissociation. Dissociating during a threatening situation may enable a person to put aside some awareness of the danger and take self-protective action. Persistent dissociation, however, may make it too easy to avoid working through the traumatic experiences later on.^22-24

Dissociation makes subsequent exposure to reminders of the trauma more similar to a reexperiencing rather than a controlled remembering of it. This can trigger physiologic stress reactions and lead to or worsen PTSD.^25-27

Dissociative disorders can be understood as chronic and severe PTSDs.²⁸ Many individuals with dissociative disorders have histories of sexual and physical abuse.^29-31 Clearly, traumatic experiences sensitize survivors to subsequent trauma through conditioned activation of fear circuitry involving the amygdala, hippocampus, and frontal lobes.³²

Hypnosis can be especially helpful—both for diagnosis and therapy.³³ It can assist the controlled recovery of memories, while allowing some images to remain dissociated from cognition until the patient is ready to deal with them. The patient can turn memories on and off by entering and exiting the hypnotic state and thereby recover and reprocess memories at a tolerable pace.

Related resources

• Society for Clinical and Experimental Hypnosis. http://ijceh.educ.wsu.edu
• American Society of Clinical Hypnosis. www.asch.net
• American Psychological Association, Division 30. Society of Psychological Hypnosis. http://www.apa.org/about/division/div30.html

Mr. M, a world-class athlete, collapsed suddenly in an alley. He was rushed to a hospital emergency room, where he nearly died of internal bleeding from a grapefruit-sized abdominal lymphoma. He was hospitalized and placed on chemotherapy.

Increasing doses of opiates hardly reduced his pain, and he became extremely anxious. Staff described him as “climbing the walls.” He lay in bed writhing, and his parents feared he was becoming a “drug addict.”

Anxiety about his life-threatening illness was clearly compounding his pain, so his attending physician ordered a psychiatric evaluation. When I interviewed the patient, I felt that hypnosis could help.

Hypnosis—as a state of highly focused attention—can help us treat patients’ anxiety, phobias, pain, posttraumatic stress disorder (PTSD), and dissociative disorders. With training, an experienced psychiatrist can quickly start using hypnosis as an adjunct to other therapies.

This article describes how hypnosis helped Mr. M and a young woman traumatized by a criminal assault. Based on my experience and the literature, I discuss what hypnosis is, what training is required, how to measure hypnotizability, and the value of hypnosis in helping patients control their anxiety, posttraumatic, and dissociative states.

Case continued: ‘Surfing’ in Hawaii

When I met Mr. M in the hospital, I acknowledged his distress and the reasons for it, saying “You don’t really want to be here, do you?”

“How many years of medical training did it take you to figure that out?” he replied.

“Well then,” I said, “let’s go somewhere else. Where would you like to be right now?”

He responded, “I’ve never surfed.”

“Good,” I replied, “let’s go to Hawaii.” In hypnosis, I had him picture himself surfing. He continued to groan, but the pattern changed. “What happened?” I asked. “I fell off the surfboard,” he replied. “OK, get back on, and do it right,” I told him.

He learned to practice self-hypnosis, which markedly reduced his anxiety and pain. Two days later he was off pain medications and joking with the nurses in the hall. The attending physician noted in the patient’s record: “Patient off pain meds. Tumor must be regressing.”

What is hypnosis?

Mr. M’s response, though unusually strong, underscores the fact that hypnosis can rapidly produce analgesia and anxiolysis in the medical setting. Hypnosis—often called “believed-in imagination”—is characterized by an ability to sustain a state of attentive, receptive, intense focal concentration with diminished peripheral awareness. The hypnotized person is awake and alert, not asleep. Hypnosis’ three main components are absorption, dissociation, and suggestibility.

Biological basis. The hypnotic state has no brain “signature” per se, but brain imaging portrays hypnosis as a state of alertness with altered anterior cingulate gyrus activation, which helps to focus attention.^1-3 Hypnotized persons can demonstrably alter blood flow in brain regions involved in perceptual processing in response to suggestions of altered perception, whether somatosensory, visual, or olfactory.^4,5 Thus, patients report not only reduced pain but changes in how they experience pain with hypnotic analgesia.

The brain’s dopamine neurotransmitter system—especially in the frontal lobes—also may be involved in hypnosis, as highly hypnotizable persons have elevated levels of dopamine metabolites in their cerebrospinal fluid.⁶

Hypnotic trance. The trance experience is often best explained to patients as similar to being absorbed in a good novel. One loses awareness of one’s surroundings and enters the imagined world. When the novel is finished, the reader requires a moment of reorientation to the surrounding world.

A trance is a state of sustained, attentive-receptive concentration in response to a signal from within or from someone else. The signal activates this shift of awareness and permits more-intensive concentration in a designated direction.

All hypnosis is self-hypnosis. Much of its clinical value is that it can be self-induced throughout the day and whenever symptoms emerge. During the first weeks, patients can be encouraged to practice every 1 or 2 hours.

Applying hypnosis to practice. A well-trained clinician can learn to use hypnosis in classes offered by the two professional hypnosis societies or the American Psychiatric Association (Box 1) Because hypnosis is not something “done to” a patient but rather a capacity to be measured, tapped, and utilized, psychiatrists can integrate hypnosis into clinical practice after some initial training, with ongoing learning and supervision.

Who can be hypnotized?

Not everyone is equally hypnotizable, and hypnotizability is a stable and measurable trait. Approximately one-quarter of adults cannot respond to hypnotic instructions, whereas 10% are extremely hypnotizable.⁷

Brief, clinically useful tests of hypnotic responsiveness have been developed, such as the Hypnotic Induction Profile (HIP).⁸ The clinician usually can induce the trance experience and systematically measure the patient’s response within 5 minutes. A HIP score of 5 indicates usable hypnotizability.

The HIP test includes instructions to produce a sense of lightness in the left arm and hand, with tests of response to this instruction. Response is characterized by dissociation, hand elevation after it is lowered, involuntariness, response to the cutoff signal, and altered sensation.

Turning hypnotic induction into a test of hypnotic capacity transforms the initial encounter by:

• removing pressure on the clinician to successfully hypnotize the subject
• reducing patients’ experiences of complying with the clinician’s wishes, rather than exploring and discovering their own hypnotic capacity.

Placing the hypnotic experience in the context of a test also makes it consonant with other medical examinations and procedures.⁸

Once a patient’s hypnotizability is determined, structured measurement is no longer necessary. The test-retest correlation for hypnotizability scores is 0.7 over 25 years, which is more consistent than IQ testing.⁷ Subsequent inductions usually can be generated by the patient or signaled by the clinician, and only seconds are required for the shift into trance.

Box 1

Reducing anxiety

Anxiety can be understood as a vaguely defined but immobilizing sense of distress. Lack of clarity about the discomfort’s source enhances the patient’s sense of helplessness and avoidance. One therapeutic challenge is to convert anxiety into fear—to give it a focus so that something can be done about it.

Box 2

Anxiety sets up a negative feedback cycle between psychological preoccupation and somatic discomfort, a “snowball effect” in which subjective anxiety and somatic tension reinforce each other. Hypnosis can help reduce anxiety and induce relaxation,⁹ and its dissociative component can help separate anxiety’s psychological and somatic components.

Hypnosis is as effective at reducing anxiety as 1 mg of alprazolam, at least in a study of college students.¹⁰ Student volunteers with high and low hypnotizability were given alprazolam, 1 mg, and a hypnotic suggestion based on their reactions to the drug. Four days later, when students received hypnosis only and hypnosis plus alprazolam:

• combination therapy reduced anxiety more effectively than did hypnosis or alprazolam alone, as measured by the Profile of Mood States tension-anxiety scale
• improvement was comparable with hypnosis or alprazolam alone
• highly hypnotizable students showed significantly greater relaxation than did those with low hypnotizability in all three treatment groups
• EEG data showed similar frontal and occipital changes in the alprazolam and hypnotic suggestion groups.

In randomized trials, simple self-hypnosis training has reduced pain and anxiety during medical procedures, reducing procedure time by an average 17 minutes and resulting in fewer complications.¹¹

A typical hypnotic instruction for managing anxiety is provided in Box 2. This approach teaches patients how to deal with stressors that complicate their anxiety and to control their somatic response. Hypnosis expands patients’ repertoire of responses and enables them to feel less helpless.

Confronting phobias

Phobic symptoms of fear and avoidance or exposure with distress respond especially well to brief hypnosis interventions. Although behavior modification and antidepressants also can treat phobias successfully, one or two hypnosis sessions often can reduce or cure phobic symptoms.

For example, one can help patients with airplane phobia prepare for flight by going into a hypnotic state and learning three concepts:

• Think of the airplane as an extension of the body, such as a bicycle.
• Float with the plane.
• Think about the difference between probability and possibility.

The hypnotic state—with its focused attention and physical relaxation—can amplify this cognitive restructuring technique. Phobic patients can feel more in control of their somatic reactions and, by extrapolation, the flying experience itself. In one study, 52% of patients taught this self-hypnosis exercise remained improved or cured at least 7 years later.¹²

Treating traumatic reactions

Evidence is growing that trauma elicits dissociation. Thus, hypnosis could help us understand and treat traumatic reactions, including patients with acute and posttraumatic stress disorder (PTSD) and dissociative disorders.

The hypnotic state’s controlled dissociation can be used to model the uncontrolled dissociation represented by posttraumatic phenomena such as flashbacks, numbing, and amnesia.¹³ This view is supported by evidence that PTSD is associated with high hypnotizability.^14,15

Acute stress disorder—as introduced in DSM-IV¹⁶—is characterized by prominent dissociative symptoms, with intrusion, avoidance, and hyperarousal. These diagnostic criteria recognize that acute dissociation is a common and predictable reaction to trauma.

Hypnosis involving grief work, exploration of trauma-related transference issues, and emotional expression are effective psychotherapies for persons exposed to trauma. Becoming familiar with hypnotic states can teach patients to recognize, understand, and control their dissociative states.

Evidence suggests that hypnosis’ intense concentration may reverse the dissociative mind fragmentation caused by trauma.¹⁷ Traumatic memories may seem less overwhelming and intrusive once patients discover they can:

• exert greater control over memory access and retrieval
• work through and assimilate disturbing thoughts.

The controlled experience of hypnotic abreaction (reliving traumatic and other memories with strong emotion) provides boundaries for psychotherapeutic grief work.^18,19 Instead of telling patients not to ruminate over a traumatic event, the clinician instructs the patient how to think about the experience.

The inferred message is that the patient can work on other things—such as relationships and daily living problems—after this therapeutic work is done.

Patients are slowly separated from the victim role. The goal is to help them restructure their memories, both cognitively and emotionally. They bear the memories’ impact, yet come to see the information differently.⁷ Traumatic input becomes more bearable when linked to a cognitively restructured recognition of an adaptive response.^,20 For example, patients may acknowledge what they did during a traumatic event that was self-protective or helped others.

PTSD. Hypnosis shares common elements with other cognitive and behavioral treatments for PTSD, including exposure to traumatic memories for cognitive and emotional processing. Few studies have examined using hypnosis to treat PTSD, but evidence suggests it is at least as effective as other cognitive-behavioral treatments.^20,21

Patients can be taught to view PTSD’s intrusive memories and bodily symptoms as re-experiencing painful memories. The memories often intrude less frequently after patients find a controlled method—such as self-hypnosis—to access and work them through.²²

Box 3

Self-blame. Many trauma victims would rather feel guilty than helpless. They blame themselves inappropriately for events over which they had no control, rather than accept their helplessness. They misuse hindsight about the trauma to assume the events were predictable and therefore avoidable. They imagine they can replay the events and change the outcome.

Such an approach to trauma can be profoundly demoralizing, leaving victims burdened by needless guilt and shame. Helping them face and bear the feelings associated with traumatic events can free them from efforts to “undo” or take responsibility for the trauma and accept what happened.

Split-screen technique. Using hypnosis with a “split-screen” technique can help patients restructure the memory of trauma. The left screen symbolizes the trauma in condensed form. The right screen helps patients focus on how they tried to master the situation. This grief work allows patients to acknowledge, bear, and put into perspective the humiliation of the experience and their loss of invulnerability, health, or loved ones (Box 3).¹⁸

Dissociation. Dissociating during a threatening situation may enable a person to put aside some awareness of the danger and take self-protective action. Persistent dissociation, however, may make it too easy to avoid working through the traumatic experiences later on.^22-24

Dissociation makes subsequent exposure to reminders of the trauma more similar to a reexperiencing rather than a controlled remembering of it. This can trigger physiologic stress reactions and lead to or worsen PTSD.^25-27

Dissociative disorders can be understood as chronic and severe PTSDs.²⁸ Many individuals with dissociative disorders have histories of sexual and physical abuse.^29-31 Clearly, traumatic experiences sensitize survivors to subsequent trauma through conditioned activation of fear circuitry involving the amygdala, hippocampus, and frontal lobes.³²

Hypnosis can be especially helpful—both for diagnosis and therapy.³³ It can assist the controlled recovery of memories, while allowing some images to remain dissociated from cognition until the patient is ready to deal with them. The patient can turn memories on and off by entering and exiting the hypnotic state and thereby recover and reprocess memories at a tolerable pace.

Related resources

• Society for Clinical and Experimental Hypnosis. http://ijceh.educ.wsu.edu
• American Society of Clinical Hypnosis. www.asch.net
• American Psychological Association, Division 30. Society of Psychological Hypnosis. http://www.apa.org/about/division/div30.html

Families and schools often pressure clinicians to “do something” when children or adolescents persistently bully, threaten, or injure others. This demand poses a treatment dilemma when psychosocial and educational interventions have failed to manage pediatric aggression.

Aggression is the main reason for drug therapy in youths with conduct disorder, but very little safety and efficacy data exist to help us choose medications. This places young patients at risk for polypharmacy, unmanaged symptoms, short-term side effects, and unknown long-term consequences of exposure to psychotropics.

Table 1

4 precautions when prescribing for pediatric aggression

This article reviews the limited data on using medications to reduce aggression in children and adolescents, focusing on double-blind, placebo-controlled trials in conduct disorder. Based on this evidence and our clinical experience, we offer a sample case and treatment recommendations.

Prescribing principles

Precautions. When prescribing drugs to treat aggressive youth, remember the American Academy of Child and Adolescent Psychiatry’s precautions (Table 1)¹ Recently published recommendations prepared by expert consensus are also valuable treatment guides.²

Linking treatment to diagnosis. Should we attempt to manage aggression as a manifestation of an underlying psychiatric disorder? Or should we treat it the same across all disorders? The latter approach is akin to the “fever model.”

Fever—regardless of cause—may be treated with a nonsteroidal anti-inflammatory drug. However, evidence from drug studies suggests that underlying psychiatric disorders should help determine the choice of aggression treatment. For example, a recent study in adults found that divalproex was effective for aggressive patients only within a specific diagnostic subgroup (in this case, cluster B personality disorders).³

Clinical experience also links aggression treatment with underlying diagnoses. For example, aggression secondary to agitated depression is treated with an antidepressant, whereas aggression secondary to command hallucinations in schizophrenia is treated with antipsychotics.

In treating aggression in conduct disorder (Table 2), first treat comorbid disorders—such as attention deficit/hyperactivity disorder (ADHD) or bipolar disorder—and address the child’s psychosocial and educational needs. Then if medication is appropriate, consider drugs with evidence of safety and efficacy, such as antipsychotics, lithium, and stimulants.

Antipsychotics

Three conventional antipsychotics—chlorpromazine, haloperidol, and thioridazine—are FDA-approved for controlling disruptive behaviors in children.⁴ No atypical antipsychotics are so indicated, but atypicals are preferred in children and adolescents because of lower risks for tardive dyskinesia, neuroleptic malignant syndrome, and extrapyramidal symptoms.²

Risperidone is the most-studied atypical antipsychotic for treating pediatric aggression, particularly in patients with low intellectual functioning or mental retardation. In a 6-week, double-blind, placebo-controlled trial, 118 children ages 5 to 12 with severely disruptive behavior and IQs of 36 to 84 were given low-dose risperidone (mean 1.16 mg/d). Risperidone reduced conduct problems significantly more than placebo, although aggression was not measured directly.⁵ Adverse events included somnolence, headache, vomiting, weight gain, and elevated serum prolactin. Similar results have been reported in other studies.⁶

Table 2

Diagnostic criteria for conduct disorder

Box 1

Risperidone also reduced aggression in children with normal intelligence in one small study.⁷ As a cautionary note, however, long-term risperidone treatment has been associated with withdrawal dyskinesias.⁸

Olanzapine, quetiapine, ziprasidone, and aripiprazole are less well-studied for treating pediatric aggression but are preferable to conventional agents when antipsychotics are considered.

Recommendation. Expert consensus opinion² recommends using atypicals when psychosocial treatments and first-line medications for primary conditions have failed. Start with low dosages, and titrate up slowly while monitoring symptoms and side effects. Because no studies have compared any atypical’s efficacy over others for aggressive behavior, base your choices on:

• discussions with the patient and family (Box 1)
• medical comorbidities
• how the patient responded to antipsychotics in the past
• side-effect profile
• long-term treatment planning.²

If the patient cannot tolerate the medication or does not respond after 4 to 6 weeks, try switching atypicals. To improve partial response, consider adding a mood stabilizer such as lithium or divalproex. If aggressive symptoms remit for 6 months or longer, attempt to taper or discontinue the antipsychotic.²

Lithium

In placebo-controlled trials, lithium reduced aggression in:

• male prisoners ages 16 to 24.⁹
• children ages 7 and 12 with conduct disorder¹⁰
• children and adolescents ages 10 to 17 with conduct disorder.¹¹

Among these studies, only ours¹¹ specifically measured aggression. We randomly assigned 40 children to receive 4 weeks of lithium, 900 to 2,100 mg/d (mean 1,425 ± 321 mg/d), or placebo. Serum lithium levels were 0.78 to 1.55 mEq/L (mean 1.07 ± 0.19 mEq/L). We used the Overt Aggression Scale (OAS)^12,13 (see Related resources) to track frequency and severity of verbal aggression, aggression against objects, aggression against others, and self-aggression.

Lithium reduced aggression more than did placebo, as measured by the clinician-rated Clinical Global Impressions (CGI) scale and staff-rated Global Clinical Judgments (Consensus) Scale (GCJCS). The CGI showed a 70% response rate with lithium and 20% with placebo. Similarly, the GCJCS scale showed 80% response with lithium and 30% with placebo.

The aggression reduction with lithium was statistically significant and clinically evident. Most subjects (37 of 40) experienced at least one adverse event, however, whether receiving lithium or placebo. Nausea, vomiting, and urinary frequency were significantly more common in the lithium-treated group than with placebo. Fewer adverse events were reported in a similar outpatient study,¹⁴ probably because of less-frequent monitoring.

Lithium did not reduce aggression in adolescent girls treated for 2 weeks¹⁵ or in an outpatient study of children with ADHD.¹⁶

Recommendation. Lithium has shown efficacy for reducing severe aggression in hospitalized children with conduct disorder but not in similar outpatients. Consider this drug to reduce severe aggression in children with conduct disorder, especially if they have failed other treatments.

Anticonvulsants

Anticonvulsants have been used to decrease aggression for more than 50 years, and epidemiologic data show their use is increasing markedly.¹⁷ Few controlled studies support this prescribing trend, however.¹⁸

Initial reports suggested that anticonvulsants reduce disruptive behaviors, but more-critically designed studies have not supported this finding. For example, phenytoin sodium (diphenylhydantoin) demonstrated efficacy in open trials, but controlled trials found this anticonvulsant no more effective than placebo. In fact, placebo may have reduced aggression more than the active drug. Likewise, earlier controlled trials of carbamazepine indicated efficacy, but more-carefully designed trials using specific measures of aggression did not.

Divalproex is the anticonvulsant most commonly used for aggression in children and adolescents. Only one small, placebo-controlled study has found it effective in reducing aggression in children.¹⁹

Twenty children ages 10 to 18 with conduct disorder or oppositional defiant disorder were randomized to divalproex, 750 to 1,500 mg/d, or placebo. Eighteen completed the first phase, and 15 crossed over to the other treatment. Concomitant drug treatment, including stimulants, was allowed. The authors reported that 12 of 15 subjects showed some response to divalproex.

A 7-week study compared divalproex in high dosages (up to 1,500 mg/d) versus low dosages (up to 250 mg/d). This study was not placebo-controlled, but aggression was reduced more in the high-dosage than in the low-dosage group.²⁰

Recommendation. If you use an anticonvulsant, first obtain informed consent from the patient and parent. Divalproex causes weight gain and has been associated with increased risk of polycystic ovary syndrome with masculinizing effects.²¹

Double-blind, placebo-controlled studies of divalproex and other anticonvulsants in treating aggression are needed, particularly as prescriptions for these agents are rising.

Stimulants

Some small controlled studies suggest that stimulants can reduce aggression in children with ADHD, but their effects on aggression in conduct disorder have not been well studied. Aggression was not measured directly in the National Institute of Mental Health Multimodal Treatment Study of Children with ADHD.²¹ Most other studies have been small and included children with ADHD but not necessarily conduct disorder.

Recommendation. Stimulants may help reduce aggression in children with ADHD, but studies gauging their effects in conduct disorder are needed.

Alpha agonists

Alpha agonists such as clonidine and guanfacine are increasingly being used to treat children with disruptive disorders, despite limited evidence. The small controlled studies that examined alpha agonists as monotherapy or add-ons in this population did not directly measure aggression.^22,23

Recommendation. Little data support alpha agonists for reducing aggression. They should probably be considered second-line treatment.

SSRIs

No double-blind, placebo-controlled studies have tested any selective serotonin reuptake inhibitor (SSRIs) for reducing aggression in conduct disorder. In a 6-week open study, citalopram (mean 27 mg/d) reduced impulsive aggression in 12 children with mixed diagnoses, as measured by the modified OAS,¹³ Child Behavior Checklist, and CGI.²⁴

Recommendation. Use caution when prescribing SSRIs to aggressive youth, as these drugs may contribute to aggression in some mood-disordered children. More evidence of SSRIs’ safety and efficacy in this population is needed.

Related resources

• Overt Aggression Scale. In: Coccaro EF, Harvey PD, Kupsaw-Lawrence E, et al. Development of neuropharmacologically-based behavioral assessments of impulsiveaggressive behavior. J Neuropsychiatry 1991;3(2):S44-S51.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Chlorpromazine • Thorazine
• Clonidine • Catapres
• Phenytoin sodium • Dilantin
• Divalproex • Depakote
• Guanfacine • Tenex
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Thioridazine • Mellaril
• Ziprasidone • Geodon

Disclosure

Dr. Malone receives research support from Pfizer Inc. and Eli Lilly and Co. and is a consultant to Janssen Pharmaceutica.

Dr. Delaney is a consultant to Shire Pharmaceuticals.

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

Families and schools often pressure clinicians to “do something” when children or adolescents persistently bully, threaten, or injure others. This demand poses a treatment dilemma when psychosocial and educational interventions have failed to manage pediatric aggression.

Aggression is the main reason for drug therapy in youths with conduct disorder, but very little safety and efficacy data exist to help us choose medications. This places young patients at risk for polypharmacy, unmanaged symptoms, short-term side effects, and unknown long-term consequences of exposure to psychotropics.

Table 1

4 precautions when prescribing for pediatric aggression

This article reviews the limited data on using medications to reduce aggression in children and adolescents, focusing on double-blind, placebo-controlled trials in conduct disorder. Based on this evidence and our clinical experience, we offer a sample case and treatment recommendations.

Prescribing principles

Precautions. When prescribing drugs to treat aggressive youth, remember the American Academy of Child and Adolescent Psychiatry’s precautions (Table 1)¹ Recently published recommendations prepared by expert consensus are also valuable treatment guides.²

Linking treatment to diagnosis. Should we attempt to manage aggression as a manifestation of an underlying psychiatric disorder? Or should we treat it the same across all disorders? The latter approach is akin to the “fever model.”

Fever—regardless of cause—may be treated with a nonsteroidal anti-inflammatory drug. However, evidence from drug studies suggests that underlying psychiatric disorders should help determine the choice of aggression treatment. For example, a recent study in adults found that divalproex was effective for aggressive patients only within a specific diagnostic subgroup (in this case, cluster B personality disorders).³

Clinical experience also links aggression treatment with underlying diagnoses. For example, aggression secondary to agitated depression is treated with an antidepressant, whereas aggression secondary to command hallucinations in schizophrenia is treated with antipsychotics.

In treating aggression in conduct disorder (Table 2), first treat comorbid disorders—such as attention deficit/hyperactivity disorder (ADHD) or bipolar disorder—and address the child’s psychosocial and educational needs. Then if medication is appropriate, consider drugs with evidence of safety and efficacy, such as antipsychotics, lithium, and stimulants.

Antipsychotics

Three conventional antipsychotics—chlorpromazine, haloperidol, and thioridazine—are FDA-approved for controlling disruptive behaviors in children.⁴ No atypical antipsychotics are so indicated, but atypicals are preferred in children and adolescents because of lower risks for tardive dyskinesia, neuroleptic malignant syndrome, and extrapyramidal symptoms.²

Risperidone is the most-studied atypical antipsychotic for treating pediatric aggression, particularly in patients with low intellectual functioning or mental retardation. In a 6-week, double-blind, placebo-controlled trial, 118 children ages 5 to 12 with severely disruptive behavior and IQs of 36 to 84 were given low-dose risperidone (mean 1.16 mg/d). Risperidone reduced conduct problems significantly more than placebo, although aggression was not measured directly.⁵ Adverse events included somnolence, headache, vomiting, weight gain, and elevated serum prolactin. Similar results have been reported in other studies.⁶

Table 2

Diagnostic criteria for conduct disorder

Box 1

Risperidone also reduced aggression in children with normal intelligence in one small study.⁷ As a cautionary note, however, long-term risperidone treatment has been associated with withdrawal dyskinesias.⁸

Olanzapine, quetiapine, ziprasidone, and aripiprazole are less well-studied for treating pediatric aggression but are preferable to conventional agents when antipsychotics are considered.

Recommendation. Expert consensus opinion² recommends using atypicals when psychosocial treatments and first-line medications for primary conditions have failed. Start with low dosages, and titrate up slowly while monitoring symptoms and side effects. Because no studies have compared any atypical’s efficacy over others for aggressive behavior, base your choices on:

• discussions with the patient and family (Box 1)
• medical comorbidities
• how the patient responded to antipsychotics in the past
• side-effect profile
• long-term treatment planning.²

If the patient cannot tolerate the medication or does not respond after 4 to 6 weeks, try switching atypicals. To improve partial response, consider adding a mood stabilizer such as lithium or divalproex. If aggressive symptoms remit for 6 months or longer, attempt to taper or discontinue the antipsychotic.²

Lithium

In placebo-controlled trials, lithium reduced aggression in:

• male prisoners ages 16 to 24.⁹
• children ages 7 and 12 with conduct disorder¹⁰
• children and adolescents ages 10 to 17 with conduct disorder.¹¹

Among these studies, only ours¹¹ specifically measured aggression. We randomly assigned 40 children to receive 4 weeks of lithium, 900 to 2,100 mg/d (mean 1,425 ± 321 mg/d), or placebo. Serum lithium levels were 0.78 to 1.55 mEq/L (mean 1.07 ± 0.19 mEq/L). We used the Overt Aggression Scale (OAS)^12,13 (see Related resources) to track frequency and severity of verbal aggression, aggression against objects, aggression against others, and self-aggression.

Lithium reduced aggression more than did placebo, as measured by the clinician-rated Clinical Global Impressions (CGI) scale and staff-rated Global Clinical Judgments (Consensus) Scale (GCJCS). The CGI showed a 70% response rate with lithium and 20% with placebo. Similarly, the GCJCS scale showed 80% response with lithium and 30% with placebo.

The aggression reduction with lithium was statistically significant and clinically evident. Most subjects (37 of 40) experienced at least one adverse event, however, whether receiving lithium or placebo. Nausea, vomiting, and urinary frequency were significantly more common in the lithium-treated group than with placebo. Fewer adverse events were reported in a similar outpatient study,¹⁴ probably because of less-frequent monitoring.

Lithium did not reduce aggression in adolescent girls treated for 2 weeks¹⁵ or in an outpatient study of children with ADHD.¹⁶

Recommendation. Lithium has shown efficacy for reducing severe aggression in hospitalized children with conduct disorder but not in similar outpatients. Consider this drug to reduce severe aggression in children with conduct disorder, especially if they have failed other treatments.

Anticonvulsants

Anticonvulsants have been used to decrease aggression for more than 50 years, and epidemiologic data show their use is increasing markedly.¹⁷ Few controlled studies support this prescribing trend, however.¹⁸

Initial reports suggested that anticonvulsants reduce disruptive behaviors, but more-critically designed studies have not supported this finding. For example, phenytoin sodium (diphenylhydantoin) demonstrated efficacy in open trials, but controlled trials found this anticonvulsant no more effective than placebo. In fact, placebo may have reduced aggression more than the active drug. Likewise, earlier controlled trials of carbamazepine indicated efficacy, but more-carefully designed trials using specific measures of aggression did not.

Divalproex is the anticonvulsant most commonly used for aggression in children and adolescents. Only one small, placebo-controlled study has found it effective in reducing aggression in children.¹⁹

Twenty children ages 10 to 18 with conduct disorder or oppositional defiant disorder were randomized to divalproex, 750 to 1,500 mg/d, or placebo. Eighteen completed the first phase, and 15 crossed over to the other treatment. Concomitant drug treatment, including stimulants, was allowed. The authors reported that 12 of 15 subjects showed some response to divalproex.

A 7-week study compared divalproex in high dosages (up to 1,500 mg/d) versus low dosages (up to 250 mg/d). This study was not placebo-controlled, but aggression was reduced more in the high-dosage than in the low-dosage group.²⁰

Recommendation. If you use an anticonvulsant, first obtain informed consent from the patient and parent. Divalproex causes weight gain and has been associated with increased risk of polycystic ovary syndrome with masculinizing effects.²¹

Double-blind, placebo-controlled studies of divalproex and other anticonvulsants in treating aggression are needed, particularly as prescriptions for these agents are rising.

Stimulants

Some small controlled studies suggest that stimulants can reduce aggression in children with ADHD, but their effects on aggression in conduct disorder have not been well studied. Aggression was not measured directly in the National Institute of Mental Health Multimodal Treatment Study of Children with ADHD.²¹ Most other studies have been small and included children with ADHD but not necessarily conduct disorder.

Recommendation. Stimulants may help reduce aggression in children with ADHD, but studies gauging their effects in conduct disorder are needed.

Alpha agonists

Alpha agonists such as clonidine and guanfacine are increasingly being used to treat children with disruptive disorders, despite limited evidence. The small controlled studies that examined alpha agonists as monotherapy or add-ons in this population did not directly measure aggression.^22,23

Recommendation. Little data support alpha agonists for reducing aggression. They should probably be considered second-line treatment.

SSRIs

No double-blind, placebo-controlled studies have tested any selective serotonin reuptake inhibitor (SSRIs) for reducing aggression in conduct disorder. In a 6-week open study, citalopram (mean 27 mg/d) reduced impulsive aggression in 12 children with mixed diagnoses, as measured by the modified OAS,¹³ Child Behavior Checklist, and CGI.²⁴

Recommendation. Use caution when prescribing SSRIs to aggressive youth, as these drugs may contribute to aggression in some mood-disordered children. More evidence of SSRIs’ safety and efficacy in this population is needed.

Related resources

• Overt Aggression Scale. In: Coccaro EF, Harvey PD, Kupsaw-Lawrence E, et al. Development of neuropharmacologically-based behavioral assessments of impulsiveaggressive behavior. J Neuropsychiatry 1991;3(2):S44-S51.

Drug brand names

• Aripiprazole • Abilify
• Carbamazepine • Tegretol
• Citalopram • Celexa
• Chlorpromazine • Thorazine
• Clonidine • Catapres
• Phenytoin sodium • Dilantin
• Divalproex • Depakote
• Guanfacine • Tenex
• Haloperidol • Haldol
• Olanzapine • Zyprexa
• Quetiapine • Seroquel
• Risperidone • Risperdal
• Thioridazine • Mellaril
• Ziprasidone • Geodon