PTSD

With all of the discussion about a truly comprehensive and inclusive psychiatry, it was sad to see the emptiness and one-sidedness of Dr. Nasrallah’s June editorial (“Innovative approaches to treatment-resistant depression,” From the Editor, Current Psychiatry, June 2012, p. 4-5; http://bit.ly/1GM92oV). Depression certainly is not a unified diagnosis such as measles or appendicitis. In the face of so-called treatment-resistance, the first step is to review the psychological and biologic formulation of the patient and the reasons for his or her depression. Dr. Nasrallah does not mention the need for a review of all aspects of the patient’s life. The approaches he suggests are dreary, dull, ineffective, and unchanging. It proves that patients are best cared for by psychiatrists who practice biopsychosocial psychiatry and not merely to pay lip service to it.

Arnold Robbins, MD
Private Practice
Cambridge, MA
Clinical Professor of Psychiatry
Boston University School of Medicine
Boston, MA

Dr. Nasrallah responds

I thank Dr. Robbins for his letter. As someone trained by the father of biopsychosocial psychiatry—George Engel, MD, at the University of Rochester—I agree that it is the optimal practice of psychiatry and I practice that approach with all my patients. However, I was describing innovative interventions and paradigm shifts for truly end-of-the-road refractory depression, where all psychosocial and pharmacotherapy treatments have failed and the patient is desperate, disabled, and at high risk for suicide. None of the available interventions work with such individuals and that’s why I regard the innovative breakthroughs I described in my editorial as a promise of hope, thanks to dedicated psychiatric neuroscientists. I hope psychotherapy researchers can achieve breakthroughs for these patients as well.

Henry A. Nasrallah, MD
Editor-in-Chief

Psychotherapy for GAD

I appreciated Dr. Barry’s in-depth review of current diagnostic criteria and therapy for generalized anxiety disorder (GAD) (“Generalized anxiety disorder: Helping patients overcome worry,” Current Psychiatry, May 2012, p. 40-44; http://bit.ly/1oUymyJ). However, I want to point out an error under the “Evidence-based treatments” section labeled “Psychotherapy.” Dr. Barry states that cognitive-behavioral therapy (CBT) is the preferred form of psychotherapy for GAD. In my 40 years of practice, I have found a combination of medication—preferably selective serotonin reuptake inhibitors—and psychodynamic psychotherapy is the most effective treatment for GAD and provides more enduring relief.

Jonathan Shedler, PhD, of the University of Colorado Denver School of Medicine reported on the efficacy of psychodynamic psychotherapy vs behavioral therapy.¹ He compiled the results of meta-analyses of psychotherapy efficacy by 18 investigators covering 792 studies. The findings show a superior result for psychodynamic psychotherapy over behavioral therapy and the effects are more lasting.

Edward L. Parsons, MD
Private Practice
Westfield, NJ

The author responds

I appreciate Dr. Parsons’ comments and his valuable contribution to the dialogue on GAD. Dr. Parsons reemphasizes the importance of psychotherapy in this chronic condition. As demonstrated by the meta-analyses reviewed by Dr. Shedler, there is sufficient evidence in the medical literature to support either psychodynamic psychotherapy or CBT. The specific therapeutic recommendation should consider unique patient variables, such as therapist availability and expertise, the presence of co-occurring conditions or dynamics that would better align with a specific modality, and patient preference and psychological mindedness, to name a few. Regardless, psychotherapy is indicated in the treatment of GAD, and both CBT and psychodynamic psychotherapy are well-supported interventions.

Matthew J. Barry, DO
Lead Psychiatrist
Rochester Veterans Affairs Outpatient Clinic
Canandaigua Veterans Affairs Medical Center
Canandaigua, NY

Caution with prazosin

We welcome the article discussing the use of prazosin and antipsychotics for posttraumatic stress disorder (PTSD)-related nightmares (Graham RL, Leckband SG, Endow-Eyer RA. “PTSD nightmares: Prazosin and atypical antipsychotics,” Current Psychiatry, June 2012, p. 59-62; http://bit.ly/LVAlSo). The favorable outcomes associated with prazosin use combined with its low cost and general tolerability give it considerable potential. Prazosin may be particularly valuable given the unfavorable cardiometabolic risks associated with antipsychotic use, especially because evidence suggests individuals with PTSD have higher rates of cardiovascular disease.¹

We believe the occurrence of adverse cardiovascular effects when starting prazosin requires further attention. As an α1-adrenergic receptor antagonist, it has been linked to orthostatic hypotension and syncope.^2,3 Its cardiovascular effects may be further complicated by concomitant use of other antihypertensive medications. Therefore, we suggest a low initiation dose and gradual titration of prazosin. In individuals who initially were normotensive but then experienced hypotension following prazosin administration, we successfully used short-term sodium chloride tablets, 4 g/d. We discontinued sodium chloride after titration was completed and no postural hypotension was evident.

To minimize polypharmacy, individuals on multiple agents for hypertension may benefit from substituting prazosin for 1 of their regular anti- hypertensives. Despite the mounting evidence supporting prazosin use, it is not indicated for PTSD.

This material is the result of work supported with resources and the use of facilities of the Mental Health and Research and Development Service Lines, Atlanta Veterans Affairs Medical Center, Decatur, GA.

Arshya Vahabzadeh, MD
PGY-2, Resident Psychiatrist
Emory University School of Medicine

Erica Duncan, MD
Attending Psychiatrist
and Associate Professor
Mental Health Service Line
Atlanta Veterans Affairs Medical Center
Decatur, GA
Department of Psychiatry and Behavioral
Sciences
Emory University School of Medicine
Atlanta, GA

The authors respond

We agree with the comments by Drs. Vahabzadeh and Duncan regarding the cardiovascular adverse effects of prazosin. It is important to assess the hemodynamic status of the patient before initiating prazosin therapy, and usually, initiation is attempted only if a patient is normotensive or hypertensive because of potential orthostatic hypotension and syncope, which can occur in up to 4% of patients.¹ As noted by Drs. Vahabzadeh and Duncan, prazosin often is viewed as a dual treatment for both nightmares and blood pressure in individuals who are hypertensive prior to initiation. Prazosin therapy usually is initiated at 1 mg at bedtime and titrated by 1 to 2 mg every 3 to 5 days.² The average dose was approximately 3 mg in studies evaluating prazosin for treating PTSD-associated nightmares (dose range: 1 to 10 mg).² Until the patient is stabilized on a prazosin dose, blood pressure should be monitored daily for inpatients. Outpatients should be educated regarding the signs and symptoms of hypotension, especially dizziness and light-headedness upon standing, along with monitoring blood pressure at his or her next clinic appointment.

Prazosin does not carry an FDA indication for PTSD. Although this is important to consider, the level of evidence in terms of treatment of nightmares also is key. Aurora et al found prazosin was the only medication with a level A rating for treating PTSD-associated nightmares, indicating it as a recommended therapy option.² Because we do not have any medications indicated for PTSD-associated nightmares, it is crucial to practice evidence-based medicine and base therapy choices on available literature supporting the most effective and safe options.

Safety is an issue in many clinicians’ minds, especially when treating geriatric patients with PTSD because of the risk of hypotensive effects with prazosin leading to negative outcomes, such as falls. In Peskind et al’s open-label study of 9 older patients (mean age: 76) with intractable PTSD-associated nightmares treated with prazosin (mean dose: 2.3 mg; increased by 1 mg per week to a maximum dose of 4 mg), 8 patients experienced >50% reduction in nightmares after 8 weeks of treatment, and 1 patient experienced transient orthostasis when starting prazosin that resolved spontaneously with only mild decreases in blood pressure noted otherwise (<20 mm Hg decrease in systolic blood pressure upon standing).³ Although this study was small, it provides evidence that prazosin can be an effective and safe treatment option in geriatric patients and is devoid of the highly sedating side effects of some other treatment options.

Rebecca L. Graham, PharmD
Second-Year Psychiatric Pharmacy Resident
Veterans Affairs San Diego Healthcare System
(VASDHS)

Susan G. Leckband, RPh, BCPP
Clinical Psychiatric Pharmacist Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego

Rene A. Endow-Eyer, PharmD, BCPP
Psychiatric Clinical Pharmacy Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego
San Diego, CA

With all of the discussion about a truly comprehensive and inclusive psychiatry, it was sad to see the emptiness and one-sidedness of Dr. Nasrallah’s June editorial (“Innovative approaches to treatment-resistant depression,” From the Editor, Current Psychiatry, June 2012, p. 4-5; http://bit.ly/1GM92oV). Depression certainly is not a unified diagnosis such as measles or appendicitis. In the face of so-called treatment-resistance, the first step is to review the psychological and biologic formulation of the patient and the reasons for his or her depression. Dr. Nasrallah does not mention the need for a review of all aspects of the patient’s life. The approaches he suggests are dreary, dull, ineffective, and unchanging. It proves that patients are best cared for by psychiatrists who practice biopsychosocial psychiatry and not merely to pay lip service to it.

Arnold Robbins, MD
Private Practice
Cambridge, MA
Clinical Professor of Psychiatry
Boston University School of Medicine
Boston, MA

Dr. Nasrallah responds

I thank Dr. Robbins for his letter. As someone trained by the father of biopsychosocial psychiatry—George Engel, MD, at the University of Rochester—I agree that it is the optimal practice of psychiatry and I practice that approach with all my patients. However, I was describing innovative interventions and paradigm shifts for truly end-of-the-road refractory depression, where all psychosocial and pharmacotherapy treatments have failed and the patient is desperate, disabled, and at high risk for suicide. None of the available interventions work with such individuals and that’s why I regard the innovative breakthroughs I described in my editorial as a promise of hope, thanks to dedicated psychiatric neuroscientists. I hope psychotherapy researchers can achieve breakthroughs for these patients as well.

Henry A. Nasrallah, MD
Editor-in-Chief

Psychotherapy for GAD

I appreciated Dr. Barry’s in-depth review of current diagnostic criteria and therapy for generalized anxiety disorder (GAD) (“Generalized anxiety disorder: Helping patients overcome worry,” Current Psychiatry, May 2012, p. 40-44; http://bit.ly/1oUymyJ). However, I want to point out an error under the “Evidence-based treatments” section labeled “Psychotherapy.” Dr. Barry states that cognitive-behavioral therapy (CBT) is the preferred form of psychotherapy for GAD. In my 40 years of practice, I have found a combination of medication—preferably selective serotonin reuptake inhibitors—and psychodynamic psychotherapy is the most effective treatment for GAD and provides more enduring relief.

Jonathan Shedler, PhD, of the University of Colorado Denver School of Medicine reported on the efficacy of psychodynamic psychotherapy vs behavioral therapy.¹ He compiled the results of meta-analyses of psychotherapy efficacy by 18 investigators covering 792 studies. The findings show a superior result for psychodynamic psychotherapy over behavioral therapy and the effects are more lasting.

Edward L. Parsons, MD
Private Practice
Westfield, NJ

The author responds

I appreciate Dr. Parsons’ comments and his valuable contribution to the dialogue on GAD. Dr. Parsons reemphasizes the importance of psychotherapy in this chronic condition. As demonstrated by the meta-analyses reviewed by Dr. Shedler, there is sufficient evidence in the medical literature to support either psychodynamic psychotherapy or CBT. The specific therapeutic recommendation should consider unique patient variables, such as therapist availability and expertise, the presence of co-occurring conditions or dynamics that would better align with a specific modality, and patient preference and psychological mindedness, to name a few. Regardless, psychotherapy is indicated in the treatment of GAD, and both CBT and psychodynamic psychotherapy are well-supported interventions.

Matthew J. Barry, DO
Lead Psychiatrist
Rochester Veterans Affairs Outpatient Clinic
Canandaigua Veterans Affairs Medical Center
Canandaigua, NY

Caution with prazosin

We welcome the article discussing the use of prazosin and antipsychotics for posttraumatic stress disorder (PTSD)-related nightmares (Graham RL, Leckband SG, Endow-Eyer RA. “PTSD nightmares: Prazosin and atypical antipsychotics,” Current Psychiatry, June 2012, p. 59-62; http://bit.ly/LVAlSo). The favorable outcomes associated with prazosin use combined with its low cost and general tolerability give it considerable potential. Prazosin may be particularly valuable given the unfavorable cardiometabolic risks associated with antipsychotic use, especially because evidence suggests individuals with PTSD have higher rates of cardiovascular disease.¹

We believe the occurrence of adverse cardiovascular effects when starting prazosin requires further attention. As an α1-adrenergic receptor antagonist, it has been linked to orthostatic hypotension and syncope.^2,3 Its cardiovascular effects may be further complicated by concomitant use of other antihypertensive medications. Therefore, we suggest a low initiation dose and gradual titration of prazosin. In individuals who initially were normotensive but then experienced hypotension following prazosin administration, we successfully used short-term sodium chloride tablets, 4 g/d. We discontinued sodium chloride after titration was completed and no postural hypotension was evident.

To minimize polypharmacy, individuals on multiple agents for hypertension may benefit from substituting prazosin for 1 of their regular anti- hypertensives. Despite the mounting evidence supporting prazosin use, it is not indicated for PTSD.

This material is the result of work supported with resources and the use of facilities of the Mental Health and Research and Development Service Lines, Atlanta Veterans Affairs Medical Center, Decatur, GA.

Arshya Vahabzadeh, MD
PGY-2, Resident Psychiatrist
Emory University School of Medicine

Erica Duncan, MD
Attending Psychiatrist
and Associate Professor
Mental Health Service Line
Atlanta Veterans Affairs Medical Center
Decatur, GA
Department of Psychiatry and Behavioral
Sciences
Emory University School of Medicine
Atlanta, GA

The authors respond

We agree with the comments by Drs. Vahabzadeh and Duncan regarding the cardiovascular adverse effects of prazosin. It is important to assess the hemodynamic status of the patient before initiating prazosin therapy, and usually, initiation is attempted only if a patient is normotensive or hypertensive because of potential orthostatic hypotension and syncope, which can occur in up to 4% of patients.¹ As noted by Drs. Vahabzadeh and Duncan, prazosin often is viewed as a dual treatment for both nightmares and blood pressure in individuals who are hypertensive prior to initiation. Prazosin therapy usually is initiated at 1 mg at bedtime and titrated by 1 to 2 mg every 3 to 5 days.² The average dose was approximately 3 mg in studies evaluating prazosin for treating PTSD-associated nightmares (dose range: 1 to 10 mg).² Until the patient is stabilized on a prazosin dose, blood pressure should be monitored daily for inpatients. Outpatients should be educated regarding the signs and symptoms of hypotension, especially dizziness and light-headedness upon standing, along with monitoring blood pressure at his or her next clinic appointment.

Prazosin does not carry an FDA indication for PTSD. Although this is important to consider, the level of evidence in terms of treatment of nightmares also is key. Aurora et al found prazosin was the only medication with a level A rating for treating PTSD-associated nightmares, indicating it as a recommended therapy option.² Because we do not have any medications indicated for PTSD-associated nightmares, it is crucial to practice evidence-based medicine and base therapy choices on available literature supporting the most effective and safe options.

Safety is an issue in many clinicians’ minds, especially when treating geriatric patients with PTSD because of the risk of hypotensive effects with prazosin leading to negative outcomes, such as falls. In Peskind et al’s open-label study of 9 older patients (mean age: 76) with intractable PTSD-associated nightmares treated with prazosin (mean dose: 2.3 mg; increased by 1 mg per week to a maximum dose of 4 mg), 8 patients experienced >50% reduction in nightmares after 8 weeks of treatment, and 1 patient experienced transient orthostasis when starting prazosin that resolved spontaneously with only mild decreases in blood pressure noted otherwise (<20 mm Hg decrease in systolic blood pressure upon standing).³ Although this study was small, it provides evidence that prazosin can be an effective and safe treatment option in geriatric patients and is devoid of the highly sedating side effects of some other treatment options.

Rebecca L. Graham, PharmD
Second-Year Psychiatric Pharmacy Resident
Veterans Affairs San Diego Healthcare System
(VASDHS)

Susan G. Leckband, RPh, BCPP
Clinical Psychiatric Pharmacist Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego

Rene A. Endow-Eyer, PharmD, BCPP
Psychiatric Clinical Pharmacy Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego
San Diego, CA

With all of the discussion about a truly comprehensive and inclusive psychiatry, it was sad to see the emptiness and one-sidedness of Dr. Nasrallah’s June editorial (“Innovative approaches to treatment-resistant depression,” From the Editor, Current Psychiatry, June 2012, p. 4-5; http://bit.ly/1GM92oV). Depression certainly is not a unified diagnosis such as measles or appendicitis. In the face of so-called treatment-resistance, the first step is to review the psychological and biologic formulation of the patient and the reasons for his or her depression. Dr. Nasrallah does not mention the need for a review of all aspects of the patient’s life. The approaches he suggests are dreary, dull, ineffective, and unchanging. It proves that patients are best cared for by psychiatrists who practice biopsychosocial psychiatry and not merely to pay lip service to it.

Arnold Robbins, MD
Private Practice
Cambridge, MA
Clinical Professor of Psychiatry
Boston University School of Medicine
Boston, MA

Dr. Nasrallah responds

I thank Dr. Robbins for his letter. As someone trained by the father of biopsychosocial psychiatry—George Engel, MD, at the University of Rochester—I agree that it is the optimal practice of psychiatry and I practice that approach with all my patients. However, I was describing innovative interventions and paradigm shifts for truly end-of-the-road refractory depression, where all psychosocial and pharmacotherapy treatments have failed and the patient is desperate, disabled, and at high risk for suicide. None of the available interventions work with such individuals and that’s why I regard the innovative breakthroughs I described in my editorial as a promise of hope, thanks to dedicated psychiatric neuroscientists. I hope psychotherapy researchers can achieve breakthroughs for these patients as well.

Henry A. Nasrallah, MD
Editor-in-Chief

Psychotherapy for GAD

I appreciated Dr. Barry’s in-depth review of current diagnostic criteria and therapy for generalized anxiety disorder (GAD) (“Generalized anxiety disorder: Helping patients overcome worry,” Current Psychiatry, May 2012, p. 40-44; http://bit.ly/1oUymyJ). However, I want to point out an error under the “Evidence-based treatments” section labeled “Psychotherapy.” Dr. Barry states that cognitive-behavioral therapy (CBT) is the preferred form of psychotherapy for GAD. In my 40 years of practice, I have found a combination of medication—preferably selective serotonin reuptake inhibitors—and psychodynamic psychotherapy is the most effective treatment for GAD and provides more enduring relief.

Jonathan Shedler, PhD, of the University of Colorado Denver School of Medicine reported on the efficacy of psychodynamic psychotherapy vs behavioral therapy.¹ He compiled the results of meta-analyses of psychotherapy efficacy by 18 investigators covering 792 studies. The findings show a superior result for psychodynamic psychotherapy over behavioral therapy and the effects are more lasting.

Edward L. Parsons, MD
Private Practice
Westfield, NJ

The author responds

I appreciate Dr. Parsons’ comments and his valuable contribution to the dialogue on GAD. Dr. Parsons reemphasizes the importance of psychotherapy in this chronic condition. As demonstrated by the meta-analyses reviewed by Dr. Shedler, there is sufficient evidence in the medical literature to support either psychodynamic psychotherapy or CBT. The specific therapeutic recommendation should consider unique patient variables, such as therapist availability and expertise, the presence of co-occurring conditions or dynamics that would better align with a specific modality, and patient preference and psychological mindedness, to name a few. Regardless, psychotherapy is indicated in the treatment of GAD, and both CBT and psychodynamic psychotherapy are well-supported interventions.

Matthew J. Barry, DO
Lead Psychiatrist
Rochester Veterans Affairs Outpatient Clinic
Canandaigua Veterans Affairs Medical Center
Canandaigua, NY

Caution with prazosin

We welcome the article discussing the use of prazosin and antipsychotics for posttraumatic stress disorder (PTSD)-related nightmares (Graham RL, Leckband SG, Endow-Eyer RA. “PTSD nightmares: Prazosin and atypical antipsychotics,” Current Psychiatry, June 2012, p. 59-62; http://bit.ly/LVAlSo). The favorable outcomes associated with prazosin use combined with its low cost and general tolerability give it considerable potential. Prazosin may be particularly valuable given the unfavorable cardiometabolic risks associated with antipsychotic use, especially because evidence suggests individuals with PTSD have higher rates of cardiovascular disease.¹

We believe the occurrence of adverse cardiovascular effects when starting prazosin requires further attention. As an α1-adrenergic receptor antagonist, it has been linked to orthostatic hypotension and syncope.^2,3 Its cardiovascular effects may be further complicated by concomitant use of other antihypertensive medications. Therefore, we suggest a low initiation dose and gradual titration of prazosin. In individuals who initially were normotensive but then experienced hypotension following prazosin administration, we successfully used short-term sodium chloride tablets, 4 g/d. We discontinued sodium chloride after titration was completed and no postural hypotension was evident.

To minimize polypharmacy, individuals on multiple agents for hypertension may benefit from substituting prazosin for 1 of their regular anti- hypertensives. Despite the mounting evidence supporting prazosin use, it is not indicated for PTSD.

This material is the result of work supported with resources and the use of facilities of the Mental Health and Research and Development Service Lines, Atlanta Veterans Affairs Medical Center, Decatur, GA.

Arshya Vahabzadeh, MD
PGY-2, Resident Psychiatrist
Emory University School of Medicine

Erica Duncan, MD
Attending Psychiatrist
and Associate Professor
Mental Health Service Line
Atlanta Veterans Affairs Medical Center
Decatur, GA
Department of Psychiatry and Behavioral
Sciences
Emory University School of Medicine
Atlanta, GA

The authors respond

We agree with the comments by Drs. Vahabzadeh and Duncan regarding the cardiovascular adverse effects of prazosin. It is important to assess the hemodynamic status of the patient before initiating prazosin therapy, and usually, initiation is attempted only if a patient is normotensive or hypertensive because of potential orthostatic hypotension and syncope, which can occur in up to 4% of patients.¹ As noted by Drs. Vahabzadeh and Duncan, prazosin often is viewed as a dual treatment for both nightmares and blood pressure in individuals who are hypertensive prior to initiation. Prazosin therapy usually is initiated at 1 mg at bedtime and titrated by 1 to 2 mg every 3 to 5 days.² The average dose was approximately 3 mg in studies evaluating prazosin for treating PTSD-associated nightmares (dose range: 1 to 10 mg).² Until the patient is stabilized on a prazosin dose, blood pressure should be monitored daily for inpatients. Outpatients should be educated regarding the signs and symptoms of hypotension, especially dizziness and light-headedness upon standing, along with monitoring blood pressure at his or her next clinic appointment.

Prazosin does not carry an FDA indication for PTSD. Although this is important to consider, the level of evidence in terms of treatment of nightmares also is key. Aurora et al found prazosin was the only medication with a level A rating for treating PTSD-associated nightmares, indicating it as a recommended therapy option.² Because we do not have any medications indicated for PTSD-associated nightmares, it is crucial to practice evidence-based medicine and base therapy choices on available literature supporting the most effective and safe options.

Safety is an issue in many clinicians’ minds, especially when treating geriatric patients with PTSD because of the risk of hypotensive effects with prazosin leading to negative outcomes, such as falls. In Peskind et al’s open-label study of 9 older patients (mean age: 76) with intractable PTSD-associated nightmares treated with prazosin (mean dose: 2.3 mg; increased by 1 mg per week to a maximum dose of 4 mg), 8 patients experienced >50% reduction in nightmares after 8 weeks of treatment, and 1 patient experienced transient orthostasis when starting prazosin that resolved spontaneously with only mild decreases in blood pressure noted otherwise (<20 mm Hg decrease in systolic blood pressure upon standing).³ Although this study was small, it provides evidence that prazosin can be an effective and safe treatment option in geriatric patients and is devoid of the highly sedating side effects of some other treatment options.

Rebecca L. Graham, PharmD
Second-Year Psychiatric Pharmacy Resident
Veterans Affairs San Diego Healthcare System
(VASDHS)

Susan G. Leckband, RPh, BCPP
Clinical Psychiatric Pharmacist Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego

Rene A. Endow-Eyer, PharmD, BCPP
Psychiatric Clinical Pharmacy Specialist
VASDHS
Assistant Clinical Professor
Skaggs School of Pharmacy and
Pharmaceutical Sciences
Department of Psychiatry
University of California, San Diego
San Diego, CA

Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

Nearly 2.5 million persons die each year in the United States.¹ For the bereaved, these deaths may be among the most painful and disruptive events they will experience. In this article, we evaluate the growing body of research on complicated grief (CG)—which also has been called prolonged grief, chronic grief, traumatic grief, and pathological grief—with an emphasis on how to identify CG and distinguish it from other adaptive and maladaptive reactions to the loss of a loved one. In addition, we review empirical evidence on treating CG, including psychotherapy, pharmacotherapy, and combined treatment approaches.

The bereavement-specific syndrome we refer to as CG currently is being reviewed for possible inclusion in DSM-5 as an official diagnosis. At press time, proposals for DSM-5 included a bereavement-related adjustment disorder within the new Trauma- and Stressor-Related Disorders category, as well as a provisional diagnosis of CG entitled Persistent Complex Bereavement-Related Disorder, which, upon acceptance, would be listed in Section III.²

What is ‘normal’ grief?

Grief is highly variable across individuals and time and may range from an absence of distress to severe and persistent pain and anguish. There’s no simple definition of “normal grief.” However, as clinicians, it’s necessary to understand the range of usual reactions. We recommend 2 considerations when evaluating grief reactions.

First, be aware that grief encompasses a range of cognitions, emotions, and behaviors. It may range from a relative lack of painful thoughts and emotions to intense and disruptive sadness, loneliness, anger, guilt, intrusive thoughts, difficulty concentrating, preoccupation with loss, social withdrawal, and a sense of being overwhelmed by the loss and its consequences. In the months after a loss, bereaved individuals may look for the deceased in a crowd, speak to them, or even experience auditory or visual hallucinations of the deceased. Nonetheless, positive feelings such as relief, peace, and happiness also are common following a loss.³ Moreover, laughter and smiling when discussing a lost loved one predicts reductions in grief symptoms over time.⁴ Overall, grief research suggests that, far from proceeding along standard and uniform stages,⁵ grief is complex and comprises a broad spectrum of thoughts, feelings, and behaviors that vary within and among individuals.

Second, note that in the absence of complications, grief progresses. For those who experience elevated levels of distress, the pain and disruption of loss initially may feel overwhelming but will subside in intensity over time for most individuals.⁵ This is not to say that an individual will never again feel sadness or longing for the deceased; elements of grief are likely to remain. Although the trajectory of grief symptoms varies among individuals and may progress in fits and starts, over time grief becomes more intermittent, less interfering, and is balanced with a sense of interest and purpose in life.

What is CG?

As research on grief experiences has grown, there’s increasing recognition that a minority of bereaved individuals experience more extreme grief symptoms that cause substantial, persistent distress and impairment despite the passage of many months or years. Shear et al⁶ proposed a set of CG diagnostic criteria (Table) in which a cluster of symptoms of intense and persistent separation distress are defined as core symptoms. Similar to other psychiatric diagnoses, the symptoms must be associated with significant distress or impairment.

Table

Proposed diagnostic criteria for complicated grief

Assessing CG symptoms

Among those with persistent elevated distress, a CG diagnosis must be considered in the context of the individual’s social and cultural environment, time since the loss, and duration of symptoms. The hallmark symptom of CG is separation distress with a focus of cognitive, behavioral, and emotional symptoms on the loss and its consequences. CG is associated with substantial distress, functional impairment, and an increased risk for suicide. See the Box for a case study.

Many individuals with CG remain undiagnosed and untreated for years despite high levels of distress and impairment and high risk for negative consequences such as suicide.⁷ Accordingly, there’s a need for greater CG screening. Clinically useful tools for assessing CG include a brief, 5-item dimensional screening assessment⁶ and the patient-rated Inventory of Complicated Grief.⁸

Distinguishing complicated and uncomplicated grief. Exhibiting CG symptoms in the first several months after a loss does not mean an individual has or will develop CG. Most bereaved adults report painful thoughts and emotions in the weeks and months following the loss, including distressed yearning, waves of intense grief, persistent and intrusive thoughts, images related to the death, somatic distress, and a feeling of being disconnected from others. For most individuals, the intensity of this response diminishes within 6 to 18 months after the loved one’s death.⁵ Although the optimal length of time to wait before establishing a diagnosis remains debatable, the earliest CG should be diagnosed is 6 months after a loss.

It’s common for grief to occasionally rise in intensity for days or weeks. This surge may occur many months or years after the loss, even in people who exhibited relatively little distress or impairment. In particular, anniversaries, holidays, or periods of stress may trigger increased grief intensity. However, these surges typically subside naturally within a short time. Accordingly, CG should be diagnosed only when symptoms persist for >1 month.

CG vs other post-loss disorders. CG, major depressive disorder (MDD), and posttraumatic stress disorder (PTSD) often are comorbid in bereaved adults. Simon et al⁹ found 72% of CG patients in a treatment- seeking sample reported a lifetime history of MDD and 53% reported a lifetime history of PTSD. However, CG can be distinguished from these disorders. In the same study, 25% of CG patients had no other axis I diagnosis.⁹ After accounting for comorbid disorders, researchers associated CG severity with work and social impairment. These findings provide clear evidence for the incremental validity of CG—ie, a CG diagnosis gives clinicians additional information that predicts impairment above and beyond other disorders. However, future research needs to further examine CG and its overlap and differentiation from MDD and PTSD.

Distinguishing CG and MDD. Intense yearning or preoccupation with the deceased is a common symptom of CG but not MDD. In addition, CG symptoms possess intentionality. For example, emotional distress such as sadness and anger are prominent features of both CG and MDD. However, in CG, these symptoms are specific to the loss or circumstances of the loss, whereas in MDD they generally are more nebulous and generalized. Similarly, CG entails proximity seeking related to the deceased, and avoidance of reminders of the deceased, whereas MDD includes a more general social withdrawal and anhedonia.

Distinguishing CG and PTSD. CG and loss-related PTSD are distinguished by the predominant emotions and focus of concern associated with each disorder. The predominant emotion in PTSD is fear, whereas in CG it is sadness and longing. In PTSD, intrusive thoughts and memories associated with the trauma generally are associated with the event itself and produce an ongoing sense of threat.¹⁰ Avoidance in PTSD is intended to reduce this threat feeling. By contrast, in CG, intrusive memories focus on the deceased or the circumstances of the death, and avoidance is aimed at preventing painful reminders of the loss or its permanence. Importantly, both syndromes may be present.

Box

Treating CG

When is treatment indicated? For years, bereavement theorists emphasized the need to work through emotions and memories related to the deceased with particular focus on negative material. However, evidence suggests that universal application of treatment to all bereaved individuals is unhelpful. In a recent meta-analysis, Neimeyer et al¹¹ found that the outcomes of grief therapy applied indiscriminately to all bereaved adults or all members of high-risk populations—such as parents whose child experienced a violent death—were no better than would be expected by the passage of time. In contrast, grief therapy applied only to those who develop elevated and persistent distress (eg, CG) led to greater and more enduring improvement in post-loss distress than was observed in control conditions.

These results suggest that most grieving individuals who do not meet criteria for CG (or other psychiatric disorders) will not require intervention. Those who do seek treatment for grief-related distress in the acute grief period should be assessed for bereavement-related depression, anxiety, and suicidality, and treated or referred to professional or community-based resources for support or counseling as clinically indicated.

Evidence for psychotherapy. For those who meet CG criteria, psychotherapy targeting the specific symptoms of CG is helpful. The evidence is strongest for CG treatment (CGT), a 16-session, manualized psychotherapy developed by M. Katherine Shear, MD.¹² CGT is based on an attachment model and cognitive-behavioral therapy (CBT) principles, and is informed by the dual-process theory proposed by Stroebe et al.¹³ According to this theory, natural healing following loss comprises 2 processes:

• a loss-oriented process in which the patient comes to terms with the loss, and
• a restoration-oriented process in which the patient reinvigorates a sense of purpose and meaning in life without the deceased.

CGT focuses on both processes. To address the former, it includes clinician-guided exercises in which the patient revisits the time of the death and planned activities in which the patient reengages with people, places, or thoughts that remind him or her of the deceased. CGT aims to allow the patient to gain an increased tolerance of the distressing thoughts and emotions associated with the loss so that these thoughts can be processed and the finality of the death and its circumstances can be accepted.

The restoration process is addressed by having patients generate and discuss personal goals and aspirations for the near and distant future, as well as scheduling pleasurable and rewarding events. This is accomplished by having patients imagine what they would want for themselves if their grief was less intense and planning concrete steps to take toward these goals. The restoration-oriented process is addressed concurrent with the loss-oriented process to encourage the oscillation between processes thought to be characteristic of a natural healing process following the loss of a loved one.

Other psychotherapy approaches (eg, support groups) may have a role for some individuals, and future research may suggest alternative approaches to CGT. To date, CGT is the most targeted evidence-based psychotherapy with randomized controlled data supporting its use in CG.

Pharmacotherapy for CG. Early research suggested that antidepressants—in particular tricyclics—may effectively reduce depressive symptoms in bereavement-related depression; their effect on CG symptoms, however, may not be as strong.¹⁴ Research on pharmacologic treatment that targets CG symptoms is developing. Because of the overlap between CG, PTSD, and MDD, researchers have hypothesized that antidepressants may be effective. Two open-label studies reported that the selective serotonin reuptake inhibitor (SSRI) escitalopram may be effective for CG.^15,16 Although a post-hoc comparison of paroxetine and nortriptyline¹⁷ showed significant reduction in CG and depressive symptoms with both agents, effects could not be separated from concomitant psychotherapy. Furthermore, an examination of naturalistic data on combining antidepressants with CGT suggested that antidepressants may improve outcomes for individuals receiving CGT.¹⁸ A multicenter, randomized controlled trial funded by the National Institute of Mental Health is examining the potential efficacy of citalopram, an SSRI, alone or in combination with CGT.¹⁹

The efficacy of benzodiazepines, which commonly are prescribed for bereaved individuals, has not been assessed in CG. However, recent research suggests they may not be useful for medically managing recent grief²⁰ and that their use in the aftermath of a loss may lead to long-term dependence in geriatric patients.²¹

Related Resources

• Center for Anxiety and Traumatic Stress Disorders. Massachusetts General Hospital. www.bostongrief.com.
• Zisook S, Shear K. Grief and bereavement: what psychiatrists need to know. World Psychiatry. 2009;8(2):67-74.
• Bonanno G. The other side of sadness: what the new science of bereavement tells us about loss. New York, NY: Basic Books; 2009.

Drug Brand Names

• Citalopram • Celexa
• Nortriptyline • Aventyl, Pamelor
• Escitalopram • Lexapro
• Paroxetine • Paxil

Disclosures

Dr. Simon receives grant or research support from the American Cancer Society, the American Foundation for Suicide Prevention, the Department of Defense, Forest Laboratories, and the National Institute of Mental Health.

Although the title of April’s cover story (“Benzodiazepines: A versatile clinical tool,” Current Psychiatry, April 2012, p. 54-63; http://bit.ly/1zkanU3) seems to encourage the use of benzodiazepines, the authors state benzodiazepines are second-or third-line treatments for most conditions, particularly for chronic problems.

As an addiction medicine physician, I see well-intentioned doctors prescribing benzodiazepines to patients with chronic ailments. I would like to emphasize the addictive nature of benzodiazepines. “When used appropriately” is contradictory if benzodiazepines are used daily. Tolerance manifests as an exacerbation of the original symptoms, usually leading to a dosage increase. Every day, I see patients in a state of chronic withdrawal manifested in unpleasant ways because they took benzodiazepines “exactly as prescribed, 3 times per day for 4 years.”

Alprazolam is the bane of an addiction medicine practice because it crosses the blood-brain barrier immediately and is relatively short acting. This is a recipe for almost certain addiction, and there are better medications. I regularly transition patients from addictive substances, including benzodiazepines, and no matter what condition I am treating—panic attacks, obsessive-compulsive disorder, depression, generalized anxiety, social anxiety, posttraumatic stress disorder, or situational anxiety—I can almost always control the patient’s symptoms using non-addictive medications.

If benzodiazepines are used for almost anything other than a short-lived condition, we are doing a tremendous disservice to our patients and exhibiting the “just give them a pill and get to the next patient” mentality we are accused of.

Terrance Reeves, MD, ABAM
Medical Director
South Walton Medical Center
Miramar Beach, FL

The authors respond

We thank Dr. Reeves for his comments and reminders of the downside to routine and long-term prescribing of benzodiazepines. As an addiction specialist, he is well positioned to see patients who are struggling with syndromes related to benzodiazepine abuse. We stand by our review of the evidence-based studies of the appropriateness of judicious benzodiazepine use in various psychiatric syndromes. The section of our article labeled “Risks of benzodiazepine use” addresses Dr. Reeves’ concerns.

Jolene R. Bostwick, PharmD, BCPS, BCPP
Clinical Assistant Professor of Pharmacy
University of Michigan College of Pharmacy
Clinical Pharmacist

Michael I. Casher, MD
Clinical Assistant Professor
Department of Psychiatry
University of Michigan Medical School
Director of Inpatient Adult Psychiatry

Shinji Yasugi, MDFirst-Year Psychiatry ResidentUniversity of Michigan Health SystemAnn Arbor, MI

Although the title of April’s cover story (“Benzodiazepines: A versatile clinical tool,” Current Psychiatry, April 2012, p. 54-63; http://bit.ly/1zkanU3) seems to encourage the use of benzodiazepines, the authors state benzodiazepines are second-or third-line treatments for most conditions, particularly for chronic problems.

As an addiction medicine physician, I see well-intentioned doctors prescribing benzodiazepines to patients with chronic ailments. I would like to emphasize the addictive nature of benzodiazepines. “When used appropriately” is contradictory if benzodiazepines are used daily. Tolerance manifests as an exacerbation of the original symptoms, usually leading to a dosage increase. Every day, I see patients in a state of chronic withdrawal manifested in unpleasant ways because they took benzodiazepines “exactly as prescribed, 3 times per day for 4 years.”

Alprazolam is the bane of an addiction medicine practice because it crosses the blood-brain barrier immediately and is relatively short acting. This is a recipe for almost certain addiction, and there are better medications. I regularly transition patients from addictive substances, including benzodiazepines, and no matter what condition I am treating—panic attacks, obsessive-compulsive disorder, depression, generalized anxiety, social anxiety, posttraumatic stress disorder, or situational anxiety—I can almost always control the patient’s symptoms using non-addictive medications.

If benzodiazepines are used for almost anything other than a short-lived condition, we are doing a tremendous disservice to our patients and exhibiting the “just give them a pill and get to the next patient” mentality we are accused of.

Terrance Reeves, MD, ABAM
Medical Director
South Walton Medical Center
Miramar Beach, FL

The authors respond

We thank Dr. Reeves for his comments and reminders of the downside to routine and long-term prescribing of benzodiazepines. As an addiction specialist, he is well positioned to see patients who are struggling with syndromes related to benzodiazepine abuse. We stand by our review of the evidence-based studies of the appropriateness of judicious benzodiazepine use in various psychiatric syndromes. The section of our article labeled “Risks of benzodiazepine use” addresses Dr. Reeves’ concerns.

Jolene R. Bostwick, PharmD, BCPS, BCPP
Clinical Assistant Professor of Pharmacy
University of Michigan College of Pharmacy
Clinical Pharmacist

Michael I. Casher, MD
Clinical Assistant Professor
Department of Psychiatry
University of Michigan Medical School
Director of Inpatient Adult Psychiatry

Shinji Yasugi, MDFirst-Year Psychiatry ResidentUniversity of Michigan Health SystemAnn Arbor, MI

Although the title of April’s cover story (“Benzodiazepines: A versatile clinical tool,” Current Psychiatry, April 2012, p. 54-63; http://bit.ly/1zkanU3) seems to encourage the use of benzodiazepines, the authors state benzodiazepines are second-or third-line treatments for most conditions, particularly for chronic problems.

As an addiction medicine physician, I see well-intentioned doctors prescribing benzodiazepines to patients with chronic ailments. I would like to emphasize the addictive nature of benzodiazepines. “When used appropriately” is contradictory if benzodiazepines are used daily. Tolerance manifests as an exacerbation of the original symptoms, usually leading to a dosage increase. Every day, I see patients in a state of chronic withdrawal manifested in unpleasant ways because they took benzodiazepines “exactly as prescribed, 3 times per day for 4 years.”

Alprazolam is the bane of an addiction medicine practice because it crosses the blood-brain barrier immediately and is relatively short acting. This is a recipe for almost certain addiction, and there are better medications. I regularly transition patients from addictive substances, including benzodiazepines, and no matter what condition I am treating—panic attacks, obsessive-compulsive disorder, depression, generalized anxiety, social anxiety, posttraumatic stress disorder, or situational anxiety—I can almost always control the patient’s symptoms using non-addictive medications.

If benzodiazepines are used for almost anything other than a short-lived condition, we are doing a tremendous disservice to our patients and exhibiting the “just give them a pill and get to the next patient” mentality we are accused of.

Terrance Reeves, MD, ABAM
Medical Director
South Walton Medical Center
Miramar Beach, FL

The authors respond

We thank Dr. Reeves for his comments and reminders of the downside to routine and long-term prescribing of benzodiazepines. As an addiction specialist, he is well positioned to see patients who are struggling with syndromes related to benzodiazepine abuse. We stand by our review of the evidence-based studies of the appropriateness of judicious benzodiazepine use in various psychiatric syndromes. The section of our article labeled “Risks of benzodiazepine use” addresses Dr. Reeves’ concerns.

Jolene R. Bostwick, PharmD, BCPS, BCPP
Clinical Assistant Professor of Pharmacy
University of Michigan College of Pharmacy
Clinical Pharmacist

Michael I. Casher, MD
Clinical Assistant Professor
Department of Psychiatry
University of Michigan Medical School
Director of Inpatient Adult Psychiatry

Shinji Yasugi, MDFirst-Year Psychiatry ResidentUniversity of Michigan Health SystemAnn Arbor, MI

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Suck it up. Tough it out. There is no “I” in team. These are a few of the messages athletes receive from coaches, teammates, and fans. There are norms, values, and expectations in every culture, including sports, that affect behavior and emotional expression. When taking a patient’s history, clinicians may ask about participation in sports because it provides health and lifestyle information. However, many clinicians fail to consider the extent to which sport participation can influence a person’s explanatory style, experience of injury, and attitude toward medications. Whether your patient is an elite athlete or someone who participates in sports solely for exercise, the extent to which he or she identifies as an athlete is worth exploring.

Research on athletes has focused on physical aspects of injury, but this may be just a small component of an athlete’s devastation after serious injury. In this article, we discuss athletes’:

• psychiatric risks after injury
• expression of pain
• risks of having an identity driven solely by sports
• distress tolerance.

We also provide tips for making a differential diagnosis and providing treatment. This information is based on our experience treating athletes, supplemented by relevant literature.

Psychiatric risks after injury

Research has explored eating disorders and substance use among athletes, but clinicians generally are less aware of the prevalence of mood and anxiety disorders in this population. Although participating in sports can protect against emotional distress, athletes who sustain an injury are at risk for major depressive disorder, posttraumatic stress disorder (PTSD), or an adjustment disorder.¹ Only about 10% of injured athletes have severe, long-term psychological consequences,² but the prevalence of anger and depression after an injury is well documented.^3,4 Researchers have found that injured athletes experience clinically significant depression 6 times as often as non-injured athletes.⁵ Injured athletes also exhibit significantly greater anxiety and lower self-esteem than non-injured controls immediately after injury and at 2-month follow-up; those with more severe injuries are more likely to become depressed.⁶ Non-injured athletes seem to experience depression at the same rate as the general population.⁷

Injury and expression of pain

Psychiatric illnesses often are underreported and undertreated in athletes.⁸ This may be because athletes feel that admitting they have a psychiatric illness or symptoms could threaten their status with their team. One professional figure skater we treated failed to seek recommended treatment for a psychiatric disorder because she feared she would be asked to leave her skating company. Her symptoms dangerously escalated before she was hospitalized.

Based on our clinical experience, many athletes feel acute pressure to play through psychological and physical pain. Some athletes continue to play with an injury to hold on to a paycheck or scholarship. Some continue to play even though they no longer enjoy the sport to prevent letting down parents or coaches; others know no other way but to “tough it out.” Supporters such as coaches, parents, or teammates may encourage athletes to play with injury, and sometimes provide medication to do so.

Mostly, however, the pressure to continue to play despite injury comes from athletes themselves. The culture of sport may lead athletes to minimize pain, fear, and self doubt.⁹ Athletes who fuse the culture of sport with their own being may underreport physical and psychiatric symptoms. In a survey of National Collegiate Athletic Association Division I athletes, Nixon⁹ found that 70% of respondents reported having been injured at least once, and more than one-half felt pressure to play while injured. Feeling pressure to perform with injury was affected by “starter” status, and whites and men scored highest on pressure scales, although women showed a roughly equal probability of playing through injury. Students who received an athletic scholarship experienced more injuries that required surgery. There was no difference in pain expression between players of contact and non-contact sports. Finally, athletes may be less likely to seek pharmacologic treatments because of cultural messages that emphasize ideas such as “the body is a temple.”

Loss of identity

An athlete’s injury should be analyzed for meaning; what may seem insignificant to one person may be quite different for another. When injury makes athletic activity impossible, an athlete may suffer more distress than someone who does not exercise regularly. Understanding the significance of the experience for an athlete is crucial to achieving recovery.¹⁰ For example, to a non-athlete a fractured wrist may be an annoyance, but it may be disastrous to a collegiate pitcher who is forced to be inactive when scouts for Major League Baseball teams search for prospects.

To an athlete, injury can mean loss of identity. Whereas most people become competent in many aspects of life, and develop support systems across multiple contexts, an athlete—particularly an extraordinarily talented one—may have focused only on his or her sport. Although athletics can help young people develop confidence, participation also can be a trap. Individuals with strong athletic identities are less likely to explore other career, educational, and lifestyle options.¹¹ In the context of team sports, an athlete may feel less emotionally supported if an injury results in the loss of his or her central role with the team. Helping athletes form an identity that is not based solely on sports is ideal because subsequent injuries could lead to recurrent struggles with loss of identity.

Athletes who achieve higher levels of success have higher levels of depression and higher suicidal ideation after injury.¹² An athlete may attempt or complete suicide, particularly those who are injured (Box).^13-16

Student athletes. When working with student athletes, it is crucial to understand the lifestyle that promotes forming a single-factor identity. Student athletes may be required to train 2 or 3 times a day, rarely spend their school breaks in tropical locations, often miss social events, and may forgo commencement ceremonies. When an injury suddenly makes these perpetual sacrifices seem to be in vain, the risk of psychiatric illness may increase.

Box

Tolerating distress

Athletes often use their sport as an outlet for emotional expression. When an injury removes that outlet, an athlete may develop anxiety and disappointment. Left alone to manage these emotions, an athlete may become irritable, passive, socially isolated, depressed, or suicidal.¹⁷ Trying but failing to find socially acceptable ways to express these feelings may intensify depression or anger. Difficult life issues, such as avoided losses, relationship issues, or various insecurities, may come to the surface when an athlete’s primary coping skill is lost. In addition, without the support of the athletic “family” (eg, teammates, coaches, staff) many athletes turn to alcohol or drugs unless they have alternate coping strategies and social supports.¹⁸

Overtraining and stress

The differential diagnosis for athletes who present with psychiatric symptoms includes several mood and anxiety disorders and other conditions (Table). When evaluating athletes who have depressive symptoms, it is essential to rule out overtraining syndrome (OTS). A common phenomenon among athletes, OTS is characterized by athletic “staleness” and chronic fatigue.¹⁹ Although there are no official OTS diagnostic criteria, characteristic symptoms include decreased physical performance or stamina, fatigue, insomnia, change in appetite, irritability, restlessness, excitability, anxiety, weight loss, loss of motivation, and poor concentration.¹⁹ The primary distinction between OTS and depression is that OTS results from athletic endeavors and can be reversed by reducing activity.

Experiencing an injury—or even a near-miss—can be terrifying to a person who derives his or her identity from a fully functioning body and feels that a perfectly working body is essential to an acceptable life. Such athletes may develop acute stress disorder or PTSD.^20,21 We treated a hockey player who just missed being involved in a serious incident on the ice. “I watched my whole athletic career up to that point flash before my eyes.… I keep getting flashes of that,” he said. After the incident, he experienced hypervigilance, avoidance, and anxiety—both on and off the ice—and was diagnosed with acute stress disorder. Similarly, we cared for a young running back whose physical symptoms had abated after experiencing a concussion. He developed an irrational fear that he would become injured again. Neither athlete had a history of psychiatric illness or serious injury, and both were paralyzed by the idea of returning to play. One of these athletes successfully engaged in exposure therapy, and the other experienced severe avoidance, hopelessness, depression, nightmares, and flashbacks before seeking treatment.

Table

Differential diagnosis of conditions associated with athletic injury

Substance use: Common and risky

Anecdotal and clinical evidence suggests that athletes in different sports engage in different substance abuse patterns. Studies show that college athletes use alcohol at higher rates than non-athletes.^22,23 In 2000, the American College of Sports Medicine reported that athletes’ abuse of recreational drugs far surpasses their abuse of performance-enhancing drugs.²⁴ Some athletes may use prescription pain medications recreationally or to self-medicate emotional pain as a result of injury. Athletes may not understand the risks of recreational use of prescription medications or illicit substances—such as cocaine’s deleterious cardiovascular effects—and may hesitate to discuss their self-medicating with physicians.

Some athletes abuse performance-enhancing drugs, such as anabolic steroids, androstenedione, stimulants, diuretics, and creatine.²⁵ Side effects of these substances include liver disease, brain hemorrhage, weight loss, and depression.²⁵

Our recommendations

Working with athletes—particularly injured athletes who have internalized sports culture—requires informed clinical effort, whether your patient is a student athlete, elite athlete, leisure athlete, or former athlete. Successful diagnosis and treatment requires understanding the meaning of athletics in your patient’s life and the extent to which he or she has “back-up” stress relievers and support systems, and assessing for cognitive dysfunction that may contribute to mood or anxiety symptoms. During evaluation, take a careful history to distinguish major depression or adjustment disorders from OTS, and assess for PTSD symptoms. When treating an injured athlete, help the patient determine whether he or she can find another outlet—preferably more than one—to replace athletics.

For an athlete who has depressive symptoms, we recommend determining whether the patient’s symptoms remit after a brief period of rest before initiating pharmacotherapy. For patients who exhibit minimal neurovegetative features, we recommend psychotherapy as a first-line treatment. Many athletes are reluctant to take medication and would be more likely to follow through with cognitive-behavioral and biofeedback interventions.

If a patient requires pharmacotherapy, ask about his or her feelings toward medications that may impact adherence. For example, is a gymnast worried about weight gain? Is a sprinter concerned with lethargy? When prescribing, be aware of the prevalence of drug and alcohol problems among athletes, understand how habits and temptations differ among sports cultures, and provide patients with psychoeducation about substance abuse when appropriate.

Related Resources

• International Society for Sports Psychiatry. http://sportspsychiatry.org.
• Sabo D, Miller KE, Melnick MJ, et al. High school athletic participation and adolescent suicide: a nationwide U.S. study. Int Rev Sociol Sport. 2005;40(1):5-23. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563797. Accessed June 7, 2012.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Suck it up. Tough it out. There is no “I” in team. These are a few of the messages athletes receive from coaches, teammates, and fans. There are norms, values, and expectations in every culture, including sports, that affect behavior and emotional expression. When taking a patient’s history, clinicians may ask about participation in sports because it provides health and lifestyle information. However, many clinicians fail to consider the extent to which sport participation can influence a person’s explanatory style, experience of injury, and attitude toward medications. Whether your patient is an elite athlete or someone who participates in sports solely for exercise, the extent to which he or she identifies as an athlete is worth exploring.

Research on athletes has focused on physical aspects of injury, but this may be just a small component of an athlete’s devastation after serious injury. In this article, we discuss athletes’:

• psychiatric risks after injury
• expression of pain
• risks of having an identity driven solely by sports
• distress tolerance.

We also provide tips for making a differential diagnosis and providing treatment. This information is based on our experience treating athletes, supplemented by relevant literature.

Psychiatric risks after injury

Research has explored eating disorders and substance use among athletes, but clinicians generally are less aware of the prevalence of mood and anxiety disorders in this population. Although participating in sports can protect against emotional distress, athletes who sustain an injury are at risk for major depressive disorder, posttraumatic stress disorder (PTSD), or an adjustment disorder.¹ Only about 10% of injured athletes have severe, long-term psychological consequences,² but the prevalence of anger and depression after an injury is well documented.^3,4 Researchers have found that injured athletes experience clinically significant depression 6 times as often as non-injured athletes.⁵ Injured athletes also exhibit significantly greater anxiety and lower self-esteem than non-injured controls immediately after injury and at 2-month follow-up; those with more severe injuries are more likely to become depressed.⁶ Non-injured athletes seem to experience depression at the same rate as the general population.⁷

Injury and expression of pain

Psychiatric illnesses often are underreported and undertreated in athletes.⁸ This may be because athletes feel that admitting they have a psychiatric illness or symptoms could threaten their status with their team. One professional figure skater we treated failed to seek recommended treatment for a psychiatric disorder because she feared she would be asked to leave her skating company. Her symptoms dangerously escalated before she was hospitalized.

Based on our clinical experience, many athletes feel acute pressure to play through psychological and physical pain. Some athletes continue to play with an injury to hold on to a paycheck or scholarship. Some continue to play even though they no longer enjoy the sport to prevent letting down parents or coaches; others know no other way but to “tough it out.” Supporters such as coaches, parents, or teammates may encourage athletes to play with injury, and sometimes provide medication to do so.

Mostly, however, the pressure to continue to play despite injury comes from athletes themselves. The culture of sport may lead athletes to minimize pain, fear, and self doubt.⁹ Athletes who fuse the culture of sport with their own being may underreport physical and psychiatric symptoms. In a survey of National Collegiate Athletic Association Division I athletes, Nixon⁹ found that 70% of respondents reported having been injured at least once, and more than one-half felt pressure to play while injured. Feeling pressure to perform with injury was affected by “starter” status, and whites and men scored highest on pressure scales, although women showed a roughly equal probability of playing through injury. Students who received an athletic scholarship experienced more injuries that required surgery. There was no difference in pain expression between players of contact and non-contact sports. Finally, athletes may be less likely to seek pharmacologic treatments because of cultural messages that emphasize ideas such as “the body is a temple.”

Loss of identity

An athlete’s injury should be analyzed for meaning; what may seem insignificant to one person may be quite different for another. When injury makes athletic activity impossible, an athlete may suffer more distress than someone who does not exercise regularly. Understanding the significance of the experience for an athlete is crucial to achieving recovery.¹⁰ For example, to a non-athlete a fractured wrist may be an annoyance, but it may be disastrous to a collegiate pitcher who is forced to be inactive when scouts for Major League Baseball teams search for prospects.

To an athlete, injury can mean loss of identity. Whereas most people become competent in many aspects of life, and develop support systems across multiple contexts, an athlete—particularly an extraordinarily talented one—may have focused only on his or her sport. Although athletics can help young people develop confidence, participation also can be a trap. Individuals with strong athletic identities are less likely to explore other career, educational, and lifestyle options.¹¹ In the context of team sports, an athlete may feel less emotionally supported if an injury results in the loss of his or her central role with the team. Helping athletes form an identity that is not based solely on sports is ideal because subsequent injuries could lead to recurrent struggles with loss of identity.

Athletes who achieve higher levels of success have higher levels of depression and higher suicidal ideation after injury.¹² An athlete may attempt or complete suicide, particularly those who are injured (Box).^13-16

Student athletes. When working with student athletes, it is crucial to understand the lifestyle that promotes forming a single-factor identity. Student athletes may be required to train 2 or 3 times a day, rarely spend their school breaks in tropical locations, often miss social events, and may forgo commencement ceremonies. When an injury suddenly makes these perpetual sacrifices seem to be in vain, the risk of psychiatric illness may increase.

Box

Tolerating distress

Athletes often use their sport as an outlet for emotional expression. When an injury removes that outlet, an athlete may develop anxiety and disappointment. Left alone to manage these emotions, an athlete may become irritable, passive, socially isolated, depressed, or suicidal.¹⁷ Trying but failing to find socially acceptable ways to express these feelings may intensify depression or anger. Difficult life issues, such as avoided losses, relationship issues, or various insecurities, may come to the surface when an athlete’s primary coping skill is lost. In addition, without the support of the athletic “family” (eg, teammates, coaches, staff) many athletes turn to alcohol or drugs unless they have alternate coping strategies and social supports.¹⁸

Overtraining and stress

The differential diagnosis for athletes who present with psychiatric symptoms includes several mood and anxiety disorders and other conditions (Table). When evaluating athletes who have depressive symptoms, it is essential to rule out overtraining syndrome (OTS). A common phenomenon among athletes, OTS is characterized by athletic “staleness” and chronic fatigue.¹⁹ Although there are no official OTS diagnostic criteria, characteristic symptoms include decreased physical performance or stamina, fatigue, insomnia, change in appetite, irritability, restlessness, excitability, anxiety, weight loss, loss of motivation, and poor concentration.¹⁹ The primary distinction between OTS and depression is that OTS results from athletic endeavors and can be reversed by reducing activity.

Experiencing an injury—or even a near-miss—can be terrifying to a person who derives his or her identity from a fully functioning body and feels that a perfectly working body is essential to an acceptable life. Such athletes may develop acute stress disorder or PTSD.^20,21 We treated a hockey player who just missed being involved in a serious incident on the ice. “I watched my whole athletic career up to that point flash before my eyes.… I keep getting flashes of that,” he said. After the incident, he experienced hypervigilance, avoidance, and anxiety—both on and off the ice—and was diagnosed with acute stress disorder. Similarly, we cared for a young running back whose physical symptoms had abated after experiencing a concussion. He developed an irrational fear that he would become injured again. Neither athlete had a history of psychiatric illness or serious injury, and both were paralyzed by the idea of returning to play. One of these athletes successfully engaged in exposure therapy, and the other experienced severe avoidance, hopelessness, depression, nightmares, and flashbacks before seeking treatment.

Table

Differential diagnosis of conditions associated with athletic injury

Substance use: Common and risky

Anecdotal and clinical evidence suggests that athletes in different sports engage in different substance abuse patterns. Studies show that college athletes use alcohol at higher rates than non-athletes.^22,23 In 2000, the American College of Sports Medicine reported that athletes’ abuse of recreational drugs far surpasses their abuse of performance-enhancing drugs.²⁴ Some athletes may use prescription pain medications recreationally or to self-medicate emotional pain as a result of injury. Athletes may not understand the risks of recreational use of prescription medications or illicit substances—such as cocaine’s deleterious cardiovascular effects—and may hesitate to discuss their self-medicating with physicians.

Some athletes abuse performance-enhancing drugs, such as anabolic steroids, androstenedione, stimulants, diuretics, and creatine.²⁵ Side effects of these substances include liver disease, brain hemorrhage, weight loss, and depression.²⁵

Our recommendations

Working with athletes—particularly injured athletes who have internalized sports culture—requires informed clinical effort, whether your patient is a student athlete, elite athlete, leisure athlete, or former athlete. Successful diagnosis and treatment requires understanding the meaning of athletics in your patient’s life and the extent to which he or she has “back-up” stress relievers and support systems, and assessing for cognitive dysfunction that may contribute to mood or anxiety symptoms. During evaluation, take a careful history to distinguish major depression or adjustment disorders from OTS, and assess for PTSD symptoms. When treating an injured athlete, help the patient determine whether he or she can find another outlet—preferably more than one—to replace athletics.

For an athlete who has depressive symptoms, we recommend determining whether the patient’s symptoms remit after a brief period of rest before initiating pharmacotherapy. For patients who exhibit minimal neurovegetative features, we recommend psychotherapy as a first-line treatment. Many athletes are reluctant to take medication and would be more likely to follow through with cognitive-behavioral and biofeedback interventions.

If a patient requires pharmacotherapy, ask about his or her feelings toward medications that may impact adherence. For example, is a gymnast worried about weight gain? Is a sprinter concerned with lethargy? When prescribing, be aware of the prevalence of drug and alcohol problems among athletes, understand how habits and temptations differ among sports cultures, and provide patients with psychoeducation about substance abuse when appropriate.

Related Resources

• International Society for Sports Psychiatry. http://sportspsychiatry.org.
• Sabo D, Miller KE, Melnick MJ, et al. High school athletic participation and adolescent suicide: a nationwide U.S. study. Int Rev Sociol Sport. 2005;40(1):5-23. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563797. Accessed June 7, 2012.

Disclosure

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

Discuss this article at www.facebook.com/CurrentPsychiatry

Suck it up. Tough it out. There is no “I” in team. These are a few of the messages athletes receive from coaches, teammates, and fans. There are norms, values, and expectations in every culture, including sports, that affect behavior and emotional expression. When taking a patient’s history, clinicians may ask about participation in sports because it provides health and lifestyle information. However, many clinicians fail to consider the extent to which sport participation can influence a person’s explanatory style, experience of injury, and attitude toward medications. Whether your patient is an elite athlete or someone who participates in sports solely for exercise, the extent to which he or she identifies as an athlete is worth exploring.

Research on athletes has focused on physical aspects of injury, but this may be just a small component of an athlete’s devastation after serious injury. In this article, we discuss athletes’:

• psychiatric risks after injury
• expression of pain
• risks of having an identity driven solely by sports
• distress tolerance.

We also provide tips for making a differential diagnosis and providing treatment. This information is based on our experience treating athletes, supplemented by relevant literature.

Psychiatric risks after injury

Research has explored eating disorders and substance use among athletes, but clinicians generally are less aware of the prevalence of mood and anxiety disorders in this population. Although participating in sports can protect against emotional distress, athletes who sustain an injury are at risk for major depressive disorder, posttraumatic stress disorder (PTSD), or an adjustment disorder.¹ Only about 10% of injured athletes have severe, long-term psychological consequences,² but the prevalence of anger and depression after an injury is well documented.^3,4 Researchers have found that injured athletes experience clinically significant depression 6 times as often as non-injured athletes.⁵ Injured athletes also exhibit significantly greater anxiety and lower self-esteem than non-injured controls immediately after injury and at 2-month follow-up; those with more severe injuries are more likely to become depressed.⁶ Non-injured athletes seem to experience depression at the same rate as the general population.⁷

Injury and expression of pain

Psychiatric illnesses often are underreported and undertreated in athletes.⁸ This may be because athletes feel that admitting they have a psychiatric illness or symptoms could threaten their status with their team. One professional figure skater we treated failed to seek recommended treatment for a psychiatric disorder because she feared she would be asked to leave her skating company. Her symptoms dangerously escalated before she was hospitalized.

Based on our clinical experience, many athletes feel acute pressure to play through psychological and physical pain. Some athletes continue to play with an injury to hold on to a paycheck or scholarship. Some continue to play even though they no longer enjoy the sport to prevent letting down parents or coaches; others know no other way but to “tough it out.” Supporters such as coaches, parents, or teammates may encourage athletes to play with injury, and sometimes provide medication to do so.

Mostly, however, the pressure to continue to play despite injury comes from athletes themselves. The culture of sport may lead athletes to minimize pain, fear, and self doubt.⁹ Athletes who fuse the culture of sport with their own being may underreport physical and psychiatric symptoms. In a survey of National Collegiate Athletic Association Division I athletes, Nixon⁹ found that 70% of respondents reported having been injured at least once, and more than one-half felt pressure to play while injured. Feeling pressure to perform with injury was affected by “starter” status, and whites and men scored highest on pressure scales, although women showed a roughly equal probability of playing through injury. Students who received an athletic scholarship experienced more injuries that required surgery. There was no difference in pain expression between players of contact and non-contact sports. Finally, athletes may be less likely to seek pharmacologic treatments because of cultural messages that emphasize ideas such as “the body is a temple.”

Loss of identity

An athlete’s injury should be analyzed for meaning; what may seem insignificant to one person may be quite different for another. When injury makes athletic activity impossible, an athlete may suffer more distress than someone who does not exercise regularly. Understanding the significance of the experience for an athlete is crucial to achieving recovery.¹⁰ For example, to a non-athlete a fractured wrist may be an annoyance, but it may be disastrous to a collegiate pitcher who is forced to be inactive when scouts for Major League Baseball teams search for prospects.

To an athlete, injury can mean loss of identity. Whereas most people become competent in many aspects of life, and develop support systems across multiple contexts, an athlete—particularly an extraordinarily talented one—may have focused only on his or her sport. Although athletics can help young people develop confidence, participation also can be a trap. Individuals with strong athletic identities are less likely to explore other career, educational, and lifestyle options.¹¹ In the context of team sports, an athlete may feel less emotionally supported if an injury results in the loss of his or her central role with the team. Helping athletes form an identity that is not based solely on sports is ideal because subsequent injuries could lead to recurrent struggles with loss of identity.

Athletes who achieve higher levels of success have higher levels of depression and higher suicidal ideation after injury.¹² An athlete may attempt or complete suicide, particularly those who are injured (Box).^13-16

Student athletes. When working with student athletes, it is crucial to understand the lifestyle that promotes forming a single-factor identity. Student athletes may be required to train 2 or 3 times a day, rarely spend their school breaks in tropical locations, often miss social events, and may forgo commencement ceremonies. When an injury suddenly makes these perpetual sacrifices seem to be in vain, the risk of psychiatric illness may increase.

Box

Tolerating distress

Athletes often use their sport as an outlet for emotional expression. When an injury removes that outlet, an athlete may develop anxiety and disappointment. Left alone to manage these emotions, an athlete may become irritable, passive, socially isolated, depressed, or suicidal.¹⁷ Trying but failing to find socially acceptable ways to express these feelings may intensify depression or anger. Difficult life issues, such as avoided losses, relationship issues, or various insecurities, may come to the surface when an athlete’s primary coping skill is lost. In addition, without the support of the athletic “family” (eg, teammates, coaches, staff) many athletes turn to alcohol or drugs unless they have alternate coping strategies and social supports.¹⁸

Overtraining and stress

The differential diagnosis for athletes who present with psychiatric symptoms includes several mood and anxiety disorders and other conditions (Table). When evaluating athletes who have depressive symptoms, it is essential to rule out overtraining syndrome (OTS). A common phenomenon among athletes, OTS is characterized by athletic “staleness” and chronic fatigue.¹⁹ Although there are no official OTS diagnostic criteria, characteristic symptoms include decreased physical performance or stamina, fatigue, insomnia, change in appetite, irritability, restlessness, excitability, anxiety, weight loss, loss of motivation, and poor concentration.¹⁹ The primary distinction between OTS and depression is that OTS results from athletic endeavors and can be reversed by reducing activity.

Experiencing an injury—or even a near-miss—can be terrifying to a person who derives his or her identity from a fully functioning body and feels that a perfectly working body is essential to an acceptable life. Such athletes may develop acute stress disorder or PTSD.^20,21 We treated a hockey player who just missed being involved in a serious incident on the ice. “I watched my whole athletic career up to that point flash before my eyes.… I keep getting flashes of that,” he said. After the incident, he experienced hypervigilance, avoidance, and anxiety—both on and off the ice—and was diagnosed with acute stress disorder. Similarly, we cared for a young running back whose physical symptoms had abated after experiencing a concussion. He developed an irrational fear that he would become injured again. Neither athlete had a history of psychiatric illness or serious injury, and both were paralyzed by the idea of returning to play. One of these athletes successfully engaged in exposure therapy, and the other experienced severe avoidance, hopelessness, depression, nightmares, and flashbacks before seeking treatment.

Table

Differential diagnosis of conditions associated with athletic injury

Substance use: Common and risky

Anecdotal and clinical evidence suggests that athletes in different sports engage in different substance abuse patterns. Studies show that college athletes use alcohol at higher rates than non-athletes.^22,23 In 2000, the American College of Sports Medicine reported that athletes’ abuse of recreational drugs far surpasses their abuse of performance-enhancing drugs.²⁴ Some athletes may use prescription pain medications recreationally or to self-medicate emotional pain as a result of injury. Athletes may not understand the risks of recreational use of prescription medications or illicit substances—such as cocaine’s deleterious cardiovascular effects—and may hesitate to discuss their self-medicating with physicians.

Some athletes abuse performance-enhancing drugs, such as anabolic steroids, androstenedione, stimulants, diuretics, and creatine.²⁵ Side effects of these substances include liver disease, brain hemorrhage, weight loss, and depression.²⁵

Our recommendations

Working with athletes—particularly injured athletes who have internalized sports culture—requires informed clinical effort, whether your patient is a student athlete, elite athlete, leisure athlete, or former athlete. Successful diagnosis and treatment requires understanding the meaning of athletics in your patient’s life and the extent to which he or she has “back-up” stress relievers and support systems, and assessing for cognitive dysfunction that may contribute to mood or anxiety symptoms. During evaluation, take a careful history to distinguish major depression or adjustment disorders from OTS, and assess for PTSD symptoms. When treating an injured athlete, help the patient determine whether he or she can find another outlet—preferably more than one—to replace athletics.

For an athlete who has depressive symptoms, we recommend determining whether the patient’s symptoms remit after a brief period of rest before initiating pharmacotherapy. For patients who exhibit minimal neurovegetative features, we recommend psychotherapy as a first-line treatment. Many athletes are reluctant to take medication and would be more likely to follow through with cognitive-behavioral and biofeedback interventions.

If a patient requires pharmacotherapy, ask about his or her feelings toward medications that may impact adherence. For example, is a gymnast worried about weight gain? Is a sprinter concerned with lethargy? When prescribing, be aware of the prevalence of drug and alcohol problems among athletes, understand how habits and temptations differ among sports cultures, and provide patients with psychoeducation about substance abuse when appropriate.

Related Resources

• International Society for Sports Psychiatry. http://sportspsychiatry.org.
• Sabo D, Miller KE, Melnick MJ, et al. High school athletic participation and adolescent suicide: a nationwide U.S. study. Int Rev Sociol Sport. 2005;40(1):5-23. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563797. Accessed June 7, 2012.

Disclosure

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

Mr. S, a 45-year-old veteran, was diagnosed with posttraumatic stress disorder (PTSD) 18 years ago after a tour of duty in the Persian Gulf. He had combat-related flashbacks triggered by the smell of gasoline or smoke from a fire, was easily startled, and began to isolate himself socially. However, his symptoms improved when he started volunteering at his local Veterans Affairs Medical Center. After he lost his job 3 years ago, Mr. S started experiencing flashbacks. He was irritable, easily startled, and avoided things that reminded him of his time in the Persian Gulf. His psychiatrist prescribed sertraline, titrated to 200 mg/d. The drug reduced the severity of his avoidance and hyperarousal symptoms and improved his mood.

During a clinic visit, Mr. S says he is doing well and can fall asleep at night but is having recurring nightmares about traumatic events that occurred during combat. These nightmares wake him up and have become more frequent, occurring once per night for the past month. Mr. S says he has been watching more news programs about conflicts in Afghanistan and Iraq since the nightmares began. His psychiatrist starts quetiapine, 50 mg at bedtime for 7 nights then 100 mg at bedtime, but after 6 weeks Mr. S says his nightmares continue.

PTSD occurs in approximately 19% of Vietnam war combat veterans¹ and 14% of service members returning from Iraq and Afghanistan.² PTSD symptoms are classified into clusters: intrusive/re-experiencing; avoidant/numbing; and hyperarousal.³ Nightmares are part of the intrusive/re-experiencing cluster, which is Criterion B in DSM-IV-TR. See Table 1 for a description of DSM-IV-TR PTSD criteria. Among PTSD patients, 50% to 70% report PTSD-associated nightmares.⁴ Despite adequate treatment targeted to improve PTSD’s core symptoms, symptoms such as sleep disturbances or nightmares often persist.

Table 1

DSM-IV-TR diagnostic criteria for posttraumatic stress disorder

Nightmares and other sleep disturbances are associated with significant distress and daytime impairment and can interfere with PTSD recovery^4-8 by disrupting sleep-dependent processing of emotional experiences and causing repeated resensitization to trauma cues (Table 2).⁸

Table 2

Psychosocial consequences of sleep disruption in PTSD

Few randomized controlled medication trials specifically address PTSD-related nightmares. Most PTSD studies do not examine sleep outcomes as a primary measure, and comprehensive literature reviews could not offer evidence-based recommendations.^9,10 The American Academy of Sleep Medicine (AASM) also noted a paucity of PTSD studies that identified nightmares as a primary outcome measure.¹¹ See Table 3 for a list of recommended medication options for PTSD-associated nightmares.

Table 3

Recommended medication treatments for PTSD-associated nightmares

CASE CONTINUED: Medication change, improvement

After reviewing AASM’s treatment recommendations, we prescribe prazosin, 1 mg at bedtime for 7 nights, then increase by 1 mg at bedtime each week until Mr. S’s nightmares improve. He reports a substantial improvement in nightmare severity and frequency after a few weeks of treatment with prazosin, 5 mg at bedtime.

Prazosin

Prazosin is an α1-adrenergic receptor antagonist with good CNS penetrability. The rationale for reducing adrenergic activity to address intrusive PTSD symptoms has been well documented.^12,13 In open-label trials,^14-18 a chart review,¹⁹ and placebo-controlled trials,^20-22prazosin reduced trauma nightmares and improved sleep quality and global clinical status more than placebo (Table 4). In these studies, prazosin doses ranged from 1 to 20 mg/d, with an average of 3 mg at bedtime and a starting dose of 1 mg. Prazosin is the only agent recommended in the AASM’s Best Practice Guide for treating PTSD-related nightmares.¹¹

Table 4

RCTs of prazosin for trauma-related nightmares

Atypical antipsychotics

Atypical antipsychotics have been used to reduce nightmares in PTSD; however, most of the evidence from studies evaluated in the AASM’s Best Practice Guide were considered to be low quality.¹¹ Quetiapine and ziprasidone were not included in the AASM review. See (Table 5) for a review of the evidence for atypical antipsychotics for treating PTSD nightmares.

Table 5

Combat-related nightmares: Evidence for atypical antipsychotics

Comparing prazosin and quetiapine. A historical prospective cohort study of 237 veterans with PTSD receiving prazosin or quetiapine for nighttime PTSD symptoms demonstrated that although the 2 drugs have similar efficacy (defined as symptomatic improvement) for short-term, 6-month treatment (61% vs 62%; P=.54), a higher percentage of patients continued prazosin long-term (3 to 6 years) than those taking quetiapine (48% vs 24%; P < .001).²³ Twenty-five percent of patients taking quetiapine switched to prazosin during the study, and approximately one-half of these patients remained on prazosin until the study’s end. Only 8% of prazosin patients switched to quetiapine, and none continued this therapy until study end.²³ Patients in the quetiapine group were more likely to discontinue the drug because of lack of efficacy (13% vs 3%; P=.03) and adverse effects (35% vs 18%; P=.008), specifically sedation (21% vs 2%; P < .001) and metabolic effects (9% vs 0%; P=.014), compared with prazosin. Although this trial may be the only published comparison study of prazosin and quetiapine, its methodological quality has been questioned, which makes it difficult to draw definitive conclusions.

Metabolic syndrome—elevated diastolic blood pressure, increased waist circumference, and low high-density lipoprotein cholesterol—is common among PTSD patients treated with antipsychotics.²⁴ This syndrome may be caused by medications, lifestyle factors, or long-term overactivation of stress-response pathways. A retrospective chart review at a community mental health center revealed that patients taking even low doses of quetiapine for insomnia gained an average of 5 lbs (P=.037).²⁵ Another retrospective chart review at 2 military hospitals reported that patients receiving low-dose quetiapine (≤100 mg/d) gained an average of slightly less than 1 lb per month, which adds up to approximately 10 lbs per year (P < .001).²⁶ The benefit of using atypical antipsychotics may be outweighed by metabolic risks such as obesity, new-onset diabetes, and dyslipidemia.²⁷

Prazosin is considered a first-line treatment for sleep disturbances and nightmares in PTSD because of its superior long-term efficacy and decreased adverse effects compared with quetiapine.

Related Resources

• American Psychiatric Association. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Arlington, VA: American Psychiatric Publishing, Inc.; 2004.
• Veterans Affairs/Department of Defense clinical practice guidelines. Management of traumatic stress disorder and acute stress reaction. www.healthquality.va.gov/Post_Traumatic_Stress_Disorder_PTSD.asp.

Drug Brand Names

• Prazosin • Minipress
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Ziprasidone • Geodon

Disclosure

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

Mr. S, a 45-year-old veteran, was diagnosed with posttraumatic stress disorder (PTSD) 18 years ago after a tour of duty in the Persian Gulf. He had combat-related flashbacks triggered by the smell of gasoline or smoke from a fire, was easily startled, and began to isolate himself socially. However, his symptoms improved when he started volunteering at his local Veterans Affairs Medical Center. After he lost his job 3 years ago, Mr. S started experiencing flashbacks. He was irritable, easily startled, and avoided things that reminded him of his time in the Persian Gulf. His psychiatrist prescribed sertraline, titrated to 200 mg/d. The drug reduced the severity of his avoidance and hyperarousal symptoms and improved his mood.

During a clinic visit, Mr. S says he is doing well and can fall asleep at night but is having recurring nightmares about traumatic events that occurred during combat. These nightmares wake him up and have become more frequent, occurring once per night for the past month. Mr. S says he has been watching more news programs about conflicts in Afghanistan and Iraq since the nightmares began. His psychiatrist starts quetiapine, 50 mg at bedtime for 7 nights then 100 mg at bedtime, but after 6 weeks Mr. S says his nightmares continue.

PTSD occurs in approximately 19% of Vietnam war combat veterans¹ and 14% of service members returning from Iraq and Afghanistan.² PTSD symptoms are classified into clusters: intrusive/re-experiencing; avoidant/numbing; and hyperarousal.³ Nightmares are part of the intrusive/re-experiencing cluster, which is Criterion B in DSM-IV-TR. See Table 1 for a description of DSM-IV-TR PTSD criteria. Among PTSD patients, 50% to 70% report PTSD-associated nightmares.⁴ Despite adequate treatment targeted to improve PTSD’s core symptoms, symptoms such as sleep disturbances or nightmares often persist.

Table 1

DSM-IV-TR diagnostic criteria for posttraumatic stress disorder

Nightmares and other sleep disturbances are associated with significant distress and daytime impairment and can interfere with PTSD recovery^4-8 by disrupting sleep-dependent processing of emotional experiences and causing repeated resensitization to trauma cues (Table 2).⁸

Table 2

Psychosocial consequences of sleep disruption in PTSD

Few randomized controlled medication trials specifically address PTSD-related nightmares. Most PTSD studies do not examine sleep outcomes as a primary measure, and comprehensive literature reviews could not offer evidence-based recommendations.^9,10 The American Academy of Sleep Medicine (AASM) also noted a paucity of PTSD studies that identified nightmares as a primary outcome measure.¹¹ See Table 3 for a list of recommended medication options for PTSD-associated nightmares.

Table 3

Recommended medication treatments for PTSD-associated nightmares

CASE CONTINUED: Medication change, improvement

After reviewing AASM’s treatment recommendations, we prescribe prazosin, 1 mg at bedtime for 7 nights, then increase by 1 mg at bedtime each week until Mr. S’s nightmares improve. He reports a substantial improvement in nightmare severity and frequency after a few weeks of treatment with prazosin, 5 mg at bedtime.

Prazosin

Prazosin is an α1-adrenergic receptor antagonist with good CNS penetrability. The rationale for reducing adrenergic activity to address intrusive PTSD symptoms has been well documented.^12,13 In open-label trials,^14-18 a chart review,¹⁹ and placebo-controlled trials,^20-22prazosin reduced trauma nightmares and improved sleep quality and global clinical status more than placebo (Table 4). In these studies, prazosin doses ranged from 1 to 20 mg/d, with an average of 3 mg at bedtime and a starting dose of 1 mg. Prazosin is the only agent recommended in the AASM’s Best Practice Guide for treating PTSD-related nightmares.¹¹

Table 4

RCTs of prazosin for trauma-related nightmares

Atypical antipsychotics

Atypical antipsychotics have been used to reduce nightmares in PTSD; however, most of the evidence from studies evaluated in the AASM’s Best Practice Guide were considered to be low quality.¹¹ Quetiapine and ziprasidone were not included in the AASM review. See (Table 5) for a review of the evidence for atypical antipsychotics for treating PTSD nightmares.

Table 5

Combat-related nightmares: Evidence for atypical antipsychotics

Comparing prazosin and quetiapine. A historical prospective cohort study of 237 veterans with PTSD receiving prazosin or quetiapine for nighttime PTSD symptoms demonstrated that although the 2 drugs have similar efficacy (defined as symptomatic improvement) for short-term, 6-month treatment (61% vs 62%; P=.54), a higher percentage of patients continued prazosin long-term (3 to 6 years) than those taking quetiapine (48% vs 24%; P < .001).²³ Twenty-five percent of patients taking quetiapine switched to prazosin during the study, and approximately one-half of these patients remained on prazosin until the study’s end. Only 8% of prazosin patients switched to quetiapine, and none continued this therapy until study end.²³ Patients in the quetiapine group were more likely to discontinue the drug because of lack of efficacy (13% vs 3%; P=.03) and adverse effects (35% vs 18%; P=.008), specifically sedation (21% vs 2%; P < .001) and metabolic effects (9% vs 0%; P=.014), compared with prazosin. Although this trial may be the only published comparison study of prazosin and quetiapine, its methodological quality has been questioned, which makes it difficult to draw definitive conclusions.

Metabolic syndrome—elevated diastolic blood pressure, increased waist circumference, and low high-density lipoprotein cholesterol—is common among PTSD patients treated with antipsychotics.²⁴ This syndrome may be caused by medications, lifestyle factors, or long-term overactivation of stress-response pathways. A retrospective chart review at a community mental health center revealed that patients taking even low doses of quetiapine for insomnia gained an average of 5 lbs (P=.037).²⁵ Another retrospective chart review at 2 military hospitals reported that patients receiving low-dose quetiapine (≤100 mg/d) gained an average of slightly less than 1 lb per month, which adds up to approximately 10 lbs per year (P < .001).²⁶ The benefit of using atypical antipsychotics may be outweighed by metabolic risks such as obesity, new-onset diabetes, and dyslipidemia.²⁷

Prazosin is considered a first-line treatment for sleep disturbances and nightmares in PTSD because of its superior long-term efficacy and decreased adverse effects compared with quetiapine.

Related Resources

• American Psychiatric Association. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Arlington, VA: American Psychiatric Publishing, Inc.; 2004.
• Veterans Affairs/Department of Defense clinical practice guidelines. Management of traumatic stress disorder and acute stress reaction. www.healthquality.va.gov/Post_Traumatic_Stress_Disorder_PTSD.asp.

Drug Brand Names

• Prazosin • Minipress
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Ziprasidone • Geodon

Disclosure

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

Mr. S, a 45-year-old veteran, was diagnosed with posttraumatic stress disorder (PTSD) 18 years ago after a tour of duty in the Persian Gulf. He had combat-related flashbacks triggered by the smell of gasoline or smoke from a fire, was easily startled, and began to isolate himself socially. However, his symptoms improved when he started volunteering at his local Veterans Affairs Medical Center. After he lost his job 3 years ago, Mr. S started experiencing flashbacks. He was irritable, easily startled, and avoided things that reminded him of his time in the Persian Gulf. His psychiatrist prescribed sertraline, titrated to 200 mg/d. The drug reduced the severity of his avoidance and hyperarousal symptoms and improved his mood.

During a clinic visit, Mr. S says he is doing well and can fall asleep at night but is having recurring nightmares about traumatic events that occurred during combat. These nightmares wake him up and have become more frequent, occurring once per night for the past month. Mr. S says he has been watching more news programs about conflicts in Afghanistan and Iraq since the nightmares began. His psychiatrist starts quetiapine, 50 mg at bedtime for 7 nights then 100 mg at bedtime, but after 6 weeks Mr. S says his nightmares continue.

PTSD occurs in approximately 19% of Vietnam war combat veterans¹ and 14% of service members returning from Iraq and Afghanistan.² PTSD symptoms are classified into clusters: intrusive/re-experiencing; avoidant/numbing; and hyperarousal.³ Nightmares are part of the intrusive/re-experiencing cluster, which is Criterion B in DSM-IV-TR. See Table 1 for a description of DSM-IV-TR PTSD criteria. Among PTSD patients, 50% to 70% report PTSD-associated nightmares.⁴ Despite adequate treatment targeted to improve PTSD’s core symptoms, symptoms such as sleep disturbances or nightmares often persist.

Table 1

DSM-IV-TR diagnostic criteria for posttraumatic stress disorder

Nightmares and other sleep disturbances are associated with significant distress and daytime impairment and can interfere with PTSD recovery^4-8 by disrupting sleep-dependent processing of emotional experiences and causing repeated resensitization to trauma cues (Table 2).⁸

Table 2

Psychosocial consequences of sleep disruption in PTSD

Few randomized controlled medication trials specifically address PTSD-related nightmares. Most PTSD studies do not examine sleep outcomes as a primary measure, and comprehensive literature reviews could not offer evidence-based recommendations.^9,10 The American Academy of Sleep Medicine (AASM) also noted a paucity of PTSD studies that identified nightmares as a primary outcome measure.¹¹ See Table 3 for a list of recommended medication options for PTSD-associated nightmares.

Table 3

Recommended medication treatments for PTSD-associated nightmares

CASE CONTINUED: Medication change, improvement

After reviewing AASM’s treatment recommendations, we prescribe prazosin, 1 mg at bedtime for 7 nights, then increase by 1 mg at bedtime each week until Mr. S’s nightmares improve. He reports a substantial improvement in nightmare severity and frequency after a few weeks of treatment with prazosin, 5 mg at bedtime.

Prazosin

Prazosin is an α1-adrenergic receptor antagonist with good CNS penetrability. The rationale for reducing adrenergic activity to address intrusive PTSD symptoms has been well documented.^12,13 In open-label trials,^14-18 a chart review,¹⁹ and placebo-controlled trials,^20-22prazosin reduced trauma nightmares and improved sleep quality and global clinical status more than placebo (Table 4). In these studies, prazosin doses ranged from 1 to 20 mg/d, with an average of 3 mg at bedtime and a starting dose of 1 mg. Prazosin is the only agent recommended in the AASM’s Best Practice Guide for treating PTSD-related nightmares.¹¹

Table 4

RCTs of prazosin for trauma-related nightmares

Atypical antipsychotics

Atypical antipsychotics have been used to reduce nightmares in PTSD; however, most of the evidence from studies evaluated in the AASM’s Best Practice Guide were considered to be low quality.¹¹ Quetiapine and ziprasidone were not included in the AASM review. See (Table 5) for a review of the evidence for atypical antipsychotics for treating PTSD nightmares.

Table 5

Combat-related nightmares: Evidence for atypical antipsychotics

Comparing prazosin and quetiapine. A historical prospective cohort study of 237 veterans with PTSD receiving prazosin or quetiapine for nighttime PTSD symptoms demonstrated that although the 2 drugs have similar efficacy (defined as symptomatic improvement) for short-term, 6-month treatment (61% vs 62%; P=.54), a higher percentage of patients continued prazosin long-term (3 to 6 years) than those taking quetiapine (48% vs 24%; P < .001).²³ Twenty-five percent of patients taking quetiapine switched to prazosin during the study, and approximately one-half of these patients remained on prazosin until the study’s end. Only 8% of prazosin patients switched to quetiapine, and none continued this therapy until study end.²³ Patients in the quetiapine group were more likely to discontinue the drug because of lack of efficacy (13% vs 3%; P=.03) and adverse effects (35% vs 18%; P=.008), specifically sedation (21% vs 2%; P < .001) and metabolic effects (9% vs 0%; P=.014), compared with prazosin. Although this trial may be the only published comparison study of prazosin and quetiapine, its methodological quality has been questioned, which makes it difficult to draw definitive conclusions.

Metabolic syndrome—elevated diastolic blood pressure, increased waist circumference, and low high-density lipoprotein cholesterol—is common among PTSD patients treated with antipsychotics.²⁴ This syndrome may be caused by medications, lifestyle factors, or long-term overactivation of stress-response pathways. A retrospective chart review at a community mental health center revealed that patients taking even low doses of quetiapine for insomnia gained an average of 5 lbs (P=.037).²⁵ Another retrospective chart review at 2 military hospitals reported that patients receiving low-dose quetiapine (≤100 mg/d) gained an average of slightly less than 1 lb per month, which adds up to approximately 10 lbs per year (P < .001).²⁶ The benefit of using atypical antipsychotics may be outweighed by metabolic risks such as obesity, new-onset diabetes, and dyslipidemia.²⁷

Prazosin is considered a first-line treatment for sleep disturbances and nightmares in PTSD because of its superior long-term efficacy and decreased adverse effects compared with quetiapine.

Related Resources

• American Psychiatric Association. Practice guidelines for the treatment of patients with acute stress disorder and posttraumatic stress disorder. Arlington, VA: American Psychiatric Publishing, Inc.; 2004.
• Veterans Affairs/Department of Defense clinical practice guidelines. Management of traumatic stress disorder and acute stress reaction. www.healthquality.va.gov/Post_Traumatic_Stress_Disorder_PTSD.asp.

Drug Brand Names

• Prazosin • Minipress
• Quetiapine • Seroquel
• Sertraline • Zoloft
• Ziprasidone • Geodon

Disclosure

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