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What about Mr. D’s sleep apnea?
I wish to comment on “When Depression Treatment Goes Nowhere” by Drs. Ahsan Khan and Katherine Grimsley (Current Psychiatry, August 2005).
I’m surprised the authors did not mention Mr. D’s untreated (presumably obstructive) sleep apnea after reporting that he could not use nasal positive airway pressure because of his work schedule.
Untreated apnea symptoms overlap many of the symptoms and concepts addressed in the article. Mr. D’s eventual weight loss could have helped resolve those symptoms, at least partially.
Did the treating physicians get Mr. D involved with effective apnea treatment but just not mention it in the article? Could his brother’s motor vehicle accident have been caused by apnea-related sleepiness as well?
Kenneth N. Wiesert, MD
Indianapolis, IN
The authors respond
We appreciate Dr. Wiesert’s thoughtful comments on the role sleep apnea may have played in Mr. D’s symptoms.
Mr. D’s excessive fatigue, decreased energy and concentration, and mood symptoms could have been attributed to sleep apnea alone. Because his medical workup uncovered strikingly elevated blood glucose and poorly treated hypertension, we chose to highlight these findings.
Although we did not mention it in our article, Mr. D was urged early in treatment to maintain his continuous positive airway pressure (CPAP) regimen, and was educated on the importance of proper adherence to decrease his daytime sleepiness and other problems.
We addressed Mr. D’s noncompliance with CPAP during his care, but he recovered significantly after he began managing his diabetes and hypertension and abstaining from drug use. Further, even if Mr. D had been using his CPAP as recommended, his symptoms would have improved minimally or not at all because of his uncontrolled diabetes and hypertension.
Ahsan Y. Khan, MD
Katherine Grimsley, MD
Department of psychiatry and behavioral health
University of Kansas School of Medicine, Wichita
I wish to comment on “When Depression Treatment Goes Nowhere” by Drs. Ahsan Khan and Katherine Grimsley (Current Psychiatry, August 2005).
I’m surprised the authors did not mention Mr. D’s untreated (presumably obstructive) sleep apnea after reporting that he could not use nasal positive airway pressure because of his work schedule.
Untreated apnea symptoms overlap many of the symptoms and concepts addressed in the article. Mr. D’s eventual weight loss could have helped resolve those symptoms, at least partially.
Did the treating physicians get Mr. D involved with effective apnea treatment but just not mention it in the article? Could his brother’s motor vehicle accident have been caused by apnea-related sleepiness as well?
Kenneth N. Wiesert, MD
Indianapolis, IN
The authors respond
We appreciate Dr. Wiesert’s thoughtful comments on the role sleep apnea may have played in Mr. D’s symptoms.
Mr. D’s excessive fatigue, decreased energy and concentration, and mood symptoms could have been attributed to sleep apnea alone. Because his medical workup uncovered strikingly elevated blood glucose and poorly treated hypertension, we chose to highlight these findings.
Although we did not mention it in our article, Mr. D was urged early in treatment to maintain his continuous positive airway pressure (CPAP) regimen, and was educated on the importance of proper adherence to decrease his daytime sleepiness and other problems.
We addressed Mr. D’s noncompliance with CPAP during his care, but he recovered significantly after he began managing his diabetes and hypertension and abstaining from drug use. Further, even if Mr. D had been using his CPAP as recommended, his symptoms would have improved minimally or not at all because of his uncontrolled diabetes and hypertension.
Ahsan Y. Khan, MD
Katherine Grimsley, MD
Department of psychiatry and behavioral health
University of Kansas School of Medicine, Wichita
I wish to comment on “When Depression Treatment Goes Nowhere” by Drs. Ahsan Khan and Katherine Grimsley (Current Psychiatry, August 2005).
I’m surprised the authors did not mention Mr. D’s untreated (presumably obstructive) sleep apnea after reporting that he could not use nasal positive airway pressure because of his work schedule.
Untreated apnea symptoms overlap many of the symptoms and concepts addressed in the article. Mr. D’s eventual weight loss could have helped resolve those symptoms, at least partially.
Did the treating physicians get Mr. D involved with effective apnea treatment but just not mention it in the article? Could his brother’s motor vehicle accident have been caused by apnea-related sleepiness as well?
Kenneth N. Wiesert, MD
Indianapolis, IN
The authors respond
We appreciate Dr. Wiesert’s thoughtful comments on the role sleep apnea may have played in Mr. D’s symptoms.
Mr. D’s excessive fatigue, decreased energy and concentration, and mood symptoms could have been attributed to sleep apnea alone. Because his medical workup uncovered strikingly elevated blood glucose and poorly treated hypertension, we chose to highlight these findings.
Although we did not mention it in our article, Mr. D was urged early in treatment to maintain his continuous positive airway pressure (CPAP) regimen, and was educated on the importance of proper adherence to decrease his daytime sleepiness and other problems.
We addressed Mr. D’s noncompliance with CPAP during his care, but he recovered significantly after he began managing his diabetes and hypertension and abstaining from drug use. Further, even if Mr. D had been using his CPAP as recommended, his symptoms would have improved minimally or not at all because of his uncontrolled diabetes and hypertension.
Ahsan Y. Khan, MD
Katherine Grimsley, MD
Department of psychiatry and behavioral health
University of Kansas School of Medicine, Wichita
Why MDs—not psychologists—prescribe
Granting prescribing privileges to psychologists, particularly in “underserved” areas, is a popular topic. Psychologists and social workers are integral treatment team players and in many cases know more about the patient than the psychiatrist does.
I recall, however, when I was a second-year resident in a crisis clinic. Police brought in a man who was floridly psychotic, out of control, talking nonsense, and behaving lewdly. He was a police officer who had just finished an extra shift. His fellow officers were concerned; they said he had never behaved like this, and they were reluctant to believe he had “gone crazy.” He was about age 30, an Army veteran, a decorated police officer, well-liked and dependable. After much effort, we got him into an interview room.
I was not afraid of him, but was a little irritated that he could not give me a coherent story. Then I asked him if he had any medical problems. Between the slurred words, nonsensical phrases and sexual suggestions, I heard “insulin-dependent diabetic.”
I requested a blood glucose check and got a reading of 39 mg/dL. I gave the patient some orange juice and told the officers to drive him across the parking lot to the ER. They were surprised; they had expected him to be admitted to the locked psychiatric unit, though they acknowledged that he had skipped his last meal and had given himself insulin.
The patient was admitted to the medicine floor, where he recovered quickly and was discharged. If not for the glucose check, we might have given him an antipsychotic and transferred him to inpatient psychiatry—and he could have died in the process.
A psychologist could very easily have missed this diagnosis. Psychologists who want prescribing privileges need to go to medical school first, regardless of how well trained and experienced they are.
Susan Redge, MD
Rochester Hills, MI
Granting prescribing privileges to psychologists, particularly in “underserved” areas, is a popular topic. Psychologists and social workers are integral treatment team players and in many cases know more about the patient than the psychiatrist does.
I recall, however, when I was a second-year resident in a crisis clinic. Police brought in a man who was floridly psychotic, out of control, talking nonsense, and behaving lewdly. He was a police officer who had just finished an extra shift. His fellow officers were concerned; they said he had never behaved like this, and they were reluctant to believe he had “gone crazy.” He was about age 30, an Army veteran, a decorated police officer, well-liked and dependable. After much effort, we got him into an interview room.
I was not afraid of him, but was a little irritated that he could not give me a coherent story. Then I asked him if he had any medical problems. Between the slurred words, nonsensical phrases and sexual suggestions, I heard “insulin-dependent diabetic.”
I requested a blood glucose check and got a reading of 39 mg/dL. I gave the patient some orange juice and told the officers to drive him across the parking lot to the ER. They were surprised; they had expected him to be admitted to the locked psychiatric unit, though they acknowledged that he had skipped his last meal and had given himself insulin.
The patient was admitted to the medicine floor, where he recovered quickly and was discharged. If not for the glucose check, we might have given him an antipsychotic and transferred him to inpatient psychiatry—and he could have died in the process.
A psychologist could very easily have missed this diagnosis. Psychologists who want prescribing privileges need to go to medical school first, regardless of how well trained and experienced they are.
Susan Redge, MD
Rochester Hills, MI
Granting prescribing privileges to psychologists, particularly in “underserved” areas, is a popular topic. Psychologists and social workers are integral treatment team players and in many cases know more about the patient than the psychiatrist does.
I recall, however, when I was a second-year resident in a crisis clinic. Police brought in a man who was floridly psychotic, out of control, talking nonsense, and behaving lewdly. He was a police officer who had just finished an extra shift. His fellow officers were concerned; they said he had never behaved like this, and they were reluctant to believe he had “gone crazy.” He was about age 30, an Army veteran, a decorated police officer, well-liked and dependable. After much effort, we got him into an interview room.
I was not afraid of him, but was a little irritated that he could not give me a coherent story. Then I asked him if he had any medical problems. Between the slurred words, nonsensical phrases and sexual suggestions, I heard “insulin-dependent diabetic.”
I requested a blood glucose check and got a reading of 39 mg/dL. I gave the patient some orange juice and told the officers to drive him across the parking lot to the ER. They were surprised; they had expected him to be admitted to the locked psychiatric unit, though they acknowledged that he had skipped his last meal and had given himself insulin.
The patient was admitted to the medicine floor, where he recovered quickly and was discharged. If not for the glucose check, we might have given him an antipsychotic and transferred him to inpatient psychiatry—and he could have died in the process.
A psychologist could very easily have missed this diagnosis. Psychologists who want prescribing privileges need to go to medical school first, regardless of how well trained and experienced they are.
Susan Redge, MD
Rochester Hills, MI
Inpatient suicide: Who is liable, and how can we prevent it?
Dr. Jon Grant describes a 26-year-old Texas psychiatric inpatient who suffocated himself with cellophane wrap and a pillowcase (Malpractice Verdicts, Current Psychiatry, November 2005). As a forensic psychiatrist, let me offer some insights regarding this case.
A psychiatrist expects that hospitalization will prevent a patient’s suicide. Based on the facts Dr. Grant presented, however, the staff did not follow the standard of care and was obviously negligent:
- The patient was not adequately supervised, nor were the 15-minute checks properly documented.
- The rigor mortis is evidence that, contrary to the staff’s report, the patient could not have been checked 5 minutes before he was found dead.
The level of negligence appears clear enough not to require an expert witness to testify about the standard of care.
More information is needed before determining liability, however. Did the suicidality assessment contain factual errors? Did the patient reveal suicidal thoughts? Why wasn’t he assigned to onetoone observation? If the patient denied that he was suicidal and had not previously tried to kill himself, this case would be viewed differently.
Also, did lapses in the patient’s outpatient care lead to his hospitalization? In studying 481 suicides, Desai et al1 uncovered variables that increase suicide risk, including poor continuity of care and failure to readmit within 6 months. We need to be aware that borderline personality disorder or major depressive disorder enhances a patient’s ability to plan a suicide.2
As Dr. Grant notes, we can decrease suicide risk by identifying and minimizing risk factors, such as withholding potentially injurious material objects. Patients, however, can find many other ways to harm themselves. The patient Dr. Grant describes used a seemingly harmless object—a pillowcase—for his suicide.
Finally, as psychiatrists we find it fundamentally difficult to act on our suspiciousness, probably because of our positive countertransference toward patients and our trust in therapeutic alliances. We need to remember that acutely suicidal patients view us as obstacles to suicide, and that they probably will not give us reliable information.
Theodor Rais, MD
Assistant professor of psychiatry
Director, outpatient and partial hospitalization services
Medical University of Ohio at Toledo
1. Desai RA, Dausey RJ, Rosenbeck RA. Mental health services delivery and suicide risk: the role of individual patient and facility factors. Am J Psychiatry 2005;162:311-18.
2. Soloff PH, Lynch KG, Kelly TM, et al. Characteristics of suicide attempts of patients with major depressive episode and borderline personality disorders: a comparative study. Am J Psychiatry 2000;157:601-8.
Dr. Jon Grant describes a 26-year-old Texas psychiatric inpatient who suffocated himself with cellophane wrap and a pillowcase (Malpractice Verdicts, Current Psychiatry, November 2005). As a forensic psychiatrist, let me offer some insights regarding this case.
A psychiatrist expects that hospitalization will prevent a patient’s suicide. Based on the facts Dr. Grant presented, however, the staff did not follow the standard of care and was obviously negligent:
- The patient was not adequately supervised, nor were the 15-minute checks properly documented.
- The rigor mortis is evidence that, contrary to the staff’s report, the patient could not have been checked 5 minutes before he was found dead.
The level of negligence appears clear enough not to require an expert witness to testify about the standard of care.
More information is needed before determining liability, however. Did the suicidality assessment contain factual errors? Did the patient reveal suicidal thoughts? Why wasn’t he assigned to onetoone observation? If the patient denied that he was suicidal and had not previously tried to kill himself, this case would be viewed differently.
Also, did lapses in the patient’s outpatient care lead to his hospitalization? In studying 481 suicides, Desai et al1 uncovered variables that increase suicide risk, including poor continuity of care and failure to readmit within 6 months. We need to be aware that borderline personality disorder or major depressive disorder enhances a patient’s ability to plan a suicide.2
As Dr. Grant notes, we can decrease suicide risk by identifying and minimizing risk factors, such as withholding potentially injurious material objects. Patients, however, can find many other ways to harm themselves. The patient Dr. Grant describes used a seemingly harmless object—a pillowcase—for his suicide.
Finally, as psychiatrists we find it fundamentally difficult to act on our suspiciousness, probably because of our positive countertransference toward patients and our trust in therapeutic alliances. We need to remember that acutely suicidal patients view us as obstacles to suicide, and that they probably will not give us reliable information.
Theodor Rais, MD
Assistant professor of psychiatry
Director, outpatient and partial hospitalization services
Medical University of Ohio at Toledo
Dr. Jon Grant describes a 26-year-old Texas psychiatric inpatient who suffocated himself with cellophane wrap and a pillowcase (Malpractice Verdicts, Current Psychiatry, November 2005). As a forensic psychiatrist, let me offer some insights regarding this case.
A psychiatrist expects that hospitalization will prevent a patient’s suicide. Based on the facts Dr. Grant presented, however, the staff did not follow the standard of care and was obviously negligent:
- The patient was not adequately supervised, nor were the 15-minute checks properly documented.
- The rigor mortis is evidence that, contrary to the staff’s report, the patient could not have been checked 5 minutes before he was found dead.
The level of negligence appears clear enough not to require an expert witness to testify about the standard of care.
More information is needed before determining liability, however. Did the suicidality assessment contain factual errors? Did the patient reveal suicidal thoughts? Why wasn’t he assigned to onetoone observation? If the patient denied that he was suicidal and had not previously tried to kill himself, this case would be viewed differently.
Also, did lapses in the patient’s outpatient care lead to his hospitalization? In studying 481 suicides, Desai et al1 uncovered variables that increase suicide risk, including poor continuity of care and failure to readmit within 6 months. We need to be aware that borderline personality disorder or major depressive disorder enhances a patient’s ability to plan a suicide.2
As Dr. Grant notes, we can decrease suicide risk by identifying and minimizing risk factors, such as withholding potentially injurious material objects. Patients, however, can find many other ways to harm themselves. The patient Dr. Grant describes used a seemingly harmless object—a pillowcase—for his suicide.
Finally, as psychiatrists we find it fundamentally difficult to act on our suspiciousness, probably because of our positive countertransference toward patients and our trust in therapeutic alliances. We need to remember that acutely suicidal patients view us as obstacles to suicide, and that they probably will not give us reliable information.
Theodor Rais, MD
Assistant professor of psychiatry
Director, outpatient and partial hospitalization services
Medical University of Ohio at Toledo
1. Desai RA, Dausey RJ, Rosenbeck RA. Mental health services delivery and suicide risk: the role of individual patient and facility factors. Am J Psychiatry 2005;162:311-18.
2. Soloff PH, Lynch KG, Kelly TM, et al. Characteristics of suicide attempts of patients with major depressive episode and borderline personality disorders: a comparative study. Am J Psychiatry 2000;157:601-8.
1. Desai RA, Dausey RJ, Rosenbeck RA. Mental health services delivery and suicide risk: the role of individual patient and facility factors. Am J Psychiatry 2005;162:311-18.
2. Soloff PH, Lynch KG, Kelly TM, et al. Characteristics of suicide attempts of patients with major depressive episode and borderline personality disorders: a comparative study. Am J Psychiatry 2000;157:601-8.
For 8 years, she’s been ‘spellbound’
History: A tortured past
Ms. A, age 46, is referred to us by her primary care physician for a psychiatric evaluation. The patient endorses longstanding depression but has never seen a psychiatrist. She also reports that she was raped several years ago.
Ms. A meets DSM-IV-TR criteria for major depressive disorder, recurrent moderate; and posttraumatic stress disorder (PTSD). She complains of depressed mood, lack of energy, poor concentration and memory, anxiety, feelings of hopelessness and worthlessness, insomnia, and poor appetite. She has nightmares, flashbacks of her rape, and decreased interest in activities. She says she tries to avoid thoughts associated with her rape, feels detached from others, is easily startled, and at times is irritable.
Approximately 8 years ago—shortly after she started taking bupropion, 150 mg/d, to help her quit smoking—Ms. A suffered her first seizure-like episode. A neurologist diagnosed her with epilepsy based on EEG findings. He started her on carbamazepine, 200 mg bid, and titrated the dosage to 900 mg/d. After 2 years, however, her spells continued. Usually, she would black out for a few minutes and forget what she was doing. During some spells she would jerk her hands and feet, stare into space, repeat words over and over, and/or fumble with her hands.
After changing health insurance plans, Ms. A saw another neurologist who switched her to divalproex, 250 mg bid. She began having nausea, vomiting, and alopecia, so she stopped taking divalproex after 2 weeks. The neurologist switched her to topiramate, 25 mg bid, and titrated the dosage to 400 mg/d over 8 weeks with no side effects but minimal response. Reducing topiramate to 200 mg/d and adding phenytoin, 300 mg/d, produced little improvement.
Ms. A says these spells now come once or twice daily. She denies aura, loss of consciousness, tongue biting, or incontinence during seizures.
Medical history. Ms. A has undergone posterior fossa decompression for Arnold-Chiari type I malformation, right nephrectomy for renal cell carcinoma, a complete hysterectomy, an appendectomy, and bilateral breast implants. She has also had venous angiomas with head and neck pain.
Ms. A is frustrated over her lack of independence, her limited social life, and her inability to drive because of her seizure disorder. Once employed full-time for 12 years in a doctor’s office, she now gets by on disability benefits, which she finds degrading. She feels hopeless and helpless, as antiepileptics have not worked.
poll here
The authors’ observations
Ms. A complained of depression, sleep problems secondary to depression and PTSD, poor appetite, underlying anxiety, and decreased concentration, energy, and interest. We decided to address these symptoms with mirtazapine. Because she is thin (126 lb, body mass index 19.2 kg/m2), potential for weight gain with mirtazapine was not a concern.
We gauged Ms. A’s response to mirtazapine and her seizure history at our next visit, during which we customarily continue taking the patient’s history.
Treatment: Marriage by force?
Ms. A begins taking mirtazapine, 15 mg/d. At her next appointment the following week, she says she has stopped it because it has increased her appetite, which she fears will cause weight gain. She says her seizures, which usually occur at home, have continued with the same frequency.
Upon exploring her history further, we discover that Ms. A’s father was rarely around, and when he was he physically abused her. As a child she struggled with dyslexia, for which she received special education. She became pregnant while finishing high school and feels her mother forced her to marry her first husband.
Ms. A added that her three former husbands were physically and/or emotionally abusive toward her. About 10 years ago, she says, her third husband raped her.
We begin to suspect that Ms. A might not have epilepsy because of the seizures’ distinct nature, her vague symptoms, minimal or no response to antiepileptics, and comorbid mood and anxiety disorders. We refer her to another neurologist for video EEG (VEEG). She reluctantly agrees to the test, unwilling to believe that her seizures might have a psychiatric cause.
poll here
The authors’ observations
Recurrent seizures characteristic of epilepsy can significantly impair quality of life. Although the diagnosis often is straightforward, distinguishing epilepsy from psychogenic nonepileptic seizures (PNES) can be difficult.
PNES are sudden, episodic changes in behavior, perception, thinking, or feeling. These changes resemble epileptic events but are not prompted by abnormal brain electrical discharges as measured by EEG.1
Formerly called pseudoseizures, PNES can have a physiologic or psychological cause (Table 1). They often are a somatic response to unbearable past events and/or current psychological tension or conflict. Most patients with PNES cite domestic abuse or family conflicts as key stressors.2
Few systematic studies have addressed how life events contribute to PNES. Associated life events—described mostly in case reports—fall into three general categories:
- childhood and adult trauma
- bereavement or loss
- acute or situational stressors.3
Table 1
Physiologic and psychological causes of nonepileptic seizures
| Physiologic |
| Autonomic disorders |
| Cerebrovascular disease |
| Cardiac disorders |
| Vasovagal syncope |
| Ischemic heart disease |
| Valvular heart disease |
| Arrythmias |
| Drug toxicity |
| Endocrine disturbance |
| Metabolic disorders |
| Migraines |
| Paroxysmal movement disorder |
| Sleep disorder |
| Psychological |
| Anxiety disorders |
| Conversion disorder |
| Dissociative disorder |
| Factitious disorder |
| Malingering |
| Victim of physical, emotional, or sexual abuse |
| Posttraumatic stress disorder |
| Psychotic disorder |
| Somatoform disorder |
| Substance abuse/dependence |
Continued treatment: Wasted years
Two weeks after our referral, Ms. A reports that the neurologist discontinued topiramate and phenytoin after VEEG showed no epileptic activity.
Ms. A now realizes she does not have epilepsy. She is angry that her first neurologist had misdiag-nosed her, effectively sentencing her to 8 years of needless dependency and disability.
We prescribe escitalopram, starting at 10 mg/d and titrating to 20 mg/d, to address Ms. A’s depressive/PTSD symptoms. We also refer her to a psychotherapist, who schedules twice-weekly supportive psychotherapy sessions. The therapist plans to teach her coping techniques and provide ego support and encouragement.
Ms. A’s psychotherapy progresses slowly at first, but by the fourth session she sets goals, which include getting off disability as soon as possible. With careful ego strengthening, she resumes driving and searches for a job. During one session, she tells her therapist she has long wanted to become a nurse, so she is encouraged to see a nursing school counselor for advice on selecting prerequisite nursing classes.
The authors’ observations
As with Ms. A, an erroneous epilepsy diagnosis can cause physical, psychosocial, and socioeconomic grief for the patient and can lead to needless restrictions, unemployment or underemployment, and dependence on disability benefits. After the misdiagnosis, Ms. A lost control of her future and considered her life a burden, leading to depression and anxiety. Her seizures caused most of her physical and psychological disturbances and diminished her overall function.
PNES are often mistaken for epileptic seizures, and 26% of seizure patients experience both.6 In a study of 50 patients, between 5% and 20% of patients evaluated for epilepsy and 10% to 40% of patients referred to comprehensive epilepsy centers were later found to have PNES.7
Like Ms. A, many patients with undiagnosed PNES receive antiepileptics to treat apparent epilepsy. These medications can cause troublesome side effects—from GI problems, to respiratory arrest in patients with pseudostatus, to potential teratogenicity.
In addition, comorbid epilepsy often goes undetected in patients with PNES. This could lead to inadequate treatment, increasing the patient’s morbidity and mortality risk.8
poll here
The authors’ observations
Patient history. Take a thorough history for patients with a history of seizures.
Too often, doctors assume a previous epilepsy diagnosis is correct, especially if rendered by a neurologist. In the United Kingdom, 20% to 31% of epilepsy diagnoses are incorrect because of incomplete history and misinterpreted EEG findings.8 When taking a patient’s seizure history, clinicians often do not get:
- a detailed history of seizures or seizurelike events, including onset, frequency, observations from family or friends, and seizure duration
- information on whether the patient remembers seizure details; has had prespell aura or loss of consciousness, or cries during the spells
- history of physical and/or sexual abuse.
Refer patients with features that may suggest PNES to a neurologist for VEEG to confirm or rule out epilepsy, because roughly one-quarter of seizure patients can have both.
Table 2
Patient features that suggest nonepileptic seizures
| Comorbid psychiatric disorder(s) |
| Events occur only in presence of others or only when alone |
| Lack of concern or excessive emotional response to seizures |
| Minimal or no response to antiepileptics |
| Multiple daily seizures |
| No history of injury resulting from seizures |
| Normal neurologic history and examination |
| Repeated hospitalizations or emergency room visits |
| Unremarkable EEG and MRI findings |
| Victim of sexual abuse |
The Minnesota Multiphasic Personality Inventory (MMPI) is often used to discriminate PNES from epilepsy. Wilkus et al9 reported significant differences in scores of MMPI hypochondriasis, hysteria, and schizophrenia scales among patients with PNES and epilepsy. Patients with PNES may have higher MMPI hypochondriasis, hysteria, schizophrenia, and psychopathic deviate scores than do patients with epilepsy.
Other authors, however, have found more variable MMPI results when using the test to distinguish PNES from epilepsy. Thus, the MMPI may provide supportive data for PNES diagnosis but is not a definitive tool.
Explaining the findings. Getting the patient to accept that the epilepsy is “in your head” is crucial to engaging him or her in treatment. The clinician needs to be honest with the patient while projecting a positive approach to the diagnosis. Tell the patient that not having epilepsy is “good news,” that antiepileptics are not needed, and that he or she can gain better control once stress or emotional issues are resolved.10
Follow-up: A learning experience
Within 4 months of her last seizure, Ms. A showed dramatic improvement. She began driving, working part-time and enrolled in nursing school. Her disability benefits program provided tuition assistance.
Ms. A has now been seizure-free for 1 year. Motivated and determined, she is taking up to 8 credit hours per semester and earning As and Bs but at times is anxious and fears failure. She needs much support and encouragement. Multiple therapy techniques—including direct teaching, admiring her progress, offering support, explaining, and ego strengthening—have produced good results. She is still taking escitalopram, 20 mg/d, and sees her therapist every 2 weeks.
Related resources
- Adetunji B, Mathews M, Williams A, Verma S. Psychogenic or epileptic seizures? How to clinch the diagnosis. Current Psychiatry 2004;3(11):25-35.
- Privitera MD. EEGs and epilepsy: When seizures mimic psychiatric illness. Current Psychiatry 2002;1(9):14-21.
- Bupropion • Wellbutrin, Zyban
- Carbamazepine • Tegretol
- Divalproex sodium • Depakote
- Escitalopram • Lexapro
- Mirtazapine • Remeron
- Phenytoin • Dilantin
- Topiramate • Topamax
Dr. Khan is a speaker for Pfizer and Wyeth.
Drs. Aziz and Syed report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Chabolla DR, Krahn LE, So EL, Rummans TA. Psychogenic nonepileptic seizures. Mayo Clin Proc 1996;71:493-500.
2. King DW, Gallagher BB, Murvin AJ, et al. Pseudoseizures: diagnostic evaluation. Neurology 1982;32:18-23.
3. Bowman ES, Markand ON. Psychodynamics and psychiatric diagnoses of pseudoseizure subjects. Am J Psychiatry 1996;153:57-63.
4. Ettinger AB, Devinsky O, Weisbrot DM, et al. A comprehensive profile of clinical, psychiatric, and psychosocial characteristics of patients with psychogenic nonepileptic seizures. Epilepsia 1999;40:1292-8.
5. Alsaadi TM, Thieman C, Shatzel A, Farias S. Video-EEG telemetry can be a crucial tool for neurologists experienced in epilepsy when diagnosing seizure disorders. Seizure 2004;13:32-4.
6. Chadwick D, Smith D. The misdiagnosis of epilepsy. BMJ 2002;324:495-6.
7. Lempert T, Schmidt D. Natural history and outcome of psychogenic seizures: a clinical study in 50 patients. J Neurol 1990;237:35-8.
8. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: findings of a population study. Seizure 1998;7:403-6.
9. Wilkus RJ, Dodrill CB. Factors affecting the outcome of MMPI and neurosychological assessments of psychogenic and epileptic seizure patients. Epilepsia 1989;30:339-47.
10. Walczak TS, Papacostas S, Williams DT, et al. Outcome after diagnosis of psychogenic nonepileptic seizures. Epilepsia 1995;36:1131-7.
History: A tortured past
Ms. A, age 46, is referred to us by her primary care physician for a psychiatric evaluation. The patient endorses longstanding depression but has never seen a psychiatrist. She also reports that she was raped several years ago.
Ms. A meets DSM-IV-TR criteria for major depressive disorder, recurrent moderate; and posttraumatic stress disorder (PTSD). She complains of depressed mood, lack of energy, poor concentration and memory, anxiety, feelings of hopelessness and worthlessness, insomnia, and poor appetite. She has nightmares, flashbacks of her rape, and decreased interest in activities. She says she tries to avoid thoughts associated with her rape, feels detached from others, is easily startled, and at times is irritable.
Approximately 8 years ago—shortly after she started taking bupropion, 150 mg/d, to help her quit smoking—Ms. A suffered her first seizure-like episode. A neurologist diagnosed her with epilepsy based on EEG findings. He started her on carbamazepine, 200 mg bid, and titrated the dosage to 900 mg/d. After 2 years, however, her spells continued. Usually, she would black out for a few minutes and forget what she was doing. During some spells she would jerk her hands and feet, stare into space, repeat words over and over, and/or fumble with her hands.
After changing health insurance plans, Ms. A saw another neurologist who switched her to divalproex, 250 mg bid. She began having nausea, vomiting, and alopecia, so she stopped taking divalproex after 2 weeks. The neurologist switched her to topiramate, 25 mg bid, and titrated the dosage to 400 mg/d over 8 weeks with no side effects but minimal response. Reducing topiramate to 200 mg/d and adding phenytoin, 300 mg/d, produced little improvement.
Ms. A says these spells now come once or twice daily. She denies aura, loss of consciousness, tongue biting, or incontinence during seizures.
Medical history. Ms. A has undergone posterior fossa decompression for Arnold-Chiari type I malformation, right nephrectomy for renal cell carcinoma, a complete hysterectomy, an appendectomy, and bilateral breast implants. She has also had venous angiomas with head and neck pain.
Ms. A is frustrated over her lack of independence, her limited social life, and her inability to drive because of her seizure disorder. Once employed full-time for 12 years in a doctor’s office, she now gets by on disability benefits, which she finds degrading. She feels hopeless and helpless, as antiepileptics have not worked.
poll here
The authors’ observations
Ms. A complained of depression, sleep problems secondary to depression and PTSD, poor appetite, underlying anxiety, and decreased concentration, energy, and interest. We decided to address these symptoms with mirtazapine. Because she is thin (126 lb, body mass index 19.2 kg/m2), potential for weight gain with mirtazapine was not a concern.
We gauged Ms. A’s response to mirtazapine and her seizure history at our next visit, during which we customarily continue taking the patient’s history.
Treatment: Marriage by force?
Ms. A begins taking mirtazapine, 15 mg/d. At her next appointment the following week, she says she has stopped it because it has increased her appetite, which she fears will cause weight gain. She says her seizures, which usually occur at home, have continued with the same frequency.
Upon exploring her history further, we discover that Ms. A’s father was rarely around, and when he was he physically abused her. As a child she struggled with dyslexia, for which she received special education. She became pregnant while finishing high school and feels her mother forced her to marry her first husband.
Ms. A added that her three former husbands were physically and/or emotionally abusive toward her. About 10 years ago, she says, her third husband raped her.
We begin to suspect that Ms. A might not have epilepsy because of the seizures’ distinct nature, her vague symptoms, minimal or no response to antiepileptics, and comorbid mood and anxiety disorders. We refer her to another neurologist for video EEG (VEEG). She reluctantly agrees to the test, unwilling to believe that her seizures might have a psychiatric cause.
poll here
The authors’ observations
Recurrent seizures characteristic of epilepsy can significantly impair quality of life. Although the diagnosis often is straightforward, distinguishing epilepsy from psychogenic nonepileptic seizures (PNES) can be difficult.
PNES are sudden, episodic changes in behavior, perception, thinking, or feeling. These changes resemble epileptic events but are not prompted by abnormal brain electrical discharges as measured by EEG.1
Formerly called pseudoseizures, PNES can have a physiologic or psychological cause (Table 1). They often are a somatic response to unbearable past events and/or current psychological tension or conflict. Most patients with PNES cite domestic abuse or family conflicts as key stressors.2
Few systematic studies have addressed how life events contribute to PNES. Associated life events—described mostly in case reports—fall into three general categories:
- childhood and adult trauma
- bereavement or loss
- acute or situational stressors.3
Table 1
Physiologic and psychological causes of nonepileptic seizures
| Physiologic |
| Autonomic disorders |
| Cerebrovascular disease |
| Cardiac disorders |
| Vasovagal syncope |
| Ischemic heart disease |
| Valvular heart disease |
| Arrythmias |
| Drug toxicity |
| Endocrine disturbance |
| Metabolic disorders |
| Migraines |
| Paroxysmal movement disorder |
| Sleep disorder |
| Psychological |
| Anxiety disorders |
| Conversion disorder |
| Dissociative disorder |
| Factitious disorder |
| Malingering |
| Victim of physical, emotional, or sexual abuse |
| Posttraumatic stress disorder |
| Psychotic disorder |
| Somatoform disorder |
| Substance abuse/dependence |
Continued treatment: Wasted years
Two weeks after our referral, Ms. A reports that the neurologist discontinued topiramate and phenytoin after VEEG showed no epileptic activity.
Ms. A now realizes she does not have epilepsy. She is angry that her first neurologist had misdiag-nosed her, effectively sentencing her to 8 years of needless dependency and disability.
We prescribe escitalopram, starting at 10 mg/d and titrating to 20 mg/d, to address Ms. A’s depressive/PTSD symptoms. We also refer her to a psychotherapist, who schedules twice-weekly supportive psychotherapy sessions. The therapist plans to teach her coping techniques and provide ego support and encouragement.
Ms. A’s psychotherapy progresses slowly at first, but by the fourth session she sets goals, which include getting off disability as soon as possible. With careful ego strengthening, she resumes driving and searches for a job. During one session, she tells her therapist she has long wanted to become a nurse, so she is encouraged to see a nursing school counselor for advice on selecting prerequisite nursing classes.
The authors’ observations
As with Ms. A, an erroneous epilepsy diagnosis can cause physical, psychosocial, and socioeconomic grief for the patient and can lead to needless restrictions, unemployment or underemployment, and dependence on disability benefits. After the misdiagnosis, Ms. A lost control of her future and considered her life a burden, leading to depression and anxiety. Her seizures caused most of her physical and psychological disturbances and diminished her overall function.
PNES are often mistaken for epileptic seizures, and 26% of seizure patients experience both.6 In a study of 50 patients, between 5% and 20% of patients evaluated for epilepsy and 10% to 40% of patients referred to comprehensive epilepsy centers were later found to have PNES.7
Like Ms. A, many patients with undiagnosed PNES receive antiepileptics to treat apparent epilepsy. These medications can cause troublesome side effects—from GI problems, to respiratory arrest in patients with pseudostatus, to potential teratogenicity.
In addition, comorbid epilepsy often goes undetected in patients with PNES. This could lead to inadequate treatment, increasing the patient’s morbidity and mortality risk.8
poll here
The authors’ observations
Patient history. Take a thorough history for patients with a history of seizures.
Too often, doctors assume a previous epilepsy diagnosis is correct, especially if rendered by a neurologist. In the United Kingdom, 20% to 31% of epilepsy diagnoses are incorrect because of incomplete history and misinterpreted EEG findings.8 When taking a patient’s seizure history, clinicians often do not get:
- a detailed history of seizures or seizurelike events, including onset, frequency, observations from family or friends, and seizure duration
- information on whether the patient remembers seizure details; has had prespell aura or loss of consciousness, or cries during the spells
- history of physical and/or sexual abuse.
Refer patients with features that may suggest PNES to a neurologist for VEEG to confirm or rule out epilepsy, because roughly one-quarter of seizure patients can have both.
Table 2
Patient features that suggest nonepileptic seizures
| Comorbid psychiatric disorder(s) |
| Events occur only in presence of others or only when alone |
| Lack of concern or excessive emotional response to seizures |
| Minimal or no response to antiepileptics |
| Multiple daily seizures |
| No history of injury resulting from seizures |
| Normal neurologic history and examination |
| Repeated hospitalizations or emergency room visits |
| Unremarkable EEG and MRI findings |
| Victim of sexual abuse |
The Minnesota Multiphasic Personality Inventory (MMPI) is often used to discriminate PNES from epilepsy. Wilkus et al9 reported significant differences in scores of MMPI hypochondriasis, hysteria, and schizophrenia scales among patients with PNES and epilepsy. Patients with PNES may have higher MMPI hypochondriasis, hysteria, schizophrenia, and psychopathic deviate scores than do patients with epilepsy.
Other authors, however, have found more variable MMPI results when using the test to distinguish PNES from epilepsy. Thus, the MMPI may provide supportive data for PNES diagnosis but is not a definitive tool.
Explaining the findings. Getting the patient to accept that the epilepsy is “in your head” is crucial to engaging him or her in treatment. The clinician needs to be honest with the patient while projecting a positive approach to the diagnosis. Tell the patient that not having epilepsy is “good news,” that antiepileptics are not needed, and that he or she can gain better control once stress or emotional issues are resolved.10
Follow-up: A learning experience
Within 4 months of her last seizure, Ms. A showed dramatic improvement. She began driving, working part-time and enrolled in nursing school. Her disability benefits program provided tuition assistance.
Ms. A has now been seizure-free for 1 year. Motivated and determined, she is taking up to 8 credit hours per semester and earning As and Bs but at times is anxious and fears failure. She needs much support and encouragement. Multiple therapy techniques—including direct teaching, admiring her progress, offering support, explaining, and ego strengthening—have produced good results. She is still taking escitalopram, 20 mg/d, and sees her therapist every 2 weeks.
Related resources
- Adetunji B, Mathews M, Williams A, Verma S. Psychogenic or epileptic seizures? How to clinch the diagnosis. Current Psychiatry 2004;3(11):25-35.
- Privitera MD. EEGs and epilepsy: When seizures mimic psychiatric illness. Current Psychiatry 2002;1(9):14-21.
- Bupropion • Wellbutrin, Zyban
- Carbamazepine • Tegretol
- Divalproex sodium • Depakote
- Escitalopram • Lexapro
- Mirtazapine • Remeron
- Phenytoin • Dilantin
- Topiramate • Topamax
Dr. Khan is a speaker for Pfizer and Wyeth.
Drs. Aziz and Syed report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
History: A tortured past
Ms. A, age 46, is referred to us by her primary care physician for a psychiatric evaluation. The patient endorses longstanding depression but has never seen a psychiatrist. She also reports that she was raped several years ago.
Ms. A meets DSM-IV-TR criteria for major depressive disorder, recurrent moderate; and posttraumatic stress disorder (PTSD). She complains of depressed mood, lack of energy, poor concentration and memory, anxiety, feelings of hopelessness and worthlessness, insomnia, and poor appetite. She has nightmares, flashbacks of her rape, and decreased interest in activities. She says she tries to avoid thoughts associated with her rape, feels detached from others, is easily startled, and at times is irritable.
Approximately 8 years ago—shortly after she started taking bupropion, 150 mg/d, to help her quit smoking—Ms. A suffered her first seizure-like episode. A neurologist diagnosed her with epilepsy based on EEG findings. He started her on carbamazepine, 200 mg bid, and titrated the dosage to 900 mg/d. After 2 years, however, her spells continued. Usually, she would black out for a few minutes and forget what she was doing. During some spells she would jerk her hands and feet, stare into space, repeat words over and over, and/or fumble with her hands.
After changing health insurance plans, Ms. A saw another neurologist who switched her to divalproex, 250 mg bid. She began having nausea, vomiting, and alopecia, so she stopped taking divalproex after 2 weeks. The neurologist switched her to topiramate, 25 mg bid, and titrated the dosage to 400 mg/d over 8 weeks with no side effects but minimal response. Reducing topiramate to 200 mg/d and adding phenytoin, 300 mg/d, produced little improvement.
Ms. A says these spells now come once or twice daily. She denies aura, loss of consciousness, tongue biting, or incontinence during seizures.
Medical history. Ms. A has undergone posterior fossa decompression for Arnold-Chiari type I malformation, right nephrectomy for renal cell carcinoma, a complete hysterectomy, an appendectomy, and bilateral breast implants. She has also had venous angiomas with head and neck pain.
Ms. A is frustrated over her lack of independence, her limited social life, and her inability to drive because of her seizure disorder. Once employed full-time for 12 years in a doctor’s office, she now gets by on disability benefits, which she finds degrading. She feels hopeless and helpless, as antiepileptics have not worked.
poll here
The authors’ observations
Ms. A complained of depression, sleep problems secondary to depression and PTSD, poor appetite, underlying anxiety, and decreased concentration, energy, and interest. We decided to address these symptoms with mirtazapine. Because she is thin (126 lb, body mass index 19.2 kg/m2), potential for weight gain with mirtazapine was not a concern.
We gauged Ms. A’s response to mirtazapine and her seizure history at our next visit, during which we customarily continue taking the patient’s history.
Treatment: Marriage by force?
Ms. A begins taking mirtazapine, 15 mg/d. At her next appointment the following week, she says she has stopped it because it has increased her appetite, which she fears will cause weight gain. She says her seizures, which usually occur at home, have continued with the same frequency.
Upon exploring her history further, we discover that Ms. A’s father was rarely around, and when he was he physically abused her. As a child she struggled with dyslexia, for which she received special education. She became pregnant while finishing high school and feels her mother forced her to marry her first husband.
Ms. A added that her three former husbands were physically and/or emotionally abusive toward her. About 10 years ago, she says, her third husband raped her.
We begin to suspect that Ms. A might not have epilepsy because of the seizures’ distinct nature, her vague symptoms, minimal or no response to antiepileptics, and comorbid mood and anxiety disorders. We refer her to another neurologist for video EEG (VEEG). She reluctantly agrees to the test, unwilling to believe that her seizures might have a psychiatric cause.
poll here
The authors’ observations
Recurrent seizures characteristic of epilepsy can significantly impair quality of life. Although the diagnosis often is straightforward, distinguishing epilepsy from psychogenic nonepileptic seizures (PNES) can be difficult.
PNES are sudden, episodic changes in behavior, perception, thinking, or feeling. These changes resemble epileptic events but are not prompted by abnormal brain electrical discharges as measured by EEG.1
Formerly called pseudoseizures, PNES can have a physiologic or psychological cause (Table 1). They often are a somatic response to unbearable past events and/or current psychological tension or conflict. Most patients with PNES cite domestic abuse or family conflicts as key stressors.2
Few systematic studies have addressed how life events contribute to PNES. Associated life events—described mostly in case reports—fall into three general categories:
- childhood and adult trauma
- bereavement or loss
- acute or situational stressors.3
Table 1
Physiologic and psychological causes of nonepileptic seizures
| Physiologic |
| Autonomic disorders |
| Cerebrovascular disease |
| Cardiac disorders |
| Vasovagal syncope |
| Ischemic heart disease |
| Valvular heart disease |
| Arrythmias |
| Drug toxicity |
| Endocrine disturbance |
| Metabolic disorders |
| Migraines |
| Paroxysmal movement disorder |
| Sleep disorder |
| Psychological |
| Anxiety disorders |
| Conversion disorder |
| Dissociative disorder |
| Factitious disorder |
| Malingering |
| Victim of physical, emotional, or sexual abuse |
| Posttraumatic stress disorder |
| Psychotic disorder |
| Somatoform disorder |
| Substance abuse/dependence |
Continued treatment: Wasted years
Two weeks after our referral, Ms. A reports that the neurologist discontinued topiramate and phenytoin after VEEG showed no epileptic activity.
Ms. A now realizes she does not have epilepsy. She is angry that her first neurologist had misdiag-nosed her, effectively sentencing her to 8 years of needless dependency and disability.
We prescribe escitalopram, starting at 10 mg/d and titrating to 20 mg/d, to address Ms. A’s depressive/PTSD symptoms. We also refer her to a psychotherapist, who schedules twice-weekly supportive psychotherapy sessions. The therapist plans to teach her coping techniques and provide ego support and encouragement.
Ms. A’s psychotherapy progresses slowly at first, but by the fourth session she sets goals, which include getting off disability as soon as possible. With careful ego strengthening, she resumes driving and searches for a job. During one session, she tells her therapist she has long wanted to become a nurse, so she is encouraged to see a nursing school counselor for advice on selecting prerequisite nursing classes.
The authors’ observations
As with Ms. A, an erroneous epilepsy diagnosis can cause physical, psychosocial, and socioeconomic grief for the patient and can lead to needless restrictions, unemployment or underemployment, and dependence on disability benefits. After the misdiagnosis, Ms. A lost control of her future and considered her life a burden, leading to depression and anxiety. Her seizures caused most of her physical and psychological disturbances and diminished her overall function.
PNES are often mistaken for epileptic seizures, and 26% of seizure patients experience both.6 In a study of 50 patients, between 5% and 20% of patients evaluated for epilepsy and 10% to 40% of patients referred to comprehensive epilepsy centers were later found to have PNES.7
Like Ms. A, many patients with undiagnosed PNES receive antiepileptics to treat apparent epilepsy. These medications can cause troublesome side effects—from GI problems, to respiratory arrest in patients with pseudostatus, to potential teratogenicity.
In addition, comorbid epilepsy often goes undetected in patients with PNES. This could lead to inadequate treatment, increasing the patient’s morbidity and mortality risk.8
poll here
The authors’ observations
Patient history. Take a thorough history for patients with a history of seizures.
Too often, doctors assume a previous epilepsy diagnosis is correct, especially if rendered by a neurologist. In the United Kingdom, 20% to 31% of epilepsy diagnoses are incorrect because of incomplete history and misinterpreted EEG findings.8 When taking a patient’s seizure history, clinicians often do not get:
- a detailed history of seizures or seizurelike events, including onset, frequency, observations from family or friends, and seizure duration
- information on whether the patient remembers seizure details; has had prespell aura or loss of consciousness, or cries during the spells
- history of physical and/or sexual abuse.
Refer patients with features that may suggest PNES to a neurologist for VEEG to confirm or rule out epilepsy, because roughly one-quarter of seizure patients can have both.
Table 2
Patient features that suggest nonepileptic seizures
| Comorbid psychiatric disorder(s) |
| Events occur only in presence of others or only when alone |
| Lack of concern or excessive emotional response to seizures |
| Minimal or no response to antiepileptics |
| Multiple daily seizures |
| No history of injury resulting from seizures |
| Normal neurologic history and examination |
| Repeated hospitalizations or emergency room visits |
| Unremarkable EEG and MRI findings |
| Victim of sexual abuse |
The Minnesota Multiphasic Personality Inventory (MMPI) is often used to discriminate PNES from epilepsy. Wilkus et al9 reported significant differences in scores of MMPI hypochondriasis, hysteria, and schizophrenia scales among patients with PNES and epilepsy. Patients with PNES may have higher MMPI hypochondriasis, hysteria, schizophrenia, and psychopathic deviate scores than do patients with epilepsy.
Other authors, however, have found more variable MMPI results when using the test to distinguish PNES from epilepsy. Thus, the MMPI may provide supportive data for PNES diagnosis but is not a definitive tool.
Explaining the findings. Getting the patient to accept that the epilepsy is “in your head” is crucial to engaging him or her in treatment. The clinician needs to be honest with the patient while projecting a positive approach to the diagnosis. Tell the patient that not having epilepsy is “good news,” that antiepileptics are not needed, and that he or she can gain better control once stress or emotional issues are resolved.10
Follow-up: A learning experience
Within 4 months of her last seizure, Ms. A showed dramatic improvement. She began driving, working part-time and enrolled in nursing school. Her disability benefits program provided tuition assistance.
Ms. A has now been seizure-free for 1 year. Motivated and determined, she is taking up to 8 credit hours per semester and earning As and Bs but at times is anxious and fears failure. She needs much support and encouragement. Multiple therapy techniques—including direct teaching, admiring her progress, offering support, explaining, and ego strengthening—have produced good results. She is still taking escitalopram, 20 mg/d, and sees her therapist every 2 weeks.
Related resources
- Adetunji B, Mathews M, Williams A, Verma S. Psychogenic or epileptic seizures? How to clinch the diagnosis. Current Psychiatry 2004;3(11):25-35.
- Privitera MD. EEGs and epilepsy: When seizures mimic psychiatric illness. Current Psychiatry 2002;1(9):14-21.
- Bupropion • Wellbutrin, Zyban
- Carbamazepine • Tegretol
- Divalproex sodium • Depakote
- Escitalopram • Lexapro
- Mirtazapine • Remeron
- Phenytoin • Dilantin
- Topiramate • Topamax
Dr. Khan is a speaker for Pfizer and Wyeth.
Drs. Aziz and Syed report no financial relationship with any company whose products are mentioned in this article, or with manufacturers of competing products.
1. Chabolla DR, Krahn LE, So EL, Rummans TA. Psychogenic nonepileptic seizures. Mayo Clin Proc 1996;71:493-500.
2. King DW, Gallagher BB, Murvin AJ, et al. Pseudoseizures: diagnostic evaluation. Neurology 1982;32:18-23.
3. Bowman ES, Markand ON. Psychodynamics and psychiatric diagnoses of pseudoseizure subjects. Am J Psychiatry 1996;153:57-63.
4. Ettinger AB, Devinsky O, Weisbrot DM, et al. A comprehensive profile of clinical, psychiatric, and psychosocial characteristics of patients with psychogenic nonepileptic seizures. Epilepsia 1999;40:1292-8.
5. Alsaadi TM, Thieman C, Shatzel A, Farias S. Video-EEG telemetry can be a crucial tool for neurologists experienced in epilepsy when diagnosing seizure disorders. Seizure 2004;13:32-4.
6. Chadwick D, Smith D. The misdiagnosis of epilepsy. BMJ 2002;324:495-6.
7. Lempert T, Schmidt D. Natural history and outcome of psychogenic seizures: a clinical study in 50 patients. J Neurol 1990;237:35-8.
8. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: findings of a population study. Seizure 1998;7:403-6.
9. Wilkus RJ, Dodrill CB. Factors affecting the outcome of MMPI and neurosychological assessments of psychogenic and epileptic seizure patients. Epilepsia 1989;30:339-47.
10. Walczak TS, Papacostas S, Williams DT, et al. Outcome after diagnosis of psychogenic nonepileptic seizures. Epilepsia 1995;36:1131-7.
1. Chabolla DR, Krahn LE, So EL, Rummans TA. Psychogenic nonepileptic seizures. Mayo Clin Proc 1996;71:493-500.
2. King DW, Gallagher BB, Murvin AJ, et al. Pseudoseizures: diagnostic evaluation. Neurology 1982;32:18-23.
3. Bowman ES, Markand ON. Psychodynamics and psychiatric diagnoses of pseudoseizure subjects. Am J Psychiatry 1996;153:57-63.
4. Ettinger AB, Devinsky O, Weisbrot DM, et al. A comprehensive profile of clinical, psychiatric, and psychosocial characteristics of patients with psychogenic nonepileptic seizures. Epilepsia 1999;40:1292-8.
5. Alsaadi TM, Thieman C, Shatzel A, Farias S. Video-EEG telemetry can be a crucial tool for neurologists experienced in epilepsy when diagnosing seizure disorders. Seizure 2004;13:32-4.
6. Chadwick D, Smith D. The misdiagnosis of epilepsy. BMJ 2002;324:495-6.
7. Lempert T, Schmidt D. Natural history and outcome of psychogenic seizures: a clinical study in 50 patients. J Neurol 1990;237:35-8.
8. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: findings of a population study. Seizure 1998;7:403-6.
9. Wilkus RJ, Dodrill CB. Factors affecting the outcome of MMPI and neurosychological assessments of psychogenic and epileptic seizure patients. Epilepsia 1989;30:339-47.
10. Walczak TS, Papacostas S, Williams DT, et al. Outcome after diagnosis of psychogenic nonepileptic seizures. Epilepsia 1995;36:1131-7.
When patients can’t sleep
Careful investigation can often reveal insomnia’s cause1—whether a medical or psychiatric condition or poor sleep habits. Understanding why patients can’t sleep is key to effective therapy.
Insomnia is associated with increased risk of accidents, work-related difficulties, and relationship problems.2 Long-term sleeplessness may even increase risk of new psychiatric disorders—most notably major depression.3
Primary Insomnia
DSM-IV-TR criteria for primary insomnia include:4
- For at least 1 month, the patient’s main complaint has been trouble going to sleep, staying asleep, or feeling unrested.
- The insomnia or resulting daytime fatigue causes clinically important distress or impairs work, social, or personal functioning.
- The insomnia does not occur solely in the course of a breathing-related or circadian rhythm sleep disorder, a parasomnia, or as part of another mental disorder such as delirium, generalized anxiety disorder, or major depressive disorder.
Adjustment sleep disorder. Acute emotional stressors—such as bereavement, job loss, or hospitalization—can cause insomnia or daytime sleepiness. Symptoms typically remit soon after the stressors abate, so this insomnia usually lasts a few days (acute) to a few months (short-term). It can also become chronic, lasting3 months or longer.
Psychophysiologic insomnia. Once insomnia begins—regardless of its cause—sleep problems may persist well after precipitating factors resolve. The mechanism may be related to somatized tension and learned sleep-preventing associations (trying too hard to sleep and conditioned arousal to the bedroom). Thus, short-term insomnia may develop into long-term, chronic difficulty with recurring episodes or a constant, daily pattern of insomnia.
Treatment for both adjustment sleep disorder and psychophysiologic insomnia with behavioral therapies and hypnotics6 is warranted if:
- sleepiness and fatigue interfere with daytime function
- the patient is significantly distressed
- a pattern of recurring episodes develops.5
Psychiatric Disorders and Insomnia
Depression. Up to 80% of depressed persons experience insomnia, although no one sleep pattern seems typical.7 Depression may be associated with:
- difficulties in falling asleep
- interrupted nocturnal sleep
- early morning awakening.
Some patients experience panic symptoms while sleeping, possibly in association with mild hypercapnia. Those patients tend to have earlier onset of panic disorder and a higher likelihood of comorbid mood and other anxiety disorders.8
In patients with PTSD, disturbed sleep continuity and increased REM phasic activity—such as eye movements—are directly correlated with PTSD symptom severity. Nightmares and disturbed REM sleep are hallmarks of PTSD.9
Workup of Sleep Complaints
The patient history is an important part of the evaluation and treatment of insomnia and other sleep disturbances (Algorithm).12
Acute. Many short-term insomnias—lasting a few weeks or less—are caused by situational stressors, circadian rhythm changes, or poor sleep hygiene (Table 1).1 A logical approach is to begin sleep hygiene measures and explore the patient’s life situation to uncover what might be causing the insomnia. Hypnotic agents may be considered if insomnia is associated with daytime sleepiness or occupational impairment or if it seems to be escalating and your assessment indicates that it is a primary condition.
Chronic. For longer-term insomnias—lasting more than a few months—consider a more thorough evaluation, including medical and psychiatric history, physical examination, and mental status examination. A differential assessment can be made on the basis of whether a patient has difficulty falling or staying asleep (Table 1). Ask about cardinal symptoms of disorders associated with insomnia, including:
- snoring or breathing pauses during sleep (sleep apnea syndrome)
- restlessness or twitching in the lower extremities (PLMD/RLS).
Carefully review the patient’s weekday and weekend sleep patterns, bedtime habits, sleep hygiene habits, and substance and medication use.
Sleep clinic referrals. Consider an evaluation by a sleep disorders center when the diagnosis remains unclear or treatment of the presumed condition fails after a reasonable time.
Table 1
Possible causes of sleep complaints
| Acute, transient | Recent or recurring stress | |
| Change in sleeping environment | ||
| Acute illness or injury | ||
| New medications | ||
| Jet lag or shift change | ||
| Chronic | Difficulty staying asleep | Difficulty falling asleep |
| Medications | Poor sleep hygiene | |
| Drug or alcohol use | Conditioned insomnia | |
| Psychiatric disorder | Restless legs syndrome | |
| Medical disorder | Circadian rhythm disorder | |
| Sleep-disordered breathing | Advanced sleep-phase syndrome | |
| Periodic limb movement disorder | ||
| Restless legs syndrome | ||
| Source: Adapted and reprinted with permission from reference 13 | ||
Behavioral Treatments
Behavioral treatments—with or without hypnotics—are appropriate for many insomnia complaints, including adjustment sleep disorder and psychophysiologic insomnia. Behavioral measures may work more slowly than drug therapy, but their effects have been shown to last longer in patients with primary insomnia. It may be useful to start with both hypnotic and behavioral treatments and withdraw the hypnotic after behavioral measures take effect.
Sleep hygiene. Many individuals unknowingly engage in habits that impair sleep. Those with insomnia, for example, often try to compensate for lost sleep by staying in bed later in the morning or by napping, which further fragment nocturnal sleep. Advise these patients to adhere to a regular awakening time—regardless of how long they slept the night before—and to avoid naps. Other tips for getting a good night’s sleep are outlined in Table 2.14
Caffeine has a plasma half-life of 3 to 7 hours, although individual sensitivity varies widely and caffeine’s erratic absorption can prolong its effects. Advise patients with insomnia to avoid caffeine-containing beverages—including coffee, tea, and soft drinks—after noon.
Relaxation training. Muscle tension can be reduced through techniques such as electromyography (EMG) biofeedback, abdominal breathing exercises, or progressive muscle relaxation. Relaxation training is usually effective within a few weeks.
Psychological counseling. Counseling can help identify and dispel tension-producing thoughts that may be disrupting sleep, such as preoccupation with unpleasant work experiences or school examinations. Reassurance may help patients overcome fears about sleeplessness; suggest that they deal with anxiety-producing thoughts during counseling sessions and at times other than bedtime.
Table 2
How to get a good night’s sleep
|
Prescribing Hypnotics
Sedative-hypnotics are indicated primarily for short-term insomnia management. Most are used at bedtime until insomnia dissipates or the physician advises the patient to take a break.
Treatment principles. Because many insomnias are recurrent, prolonged hypnotic treatment given in short bouts is often optimal. Longer treatment—months to years—is clearly needed by a few patients with chronic insomnia. In these cases, carefully monitor for tolerance, as manifested by dosage escalation. Hypnotic treatment is generally not suitable for patients with drug abuse or dependence histories.
Although chloral hydrate and barbiturates are effective hypnotics, adverse effects limit their safety and usefulness. Benzodiazepines and more recently introduced agents have milder side-effect profiles (Table 3). Choose agents based on the patient’s situation, preferences, and effects of prior trials with similar agents. Guidelines for hypnotics discourage chronic use to minimize abuse, misuse, and habituation (Table 4).
Elimination half-life is one of the most important pharmacological properties that differentiates the hypnotics from each other:15
- longer half-life: flurazepam, quazepam
- intermediate half-life: estazolam, temazepam, eszopiclone
- short half-life: triazolam, zolpidem, zolpidem ER, zaleplon, ramelteon.
Benzodiazepine receptor agonists. Of the all the drugs in class, zalepon—because of its ultra-short half-life—is least likely to cause residual daytime effects when administered at bedtime. At 10-mg doses, its side effects seem to last no more than 4 hours after administration. Zaleplon can be safely taken after nocturnal awakenings if the patient remains in bed 4 hours or longer after taking it.17
An ultra-short half life is less desirable for patients with difficulty with sleep initiation and discontinuous sleep throughout the night. For them, longer elimination half-life agents—such as zolpidem, zolpidem extended release (ER), and eszopiclone—may be more predictably effective for the entire night.18
Short half-life hypnotics do not offer anxiolysis for patients with daytime anxiety, as the longer half-life agents do.
Zolpidem ER and eszopiclone do not have a limitation imposed on duration of use. Although zolpidem ER has not been investigated in controlled trials greater than 3 weeks, eszopiclone was evaluated during a 6-month study that demonstrated lack of tolerance during the entire period, and lack of rebound after rapid discontinuation.19 Eszopiclone is the only hypnotic indicated for long-term (lasting > 3 weeks) insomnia.
Melatonin receptor agonists. Ramelteon’s activity at MT1 and MT2 receptors is believed to contribute to its sleep-promoting properties. This agent has been found to reduce sleep latency,20,21 and it is indicated to treat insomnia characterized by sleep-onset delays. Although controlled, longterm studies are lacking, ramelteon does not have a limit on duration of use. It demonstrated a lack of abuse liability when compared with triazolam and placebo in subjects with a history of sedative/hypnotic or anxiolytic drug abuse.22
Tolerance and rebound. Tolerance can develop after repeated dosing with benzodiazepines—primarily triazolam—and rebound insomnia can follow abrupt discontinuation. Both can be minimized by using benzodiazepines at the lowest effective dosages and for brief periods. Gradual tapering when discontinuing the drug can help control rebound.
Tolerance and rebound seem to be less of a concern with the newer hypnotics than with benzodiazepines, as shown by controlled studies of eszopiclone19, zolpidem23, and zaleplon.24 However, periodic re-evaluation is still the prudent clinical standard for hypnotics prescribed over long periods of time.
Table 3
Actions and available doses of common hypnotics
| Class/drug | Onset of action | Half-life (hrs) | Active metabolites | Doses (mg) |
|---|---|---|---|---|
| Benzodiazepines | ||||
| Flurazepam | Rapid | 40 to 250 | Yes | 15, 30 |
| Quazepam | Rapid | 40 to 250 | Yes | 7.5, 15 |
| Estazolam | Rapid | 10 to 24 | Yes | 0.5, 1, 2 |
| Temazepam | Intermediate | 8 to 22 | No | 7.5, 15 |
| Triazolam | Rapid | No | 0.125, 0.25, 0.5 | |
| Imidazopyridine | ||||
| Zolpidem | Rapid | 2.5 | No | 5, 10 |
| Zolpidem ER | Rapid | 2.5 | No | 6.25, 12.5 |
| Pyrazolopyrimidines | ||||
| Zaleplon | Rapid | 1 | No | 5, 10, 20 |
| Cyclopyrrolone | ||||
| Eszopiclone | Rapid | 6 | Minor | 2,3 |
| Melatonin receptor agonist | ||||
| Ramelteon | Rapid | 1 to 2.6 | No | 8 |
Guidelines for safe use of hypnotics
|
Nonhypnotic Sleep AIDS
Sedating antidepressants. Some physicians prescribe low doses of sedating antidepressants to control insomnia, a practice supported by controlled clinical trials of some tricyclic antidepressants (TCAs) such as doxepin,25 trazodone,26 and trimipramine.27 Some physicians also advocate using more-sedating antidepressants—at dosages needed to treat depression—to control insomnia in depressed patients.
Evening dosing can minimize daytime sedation. If you choose an activating antidepressant, the potential side effect of insomnia can be managed by judicious use of hypnotic agents. Little is known about antidepressants’ effects on sleep quality after the first 6 to 8 weeks of treatment.28
Although possibly helpful as sleep aids, TCAs are associated with anticholinergic effects such as dry mouth, urinary flow difficulties, and cardiac dysrhythmias.
Alcohol. Patients with insomnia sometimes selfmedicate with alcohol at bedtime because it enhances sleepiness and induces a more rapid sleep onset.29 Drinking a “nightcap” is a poor choice, however, because alcohol can impair sleep quality, resulting in daytime somnolence. Alcohol is also associated with rapid development of tolerance.
Antihistamines and over-the-counter products whose main active ingredients are antihistamines—such as doxylamine and diphenhydramine—are used for insomnia and may help individuals fall asleep and stay asleep. However, antihistamine use is complicated by unpredictable efficacy and side effects such as daytime sedation, confusion, and systemic anticholinergic effects.30
Melatonin is a nonprescription dietary supplement used in dosages of 0.5 to 3,000 mg. Anecdotal reports indicate it may be efficacious in certain subtypes of insomnia—such as shift work, jet lag, blindness, delayed sleep phase syndrome—and in older patients with sleep complaints.
Melatonin’s efficacy has not been established conclusively, however, and concerns have been expressed regarding the purity of over-the-counter preparations and possible coronary artery tissue stimulation, as observed in animal studies.
Related resources
- American Academy of Sleep Medicine. Sleep logs, patient education materials. www.aasmnet.org
- American Sleep Apnea Association. National Sleep Foundation. www.sleepapnea.org
- Doxepin • Inequan
- Estazolam • Prosom
- Eszopiclone • Lunesta
- Flurazepam • Dalmane
- Quazepam • Doral
- Ramelteon • Rozerem
- Temazepam • Restoril
- Trazodone • Desyrel
- Triazolam • Halcion
- Trimipramine • Surmontil
- Zaleplon • Sonata
- Zolpidem • Ambien
Dr. Doghramji receives research grant support from Cephalon, GlaxoSmithKline, Merck & Co., and Sanofi-Synthelabo
1. Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. Sleep 2000;23:243-81.
2. Zammit GK, Weiner J, Damato N, et al. Quality of life in people with insomnia. Sleep 1999;22(suppl 2):S379-385.
3. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. JAMA 1989;262:1479-84.
4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington DC: American Psychiatric Association, 2000.
5. International Classification of Sleep Disorders: Diagnostic and Coding Manual, (2nd ed.) Westchester, IL: The American Academy of Sleep Medicine, 2005.
6. Spielman AJ, Glovinsky P. The varied nature of insomnia. In: Hauri P (ed). Case studies in insomnia. New York: Plenum Press, 1991;1:15.-
7. Reynolds CF, III, Kupfer DJ. Sleep research in affective illness: state of the art circa 1987. Sleep 1987;10:199-215.
8. Labbate LA, Pollack MH, Otto MW, et al. Sleep panic attacks: an association with childhood anxiety and adult psychopathology. Biol Psychiatry 1994;43:840-2.
9. Ross RJ, Ball WA, Sullivan KA, et al. Sleep disturbance as the hallmark of posttraumatic stress disorder. Am J Psychiatry 1989;146:697-707.
10. Winokur A, Reynolds CF. The effects of antidepressants on sleep physiology. Primary Psychiatry 1994;6:22-7.
11. Gillin JC, Rapaport M, Erman MK, et al. A comparison of nefazodone and fluoxetine on mood and on objective, subjective, and clinician-rated measures of sleep in depressed patients: a double blind, 8-week clinical trial. J Clin Psychiatry 1997;58(5):185-92.
12. Erman M. Clinical update. Diagnosis of insomnia in the primary care practice. Available at: http://www.medscape.com/viewarticle/478849. Accessed Jan. 18, 2005.
13. Rajput V, Bromley SM. Chronic insomnia: A practical review. Am Fam Physician 1999;60:1431-8.
14. Doghramji K. The evaluation and management of sleep disorders. In: Stoudemire A (ed). Clinical psychiatry for medical students (3rd ed). Philadelphia: JB Lippincott, 1998;783-818.
15. Gillin JC. The long and short of sleeping pills. N Engl J Med 1991;324:1735-7.
16. Lunesta (eszopiclone). Approved labeling text. Marlborough, MA: Sepracor, Inc., 2005.
17. Corser B, Mayleben D, Doghramji K, et al. No next-day residual sedation four hours after middle-of-the-night treatment with zaleplon. Sleep 2000;23(suppl 2):abstract 309.
18. Holm KJ, Goa KL. Zolpidem: an update of its pharmacology, therapeutic efficacy and tolerability in the treatment of insomnia. Drugs 2000;59:865-89.
19. Scarf MB, Roth T, Vogel GW, Walsh JK. A multicenter, placebocontrolled study evaluating zolpidem in the treatment of chronic insomnia. J Clin Psychiatry 1994;55:192-9.
20. Roth T, Stubbs C, Walsh JK. Ramelteon (TAK-375), a selective MT1/MT2-receptor agonist, reduces sleep latency to persistent sleep in a model of transient insomnia related to a novel sleep environment. Sleep 2005;28:303-7.
21. Roth T, Seiden D, Sainati S, et al. Phase III outpatient trial of ramelteon for the treatment of chronic insomniain elderly patients (poster presentation). Orlando, FL: American Geriatric Society annual meeting, 2005.
22. Griffiths R, Seuss P. Ramelteonand triazolam in humans: behavioral effectsand abuse potential (poster presentation). Atlanta, GA: American Psychiatric Association annual meeting, 2005.
23. Elie R, Ruther E, Farr I, et al. Sleep latency is shortened during 4 weeks of treatment with zaleplon, a novel nonbenzodiazepine hypnotic. Zaleplon Clinical Study Group. J Clin Psychiatry 1999;60:536-44.
24. Krystal A, Walsh J, Laska E, et al. Sustained efficacy of eszopiclone over six months of nightly treatment: results of a randomized, double-blind, placebo-controlled study in adults with chronic insomnia. Sleep 2003;26:793-9.
25. Hajak G, Rodenbeck A, Voderholzer U, et al. Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study. J Clin Psychiatry 2001;62:453-63.
26. Walsh JK, Erman M, Erwin CE, et al. Subjective hypnotic efficacy of trazodone and zolpidem in DSM-III-R primary insomnia. Hum Psychopharmacol 1998;13(3):191-8.
27. Hohagen F, Monero RF, Weiss E, et al. Treatment of primary insomnia with trimipramine: an alternative to benzodiazepine hypnotics? Eur Arch Psychiatry Clin Neurosci 1994;244(2):65-72.
28. Thase ME. Antidepressant treatment of the depressed patient with insomnia. J Clin Psychiatry 1999;60(suppl 17):28-31.
29. Johnson EO, Roehrs T, Roth T, Breslau N. Epidemiology of alcohol and medication as aids to sleep in early adulthood. Sleep 1998;21:178-86.
30. Gengo F, Gabos C, Miller JK. The pharmacodynamics of diphenhydramine-induced drowsiness and changes in mental performance. Clin Pharmacol Ther 1989;45:15-21.
Careful investigation can often reveal insomnia’s cause1—whether a medical or psychiatric condition or poor sleep habits. Understanding why patients can’t sleep is key to effective therapy.
Insomnia is associated with increased risk of accidents, work-related difficulties, and relationship problems.2 Long-term sleeplessness may even increase risk of new psychiatric disorders—most notably major depression.3
Primary Insomnia
DSM-IV-TR criteria for primary insomnia include:4
- For at least 1 month, the patient’s main complaint has been trouble going to sleep, staying asleep, or feeling unrested.
- The insomnia or resulting daytime fatigue causes clinically important distress or impairs work, social, or personal functioning.
- The insomnia does not occur solely in the course of a breathing-related or circadian rhythm sleep disorder, a parasomnia, or as part of another mental disorder such as delirium, generalized anxiety disorder, or major depressive disorder.
Adjustment sleep disorder. Acute emotional stressors—such as bereavement, job loss, or hospitalization—can cause insomnia or daytime sleepiness. Symptoms typically remit soon after the stressors abate, so this insomnia usually lasts a few days (acute) to a few months (short-term). It can also become chronic, lasting3 months or longer.
Psychophysiologic insomnia. Once insomnia begins—regardless of its cause—sleep problems may persist well after precipitating factors resolve. The mechanism may be related to somatized tension and learned sleep-preventing associations (trying too hard to sleep and conditioned arousal to the bedroom). Thus, short-term insomnia may develop into long-term, chronic difficulty with recurring episodes or a constant, daily pattern of insomnia.
Treatment for both adjustment sleep disorder and psychophysiologic insomnia with behavioral therapies and hypnotics6 is warranted if:
- sleepiness and fatigue interfere with daytime function
- the patient is significantly distressed
- a pattern of recurring episodes develops.5
Psychiatric Disorders and Insomnia
Depression. Up to 80% of depressed persons experience insomnia, although no one sleep pattern seems typical.7 Depression may be associated with:
- difficulties in falling asleep
- interrupted nocturnal sleep
- early morning awakening.
Some patients experience panic symptoms while sleeping, possibly in association with mild hypercapnia. Those patients tend to have earlier onset of panic disorder and a higher likelihood of comorbid mood and other anxiety disorders.8
In patients with PTSD, disturbed sleep continuity and increased REM phasic activity—such as eye movements—are directly correlated with PTSD symptom severity. Nightmares and disturbed REM sleep are hallmarks of PTSD.9
Workup of Sleep Complaints
The patient history is an important part of the evaluation and treatment of insomnia and other sleep disturbances (Algorithm).12
Acute. Many short-term insomnias—lasting a few weeks or less—are caused by situational stressors, circadian rhythm changes, or poor sleep hygiene (Table 1).1 A logical approach is to begin sleep hygiene measures and explore the patient’s life situation to uncover what might be causing the insomnia. Hypnotic agents may be considered if insomnia is associated with daytime sleepiness or occupational impairment or if it seems to be escalating and your assessment indicates that it is a primary condition.
Chronic. For longer-term insomnias—lasting more than a few months—consider a more thorough evaluation, including medical and psychiatric history, physical examination, and mental status examination. A differential assessment can be made on the basis of whether a patient has difficulty falling or staying asleep (Table 1). Ask about cardinal symptoms of disorders associated with insomnia, including:
- snoring or breathing pauses during sleep (sleep apnea syndrome)
- restlessness or twitching in the lower extremities (PLMD/RLS).
Carefully review the patient’s weekday and weekend sleep patterns, bedtime habits, sleep hygiene habits, and substance and medication use.
Sleep clinic referrals. Consider an evaluation by a sleep disorders center when the diagnosis remains unclear or treatment of the presumed condition fails after a reasonable time.
Table 1
Possible causes of sleep complaints
| Acute, transient | Recent or recurring stress | |
| Change in sleeping environment | ||
| Acute illness or injury | ||
| New medications | ||
| Jet lag or shift change | ||
| Chronic | Difficulty staying asleep | Difficulty falling asleep |
| Medications | Poor sleep hygiene | |
| Drug or alcohol use | Conditioned insomnia | |
| Psychiatric disorder | Restless legs syndrome | |
| Medical disorder | Circadian rhythm disorder | |
| Sleep-disordered breathing | Advanced sleep-phase syndrome | |
| Periodic limb movement disorder | ||
| Restless legs syndrome | ||
| Source: Adapted and reprinted with permission from reference 13 | ||
Behavioral Treatments
Behavioral treatments—with or without hypnotics—are appropriate for many insomnia complaints, including adjustment sleep disorder and psychophysiologic insomnia. Behavioral measures may work more slowly than drug therapy, but their effects have been shown to last longer in patients with primary insomnia. It may be useful to start with both hypnotic and behavioral treatments and withdraw the hypnotic after behavioral measures take effect.
Sleep hygiene. Many individuals unknowingly engage in habits that impair sleep. Those with insomnia, for example, often try to compensate for lost sleep by staying in bed later in the morning or by napping, which further fragment nocturnal sleep. Advise these patients to adhere to a regular awakening time—regardless of how long they slept the night before—and to avoid naps. Other tips for getting a good night’s sleep are outlined in Table 2.14
Caffeine has a plasma half-life of 3 to 7 hours, although individual sensitivity varies widely and caffeine’s erratic absorption can prolong its effects. Advise patients with insomnia to avoid caffeine-containing beverages—including coffee, tea, and soft drinks—after noon.
Relaxation training. Muscle tension can be reduced through techniques such as electromyography (EMG) biofeedback, abdominal breathing exercises, or progressive muscle relaxation. Relaxation training is usually effective within a few weeks.
Psychological counseling. Counseling can help identify and dispel tension-producing thoughts that may be disrupting sleep, such as preoccupation with unpleasant work experiences or school examinations. Reassurance may help patients overcome fears about sleeplessness; suggest that they deal with anxiety-producing thoughts during counseling sessions and at times other than bedtime.
Table 2
How to get a good night’s sleep
|
Prescribing Hypnotics
Sedative-hypnotics are indicated primarily for short-term insomnia management. Most are used at bedtime until insomnia dissipates or the physician advises the patient to take a break.
Treatment principles. Because many insomnias are recurrent, prolonged hypnotic treatment given in short bouts is often optimal. Longer treatment—months to years—is clearly needed by a few patients with chronic insomnia. In these cases, carefully monitor for tolerance, as manifested by dosage escalation. Hypnotic treatment is generally not suitable for patients with drug abuse or dependence histories.
Although chloral hydrate and barbiturates are effective hypnotics, adverse effects limit their safety and usefulness. Benzodiazepines and more recently introduced agents have milder side-effect profiles (Table 3). Choose agents based on the patient’s situation, preferences, and effects of prior trials with similar agents. Guidelines for hypnotics discourage chronic use to minimize abuse, misuse, and habituation (Table 4).
Elimination half-life is one of the most important pharmacological properties that differentiates the hypnotics from each other:15
- longer half-life: flurazepam, quazepam
- intermediate half-life: estazolam, temazepam, eszopiclone
- short half-life: triazolam, zolpidem, zolpidem ER, zaleplon, ramelteon.
Benzodiazepine receptor agonists. Of the all the drugs in class, zalepon—because of its ultra-short half-life—is least likely to cause residual daytime effects when administered at bedtime. At 10-mg doses, its side effects seem to last no more than 4 hours after administration. Zaleplon can be safely taken after nocturnal awakenings if the patient remains in bed 4 hours or longer after taking it.17
An ultra-short half life is less desirable for patients with difficulty with sleep initiation and discontinuous sleep throughout the night. For them, longer elimination half-life agents—such as zolpidem, zolpidem extended release (ER), and eszopiclone—may be more predictably effective for the entire night.18
Short half-life hypnotics do not offer anxiolysis for patients with daytime anxiety, as the longer half-life agents do.
Zolpidem ER and eszopiclone do not have a limitation imposed on duration of use. Although zolpidem ER has not been investigated in controlled trials greater than 3 weeks, eszopiclone was evaluated during a 6-month study that demonstrated lack of tolerance during the entire period, and lack of rebound after rapid discontinuation.19 Eszopiclone is the only hypnotic indicated for long-term (lasting > 3 weeks) insomnia.
Melatonin receptor agonists. Ramelteon’s activity at MT1 and MT2 receptors is believed to contribute to its sleep-promoting properties. This agent has been found to reduce sleep latency,20,21 and it is indicated to treat insomnia characterized by sleep-onset delays. Although controlled, longterm studies are lacking, ramelteon does not have a limit on duration of use. It demonstrated a lack of abuse liability when compared with triazolam and placebo in subjects with a history of sedative/hypnotic or anxiolytic drug abuse.22
Tolerance and rebound. Tolerance can develop after repeated dosing with benzodiazepines—primarily triazolam—and rebound insomnia can follow abrupt discontinuation. Both can be minimized by using benzodiazepines at the lowest effective dosages and for brief periods. Gradual tapering when discontinuing the drug can help control rebound.
Tolerance and rebound seem to be less of a concern with the newer hypnotics than with benzodiazepines, as shown by controlled studies of eszopiclone19, zolpidem23, and zaleplon.24 However, periodic re-evaluation is still the prudent clinical standard for hypnotics prescribed over long periods of time.
Table 3
Actions and available doses of common hypnotics
| Class/drug | Onset of action | Half-life (hrs) | Active metabolites | Doses (mg) |
|---|---|---|---|---|
| Benzodiazepines | ||||
| Flurazepam | Rapid | 40 to 250 | Yes | 15, 30 |
| Quazepam | Rapid | 40 to 250 | Yes | 7.5, 15 |
| Estazolam | Rapid | 10 to 24 | Yes | 0.5, 1, 2 |
| Temazepam | Intermediate | 8 to 22 | No | 7.5, 15 |
| Triazolam | Rapid | No | 0.125, 0.25, 0.5 | |
| Imidazopyridine | ||||
| Zolpidem | Rapid | 2.5 | No | 5, 10 |
| Zolpidem ER | Rapid | 2.5 | No | 6.25, 12.5 |
| Pyrazolopyrimidines | ||||
| Zaleplon | Rapid | 1 | No | 5, 10, 20 |
| Cyclopyrrolone | ||||
| Eszopiclone | Rapid | 6 | Minor | 2,3 |
| Melatonin receptor agonist | ||||
| Ramelteon | Rapid | 1 to 2.6 | No | 8 |
Guidelines for safe use of hypnotics
|
Nonhypnotic Sleep AIDS
Sedating antidepressants. Some physicians prescribe low doses of sedating antidepressants to control insomnia, a practice supported by controlled clinical trials of some tricyclic antidepressants (TCAs) such as doxepin,25 trazodone,26 and trimipramine.27 Some physicians also advocate using more-sedating antidepressants—at dosages needed to treat depression—to control insomnia in depressed patients.
Evening dosing can minimize daytime sedation. If you choose an activating antidepressant, the potential side effect of insomnia can be managed by judicious use of hypnotic agents. Little is known about antidepressants’ effects on sleep quality after the first 6 to 8 weeks of treatment.28
Although possibly helpful as sleep aids, TCAs are associated with anticholinergic effects such as dry mouth, urinary flow difficulties, and cardiac dysrhythmias.
Alcohol. Patients with insomnia sometimes selfmedicate with alcohol at bedtime because it enhances sleepiness and induces a more rapid sleep onset.29 Drinking a “nightcap” is a poor choice, however, because alcohol can impair sleep quality, resulting in daytime somnolence. Alcohol is also associated with rapid development of tolerance.
Antihistamines and over-the-counter products whose main active ingredients are antihistamines—such as doxylamine and diphenhydramine—are used for insomnia and may help individuals fall asleep and stay asleep. However, antihistamine use is complicated by unpredictable efficacy and side effects such as daytime sedation, confusion, and systemic anticholinergic effects.30
Melatonin is a nonprescription dietary supplement used in dosages of 0.5 to 3,000 mg. Anecdotal reports indicate it may be efficacious in certain subtypes of insomnia—such as shift work, jet lag, blindness, delayed sleep phase syndrome—and in older patients with sleep complaints.
Melatonin’s efficacy has not been established conclusively, however, and concerns have been expressed regarding the purity of over-the-counter preparations and possible coronary artery tissue stimulation, as observed in animal studies.
Related resources
- American Academy of Sleep Medicine. Sleep logs, patient education materials. www.aasmnet.org
- American Sleep Apnea Association. National Sleep Foundation. www.sleepapnea.org
- Doxepin • Inequan
- Estazolam • Prosom
- Eszopiclone • Lunesta
- Flurazepam • Dalmane
- Quazepam • Doral
- Ramelteon • Rozerem
- Temazepam • Restoril
- Trazodone • Desyrel
- Triazolam • Halcion
- Trimipramine • Surmontil
- Zaleplon • Sonata
- Zolpidem • Ambien
Dr. Doghramji receives research grant support from Cephalon, GlaxoSmithKline, Merck & Co., and Sanofi-Synthelabo
Careful investigation can often reveal insomnia’s cause1—whether a medical or psychiatric condition or poor sleep habits. Understanding why patients can’t sleep is key to effective therapy.
Insomnia is associated with increased risk of accidents, work-related difficulties, and relationship problems.2 Long-term sleeplessness may even increase risk of new psychiatric disorders—most notably major depression.3
Primary Insomnia
DSM-IV-TR criteria for primary insomnia include:4
- For at least 1 month, the patient’s main complaint has been trouble going to sleep, staying asleep, or feeling unrested.
- The insomnia or resulting daytime fatigue causes clinically important distress or impairs work, social, or personal functioning.
- The insomnia does not occur solely in the course of a breathing-related or circadian rhythm sleep disorder, a parasomnia, or as part of another mental disorder such as delirium, generalized anxiety disorder, or major depressive disorder.
Adjustment sleep disorder. Acute emotional stressors—such as bereavement, job loss, or hospitalization—can cause insomnia or daytime sleepiness. Symptoms typically remit soon after the stressors abate, so this insomnia usually lasts a few days (acute) to a few months (short-term). It can also become chronic, lasting3 months or longer.
Psychophysiologic insomnia. Once insomnia begins—regardless of its cause—sleep problems may persist well after precipitating factors resolve. The mechanism may be related to somatized tension and learned sleep-preventing associations (trying too hard to sleep and conditioned arousal to the bedroom). Thus, short-term insomnia may develop into long-term, chronic difficulty with recurring episodes or a constant, daily pattern of insomnia.
Treatment for both adjustment sleep disorder and psychophysiologic insomnia with behavioral therapies and hypnotics6 is warranted if:
- sleepiness and fatigue interfere with daytime function
- the patient is significantly distressed
- a pattern of recurring episodes develops.5
Psychiatric Disorders and Insomnia
Depression. Up to 80% of depressed persons experience insomnia, although no one sleep pattern seems typical.7 Depression may be associated with:
- difficulties in falling asleep
- interrupted nocturnal sleep
- early morning awakening.
Some patients experience panic symptoms while sleeping, possibly in association with mild hypercapnia. Those patients tend to have earlier onset of panic disorder and a higher likelihood of comorbid mood and other anxiety disorders.8
In patients with PTSD, disturbed sleep continuity and increased REM phasic activity—such as eye movements—are directly correlated with PTSD symptom severity. Nightmares and disturbed REM sleep are hallmarks of PTSD.9
Workup of Sleep Complaints
The patient history is an important part of the evaluation and treatment of insomnia and other sleep disturbances (Algorithm).12
Acute. Many short-term insomnias—lasting a few weeks or less—are caused by situational stressors, circadian rhythm changes, or poor sleep hygiene (Table 1).1 A logical approach is to begin sleep hygiene measures and explore the patient’s life situation to uncover what might be causing the insomnia. Hypnotic agents may be considered if insomnia is associated with daytime sleepiness or occupational impairment or if it seems to be escalating and your assessment indicates that it is a primary condition.
Chronic. For longer-term insomnias—lasting more than a few months—consider a more thorough evaluation, including medical and psychiatric history, physical examination, and mental status examination. A differential assessment can be made on the basis of whether a patient has difficulty falling or staying asleep (Table 1). Ask about cardinal symptoms of disorders associated with insomnia, including:
- snoring or breathing pauses during sleep (sleep apnea syndrome)
- restlessness or twitching in the lower extremities (PLMD/RLS).
Carefully review the patient’s weekday and weekend sleep patterns, bedtime habits, sleep hygiene habits, and substance and medication use.
Sleep clinic referrals. Consider an evaluation by a sleep disorders center when the diagnosis remains unclear or treatment of the presumed condition fails after a reasonable time.
Table 1
Possible causes of sleep complaints
| Acute, transient | Recent or recurring stress | |
| Change in sleeping environment | ||
| Acute illness or injury | ||
| New medications | ||
| Jet lag or shift change | ||
| Chronic | Difficulty staying asleep | Difficulty falling asleep |
| Medications | Poor sleep hygiene | |
| Drug or alcohol use | Conditioned insomnia | |
| Psychiatric disorder | Restless legs syndrome | |
| Medical disorder | Circadian rhythm disorder | |
| Sleep-disordered breathing | Advanced sleep-phase syndrome | |
| Periodic limb movement disorder | ||
| Restless legs syndrome | ||
| Source: Adapted and reprinted with permission from reference 13 | ||
Behavioral Treatments
Behavioral treatments—with or without hypnotics—are appropriate for many insomnia complaints, including adjustment sleep disorder and psychophysiologic insomnia. Behavioral measures may work more slowly than drug therapy, but their effects have been shown to last longer in patients with primary insomnia. It may be useful to start with both hypnotic and behavioral treatments and withdraw the hypnotic after behavioral measures take effect.
Sleep hygiene. Many individuals unknowingly engage in habits that impair sleep. Those with insomnia, for example, often try to compensate for lost sleep by staying in bed later in the morning or by napping, which further fragment nocturnal sleep. Advise these patients to adhere to a regular awakening time—regardless of how long they slept the night before—and to avoid naps. Other tips for getting a good night’s sleep are outlined in Table 2.14
Caffeine has a plasma half-life of 3 to 7 hours, although individual sensitivity varies widely and caffeine’s erratic absorption can prolong its effects. Advise patients with insomnia to avoid caffeine-containing beverages—including coffee, tea, and soft drinks—after noon.
Relaxation training. Muscle tension can be reduced through techniques such as electromyography (EMG) biofeedback, abdominal breathing exercises, or progressive muscle relaxation. Relaxation training is usually effective within a few weeks.
Psychological counseling. Counseling can help identify and dispel tension-producing thoughts that may be disrupting sleep, such as preoccupation with unpleasant work experiences or school examinations. Reassurance may help patients overcome fears about sleeplessness; suggest that they deal with anxiety-producing thoughts during counseling sessions and at times other than bedtime.
Table 2
How to get a good night’s sleep
|
Prescribing Hypnotics
Sedative-hypnotics are indicated primarily for short-term insomnia management. Most are used at bedtime until insomnia dissipates or the physician advises the patient to take a break.
Treatment principles. Because many insomnias are recurrent, prolonged hypnotic treatment given in short bouts is often optimal. Longer treatment—months to years—is clearly needed by a few patients with chronic insomnia. In these cases, carefully monitor for tolerance, as manifested by dosage escalation. Hypnotic treatment is generally not suitable for patients with drug abuse or dependence histories.
Although chloral hydrate and barbiturates are effective hypnotics, adverse effects limit their safety and usefulness. Benzodiazepines and more recently introduced agents have milder side-effect profiles (Table 3). Choose agents based on the patient’s situation, preferences, and effects of prior trials with similar agents. Guidelines for hypnotics discourage chronic use to minimize abuse, misuse, and habituation (Table 4).
Elimination half-life is one of the most important pharmacological properties that differentiates the hypnotics from each other:15
- longer half-life: flurazepam, quazepam
- intermediate half-life: estazolam, temazepam, eszopiclone
- short half-life: triazolam, zolpidem, zolpidem ER, zaleplon, ramelteon.
Benzodiazepine receptor agonists. Of the all the drugs in class, zalepon—because of its ultra-short half-life—is least likely to cause residual daytime effects when administered at bedtime. At 10-mg doses, its side effects seem to last no more than 4 hours after administration. Zaleplon can be safely taken after nocturnal awakenings if the patient remains in bed 4 hours or longer after taking it.17
An ultra-short half life is less desirable for patients with difficulty with sleep initiation and discontinuous sleep throughout the night. For them, longer elimination half-life agents—such as zolpidem, zolpidem extended release (ER), and eszopiclone—may be more predictably effective for the entire night.18
Short half-life hypnotics do not offer anxiolysis for patients with daytime anxiety, as the longer half-life agents do.
Zolpidem ER and eszopiclone do not have a limitation imposed on duration of use. Although zolpidem ER has not been investigated in controlled trials greater than 3 weeks, eszopiclone was evaluated during a 6-month study that demonstrated lack of tolerance during the entire period, and lack of rebound after rapid discontinuation.19 Eszopiclone is the only hypnotic indicated for long-term (lasting > 3 weeks) insomnia.
Melatonin receptor agonists. Ramelteon’s activity at MT1 and MT2 receptors is believed to contribute to its sleep-promoting properties. This agent has been found to reduce sleep latency,20,21 and it is indicated to treat insomnia characterized by sleep-onset delays. Although controlled, longterm studies are lacking, ramelteon does not have a limit on duration of use. It demonstrated a lack of abuse liability when compared with triazolam and placebo in subjects with a history of sedative/hypnotic or anxiolytic drug abuse.22
Tolerance and rebound. Tolerance can develop after repeated dosing with benzodiazepines—primarily triazolam—and rebound insomnia can follow abrupt discontinuation. Both can be minimized by using benzodiazepines at the lowest effective dosages and for brief periods. Gradual tapering when discontinuing the drug can help control rebound.
Tolerance and rebound seem to be less of a concern with the newer hypnotics than with benzodiazepines, as shown by controlled studies of eszopiclone19, zolpidem23, and zaleplon.24 However, periodic re-evaluation is still the prudent clinical standard for hypnotics prescribed over long periods of time.
Table 3
Actions and available doses of common hypnotics
| Class/drug | Onset of action | Half-life (hrs) | Active metabolites | Doses (mg) |
|---|---|---|---|---|
| Benzodiazepines | ||||
| Flurazepam | Rapid | 40 to 250 | Yes | 15, 30 |
| Quazepam | Rapid | 40 to 250 | Yes | 7.5, 15 |
| Estazolam | Rapid | 10 to 24 | Yes | 0.5, 1, 2 |
| Temazepam | Intermediate | 8 to 22 | No | 7.5, 15 |
| Triazolam | Rapid | No | 0.125, 0.25, 0.5 | |
| Imidazopyridine | ||||
| Zolpidem | Rapid | 2.5 | No | 5, 10 |
| Zolpidem ER | Rapid | 2.5 | No | 6.25, 12.5 |
| Pyrazolopyrimidines | ||||
| Zaleplon | Rapid | 1 | No | 5, 10, 20 |
| Cyclopyrrolone | ||||
| Eszopiclone | Rapid | 6 | Minor | 2,3 |
| Melatonin receptor agonist | ||||
| Ramelteon | Rapid | 1 to 2.6 | No | 8 |
Guidelines for safe use of hypnotics
|
Nonhypnotic Sleep AIDS
Sedating antidepressants. Some physicians prescribe low doses of sedating antidepressants to control insomnia, a practice supported by controlled clinical trials of some tricyclic antidepressants (TCAs) such as doxepin,25 trazodone,26 and trimipramine.27 Some physicians also advocate using more-sedating antidepressants—at dosages needed to treat depression—to control insomnia in depressed patients.
Evening dosing can minimize daytime sedation. If you choose an activating antidepressant, the potential side effect of insomnia can be managed by judicious use of hypnotic agents. Little is known about antidepressants’ effects on sleep quality after the first 6 to 8 weeks of treatment.28
Although possibly helpful as sleep aids, TCAs are associated with anticholinergic effects such as dry mouth, urinary flow difficulties, and cardiac dysrhythmias.
Alcohol. Patients with insomnia sometimes selfmedicate with alcohol at bedtime because it enhances sleepiness and induces a more rapid sleep onset.29 Drinking a “nightcap” is a poor choice, however, because alcohol can impair sleep quality, resulting in daytime somnolence. Alcohol is also associated with rapid development of tolerance.
Antihistamines and over-the-counter products whose main active ingredients are antihistamines—such as doxylamine and diphenhydramine—are used for insomnia and may help individuals fall asleep and stay asleep. However, antihistamine use is complicated by unpredictable efficacy and side effects such as daytime sedation, confusion, and systemic anticholinergic effects.30
Melatonin is a nonprescription dietary supplement used in dosages of 0.5 to 3,000 mg. Anecdotal reports indicate it may be efficacious in certain subtypes of insomnia—such as shift work, jet lag, blindness, delayed sleep phase syndrome—and in older patients with sleep complaints.
Melatonin’s efficacy has not been established conclusively, however, and concerns have been expressed regarding the purity of over-the-counter preparations and possible coronary artery tissue stimulation, as observed in animal studies.
Related resources
- American Academy of Sleep Medicine. Sleep logs, patient education materials. www.aasmnet.org
- American Sleep Apnea Association. National Sleep Foundation. www.sleepapnea.org
- Doxepin • Inequan
- Estazolam • Prosom
- Eszopiclone • Lunesta
- Flurazepam • Dalmane
- Quazepam • Doral
- Ramelteon • Rozerem
- Temazepam • Restoril
- Trazodone • Desyrel
- Triazolam • Halcion
- Trimipramine • Surmontil
- Zaleplon • Sonata
- Zolpidem • Ambien
Dr. Doghramji receives research grant support from Cephalon, GlaxoSmithKline, Merck & Co., and Sanofi-Synthelabo
1. Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. Sleep 2000;23:243-81.
2. Zammit GK, Weiner J, Damato N, et al. Quality of life in people with insomnia. Sleep 1999;22(suppl 2):S379-385.
3. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. JAMA 1989;262:1479-84.
4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington DC: American Psychiatric Association, 2000.
5. International Classification of Sleep Disorders: Diagnostic and Coding Manual, (2nd ed.) Westchester, IL: The American Academy of Sleep Medicine, 2005.
6. Spielman AJ, Glovinsky P. The varied nature of insomnia. In: Hauri P (ed). Case studies in insomnia. New York: Plenum Press, 1991;1:15.-
7. Reynolds CF, III, Kupfer DJ. Sleep research in affective illness: state of the art circa 1987. Sleep 1987;10:199-215.
8. Labbate LA, Pollack MH, Otto MW, et al. Sleep panic attacks: an association with childhood anxiety and adult psychopathology. Biol Psychiatry 1994;43:840-2.
9. Ross RJ, Ball WA, Sullivan KA, et al. Sleep disturbance as the hallmark of posttraumatic stress disorder. Am J Psychiatry 1989;146:697-707.
10. Winokur A, Reynolds CF. The effects of antidepressants on sleep physiology. Primary Psychiatry 1994;6:22-7.
11. Gillin JC, Rapaport M, Erman MK, et al. A comparison of nefazodone and fluoxetine on mood and on objective, subjective, and clinician-rated measures of sleep in depressed patients: a double blind, 8-week clinical trial. J Clin Psychiatry 1997;58(5):185-92.
12. Erman M. Clinical update. Diagnosis of insomnia in the primary care practice. Available at: http://www.medscape.com/viewarticle/478849. Accessed Jan. 18, 2005.
13. Rajput V, Bromley SM. Chronic insomnia: A practical review. Am Fam Physician 1999;60:1431-8.
14. Doghramji K. The evaluation and management of sleep disorders. In: Stoudemire A (ed). Clinical psychiatry for medical students (3rd ed). Philadelphia: JB Lippincott, 1998;783-818.
15. Gillin JC. The long and short of sleeping pills. N Engl J Med 1991;324:1735-7.
16. Lunesta (eszopiclone). Approved labeling text. Marlborough, MA: Sepracor, Inc., 2005.
17. Corser B, Mayleben D, Doghramji K, et al. No next-day residual sedation four hours after middle-of-the-night treatment with zaleplon. Sleep 2000;23(suppl 2):abstract 309.
18. Holm KJ, Goa KL. Zolpidem: an update of its pharmacology, therapeutic efficacy and tolerability in the treatment of insomnia. Drugs 2000;59:865-89.
19. Scarf MB, Roth T, Vogel GW, Walsh JK. A multicenter, placebocontrolled study evaluating zolpidem in the treatment of chronic insomnia. J Clin Psychiatry 1994;55:192-9.
20. Roth T, Stubbs C, Walsh JK. Ramelteon (TAK-375), a selective MT1/MT2-receptor agonist, reduces sleep latency to persistent sleep in a model of transient insomnia related to a novel sleep environment. Sleep 2005;28:303-7.
21. Roth T, Seiden D, Sainati S, et al. Phase III outpatient trial of ramelteon for the treatment of chronic insomniain elderly patients (poster presentation). Orlando, FL: American Geriatric Society annual meeting, 2005.
22. Griffiths R, Seuss P. Ramelteonand triazolam in humans: behavioral effectsand abuse potential (poster presentation). Atlanta, GA: American Psychiatric Association annual meeting, 2005.
23. Elie R, Ruther E, Farr I, et al. Sleep latency is shortened during 4 weeks of treatment with zaleplon, a novel nonbenzodiazepine hypnotic. Zaleplon Clinical Study Group. J Clin Psychiatry 1999;60:536-44.
24. Krystal A, Walsh J, Laska E, et al. Sustained efficacy of eszopiclone over six months of nightly treatment: results of a randomized, double-blind, placebo-controlled study in adults with chronic insomnia. Sleep 2003;26:793-9.
25. Hajak G, Rodenbeck A, Voderholzer U, et al. Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study. J Clin Psychiatry 2001;62:453-63.
26. Walsh JK, Erman M, Erwin CE, et al. Subjective hypnotic efficacy of trazodone and zolpidem in DSM-III-R primary insomnia. Hum Psychopharmacol 1998;13(3):191-8.
27. Hohagen F, Monero RF, Weiss E, et al. Treatment of primary insomnia with trimipramine: an alternative to benzodiazepine hypnotics? Eur Arch Psychiatry Clin Neurosci 1994;244(2):65-72.
28. Thase ME. Antidepressant treatment of the depressed patient with insomnia. J Clin Psychiatry 1999;60(suppl 17):28-31.
29. Johnson EO, Roehrs T, Roth T, Breslau N. Epidemiology of alcohol and medication as aids to sleep in early adulthood. Sleep 1998;21:178-86.
30. Gengo F, Gabos C, Miller JK. The pharmacodynamics of diphenhydramine-induced drowsiness and changes in mental performance. Clin Pharmacol Ther 1989;45:15-21.
1. Sateia MJ, Doghramji K, Hauri PJ, Morin CM. Evaluation of chronic insomnia. Sleep 2000;23:243-81.
2. Zammit GK, Weiner J, Damato N, et al. Quality of life in people with insomnia. Sleep 1999;22(suppl 2):S379-385.
3. Ford DE, Kamerow DB. Epidemiologic study of sleep disturbances and psychiatric disorders. JAMA 1989;262:1479-84.
4. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington DC: American Psychiatric Association, 2000.
5. International Classification of Sleep Disorders: Diagnostic and Coding Manual, (2nd ed.) Westchester, IL: The American Academy of Sleep Medicine, 2005.
6. Spielman AJ, Glovinsky P. The varied nature of insomnia. In: Hauri P (ed). Case studies in insomnia. New York: Plenum Press, 1991;1:15.-
7. Reynolds CF, III, Kupfer DJ. Sleep research in affective illness: state of the art circa 1987. Sleep 1987;10:199-215.
8. Labbate LA, Pollack MH, Otto MW, et al. Sleep panic attacks: an association with childhood anxiety and adult psychopathology. Biol Psychiatry 1994;43:840-2.
9. Ross RJ, Ball WA, Sullivan KA, et al. Sleep disturbance as the hallmark of posttraumatic stress disorder. Am J Psychiatry 1989;146:697-707.
10. Winokur A, Reynolds CF. The effects of antidepressants on sleep physiology. Primary Psychiatry 1994;6:22-7.
11. Gillin JC, Rapaport M, Erman MK, et al. A comparison of nefazodone and fluoxetine on mood and on objective, subjective, and clinician-rated measures of sleep in depressed patients: a double blind, 8-week clinical trial. J Clin Psychiatry 1997;58(5):185-92.
12. Erman M. Clinical update. Diagnosis of insomnia in the primary care practice. Available at: http://www.medscape.com/viewarticle/478849. Accessed Jan. 18, 2005.
13. Rajput V, Bromley SM. Chronic insomnia: A practical review. Am Fam Physician 1999;60:1431-8.
14. Doghramji K. The evaluation and management of sleep disorders. In: Stoudemire A (ed). Clinical psychiatry for medical students (3rd ed). Philadelphia: JB Lippincott, 1998;783-818.
15. Gillin JC. The long and short of sleeping pills. N Engl J Med 1991;324:1735-7.
16. Lunesta (eszopiclone). Approved labeling text. Marlborough, MA: Sepracor, Inc., 2005.
17. Corser B, Mayleben D, Doghramji K, et al. No next-day residual sedation four hours after middle-of-the-night treatment with zaleplon. Sleep 2000;23(suppl 2):abstract 309.
18. Holm KJ, Goa KL. Zolpidem: an update of its pharmacology, therapeutic efficacy and tolerability in the treatment of insomnia. Drugs 2000;59:865-89.
19. Scarf MB, Roth T, Vogel GW, Walsh JK. A multicenter, placebocontrolled study evaluating zolpidem in the treatment of chronic insomnia. J Clin Psychiatry 1994;55:192-9.
20. Roth T, Stubbs C, Walsh JK. Ramelteon (TAK-375), a selective MT1/MT2-receptor agonist, reduces sleep latency to persistent sleep in a model of transient insomnia related to a novel sleep environment. Sleep 2005;28:303-7.
21. Roth T, Seiden D, Sainati S, et al. Phase III outpatient trial of ramelteon for the treatment of chronic insomniain elderly patients (poster presentation). Orlando, FL: American Geriatric Society annual meeting, 2005.
22. Griffiths R, Seuss P. Ramelteonand triazolam in humans: behavioral effectsand abuse potential (poster presentation). Atlanta, GA: American Psychiatric Association annual meeting, 2005.
23. Elie R, Ruther E, Farr I, et al. Sleep latency is shortened during 4 weeks of treatment with zaleplon, a novel nonbenzodiazepine hypnotic. Zaleplon Clinical Study Group. J Clin Psychiatry 1999;60:536-44.
24. Krystal A, Walsh J, Laska E, et al. Sustained efficacy of eszopiclone over six months of nightly treatment: results of a randomized, double-blind, placebo-controlled study in adults with chronic insomnia. Sleep 2003;26:793-9.
25. Hajak G, Rodenbeck A, Voderholzer U, et al. Doxepin in the treatment of primary insomnia: a placebo-controlled, double-blind, polysomnographic study. J Clin Psychiatry 2001;62:453-63.
26. Walsh JK, Erman M, Erwin CE, et al. Subjective hypnotic efficacy of trazodone and zolpidem in DSM-III-R primary insomnia. Hum Psychopharmacol 1998;13(3):191-8.
27. Hohagen F, Monero RF, Weiss E, et al. Treatment of primary insomnia with trimipramine: an alternative to benzodiazepine hypnotics? Eur Arch Psychiatry Clin Neurosci 1994;244(2):65-72.
28. Thase ME. Antidepressant treatment of the depressed patient with insomnia. J Clin Psychiatry 1999;60(suppl 17):28-31.
29. Johnson EO, Roehrs T, Roth T, Breslau N. Epidemiology of alcohol and medication as aids to sleep in early adulthood. Sleep 1998;21:178-86.
30. Gengo F, Gabos C, Miller JK. The pharmacodynamics of diphenhydramine-induced drowsiness and changes in mental performance. Clin Pharmacol Ther 1989;45:15-21.
How to avoid burnout and keep your spark
Burnout develops slowly and insidiously; there are no fire alarms, no smoke. It is easy to ignore the warning signs. As psychiatrists, we are at high risk for burnout, and the consequences can be devastating. We have:
- suicide rates 2 to 3 times higher than those of the general population
- higher rates of divorce and substance abuse compared with other physicians and non-physicians (Table 1).1-12
Burnout affects 25% to 57% of our profession at any given time,13 yet we seldom address it. Despite vast literature on burnout in family medicine and other medical specialties, psychiatric burnout is grossly under-recognized. It’s as if we aren’t supposed to burn out; after all, aren’t we the experts others come to when they are burned out?
If you think you may be heading toward burnout, we offer practical, evidence-based information to help you:
- prevent burnout
- diagnose burnout, “brownout,” and “compassion fatigue”
- begin to make immediate changes to over-come burnout and reclaim your life.
Table 1
Relative rates of divorce, suicide, and substance abuse among psychiatrists
| Event | Psychiatrists | Other physicians | General population |
|---|---|---|---|
| Divorce* | 50% (2.7 times risk of other physicians)3 | 22% to 24% in internists and pediatricians3 | 10% to 20% less than among physicians4 |
| Suicide | 28 to 40/100,0001 (2 to 3 times rate in general population) | May be similar to rate among psychiatrists† Equal rates in male and female physicians | 12/100,000 |
| Rate in female physicians is 2 to 4 times that of women in general population1,2,5 | |||
| Substance abuse6-10 | |||
| Benzodiazepine use (past year)6 | 26.3% | 7% to 16% (11.4% across all specialties) | |
| Lifetime abuse/dependence6 | 14.3% | 7.9% | |
| Alcohol only | 7.9% | 4.2% | |
| * Divorce risk across 30 years | |||
| † Some but not all evidence indicates psychiatrists have higher rates of suicide than other physicians1,2,11,12 | |||
Case: ‘Something in me had died’
I (PB) was 50 years old, racing along, seeing patients 45 hours a week, and keeping a full schedule of teaching and writing. Psychotherapy was my primary training and my love, but monitoring medications for other therapists—without getting to know the patients—had become unsatisfying. My practice group had exploded from 5 mental health professionals to more than 20, creating unexpected stresses and conflicts. At the same time, my marriage was failing.
Increasingly overextended, I lost my good humor. I became irritable and short with everyone, and—worse—I felt resentful and burdened by my patients. Once eager for challenges, I avoided new consults and referrals. Every hour was filled with dread, and I struggled to get through the day. Empty, numb, and miserable, I had burned out but did not realize it. I only knew that something in me had died.
I started fantasizing about retiring from clinical work, but what would I do then? What if this was the end of my career?
Burnout is a ‘heart attack’
Most burnout definitions include three features: emotional exhaustion, depersonalization, and diminished feelings of personal accomplishment.14 Some writers describe it as a state of mourning: “A grief syndrome due to loss of our dreams or sense of purpose or mission, leading to the experience of emotional depletion…expectations clash with an imposing reality.”15
Burnout represents a loss of meaning. It resembles a “spiritual heart attack,” with “referred pain” that affects our work, our relationships, and our soul. We become members of the “coronary club” (Box 1).16
- Your job comes first; personal considerations are secondary.
- Go to the office evenings, weekends, and holidays.
- Never say no to a request; always say yes.
- Accept all invitations to meetings, banquets, committees, etc.
- Do not eat a restful, relaxing meal; always plan a meeting for the meal hour.
- Never delegate responsibility to others; carry the entire load by yourself at all times.
Are you getting close to eligibility?
The “15-minute” medication check is probably the most demoralizing hazard. Pressure from managed care to focus on brief contact with patients only for medication management is dispiriting, resulting in:
- little time for empathic connection
- loss of professional autonomy
- fear of greater liability risk than when we handle psychotherapy and medication
- fear of lost income if we opt not to accept medication-only referrals.17-21
Internal causes. Approximately 60% of job satisfaction is related to internal determinants: attitudes, beliefs, lifestyle, and coping techniques. Burnout is not simply the result of overwork, underpay, or increasing demands of a changing medical culture. If all managed care hassles disappeared tomorrow—if paperwork went away and reimbursements flowed freely—burnout would continue because it is the loss of a dream. Freuden-berger23 refers to it as a loss of idealism; a loss of expected goals.
Psychiatry is about intimate human relationships, connectedness, and accompanying our patients over the complex terrain of the human condition. Often, burnout develops when something disrupts the physician-patient bond. As Irvin Yalom reminds us, “It’s the relationship that heals.” That relationship is healing to the physician as well as to the patient.24
Burnout comes from decreased quality of fulfillment we derive from our efforts. It concerns intangible phenomena such as losing our sense of purpose or feeling we are not making a difference. We wonder: Am I doing what I was born to do? Burnout is suffering that goes beyond a worn-down body and approaches “erosion of the soul.”25
Diversify your portfolio
Physician-author Rachel Naomi Remen, MD, clinical professor of family and community medicine at the University of California, San Francisco, reminds us, “Service in medicine is the work of the heart and the soul.”26 To heal ourselves, we must by nurturing and cultivating our inner life. By plumbing these depths, you may rediscover your sense of purpose.
You may need to “diversify your portfolio” with reflective and regenerative activities. These may be as varied as reading poetry, paddling canoes, spiritual practices, gardening, hiking, or visiting art museums.
More importantly, you may need to re-examine and deepen your relationships with:
- your partner (Are you spending enough time together? Is your relationship growing?)
- your patients (Are you getting to know your patients as people?)
- your sense of purpose or spirituality (Do you see a higher or transcendent meaning in your life?)
- the community, the world. (Are you making them better?).
What’s your diagnosis?
How do you know if you have brownout (mild depression; a prodromal phase), classic burnout (severe depression), or compassion fatigue (a form of burnout)?
Brownout vs burnout (Table 2). Look for depressive symptoms: sad mood, lack of pleasure, low energy or motivation, poor concentration or memory, or insomnia. In addition, you may experience a “deadness” at work, as well as “marital deadness.” The “helper’s high” has become the “helper’s low.” You may anger quickly and have tensions with your family or co-workers. Signs of burnout include disorganization and chronic lateness, absenteeism, or “presenteeism” (physically present, spiritually and go beyond the mind and body to address the soul emotionally absent).
Irritability and lack of time for family can cause extensive collateral damage:
- Wife of a burned-out doctor: “My husband wasn’t there for our son’s 6th birthday, and he missed our daughter’s high-school graduation. He’s missed half their childhoods.”
- Husband of a burned-out psychiatrist: “I’m miserable. She’s not the same woman I married. She’s such a workaholic, she’s got nothing left for us.”
- A psychiatrist’s 13-year-old daughter: “He helps his patients have a good life; why can’t he do that with us?”
Are you suffering from brownout or burnout?
| Brownout (mild depression) | Burnout (severe depression) |
|---|---|
| I feel tired | I feel exhausted, listless |
| I’m having less fun and feeling less satisfied | I feel grumpy and joyless |
| I’m drinking more caffeine and eating more junk food | I’m drinking more alcohol, taking more medications, or using illicit drugs |
| I feel less interested and less caring about my patients, residents, and coworkers | I want to leave patient care, and I don’t care about my co-workers |
| I am dissatisfied, troubled | I am impaired |
Table 3
Is it burnout or compassion fatigue?
| Burnout | Compassion fatigue |
|---|---|
| Evolves gradually | Reaction to extreme circumstances or suddenly increased work demands, such as disaster relief, crisis work |
| Loss of meaning, unmet expectations | Vicarious suffering of others’ trauma (“emotional contagion”) |
| Diminished work capacity (depression, withdrawal) | Increased, relentless work effort (ignore physical health, work-‘til-you-drop mentality, obsessive-compulsive behavior) |
Intensive care for burnout
Treating or preventing burnout requires individual solutions, peer strategies, and group/organizational techniques. The first five suggestions below relate to individual steps, and the last two to peer approaches and organizational strategy.
Stop doing what you’re doing. In her book, The Joy of Burnout, Dina Glouberman, PhD, says, “Burn-out is life catching up with us…. Stop doing, and start listening to ourselves in a completely new way, to make space for our true self.”28 Better time management is not the answer; you cannot give what you do not have.
Take time off. Most experts recommend at least 1 month off to rethink things, and 6 months off to renew. I (PB) took 6 months off to recover from my burnout and needed every minute of it.
Take a serious inventory of your life and priorities, and set limits (Box 2). One psychiatrist decided he didn’t want to be on three medical society committees, two hospital committees, and a church task force. His wife had threatened to divorce him, and he was always exhausted.
- Decline (‘Thanks for thinking of me, but I can’t do that right now’)
- Delay (‘Let me think about your request’)
- Delegate
- Dump (‘I thought I could help with this task, but I find it isn’t working for me’)
Get professional counseling. Burnout is moderate or major depression. Practice what you preach.
Join a support group. Let go of, “Real doctors handle things on their own.” Focus on introspection and solutions.
Consider stress management. Options include seminars or retreats and individual, practice-oriented, and organizational consultations (see Related resources).
Burnout as opportunity
Viewing burnout as an opportunity for transformation gives you a chance to:
Re-evaluate your life and priorities. What is most important to you: Money? Family? Making your community a better place? Spiritual growth? If you knew you had only 1 year to live, how would you be living?
Renew/reinvent yourself. One burned-out psychiatrist moved from Denver to San Francisco, where he started over with no expectations or image to uphold. This made it easier to try new professional and personal ventures.
“The geographical solution” is not necessary, however, and can add stress at a vulnerable time. You can “bloom where you’re planted” and renew yourself wherever you are.
Rediscover your passion. Teaching? Art? Part-time practice and run a bed-and-breakfast? Surfing? Guitar lessons? We know physicians who used each of these to help revitalize themselves.
Case continued: recovery
As my life got worse—a drawn-out divorce, two daughters in private universities, and by now a greatly reduced income—I felt trapped and spent. I had to change or die emotionally (possibly even physically).
Not knowing what to do, I took a leap. I cashed in my retirement fund and resigned. I took a 6-month unpaid sabbatical. With no schedule to keep, I had time to read and think. I resumed my own psychotherapy, went through deep reflection, and re-evaluated my priorities and values. I took up acting for fun and started keeping a gratitude journal.
Eventually I remarried. I started changing my workaholic tendencies, limited my practice to 20 hours a week, and established that my priorities were family, friends, and the joy of helping patients and colleagues. I re-discovered my enthusiasm for teaching, including teaching others about preventing burnout.
Preventative medicine
To prevent burnout, we must learn to recognize and address brownout. This is a much better choice than trying to recover from full-fledged burnout: less disruptive, less costly, less damaging interpersonally.
How do we prevent burnout? Several approaches are particularly useful for psychiatrists:
Self-care. Take time off, but beware of “The Vacation Solution”—psychiatrists’ most popular strategy. As one put it: “I work until I’m ready to drop, then I take 2 weeks off.” This is unhealthy:
- physically (gradually wears you down)
- emotionally (we all know the risk of repeated mild depressions, or brownout)
- interpersonally (our family members and colleagues suffer as we get exhausted).
Give and get affirmation and support. Isolating yourself socially is one of the surest roads to burnout. Compared with solo practitioners, psychiatrists working at community mental health centers often report greater career satisfaction. Although they may have difficult case loads and systemic challenges, group practitioners are supported by nurses, social workers, and case managers. The team helps dilute the stress of caring for the most difficult patients.
If you have a solo practice, try to connect and commiserate with other mental health practitioners by joining a professional organization or forming your own process group. If you prefer not to socialize professionally, consider a book club, temple, or church group.
Take time to interact meaningfully: practice appreciating others at least 3 times a day. Saying, “I really admire how you handled that situation,” or “How are you doing?” takes less than 10 seconds. Appreciate your own efforts, too. Write down—now, as you read this—the names of three people you will affirm or offer support to today. Include one person you usually wouldn’t acknowledge.
Find/create meaning in your work life. When you get tired or frustrated, remind yourself that practicing psychiatry is a privilege. We make a difference with people (service) through intimate emotional connection (relationship). Altruism confers benefits to the giver and the recipient. Some psychiatrists derive meaning by seeing our profession as fulfilling a mission or higher purpose, even as a calling.
Be grateful. Gratitude can reduce depression and boost happiness and life satisfaction.29,30 For the next month, try keeping a “gratitude journal,” writing 3 to 5 things you are grateful for each day. It can produce a positive shift in mood, even after a frustrating or demanding workday.31 Start now, by writing what you are grateful for today.
Live fully in this moment. Avoid the “someday” game, waiting to be happy until… you’re caught up with your work, your children are in (or out) of school, you’re wealthy/old enough to retire, etc. Live right now, with this patient, this colleague, this family member. Focus 100% on the person or task of the moment.
Don’t let the task get between us.32 If your spouse or friend wants to visit or share feelings, make the time, even if you’re “busy.” If your patient wants an “extra minute” to thank you for your help or to show you a picture, make time happily.
Play a little every day. Take mini-vacations: walk outside, listen to or make music (a colleague next door lightens my day playing his guitar). Call your spouse or give him/her a funny greeting card, wear a light-hearted tie, bring flowers to your nurses or receptionist. Play with your patients: read poetry; have them bring in pictures of themselves when they were young to help them remember their vitality and spirit. Create your own change of pace (Box 3).
Reading this article is a start, but enduring results will happen only if you commit to follow up. Think about each strategy and decide what appeals to you most. Commit to putting 2 to 4 ideas into practice immediately, and continue them for at least 1 month.
Display the SSPARK mnemonic somewhere to remind you to take care of yourself.
SSPARK =
- Self-care
- Support/affirm
- Purpose/meaning
- Appreciate/gratitude
- Right now
- Kid around/play
- Institute for Healing in Society and Medicine. Martin Sullivan, MD. www.healinginmedicine.org
- Center for Professional Well-Being. John-Henry Pfifferling, PhD. www.cpwb.org
- Renew. Linda Clever, MD. www.renewnow.org
- WorkLife Design. Kernan Manion, MD. www.worklifedesign.org
- Menninger Clinic. Professionals in Crisis Program. www.menningerclinic.com
- Rachel Naomi Remen. Author of Kitchen Table Wisdom: Stories That Heal. www.rachelremen.com.
1. Council on Scientific Affairs: Results and implications of the AMA-APA Physician Mortality Project Stage 2. JAMA 1987;257:2949-53.
2. Hawton K, Clements A, Sakarovitch C, et al. Suicide in doctors: A study of risk according to gender, seniority and specialty in medical practitioners in England and Wales, 1979-1995. J Epidemiol Community Health 2001;55:296-300.
3. Rollman l, Mead LA, Wang N, et al. Medical specialty and the incidence of divorce. N Engl J Med 1997;336(11):800-3.
4. Sotile WM, Sotile MO. The medical marriage: A couple’s survival guide. New York: Carol Publishing; 1996.
5. Pitts FN, Schuller AB, Rich CL, et al. Suicide among U.S. women physicians 1967-1972. Am J Psychiatry 1979;136:694-6.
6. Hughes PH, Storr CL, Brandenburg NA, et al. Physician substance use by medical specialty. J Addict Dis 1999;8(2):23-37.
7. McAuliffe W, Rohman M, Santangelo S, et al. Psychoactive drug use among practicing physicians and medical students. N Engl J Med 1986;315:805-10.
8. Hughes P, Conard S, Baldwin D, et al. Resident physician substance use by specialty. Am J Psychiatry 1992;149:1348-54.
9. Maddux J, Tinnerman I, Costello R. Use of psychoactive substances by residents. J Med Educ 1987;62:852-4.
10. O’Connor PG, Spickard A. Physician impairment by substance abuse. Med Clin North Am 1997;81:1037-52.
11. Craig AG, Pitts FN. Suicide by physicians. Dis Nerv Syst 1968;29:763-72.
12. Rich CL, Pitts FN. Suicide by psychiatrists: a study of medical specialists among 18,730 consecutive physician deaths during a five-year period, 1967-72. J Clin Psychiatry 1980;41:261-3.
13. Montenegro R. A new environmental tragedy: The burn-out of mental health workers. In: Spinetti G, Janiri L (eds). Ecologia e Psichiatria. Rome: CIC Edizioni; 2001.
14. Maslach C. Burnout: The cost of caring. New York: Prentice Hall; 1982.
15. Pfifferling JH, Gilley K. Putting ‘life’ back into your professional life. Fam Pract Manag 1999;6(6):36-42.
16. Adapted from Bits × Pieces January 7 1993. Author unknown.
17. Private Practice Holds Its Own. Psychiatric News April 7, 1995, pp 11, 28.
18. Mizner GL. Current problems in the private practice of psychotherapy. Psychiatric Times August 1994, p 19.
19. Henneberger M. Managed care changing practice of psychotherapy. The New York Times October 9, 1994, pp 1, 50.
20. Pollock EJ. Managed care’s focus on psychiatric drugs alarms many doctors. Wall Street Journal December 1, 1995, pp A1, A11.
21. Hymowitz C. High anxiety: in the name of Freud, why are patients complaining so much? Wall Street Journal December 12, 1995, pp A1, A10.
22. Kalman TP, Goldstein MA. Satisfaction of Manhattan psychiatrists with private practice: assessing the impact of managed care. Medscape Psychiatry & Mental Health eJournal 1998; 3(1).
23. Freudenberger HJ. Staff burn-out. Journal of Social Issues 1974;30:159-65.
24. Yalom ID. Love’s executioner and other tales of psychotherapy. New York: Harper Collins; 1989.
25. Maslach C, Leiter M. The truth about burnout: How organizations cause personal stress and what to do about it. San Francisco, CA: Jossey-Bass Inc.; 1997.
26. Remen RN. Recapturing the soul of medicine: Physicians need to reclaim meaning in their lives. West J Med 2001;174(1):4-5.
27. Figley CR. Compassion fatigue: Coping with secondary post traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995.
28. Glouberman D. The joy of burnout: How the end of the world can be a new beginning. Makawao, HI: Inner Ocean Publishing; 2003.
29. Emmons RA, McCullough ME. Counting blessings versus burdens: Experimental studies of gratitude and subjective well-being in daily life. J Pers Soc Psychol 2003;84(2):377-89.
30. Seligman ME. Positive psychology process: Empirical validation of interventions. Am Psychol 2005;60(5):410-21.
31. Sheldon KM, Lyubomirsky S. How to increase and sustain positive emotion: The benefits of expressing gratitude and visualizing best possible selves. Journal of Positive Psychology, in press.
32. Remen RN. Kitchen table wisdom: Stories that heal. New York: Riverhead Books; 1997.
Burnout develops slowly and insidiously; there are no fire alarms, no smoke. It is easy to ignore the warning signs. As psychiatrists, we are at high risk for burnout, and the consequences can be devastating. We have:
- suicide rates 2 to 3 times higher than those of the general population
- higher rates of divorce and substance abuse compared with other physicians and non-physicians (Table 1).1-12
Burnout affects 25% to 57% of our profession at any given time,13 yet we seldom address it. Despite vast literature on burnout in family medicine and other medical specialties, psychiatric burnout is grossly under-recognized. It’s as if we aren’t supposed to burn out; after all, aren’t we the experts others come to when they are burned out?
If you think you may be heading toward burnout, we offer practical, evidence-based information to help you:
- prevent burnout
- diagnose burnout, “brownout,” and “compassion fatigue”
- begin to make immediate changes to over-come burnout and reclaim your life.
Table 1
Relative rates of divorce, suicide, and substance abuse among psychiatrists
| Event | Psychiatrists | Other physicians | General population |
|---|---|---|---|
| Divorce* | 50% (2.7 times risk of other physicians)3 | 22% to 24% in internists and pediatricians3 | 10% to 20% less than among physicians4 |
| Suicide | 28 to 40/100,0001 (2 to 3 times rate in general population) | May be similar to rate among psychiatrists† Equal rates in male and female physicians | 12/100,000 |
| Rate in female physicians is 2 to 4 times that of women in general population1,2,5 | |||
| Substance abuse6-10 | |||
| Benzodiazepine use (past year)6 | 26.3% | 7% to 16% (11.4% across all specialties) | |
| Lifetime abuse/dependence6 | 14.3% | 7.9% | |
| Alcohol only | 7.9% | 4.2% | |
| * Divorce risk across 30 years | |||
| † Some but not all evidence indicates psychiatrists have higher rates of suicide than other physicians1,2,11,12 | |||
Case: ‘Something in me had died’
I (PB) was 50 years old, racing along, seeing patients 45 hours a week, and keeping a full schedule of teaching and writing. Psychotherapy was my primary training and my love, but monitoring medications for other therapists—without getting to know the patients—had become unsatisfying. My practice group had exploded from 5 mental health professionals to more than 20, creating unexpected stresses and conflicts. At the same time, my marriage was failing.
Increasingly overextended, I lost my good humor. I became irritable and short with everyone, and—worse—I felt resentful and burdened by my patients. Once eager for challenges, I avoided new consults and referrals. Every hour was filled with dread, and I struggled to get through the day. Empty, numb, and miserable, I had burned out but did not realize it. I only knew that something in me had died.
I started fantasizing about retiring from clinical work, but what would I do then? What if this was the end of my career?
Burnout is a ‘heart attack’
Most burnout definitions include three features: emotional exhaustion, depersonalization, and diminished feelings of personal accomplishment.14 Some writers describe it as a state of mourning: “A grief syndrome due to loss of our dreams or sense of purpose or mission, leading to the experience of emotional depletion…expectations clash with an imposing reality.”15
Burnout represents a loss of meaning. It resembles a “spiritual heart attack,” with “referred pain” that affects our work, our relationships, and our soul. We become members of the “coronary club” (Box 1).16
- Your job comes first; personal considerations are secondary.
- Go to the office evenings, weekends, and holidays.
- Never say no to a request; always say yes.
- Accept all invitations to meetings, banquets, committees, etc.
- Do not eat a restful, relaxing meal; always plan a meeting for the meal hour.
- Never delegate responsibility to others; carry the entire load by yourself at all times.
Are you getting close to eligibility?
The “15-minute” medication check is probably the most demoralizing hazard. Pressure from managed care to focus on brief contact with patients only for medication management is dispiriting, resulting in:
- little time for empathic connection
- loss of professional autonomy
- fear of greater liability risk than when we handle psychotherapy and medication
- fear of lost income if we opt not to accept medication-only referrals.17-21
Internal causes. Approximately 60% of job satisfaction is related to internal determinants: attitudes, beliefs, lifestyle, and coping techniques. Burnout is not simply the result of overwork, underpay, or increasing demands of a changing medical culture. If all managed care hassles disappeared tomorrow—if paperwork went away and reimbursements flowed freely—burnout would continue because it is the loss of a dream. Freuden-berger23 refers to it as a loss of idealism; a loss of expected goals.
Psychiatry is about intimate human relationships, connectedness, and accompanying our patients over the complex terrain of the human condition. Often, burnout develops when something disrupts the physician-patient bond. As Irvin Yalom reminds us, “It’s the relationship that heals.” That relationship is healing to the physician as well as to the patient.24
Burnout comes from decreased quality of fulfillment we derive from our efforts. It concerns intangible phenomena such as losing our sense of purpose or feeling we are not making a difference. We wonder: Am I doing what I was born to do? Burnout is suffering that goes beyond a worn-down body and approaches “erosion of the soul.”25
Diversify your portfolio
Physician-author Rachel Naomi Remen, MD, clinical professor of family and community medicine at the University of California, San Francisco, reminds us, “Service in medicine is the work of the heart and the soul.”26 To heal ourselves, we must by nurturing and cultivating our inner life. By plumbing these depths, you may rediscover your sense of purpose.
You may need to “diversify your portfolio” with reflective and regenerative activities. These may be as varied as reading poetry, paddling canoes, spiritual practices, gardening, hiking, or visiting art museums.
More importantly, you may need to re-examine and deepen your relationships with:
- your partner (Are you spending enough time together? Is your relationship growing?)
- your patients (Are you getting to know your patients as people?)
- your sense of purpose or spirituality (Do you see a higher or transcendent meaning in your life?)
- the community, the world. (Are you making them better?).
What’s your diagnosis?
How do you know if you have brownout (mild depression; a prodromal phase), classic burnout (severe depression), or compassion fatigue (a form of burnout)?
Brownout vs burnout (Table 2). Look for depressive symptoms: sad mood, lack of pleasure, low energy or motivation, poor concentration or memory, or insomnia. In addition, you may experience a “deadness” at work, as well as “marital deadness.” The “helper’s high” has become the “helper’s low.” You may anger quickly and have tensions with your family or co-workers. Signs of burnout include disorganization and chronic lateness, absenteeism, or “presenteeism” (physically present, spiritually and go beyond the mind and body to address the soul emotionally absent).
Irritability and lack of time for family can cause extensive collateral damage:
- Wife of a burned-out doctor: “My husband wasn’t there for our son’s 6th birthday, and he missed our daughter’s high-school graduation. He’s missed half their childhoods.”
- Husband of a burned-out psychiatrist: “I’m miserable. She’s not the same woman I married. She’s such a workaholic, she’s got nothing left for us.”
- A psychiatrist’s 13-year-old daughter: “He helps his patients have a good life; why can’t he do that with us?”
Are you suffering from brownout or burnout?
| Brownout (mild depression) | Burnout (severe depression) |
|---|---|
| I feel tired | I feel exhausted, listless |
| I’m having less fun and feeling less satisfied | I feel grumpy and joyless |
| I’m drinking more caffeine and eating more junk food | I’m drinking more alcohol, taking more medications, or using illicit drugs |
| I feel less interested and less caring about my patients, residents, and coworkers | I want to leave patient care, and I don’t care about my co-workers |
| I am dissatisfied, troubled | I am impaired |
Table 3
Is it burnout or compassion fatigue?
| Burnout | Compassion fatigue |
|---|---|
| Evolves gradually | Reaction to extreme circumstances or suddenly increased work demands, such as disaster relief, crisis work |
| Loss of meaning, unmet expectations | Vicarious suffering of others’ trauma (“emotional contagion”) |
| Diminished work capacity (depression, withdrawal) | Increased, relentless work effort (ignore physical health, work-‘til-you-drop mentality, obsessive-compulsive behavior) |
Intensive care for burnout
Treating or preventing burnout requires individual solutions, peer strategies, and group/organizational techniques. The first five suggestions below relate to individual steps, and the last two to peer approaches and organizational strategy.
Stop doing what you’re doing. In her book, The Joy of Burnout, Dina Glouberman, PhD, says, “Burn-out is life catching up with us…. Stop doing, and start listening to ourselves in a completely new way, to make space for our true self.”28 Better time management is not the answer; you cannot give what you do not have.
Take time off. Most experts recommend at least 1 month off to rethink things, and 6 months off to renew. I (PB) took 6 months off to recover from my burnout and needed every minute of it.
Take a serious inventory of your life and priorities, and set limits (Box 2). One psychiatrist decided he didn’t want to be on three medical society committees, two hospital committees, and a church task force. His wife had threatened to divorce him, and he was always exhausted.
- Decline (‘Thanks for thinking of me, but I can’t do that right now’)
- Delay (‘Let me think about your request’)
- Delegate
- Dump (‘I thought I could help with this task, but I find it isn’t working for me’)
Get professional counseling. Burnout is moderate or major depression. Practice what you preach.
Join a support group. Let go of, “Real doctors handle things on their own.” Focus on introspection and solutions.
Consider stress management. Options include seminars or retreats and individual, practice-oriented, and organizational consultations (see Related resources).
Burnout as opportunity
Viewing burnout as an opportunity for transformation gives you a chance to:
Re-evaluate your life and priorities. What is most important to you: Money? Family? Making your community a better place? Spiritual growth? If you knew you had only 1 year to live, how would you be living?
Renew/reinvent yourself. One burned-out psychiatrist moved from Denver to San Francisco, where he started over with no expectations or image to uphold. This made it easier to try new professional and personal ventures.
“The geographical solution” is not necessary, however, and can add stress at a vulnerable time. You can “bloom where you’re planted” and renew yourself wherever you are.
Rediscover your passion. Teaching? Art? Part-time practice and run a bed-and-breakfast? Surfing? Guitar lessons? We know physicians who used each of these to help revitalize themselves.
Case continued: recovery
As my life got worse—a drawn-out divorce, two daughters in private universities, and by now a greatly reduced income—I felt trapped and spent. I had to change or die emotionally (possibly even physically).
Not knowing what to do, I took a leap. I cashed in my retirement fund and resigned. I took a 6-month unpaid sabbatical. With no schedule to keep, I had time to read and think. I resumed my own psychotherapy, went through deep reflection, and re-evaluated my priorities and values. I took up acting for fun and started keeping a gratitude journal.
Eventually I remarried. I started changing my workaholic tendencies, limited my practice to 20 hours a week, and established that my priorities were family, friends, and the joy of helping patients and colleagues. I re-discovered my enthusiasm for teaching, including teaching others about preventing burnout.
Preventative medicine
To prevent burnout, we must learn to recognize and address brownout. This is a much better choice than trying to recover from full-fledged burnout: less disruptive, less costly, less damaging interpersonally.
How do we prevent burnout? Several approaches are particularly useful for psychiatrists:
Self-care. Take time off, but beware of “The Vacation Solution”—psychiatrists’ most popular strategy. As one put it: “I work until I’m ready to drop, then I take 2 weeks off.” This is unhealthy:
- physically (gradually wears you down)
- emotionally (we all know the risk of repeated mild depressions, or brownout)
- interpersonally (our family members and colleagues suffer as we get exhausted).
Give and get affirmation and support. Isolating yourself socially is one of the surest roads to burnout. Compared with solo practitioners, psychiatrists working at community mental health centers often report greater career satisfaction. Although they may have difficult case loads and systemic challenges, group practitioners are supported by nurses, social workers, and case managers. The team helps dilute the stress of caring for the most difficult patients.
If you have a solo practice, try to connect and commiserate with other mental health practitioners by joining a professional organization or forming your own process group. If you prefer not to socialize professionally, consider a book club, temple, or church group.
Take time to interact meaningfully: practice appreciating others at least 3 times a day. Saying, “I really admire how you handled that situation,” or “How are you doing?” takes less than 10 seconds. Appreciate your own efforts, too. Write down—now, as you read this—the names of three people you will affirm or offer support to today. Include one person you usually wouldn’t acknowledge.
Find/create meaning in your work life. When you get tired or frustrated, remind yourself that practicing psychiatry is a privilege. We make a difference with people (service) through intimate emotional connection (relationship). Altruism confers benefits to the giver and the recipient. Some psychiatrists derive meaning by seeing our profession as fulfilling a mission or higher purpose, even as a calling.
Be grateful. Gratitude can reduce depression and boost happiness and life satisfaction.29,30 For the next month, try keeping a “gratitude journal,” writing 3 to 5 things you are grateful for each day. It can produce a positive shift in mood, even after a frustrating or demanding workday.31 Start now, by writing what you are grateful for today.
Live fully in this moment. Avoid the “someday” game, waiting to be happy until… you’re caught up with your work, your children are in (or out) of school, you’re wealthy/old enough to retire, etc. Live right now, with this patient, this colleague, this family member. Focus 100% on the person or task of the moment.
Don’t let the task get between us.32 If your spouse or friend wants to visit or share feelings, make the time, even if you’re “busy.” If your patient wants an “extra minute” to thank you for your help or to show you a picture, make time happily.
Play a little every day. Take mini-vacations: walk outside, listen to or make music (a colleague next door lightens my day playing his guitar). Call your spouse or give him/her a funny greeting card, wear a light-hearted tie, bring flowers to your nurses or receptionist. Play with your patients: read poetry; have them bring in pictures of themselves when they were young to help them remember their vitality and spirit. Create your own change of pace (Box 3).
Reading this article is a start, but enduring results will happen only if you commit to follow up. Think about each strategy and decide what appeals to you most. Commit to putting 2 to 4 ideas into practice immediately, and continue them for at least 1 month.
Display the SSPARK mnemonic somewhere to remind you to take care of yourself.
SSPARK =
- Self-care
- Support/affirm
- Purpose/meaning
- Appreciate/gratitude
- Right now
- Kid around/play
- Institute for Healing in Society and Medicine. Martin Sullivan, MD. www.healinginmedicine.org
- Center for Professional Well-Being. John-Henry Pfifferling, PhD. www.cpwb.org
- Renew. Linda Clever, MD. www.renewnow.org
- WorkLife Design. Kernan Manion, MD. www.worklifedesign.org
- Menninger Clinic. Professionals in Crisis Program. www.menningerclinic.com
- Rachel Naomi Remen. Author of Kitchen Table Wisdom: Stories That Heal. www.rachelremen.com.
Burnout develops slowly and insidiously; there are no fire alarms, no smoke. It is easy to ignore the warning signs. As psychiatrists, we are at high risk for burnout, and the consequences can be devastating. We have:
- suicide rates 2 to 3 times higher than those of the general population
- higher rates of divorce and substance abuse compared with other physicians and non-physicians (Table 1).1-12
Burnout affects 25% to 57% of our profession at any given time,13 yet we seldom address it. Despite vast literature on burnout in family medicine and other medical specialties, psychiatric burnout is grossly under-recognized. It’s as if we aren’t supposed to burn out; after all, aren’t we the experts others come to when they are burned out?
If you think you may be heading toward burnout, we offer practical, evidence-based information to help you:
- prevent burnout
- diagnose burnout, “brownout,” and “compassion fatigue”
- begin to make immediate changes to over-come burnout and reclaim your life.
Table 1
Relative rates of divorce, suicide, and substance abuse among psychiatrists
| Event | Psychiatrists | Other physicians | General population |
|---|---|---|---|
| Divorce* | 50% (2.7 times risk of other physicians)3 | 22% to 24% in internists and pediatricians3 | 10% to 20% less than among physicians4 |
| Suicide | 28 to 40/100,0001 (2 to 3 times rate in general population) | May be similar to rate among psychiatrists† Equal rates in male and female physicians | 12/100,000 |
| Rate in female physicians is 2 to 4 times that of women in general population1,2,5 | |||
| Substance abuse6-10 | |||
| Benzodiazepine use (past year)6 | 26.3% | 7% to 16% (11.4% across all specialties) | |
| Lifetime abuse/dependence6 | 14.3% | 7.9% | |
| Alcohol only | 7.9% | 4.2% | |
| * Divorce risk across 30 years | |||
| † Some but not all evidence indicates psychiatrists have higher rates of suicide than other physicians1,2,11,12 | |||
Case: ‘Something in me had died’
I (PB) was 50 years old, racing along, seeing patients 45 hours a week, and keeping a full schedule of teaching and writing. Psychotherapy was my primary training and my love, but monitoring medications for other therapists—without getting to know the patients—had become unsatisfying. My practice group had exploded from 5 mental health professionals to more than 20, creating unexpected stresses and conflicts. At the same time, my marriage was failing.
Increasingly overextended, I lost my good humor. I became irritable and short with everyone, and—worse—I felt resentful and burdened by my patients. Once eager for challenges, I avoided new consults and referrals. Every hour was filled with dread, and I struggled to get through the day. Empty, numb, and miserable, I had burned out but did not realize it. I only knew that something in me had died.
I started fantasizing about retiring from clinical work, but what would I do then? What if this was the end of my career?
Burnout is a ‘heart attack’
Most burnout definitions include three features: emotional exhaustion, depersonalization, and diminished feelings of personal accomplishment.14 Some writers describe it as a state of mourning: “A grief syndrome due to loss of our dreams or sense of purpose or mission, leading to the experience of emotional depletion…expectations clash with an imposing reality.”15
Burnout represents a loss of meaning. It resembles a “spiritual heart attack,” with “referred pain” that affects our work, our relationships, and our soul. We become members of the “coronary club” (Box 1).16
- Your job comes first; personal considerations are secondary.
- Go to the office evenings, weekends, and holidays.
- Never say no to a request; always say yes.
- Accept all invitations to meetings, banquets, committees, etc.
- Do not eat a restful, relaxing meal; always plan a meeting for the meal hour.
- Never delegate responsibility to others; carry the entire load by yourself at all times.
Are you getting close to eligibility?
The “15-minute” medication check is probably the most demoralizing hazard. Pressure from managed care to focus on brief contact with patients only for medication management is dispiriting, resulting in:
- little time for empathic connection
- loss of professional autonomy
- fear of greater liability risk than when we handle psychotherapy and medication
- fear of lost income if we opt not to accept medication-only referrals.17-21
Internal causes. Approximately 60% of job satisfaction is related to internal determinants: attitudes, beliefs, lifestyle, and coping techniques. Burnout is not simply the result of overwork, underpay, or increasing demands of a changing medical culture. If all managed care hassles disappeared tomorrow—if paperwork went away and reimbursements flowed freely—burnout would continue because it is the loss of a dream. Freuden-berger23 refers to it as a loss of idealism; a loss of expected goals.
Psychiatry is about intimate human relationships, connectedness, and accompanying our patients over the complex terrain of the human condition. Often, burnout develops when something disrupts the physician-patient bond. As Irvin Yalom reminds us, “It’s the relationship that heals.” That relationship is healing to the physician as well as to the patient.24
Burnout comes from decreased quality of fulfillment we derive from our efforts. It concerns intangible phenomena such as losing our sense of purpose or feeling we are not making a difference. We wonder: Am I doing what I was born to do? Burnout is suffering that goes beyond a worn-down body and approaches “erosion of the soul.”25
Diversify your portfolio
Physician-author Rachel Naomi Remen, MD, clinical professor of family and community medicine at the University of California, San Francisco, reminds us, “Service in medicine is the work of the heart and the soul.”26 To heal ourselves, we must by nurturing and cultivating our inner life. By plumbing these depths, you may rediscover your sense of purpose.
You may need to “diversify your portfolio” with reflective and regenerative activities. These may be as varied as reading poetry, paddling canoes, spiritual practices, gardening, hiking, or visiting art museums.
More importantly, you may need to re-examine and deepen your relationships with:
- your partner (Are you spending enough time together? Is your relationship growing?)
- your patients (Are you getting to know your patients as people?)
- your sense of purpose or spirituality (Do you see a higher or transcendent meaning in your life?)
- the community, the world. (Are you making them better?).
What’s your diagnosis?
How do you know if you have brownout (mild depression; a prodromal phase), classic burnout (severe depression), or compassion fatigue (a form of burnout)?
Brownout vs burnout (Table 2). Look for depressive symptoms: sad mood, lack of pleasure, low energy or motivation, poor concentration or memory, or insomnia. In addition, you may experience a “deadness” at work, as well as “marital deadness.” The “helper’s high” has become the “helper’s low.” You may anger quickly and have tensions with your family or co-workers. Signs of burnout include disorganization and chronic lateness, absenteeism, or “presenteeism” (physically present, spiritually and go beyond the mind and body to address the soul emotionally absent).
Irritability and lack of time for family can cause extensive collateral damage:
- Wife of a burned-out doctor: “My husband wasn’t there for our son’s 6th birthday, and he missed our daughter’s high-school graduation. He’s missed half their childhoods.”
- Husband of a burned-out psychiatrist: “I’m miserable. She’s not the same woman I married. She’s such a workaholic, she’s got nothing left for us.”
- A psychiatrist’s 13-year-old daughter: “He helps his patients have a good life; why can’t he do that with us?”
Are you suffering from brownout or burnout?
| Brownout (mild depression) | Burnout (severe depression) |
|---|---|
| I feel tired | I feel exhausted, listless |
| I’m having less fun and feeling less satisfied | I feel grumpy and joyless |
| I’m drinking more caffeine and eating more junk food | I’m drinking more alcohol, taking more medications, or using illicit drugs |
| I feel less interested and less caring about my patients, residents, and coworkers | I want to leave patient care, and I don’t care about my co-workers |
| I am dissatisfied, troubled | I am impaired |
Table 3
Is it burnout or compassion fatigue?
| Burnout | Compassion fatigue |
|---|---|
| Evolves gradually | Reaction to extreme circumstances or suddenly increased work demands, such as disaster relief, crisis work |
| Loss of meaning, unmet expectations | Vicarious suffering of others’ trauma (“emotional contagion”) |
| Diminished work capacity (depression, withdrawal) | Increased, relentless work effort (ignore physical health, work-‘til-you-drop mentality, obsessive-compulsive behavior) |
Intensive care for burnout
Treating or preventing burnout requires individual solutions, peer strategies, and group/organizational techniques. The first five suggestions below relate to individual steps, and the last two to peer approaches and organizational strategy.
Stop doing what you’re doing. In her book, The Joy of Burnout, Dina Glouberman, PhD, says, “Burn-out is life catching up with us…. Stop doing, and start listening to ourselves in a completely new way, to make space for our true self.”28 Better time management is not the answer; you cannot give what you do not have.
Take time off. Most experts recommend at least 1 month off to rethink things, and 6 months off to renew. I (PB) took 6 months off to recover from my burnout and needed every minute of it.
Take a serious inventory of your life and priorities, and set limits (Box 2). One psychiatrist decided he didn’t want to be on three medical society committees, two hospital committees, and a church task force. His wife had threatened to divorce him, and he was always exhausted.
- Decline (‘Thanks for thinking of me, but I can’t do that right now’)
- Delay (‘Let me think about your request’)
- Delegate
- Dump (‘I thought I could help with this task, but I find it isn’t working for me’)
Get professional counseling. Burnout is moderate or major depression. Practice what you preach.
Join a support group. Let go of, “Real doctors handle things on their own.” Focus on introspection and solutions.
Consider stress management. Options include seminars or retreats and individual, practice-oriented, and organizational consultations (see Related resources).
Burnout as opportunity
Viewing burnout as an opportunity for transformation gives you a chance to:
Re-evaluate your life and priorities. What is most important to you: Money? Family? Making your community a better place? Spiritual growth? If you knew you had only 1 year to live, how would you be living?
Renew/reinvent yourself. One burned-out psychiatrist moved from Denver to San Francisco, where he started over with no expectations or image to uphold. This made it easier to try new professional and personal ventures.
“The geographical solution” is not necessary, however, and can add stress at a vulnerable time. You can “bloom where you’re planted” and renew yourself wherever you are.
Rediscover your passion. Teaching? Art? Part-time practice and run a bed-and-breakfast? Surfing? Guitar lessons? We know physicians who used each of these to help revitalize themselves.
Case continued: recovery
As my life got worse—a drawn-out divorce, two daughters in private universities, and by now a greatly reduced income—I felt trapped and spent. I had to change or die emotionally (possibly even physically).
Not knowing what to do, I took a leap. I cashed in my retirement fund and resigned. I took a 6-month unpaid sabbatical. With no schedule to keep, I had time to read and think. I resumed my own psychotherapy, went through deep reflection, and re-evaluated my priorities and values. I took up acting for fun and started keeping a gratitude journal.
Eventually I remarried. I started changing my workaholic tendencies, limited my practice to 20 hours a week, and established that my priorities were family, friends, and the joy of helping patients and colleagues. I re-discovered my enthusiasm for teaching, including teaching others about preventing burnout.
Preventative medicine
To prevent burnout, we must learn to recognize and address brownout. This is a much better choice than trying to recover from full-fledged burnout: less disruptive, less costly, less damaging interpersonally.
How do we prevent burnout? Several approaches are particularly useful for psychiatrists:
Self-care. Take time off, but beware of “The Vacation Solution”—psychiatrists’ most popular strategy. As one put it: “I work until I’m ready to drop, then I take 2 weeks off.” This is unhealthy:
- physically (gradually wears you down)
- emotionally (we all know the risk of repeated mild depressions, or brownout)
- interpersonally (our family members and colleagues suffer as we get exhausted).
Give and get affirmation and support. Isolating yourself socially is one of the surest roads to burnout. Compared with solo practitioners, psychiatrists working at community mental health centers often report greater career satisfaction. Although they may have difficult case loads and systemic challenges, group practitioners are supported by nurses, social workers, and case managers. The team helps dilute the stress of caring for the most difficult patients.
If you have a solo practice, try to connect and commiserate with other mental health practitioners by joining a professional organization or forming your own process group. If you prefer not to socialize professionally, consider a book club, temple, or church group.
Take time to interact meaningfully: practice appreciating others at least 3 times a day. Saying, “I really admire how you handled that situation,” or “How are you doing?” takes less than 10 seconds. Appreciate your own efforts, too. Write down—now, as you read this—the names of three people you will affirm or offer support to today. Include one person you usually wouldn’t acknowledge.
Find/create meaning in your work life. When you get tired or frustrated, remind yourself that practicing psychiatry is a privilege. We make a difference with people (service) through intimate emotional connection (relationship). Altruism confers benefits to the giver and the recipient. Some psychiatrists derive meaning by seeing our profession as fulfilling a mission or higher purpose, even as a calling.
Be grateful. Gratitude can reduce depression and boost happiness and life satisfaction.29,30 For the next month, try keeping a “gratitude journal,” writing 3 to 5 things you are grateful for each day. It can produce a positive shift in mood, even after a frustrating or demanding workday.31 Start now, by writing what you are grateful for today.
Live fully in this moment. Avoid the “someday” game, waiting to be happy until… you’re caught up with your work, your children are in (or out) of school, you’re wealthy/old enough to retire, etc. Live right now, with this patient, this colleague, this family member. Focus 100% on the person or task of the moment.
Don’t let the task get between us.32 If your spouse or friend wants to visit or share feelings, make the time, even if you’re “busy.” If your patient wants an “extra minute” to thank you for your help or to show you a picture, make time happily.
Play a little every day. Take mini-vacations: walk outside, listen to or make music (a colleague next door lightens my day playing his guitar). Call your spouse or give him/her a funny greeting card, wear a light-hearted tie, bring flowers to your nurses or receptionist. Play with your patients: read poetry; have them bring in pictures of themselves when they were young to help them remember their vitality and spirit. Create your own change of pace (Box 3).
Reading this article is a start, but enduring results will happen only if you commit to follow up. Think about each strategy and decide what appeals to you most. Commit to putting 2 to 4 ideas into practice immediately, and continue them for at least 1 month.
Display the SSPARK mnemonic somewhere to remind you to take care of yourself.
SSPARK =
- Self-care
- Support/affirm
- Purpose/meaning
- Appreciate/gratitude
- Right now
- Kid around/play
- Institute for Healing in Society and Medicine. Martin Sullivan, MD. www.healinginmedicine.org
- Center for Professional Well-Being. John-Henry Pfifferling, PhD. www.cpwb.org
- Renew. Linda Clever, MD. www.renewnow.org
- WorkLife Design. Kernan Manion, MD. www.worklifedesign.org
- Menninger Clinic. Professionals in Crisis Program. www.menningerclinic.com
- Rachel Naomi Remen. Author of Kitchen Table Wisdom: Stories That Heal. www.rachelremen.com.
1. Council on Scientific Affairs: Results and implications of the AMA-APA Physician Mortality Project Stage 2. JAMA 1987;257:2949-53.
2. Hawton K, Clements A, Sakarovitch C, et al. Suicide in doctors: A study of risk according to gender, seniority and specialty in medical practitioners in England and Wales, 1979-1995. J Epidemiol Community Health 2001;55:296-300.
3. Rollman l, Mead LA, Wang N, et al. Medical specialty and the incidence of divorce. N Engl J Med 1997;336(11):800-3.
4. Sotile WM, Sotile MO. The medical marriage: A couple’s survival guide. New York: Carol Publishing; 1996.
5. Pitts FN, Schuller AB, Rich CL, et al. Suicide among U.S. women physicians 1967-1972. Am J Psychiatry 1979;136:694-6.
6. Hughes PH, Storr CL, Brandenburg NA, et al. Physician substance use by medical specialty. J Addict Dis 1999;8(2):23-37.
7. McAuliffe W, Rohman M, Santangelo S, et al. Psychoactive drug use among practicing physicians and medical students. N Engl J Med 1986;315:805-10.
8. Hughes P, Conard S, Baldwin D, et al. Resident physician substance use by specialty. Am J Psychiatry 1992;149:1348-54.
9. Maddux J, Tinnerman I, Costello R. Use of psychoactive substances by residents. J Med Educ 1987;62:852-4.
10. O’Connor PG, Spickard A. Physician impairment by substance abuse. Med Clin North Am 1997;81:1037-52.
11. Craig AG, Pitts FN. Suicide by physicians. Dis Nerv Syst 1968;29:763-72.
12. Rich CL, Pitts FN. Suicide by psychiatrists: a study of medical specialists among 18,730 consecutive physician deaths during a five-year period, 1967-72. J Clin Psychiatry 1980;41:261-3.
13. Montenegro R. A new environmental tragedy: The burn-out of mental health workers. In: Spinetti G, Janiri L (eds). Ecologia e Psichiatria. Rome: CIC Edizioni; 2001.
14. Maslach C. Burnout: The cost of caring. New York: Prentice Hall; 1982.
15. Pfifferling JH, Gilley K. Putting ‘life’ back into your professional life. Fam Pract Manag 1999;6(6):36-42.
16. Adapted from Bits × Pieces January 7 1993. Author unknown.
17. Private Practice Holds Its Own. Psychiatric News April 7, 1995, pp 11, 28.
18. Mizner GL. Current problems in the private practice of psychotherapy. Psychiatric Times August 1994, p 19.
19. Henneberger M. Managed care changing practice of psychotherapy. The New York Times October 9, 1994, pp 1, 50.
20. Pollock EJ. Managed care’s focus on psychiatric drugs alarms many doctors. Wall Street Journal December 1, 1995, pp A1, A11.
21. Hymowitz C. High anxiety: in the name of Freud, why are patients complaining so much? Wall Street Journal December 12, 1995, pp A1, A10.
22. Kalman TP, Goldstein MA. Satisfaction of Manhattan psychiatrists with private practice: assessing the impact of managed care. Medscape Psychiatry & Mental Health eJournal 1998; 3(1).
23. Freudenberger HJ. Staff burn-out. Journal of Social Issues 1974;30:159-65.
24. Yalom ID. Love’s executioner and other tales of psychotherapy. New York: Harper Collins; 1989.
25. Maslach C, Leiter M. The truth about burnout: How organizations cause personal stress and what to do about it. San Francisco, CA: Jossey-Bass Inc.; 1997.
26. Remen RN. Recapturing the soul of medicine: Physicians need to reclaim meaning in their lives. West J Med 2001;174(1):4-5.
27. Figley CR. Compassion fatigue: Coping with secondary post traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995.
28. Glouberman D. The joy of burnout: How the end of the world can be a new beginning. Makawao, HI: Inner Ocean Publishing; 2003.
29. Emmons RA, McCullough ME. Counting blessings versus burdens: Experimental studies of gratitude and subjective well-being in daily life. J Pers Soc Psychol 2003;84(2):377-89.
30. Seligman ME. Positive psychology process: Empirical validation of interventions. Am Psychol 2005;60(5):410-21.
31. Sheldon KM, Lyubomirsky S. How to increase and sustain positive emotion: The benefits of expressing gratitude and visualizing best possible selves. Journal of Positive Psychology, in press.
32. Remen RN. Kitchen table wisdom: Stories that heal. New York: Riverhead Books; 1997.
1. Council on Scientific Affairs: Results and implications of the AMA-APA Physician Mortality Project Stage 2. JAMA 1987;257:2949-53.
2. Hawton K, Clements A, Sakarovitch C, et al. Suicide in doctors: A study of risk according to gender, seniority and specialty in medical practitioners in England and Wales, 1979-1995. J Epidemiol Community Health 2001;55:296-300.
3. Rollman l, Mead LA, Wang N, et al. Medical specialty and the incidence of divorce. N Engl J Med 1997;336(11):800-3.
4. Sotile WM, Sotile MO. The medical marriage: A couple’s survival guide. New York: Carol Publishing; 1996.
5. Pitts FN, Schuller AB, Rich CL, et al. Suicide among U.S. women physicians 1967-1972. Am J Psychiatry 1979;136:694-6.
6. Hughes PH, Storr CL, Brandenburg NA, et al. Physician substance use by medical specialty. J Addict Dis 1999;8(2):23-37.
7. McAuliffe W, Rohman M, Santangelo S, et al. Psychoactive drug use among practicing physicians and medical students. N Engl J Med 1986;315:805-10.
8. Hughes P, Conard S, Baldwin D, et al. Resident physician substance use by specialty. Am J Psychiatry 1992;149:1348-54.
9. Maddux J, Tinnerman I, Costello R. Use of psychoactive substances by residents. J Med Educ 1987;62:852-4.
10. O’Connor PG, Spickard A. Physician impairment by substance abuse. Med Clin North Am 1997;81:1037-52.
11. Craig AG, Pitts FN. Suicide by physicians. Dis Nerv Syst 1968;29:763-72.
12. Rich CL, Pitts FN. Suicide by psychiatrists: a study of medical specialists among 18,730 consecutive physician deaths during a five-year period, 1967-72. J Clin Psychiatry 1980;41:261-3.
13. Montenegro R. A new environmental tragedy: The burn-out of mental health workers. In: Spinetti G, Janiri L (eds). Ecologia e Psichiatria. Rome: CIC Edizioni; 2001.
14. Maslach C. Burnout: The cost of caring. New York: Prentice Hall; 1982.
15. Pfifferling JH, Gilley K. Putting ‘life’ back into your professional life. Fam Pract Manag 1999;6(6):36-42.
16. Adapted from Bits × Pieces January 7 1993. Author unknown.
17. Private Practice Holds Its Own. Psychiatric News April 7, 1995, pp 11, 28.
18. Mizner GL. Current problems in the private practice of psychotherapy. Psychiatric Times August 1994, p 19.
19. Henneberger M. Managed care changing practice of psychotherapy. The New York Times October 9, 1994, pp 1, 50.
20. Pollock EJ. Managed care’s focus on psychiatric drugs alarms many doctors. Wall Street Journal December 1, 1995, pp A1, A11.
21. Hymowitz C. High anxiety: in the name of Freud, why are patients complaining so much? Wall Street Journal December 12, 1995, pp A1, A10.
22. Kalman TP, Goldstein MA. Satisfaction of Manhattan psychiatrists with private practice: assessing the impact of managed care. Medscape Psychiatry & Mental Health eJournal 1998; 3(1).
23. Freudenberger HJ. Staff burn-out. Journal of Social Issues 1974;30:159-65.
24. Yalom ID. Love’s executioner and other tales of psychotherapy. New York: Harper Collins; 1989.
25. Maslach C, Leiter M. The truth about burnout: How organizations cause personal stress and what to do about it. San Francisco, CA: Jossey-Bass Inc.; 1997.
26. Remen RN. Recapturing the soul of medicine: Physicians need to reclaim meaning in their lives. West J Med 2001;174(1):4-5.
27. Figley CR. Compassion fatigue: Coping with secondary post traumatic stress disorder in those who treat the traumatized. New York: Brunner/Mazel; 1995.
28. Glouberman D. The joy of burnout: How the end of the world can be a new beginning. Makawao, HI: Inner Ocean Publishing; 2003.
29. Emmons RA, McCullough ME. Counting blessings versus burdens: Experimental studies of gratitude and subjective well-being in daily life. J Pers Soc Psychol 2003;84(2):377-89.
30. Seligman ME. Positive psychology process: Empirical validation of interventions. Am Psychol 2005;60(5):410-21.
31. Sheldon KM, Lyubomirsky S. How to increase and sustain positive emotion: The benefits of expressing gratitude and visualizing best possible selves. Journal of Positive Psychology, in press.
32. Remen RN. Kitchen table wisdom: Stories that heal. New York: Riverhead Books; 1997.
U.S. troops returning home: Are you prepared?
National Guard and Army Reserve troops constitute an estimated 30% to 40% of the 1 million-plus U.S. military personnel deployed in Iraq and Afghanistan.1-3 Many of these civilian soldiers—once considered “weekend warriors”—are serving a first combat tour, returning home, and being redeployed for additional tours of duty.
Because of these unprecedented deployment policies, civilian psychiatrists will likely play a greater role in treating combat-related mental health problems than in any previous U.S. war. You may need to provide initial and long-term psychiatric care for reservists and Guard members returning to your community during 2006 and beyond.
To help you prepare, we discuss the combat situations these soldiers are experiencing, types of psychiatric problems they are reporting in anonymous surveys, and their attitudes about seeking psychiatric care. We also offer practical resources on combat-related posttraumatic stress disorder (PTSD) for nonmilitary or Veterans Administration clinicians.
A soldier’s story: ‘He’s always jumpy’
Mr. L, age 39, is supervisor for a local construction company and a sergeant first class with 18 years of Army Reserve service who returned from Iraq 7 months ago. He tells you, “My wife made me come see you—I didn’t want to.”
Though he does not think he needs a psychiatrist, his irritability and poor sleep worry his wife. “He isn’t the same anymore,” she says. “He’s always jumpy.”
Reported psychiatric problems
Stress-related symptoms. Within 4 months of returning home from Iraq or Afghanistan, 3 in 10 soldiers have developed “stress-related mental health problems” such as anxiety, depression, nightmares, anger, and concentration difficulties, reports Army Surgeon General Lt. Gen. Kevin Kiley.4 An unknown smaller percentage were reportedly diagnosed with PTSD.
Strained marriages, suicidal thoughts/feelings, nightmares or flashbacks, and fear of losing control or injuring someone else were among problems soldiers acknowledged during post-deployment health assessments between January and August 2005. In these surveys, 28% of 193,000 returnees endorsed mental health problems, according to the Army Center for Health Promotion and Preventive Medicine (Table 1).5
Table 1
Mental health problems reported by troops returning from combat in Iraq*
| Problem | Number among 193,000 U.S. soldiers |
|---|---|
| Nightmares or unwanted war recollections | 20,000 |
| Might “hurt or lose control” with someone else | 3,700 |
| Suicidal thoughts/feeling better off dead | 1,700 |
| * 28% of returnees reported mental health problems in post-deployment surveys between January and August 2005. | |
| Source: Army Center for Health Promotion and Preventive Medicine, reference 5. | |
Unfortunately, this new information may underestimate the number of returnees with psychiatric problems and the severity of those problems. In an anonymous survey of returning Army and Marine soldiers, Hoge et al7 found that those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis (Table 2).
Table 2
Perceived barriers to seeking mental health services cited by U.S. soldiers after combat duty in Iraq and Afghanistan*
| Perceived barrier | Met screening criteria for a mental disorder? | |
|---|---|---|
| Yes (N=731) | No (N=5,422) | |
| I would be seen as weak | 65% | 31% |
| My unit leadership might treat me differently | 63% | 33% |
| Members of my unit might have less confidence in me | 59% | 31% |
| I would have difficulty getting time off work for treatment | 55% | 22% |
| My leaders would blame me for the problem | 51% | 20% |
| It would harm my career | 50% | 24% |
| It is difficult to schedule an appointment | 45% | 17% |
| It would be too embarrassing | 41% | 18% |
| I don’t trust mental health professionals | 38% | 17% |
| Mental health care costs too much money | 25% | 10% |
| Mental health care doesn’t work | 25% | 9% |
| I don’t know where to get help | 22% | 6% |
| I don’t have adequate transportation | 18% | 6% |
| * Anonymous survey. Those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis. | ||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22. | ||
Gender per se may not be the most important variable; age, number of years in the military, type of military unit, and ethnic group are also risk factors for developing a war-related psychiatric disorder. Further studies of OIF- and OEF-related psychiatric disorders are needed to determine whether female veterans’ clinical needs differ in important ways from those of male veterans.
PTSD in combat veterans
Every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences (Box).9,11 Compared with persons with PTSD from other types of trauma, combat veterans appear to have the highest rate of delayed-onset PTSD and are less responsive to treatment.9
Initial PTSD rates for soldiers returning from Iraq ranged from 12.2% (Marines) to 12.9% (Army), using diagnostic criteria requiring functional impairment.7 These rates are 2.5 times the rate observed before combat (5%) and 3 to 4 times that of the general population (3.6%), using the same methodology.10
If 12.5% of 1 million combat-exposed service members develop PTSD, 125,000 service members may be affected. This rough estimate—7 times the number of personnel officially reported as “wounded”—does not take into account the wide variability of combat exposure among deployed troops or the effects of combat stress interventions (which might decrease the rate). Nor does it consider the impact of multiple rotations and possible decreased combat simulation training in reserve troops (which might increase the rate).
During the Civil War, soldiers with pathologic reactions to combat were described as having “irritable heart” or “soldier’s heart.”9 Since then, every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences.
Affected troops in World War I were said to have “shell shock,” whereas those in World War II and the Korean War had “combat fatigue.” Those fighting in the jungles of Vietnam had posttraumatic stress disorder (PTSD).
Along with evolving psychiatric nomenclature and diagnostic schema, each war—including those in Iraq and Afghanistan—has had unique symptom constellations.11 These differences relate to the contemporary state of scientific and medical knowledge, sociocultural factors, and popular press concerns. Some differences stem from actual or perceived weapon effects (such as chemical warfare or depleted uranium).
For example, World War I physicians at first considered “shell shock” to result from traumatic effects of high-explosive shells on the brain. This explanation proved inadequate when soldiers without direct concussive exposure expressed trauma-related symptoms.12
To develop, PTSD requires synergy between a severe stressor and a neurobiologic response. Because of genetic endowment or experience, not all persons are susceptible to the high levels of stress and associated hypothalamus-pituitary-adrenal axis activation required for the disorder to occur. Specific individual differences in coping, trauma history, and biology may predispose some individuals to PTSD.11
Mr. L’s story: Detached and irritable
As a combat infantryman, Mr. L was in seven fire fights, in which three of his buddies died. In responding to your questions, he admits feeling disconnected from his children and from his old friends who did not go to Iraq. He describes frequent arguments with his wife, though they had rarely argued previously. He denies psychiatric problems before his 12-month rotation in Iraq.
Being wounded in combat, surviving multiple life-threatening events, and experiencing combat of greater intensity and duration all increase the risk of developing PTSD. Mr. L’s multiple fire fights, loss of three friends, and other combat experiences place him at high risk for developing PTSD.
Typical combat experiences in Iraq and Afghanistan reported by Army and Marine troops are outlined in Table 3.7 Familiarizing yourself with these experiences can help you interview combat-exposed patients after you develop trust and rapport with them.
Table 3
Combat experiences reported by U.S. troops
after deployment in Iraq or Afghanistan
| Experience | Army groups | Marine group | |
|---|---|---|---|
| Afghanistan | Iraq | ||
| Being attacked or ambushed | 58% | 89% | 95% |
| Receiving incoming artillery, rocket or mortar fire | 84% | 86% | 92% |
| Being shot at or receiving small-arms fire | 66% | 93% | 97% |
| Shooting or directing fire at the enemy | 27% | 77% | 87% |
| Being responsible for death of an enemy combatant | 12% | 48% | 65% |
| Being responsible for death of a noncombatant | 1% | 14% | 28% |
| Seeing dead bodies or human remains | 39% | 95% | 94% |
| Seeing dead or seriously injured Americans | 30% | 65% | 75% |
| Knowing someone seriously injured or killed | 43% | 86% | 87% |
| Participating in demining operations | 16% | 38% | 34% |
| Seeing ill or injured women or children whom you were unable to help | 46% | 69% | 83% |
| Being wounded or injured | 5% | 14% | 9% |
| Being shot or hit, but protective gear saved you | * | 8% | 10% |
| Having a buddy who was near you shot or hit | * | 22% | 26% |
| Clearing or searching homes or buildings | 57% | 80% | 86% |
| Engaging in hand-to-hand combat | 3% | 22% | 9% |
| Saved the life of a soldier or civilian | 6% | 21% | 19% |
| * Question not included in this survey | |||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004; 351:13-22. | |||
Workup of combat veterans
Military psychiatrists provide support and treatment during and immediately after combat, but they do not associate acute reactions with specific psychiatric diagnoses to avoid “pathologizing” brief reactions to combat. To provide appropriate treatment for returning troops, however, you will need to characterize clinically significant psychopathology by using DSM IV-TR criteria for acute stress disorder and PTSD.12
We recommend that you manage a returning service member according to usual clinical practice. This includes a thorough history and appropriate medical and laboratory workup. Because soldiers commonly minimize their symptoms and concerns—particularly if they fear full disclosure could jeopardize their military careers—consider including collateral history from the patient’s family and friends in your assessment.
Differential diagnosis of mental disorders in combat troops is broad. You will need to obtain a thorough substance abuse history, with particular attention to use of alcohol to self-medicate symptoms. It will be important to assess safety issues, including potential for suicide, homicide, and domestic violence.
Many soldiers report difficulties with re-entering family life. Marital and sexual problems may develop because of role changes that occurred during a long separation. Pre-existing marital problems may be exacerbated, and both military members and spouses may express concerns about infidelity. Separation and divorce rates may be high.
Mr. L’s story: Alcohol ‘helps me sleep’
When you ask Mr. L about his use of alcohol, he notes that he was cited for driving while intoxicated at age 28. “I used to have a problem with drinking, but after my ticket I didn’t drink ‘til I came back from Iraq,” he says. “Now it’s the only thing that calms me down and helps me sleep.”
Comorbid diagnoses associated with PTSD are the rule. Mr. L’s drinking to self-medicate his PTSD symptoms puts him at risk of redeveloping alcohol problems. Use current best practices for managing depression, anxiety disorders, and substance abuse (if present) to guide treatment.
Suicidal behavior has also been strongly associated with PTSD.13 Thus, address Mr. L’s access to firearms, and include suicide assessment and regular followup in any treatment plan.
Head injuries in iraq
The use of effective body armor has dramatically changed the types of wounds and injuries sustained in combat. Kevlar body armor has decreased the frequency of mortal chest and abdominal wounds, leading to an unprecedented proportion of head and neck wounds, including eye injuries. In the war in Iraq and Afghanistan, 22% of evacuated casualties have injuries to the head, neck, and face.14
At the same time, rapid treatment of open and closed head injuries—often fatal in past wars—has improved survival. As a result, the prevalence of traumatic brain injury in veteran populations is believed to be substantially higher now than in previous conflicts.15
Mr. L’s story: ‘I forget everything’
Mr. L reports that after he served 8 months in Iraq, his vehicle was destroyed by a roadside bomb. He lost consciousness and was hospitalized briefly before returning to duty and completing his tour.
“I’m having trouble concentrating at work, and it seems like I forget everything,” he says. “My boss has complained about mistakes I make when planning our construction jobs. Could that explosion be causing my problems?”
Mr. L’s loss of consciousness associated with a blast injury and his cognitive complaints suggest possible mild traumatic brain injury. Consider neuropsychological testing and brain imaging studies, along with possible referral to appropriate rehabilitation programs if needed.
Treatment resources
The Iraq War Clinician Guide16 delineates military approaches to prevention, as well as acute intervention and initial treatment after evacuation from a war zone. This guide also:
- outlines rationales for removing affected service members from combat and eventually returning them to duty or medically retiring them if severe symptoms continue to interfere with ability to function.
- describes the biopsychosocial approach used by the Walter Reed Army Medical Center Psychiatric Consultation Service to address the multifactorial needs of the traumatized amputee.
- National Center for PTSD: The War in Iraq. www.ncptsd.va.gov/topics/war.html
Comprehensive Web site designated by Congress to provide information for military veterans with PTSD. Clinician’s guide available, plus fact sheets for family and patients. - National Center for PTSD. Iraq War Clinician Guide (2nd ed). www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf
Detailed guide for treating the soldier in combat. Includes treatment options for PTSD and the veteran with amputation. - U.S. Army Center for Health Promotion and Preventive Medicine. Supporting Guidelines. www.pdhealth.mil/clinicians/support.asp
Collection of guidelines for PTSD, major depression, and medically unexplained symptoms following combat. - Military One Source. www.militaryonesource.com
Resource for active duty and reserve soldiers and family members. Portal for support services, policies, and education. Brief confidential counseling support for soldiers and family members. - Veterans Administration (VA)/Department of Defense (DOD) Clinical Practice Guideline for Management of PTSD, January 2004. www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm
Includes list of clinical trials, medication dosing, and evidence basis for treatment with pharmacotherapy and psychotherapy. - American Psychiatric Association. Practice Guideline for the Treatment of Patients With Acute Stress Disorder and Posttraumatic Stress Disorder. http://www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
Background and guidelines for managing PTSD, including treatment recommendations, evidence basis, background, and areas for future research.
Disclosure
Drs. Lineberry, Bostwick, and Rundell previously served on active duty in the U.S. Air Force for 12, 5, and 23 years, respectively.
1. Benjamin M. How many have gone to war? Salon.com April 12, 2005. Available at: http://www.salon.com/news/feature/2005/04/12/troops_numbers/index_np.html. Accessed Dec. 13, 2005.
2. United States Government Accountability Office. Testimony before the Committee on Government Reform, House of Representatives. Reserve forces. Army National Guard’s role, organization, and equipment need to be reexamined. Oct. 20, 2005. Available at: http://www.gao.gov/new.items/d06170t.pdf. Accessed Oct. 26, 2005.
3. Wetzel K. Senators told of Guard struggles. Seattle Times Oct. 20, 2005. Available at: http://seattletimes.nwsource.com/html/local-news/2002571967_soldiers20m.html. Accessed Oct. 26, 2005.
4. Associated Press. Survey: 30% of returning Iraq vets suffer mental ills. USA Today July 28, 2005. Available at: http://www.usatoday.com/news/health/2005-07-28-iraq-vets-health_x.htm?csp=34. Accessed Oct. 26, 2005.
5. Zoroya G. One in four Iraq vets ailing on return. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-side_x.htm. Accessed Oct. 26, 2005.
6. Zoroya G. Troops screened as never before. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-stress-side_x.htm. Accessed Oct. 26, 2005.
7. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22.
8. Prigerson HG, Maciejewski PK, Rosenheck RA. Combat trauma: trauma with highest risk of delayed onset and unresolved posttraumatic stress disorder symptoms, unemployment, and abuse among men. J Nerv Ment Dis 2001;189:99-108.
9. Narrow WE, Rae DS, Robins LN, Regier DA. Revised prevalence estimates of mental disorders in the United States: using a clinical significance criterion to reconcile 2 surveys’ estimates. Arch Gen Psychiatry 2002;59:115-23.
10. Lieberman HR, Bathalon GP, Falco CN, et al. Severe decrements in cognition, function and mood induced by sleep loss, heat, dehydration, and under-nutrition during simulated combat. Biol Psychiatry 2005;57:422-9.
11. Nemeroff CB, Bremner JD, Foa EB, et al. Posttraumatic stress disorder: a state-of-the-science review. J Psychiatr Res (In press; Oct 2005 epub ahead of publication).
12. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington, DC: American Psychiatric Association; 2000.
13. Sareen J, Houlahan T, Cox BJ, Asmundson GJ. Anxiety disorders associated with suicidal ideation and suicide attempts in the national comorbidity survey. J Nerv Ment Dis 2005;193:450-4.
14. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysis of battlefield head and neck injuries in Iraq and Afghanistan. Otolarnygol Head Neck Surg 2005;133:497-504.
15. Okie S. Traumatic brain injury in the war zone. N Engl J Med 2005;352(20):2043-7.
16. Cozza SJ, Benedek DM, Bradley JC, et al. Topics specific to the psychiatric treatment of military personnel. In: Schnurr PP, Cozza SJ (eds). Iraq War clinician guide (2nd ed). Washington, DC: National Center for PTSD. Walter Reed Army Medical Center; 2004:4-20. Available at: http://www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf Accessed Oct. 26, 2005.
National Guard and Army Reserve troops constitute an estimated 30% to 40% of the 1 million-plus U.S. military personnel deployed in Iraq and Afghanistan.1-3 Many of these civilian soldiers—once considered “weekend warriors”—are serving a first combat tour, returning home, and being redeployed for additional tours of duty.
Because of these unprecedented deployment policies, civilian psychiatrists will likely play a greater role in treating combat-related mental health problems than in any previous U.S. war. You may need to provide initial and long-term psychiatric care for reservists and Guard members returning to your community during 2006 and beyond.
To help you prepare, we discuss the combat situations these soldiers are experiencing, types of psychiatric problems they are reporting in anonymous surveys, and their attitudes about seeking psychiatric care. We also offer practical resources on combat-related posttraumatic stress disorder (PTSD) for nonmilitary or Veterans Administration clinicians.
A soldier’s story: ‘He’s always jumpy’
Mr. L, age 39, is supervisor for a local construction company and a sergeant first class with 18 years of Army Reserve service who returned from Iraq 7 months ago. He tells you, “My wife made me come see you—I didn’t want to.”
Though he does not think he needs a psychiatrist, his irritability and poor sleep worry his wife. “He isn’t the same anymore,” she says. “He’s always jumpy.”
Reported psychiatric problems
Stress-related symptoms. Within 4 months of returning home from Iraq or Afghanistan, 3 in 10 soldiers have developed “stress-related mental health problems” such as anxiety, depression, nightmares, anger, and concentration difficulties, reports Army Surgeon General Lt. Gen. Kevin Kiley.4 An unknown smaller percentage were reportedly diagnosed with PTSD.
Strained marriages, suicidal thoughts/feelings, nightmares or flashbacks, and fear of losing control or injuring someone else were among problems soldiers acknowledged during post-deployment health assessments between January and August 2005. In these surveys, 28% of 193,000 returnees endorsed mental health problems, according to the Army Center for Health Promotion and Preventive Medicine (Table 1).5
Table 1
Mental health problems reported by troops returning from combat in Iraq*
| Problem | Number among 193,000 U.S. soldiers |
|---|---|
| Nightmares or unwanted war recollections | 20,000 |
| Might “hurt or lose control” with someone else | 3,700 |
| Suicidal thoughts/feeling better off dead | 1,700 |
| * 28% of returnees reported mental health problems in post-deployment surveys between January and August 2005. | |
| Source: Army Center for Health Promotion and Preventive Medicine, reference 5. | |
Unfortunately, this new information may underestimate the number of returnees with psychiatric problems and the severity of those problems. In an anonymous survey of returning Army and Marine soldiers, Hoge et al7 found that those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis (Table 2).
Table 2
Perceived barriers to seeking mental health services cited by U.S. soldiers after combat duty in Iraq and Afghanistan*
| Perceived barrier | Met screening criteria for a mental disorder? | |
|---|---|---|
| Yes (N=731) | No (N=5,422) | |
| I would be seen as weak | 65% | 31% |
| My unit leadership might treat me differently | 63% | 33% |
| Members of my unit might have less confidence in me | 59% | 31% |
| I would have difficulty getting time off work for treatment | 55% | 22% |
| My leaders would blame me for the problem | 51% | 20% |
| It would harm my career | 50% | 24% |
| It is difficult to schedule an appointment | 45% | 17% |
| It would be too embarrassing | 41% | 18% |
| I don’t trust mental health professionals | 38% | 17% |
| Mental health care costs too much money | 25% | 10% |
| Mental health care doesn’t work | 25% | 9% |
| I don’t know where to get help | 22% | 6% |
| I don’t have adequate transportation | 18% | 6% |
| * Anonymous survey. Those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis. | ||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22. | ||
Gender per se may not be the most important variable; age, number of years in the military, type of military unit, and ethnic group are also risk factors for developing a war-related psychiatric disorder. Further studies of OIF- and OEF-related psychiatric disorders are needed to determine whether female veterans’ clinical needs differ in important ways from those of male veterans.
PTSD in combat veterans
Every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences (Box).9,11 Compared with persons with PTSD from other types of trauma, combat veterans appear to have the highest rate of delayed-onset PTSD and are less responsive to treatment.9
Initial PTSD rates for soldiers returning from Iraq ranged from 12.2% (Marines) to 12.9% (Army), using diagnostic criteria requiring functional impairment.7 These rates are 2.5 times the rate observed before combat (5%) and 3 to 4 times that of the general population (3.6%), using the same methodology.10
If 12.5% of 1 million combat-exposed service members develop PTSD, 125,000 service members may be affected. This rough estimate—7 times the number of personnel officially reported as “wounded”—does not take into account the wide variability of combat exposure among deployed troops or the effects of combat stress interventions (which might decrease the rate). Nor does it consider the impact of multiple rotations and possible decreased combat simulation training in reserve troops (which might increase the rate).
During the Civil War, soldiers with pathologic reactions to combat were described as having “irritable heart” or “soldier’s heart.”9 Since then, every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences.
Affected troops in World War I were said to have “shell shock,” whereas those in World War II and the Korean War had “combat fatigue.” Those fighting in the jungles of Vietnam had posttraumatic stress disorder (PTSD).
Along with evolving psychiatric nomenclature and diagnostic schema, each war—including those in Iraq and Afghanistan—has had unique symptom constellations.11 These differences relate to the contemporary state of scientific and medical knowledge, sociocultural factors, and popular press concerns. Some differences stem from actual or perceived weapon effects (such as chemical warfare or depleted uranium).
For example, World War I physicians at first considered “shell shock” to result from traumatic effects of high-explosive shells on the brain. This explanation proved inadequate when soldiers without direct concussive exposure expressed trauma-related symptoms.12
To develop, PTSD requires synergy between a severe stressor and a neurobiologic response. Because of genetic endowment or experience, not all persons are susceptible to the high levels of stress and associated hypothalamus-pituitary-adrenal axis activation required for the disorder to occur. Specific individual differences in coping, trauma history, and biology may predispose some individuals to PTSD.11
Mr. L’s story: Detached and irritable
As a combat infantryman, Mr. L was in seven fire fights, in which three of his buddies died. In responding to your questions, he admits feeling disconnected from his children and from his old friends who did not go to Iraq. He describes frequent arguments with his wife, though they had rarely argued previously. He denies psychiatric problems before his 12-month rotation in Iraq.
Being wounded in combat, surviving multiple life-threatening events, and experiencing combat of greater intensity and duration all increase the risk of developing PTSD. Mr. L’s multiple fire fights, loss of three friends, and other combat experiences place him at high risk for developing PTSD.
Typical combat experiences in Iraq and Afghanistan reported by Army and Marine troops are outlined in Table 3.7 Familiarizing yourself with these experiences can help you interview combat-exposed patients after you develop trust and rapport with them.
Table 3
Combat experiences reported by U.S. troops
after deployment in Iraq or Afghanistan
| Experience | Army groups | Marine group | |
|---|---|---|---|
| Afghanistan | Iraq | ||
| Being attacked or ambushed | 58% | 89% | 95% |
| Receiving incoming artillery, rocket or mortar fire | 84% | 86% | 92% |
| Being shot at or receiving small-arms fire | 66% | 93% | 97% |
| Shooting or directing fire at the enemy | 27% | 77% | 87% |
| Being responsible for death of an enemy combatant | 12% | 48% | 65% |
| Being responsible for death of a noncombatant | 1% | 14% | 28% |
| Seeing dead bodies or human remains | 39% | 95% | 94% |
| Seeing dead or seriously injured Americans | 30% | 65% | 75% |
| Knowing someone seriously injured or killed | 43% | 86% | 87% |
| Participating in demining operations | 16% | 38% | 34% |
| Seeing ill or injured women or children whom you were unable to help | 46% | 69% | 83% |
| Being wounded or injured | 5% | 14% | 9% |
| Being shot or hit, but protective gear saved you | * | 8% | 10% |
| Having a buddy who was near you shot or hit | * | 22% | 26% |
| Clearing or searching homes or buildings | 57% | 80% | 86% |
| Engaging in hand-to-hand combat | 3% | 22% | 9% |
| Saved the life of a soldier or civilian | 6% | 21% | 19% |
| * Question not included in this survey | |||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004; 351:13-22. | |||
Workup of combat veterans
Military psychiatrists provide support and treatment during and immediately after combat, but they do not associate acute reactions with specific psychiatric diagnoses to avoid “pathologizing” brief reactions to combat. To provide appropriate treatment for returning troops, however, you will need to characterize clinically significant psychopathology by using DSM IV-TR criteria for acute stress disorder and PTSD.12
We recommend that you manage a returning service member according to usual clinical practice. This includes a thorough history and appropriate medical and laboratory workup. Because soldiers commonly minimize their symptoms and concerns—particularly if they fear full disclosure could jeopardize their military careers—consider including collateral history from the patient’s family and friends in your assessment.
Differential diagnosis of mental disorders in combat troops is broad. You will need to obtain a thorough substance abuse history, with particular attention to use of alcohol to self-medicate symptoms. It will be important to assess safety issues, including potential for suicide, homicide, and domestic violence.
Many soldiers report difficulties with re-entering family life. Marital and sexual problems may develop because of role changes that occurred during a long separation. Pre-existing marital problems may be exacerbated, and both military members and spouses may express concerns about infidelity. Separation and divorce rates may be high.
Mr. L’s story: Alcohol ‘helps me sleep’
When you ask Mr. L about his use of alcohol, he notes that he was cited for driving while intoxicated at age 28. “I used to have a problem with drinking, but after my ticket I didn’t drink ‘til I came back from Iraq,” he says. “Now it’s the only thing that calms me down and helps me sleep.”
Comorbid diagnoses associated with PTSD are the rule. Mr. L’s drinking to self-medicate his PTSD symptoms puts him at risk of redeveloping alcohol problems. Use current best practices for managing depression, anxiety disorders, and substance abuse (if present) to guide treatment.
Suicidal behavior has also been strongly associated with PTSD.13 Thus, address Mr. L’s access to firearms, and include suicide assessment and regular followup in any treatment plan.
Head injuries in iraq
The use of effective body armor has dramatically changed the types of wounds and injuries sustained in combat. Kevlar body armor has decreased the frequency of mortal chest and abdominal wounds, leading to an unprecedented proportion of head and neck wounds, including eye injuries. In the war in Iraq and Afghanistan, 22% of evacuated casualties have injuries to the head, neck, and face.14
At the same time, rapid treatment of open and closed head injuries—often fatal in past wars—has improved survival. As a result, the prevalence of traumatic brain injury in veteran populations is believed to be substantially higher now than in previous conflicts.15
Mr. L’s story: ‘I forget everything’
Mr. L reports that after he served 8 months in Iraq, his vehicle was destroyed by a roadside bomb. He lost consciousness and was hospitalized briefly before returning to duty and completing his tour.
“I’m having trouble concentrating at work, and it seems like I forget everything,” he says. “My boss has complained about mistakes I make when planning our construction jobs. Could that explosion be causing my problems?”
Mr. L’s loss of consciousness associated with a blast injury and his cognitive complaints suggest possible mild traumatic brain injury. Consider neuropsychological testing and brain imaging studies, along with possible referral to appropriate rehabilitation programs if needed.
Treatment resources
The Iraq War Clinician Guide16 delineates military approaches to prevention, as well as acute intervention and initial treatment after evacuation from a war zone. This guide also:
- outlines rationales for removing affected service members from combat and eventually returning them to duty or medically retiring them if severe symptoms continue to interfere with ability to function.
- describes the biopsychosocial approach used by the Walter Reed Army Medical Center Psychiatric Consultation Service to address the multifactorial needs of the traumatized amputee.
- National Center for PTSD: The War in Iraq. www.ncptsd.va.gov/topics/war.html
Comprehensive Web site designated by Congress to provide information for military veterans with PTSD. Clinician’s guide available, plus fact sheets for family and patients. - National Center for PTSD. Iraq War Clinician Guide (2nd ed). www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf
Detailed guide for treating the soldier in combat. Includes treatment options for PTSD and the veteran with amputation. - U.S. Army Center for Health Promotion and Preventive Medicine. Supporting Guidelines. www.pdhealth.mil/clinicians/support.asp
Collection of guidelines for PTSD, major depression, and medically unexplained symptoms following combat. - Military One Source. www.militaryonesource.com
Resource for active duty and reserve soldiers and family members. Portal for support services, policies, and education. Brief confidential counseling support for soldiers and family members. - Veterans Administration (VA)/Department of Defense (DOD) Clinical Practice Guideline for Management of PTSD, January 2004. www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm
Includes list of clinical trials, medication dosing, and evidence basis for treatment with pharmacotherapy and psychotherapy. - American Psychiatric Association. Practice Guideline for the Treatment of Patients With Acute Stress Disorder and Posttraumatic Stress Disorder. http://www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
Background and guidelines for managing PTSD, including treatment recommendations, evidence basis, background, and areas for future research.
Disclosure
Drs. Lineberry, Bostwick, and Rundell previously served on active duty in the U.S. Air Force for 12, 5, and 23 years, respectively.
National Guard and Army Reserve troops constitute an estimated 30% to 40% of the 1 million-plus U.S. military personnel deployed in Iraq and Afghanistan.1-3 Many of these civilian soldiers—once considered “weekend warriors”—are serving a first combat tour, returning home, and being redeployed for additional tours of duty.
Because of these unprecedented deployment policies, civilian psychiatrists will likely play a greater role in treating combat-related mental health problems than in any previous U.S. war. You may need to provide initial and long-term psychiatric care for reservists and Guard members returning to your community during 2006 and beyond.
To help you prepare, we discuss the combat situations these soldiers are experiencing, types of psychiatric problems they are reporting in anonymous surveys, and their attitudes about seeking psychiatric care. We also offer practical resources on combat-related posttraumatic stress disorder (PTSD) for nonmilitary or Veterans Administration clinicians.
A soldier’s story: ‘He’s always jumpy’
Mr. L, age 39, is supervisor for a local construction company and a sergeant first class with 18 years of Army Reserve service who returned from Iraq 7 months ago. He tells you, “My wife made me come see you—I didn’t want to.”
Though he does not think he needs a psychiatrist, his irritability and poor sleep worry his wife. “He isn’t the same anymore,” she says. “He’s always jumpy.”
Reported psychiatric problems
Stress-related symptoms. Within 4 months of returning home from Iraq or Afghanistan, 3 in 10 soldiers have developed “stress-related mental health problems” such as anxiety, depression, nightmares, anger, and concentration difficulties, reports Army Surgeon General Lt. Gen. Kevin Kiley.4 An unknown smaller percentage were reportedly diagnosed with PTSD.
Strained marriages, suicidal thoughts/feelings, nightmares or flashbacks, and fear of losing control or injuring someone else were among problems soldiers acknowledged during post-deployment health assessments between January and August 2005. In these surveys, 28% of 193,000 returnees endorsed mental health problems, according to the Army Center for Health Promotion and Preventive Medicine (Table 1).5
Table 1
Mental health problems reported by troops returning from combat in Iraq*
| Problem | Number among 193,000 U.S. soldiers |
|---|---|
| Nightmares or unwanted war recollections | 20,000 |
| Might “hurt or lose control” with someone else | 3,700 |
| Suicidal thoughts/feeling better off dead | 1,700 |
| * 28% of returnees reported mental health problems in post-deployment surveys between January and August 2005. | |
| Source: Army Center for Health Promotion and Preventive Medicine, reference 5. | |
Unfortunately, this new information may underestimate the number of returnees with psychiatric problems and the severity of those problems. In an anonymous survey of returning Army and Marine soldiers, Hoge et al7 found that those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis (Table 2).
Table 2
Perceived barriers to seeking mental health services cited by U.S. soldiers after combat duty in Iraq and Afghanistan*
| Perceived barrier | Met screening criteria for a mental disorder? | |
|---|---|---|
| Yes (N=731) | No (N=5,422) | |
| I would be seen as weak | 65% | 31% |
| My unit leadership might treat me differently | 63% | 33% |
| Members of my unit might have less confidence in me | 59% | 31% |
| I would have difficulty getting time off work for treatment | 55% | 22% |
| My leaders would blame me for the problem | 51% | 20% |
| It would harm my career | 50% | 24% |
| It is difficult to schedule an appointment | 45% | 17% |
| It would be too embarrassing | 41% | 18% |
| I don’t trust mental health professionals | 38% | 17% |
| Mental health care costs too much money | 25% | 10% |
| Mental health care doesn’t work | 25% | 9% |
| I don’t know where to get help | 22% | 6% |
| I don’t have adequate transportation | 18% | 6% |
| * Anonymous survey. Those who met criteria for psychiatric diagnoses were less likely to seek assistance because of perceived stigma and concerns about their military careers than those without a psychiatric diagnosis. | ||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22. | ||
Gender per se may not be the most important variable; age, number of years in the military, type of military unit, and ethnic group are also risk factors for developing a war-related psychiatric disorder. Further studies of OIF- and OEF-related psychiatric disorders are needed to determine whether female veterans’ clinical needs differ in important ways from those of male veterans.
PTSD in combat veterans
Every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences (Box).9,11 Compared with persons with PTSD from other types of trauma, combat veterans appear to have the highest rate of delayed-onset PTSD and are less responsive to treatment.9
Initial PTSD rates for soldiers returning from Iraq ranged from 12.2% (Marines) to 12.9% (Army), using diagnostic criteria requiring functional impairment.7 These rates are 2.5 times the rate observed before combat (5%) and 3 to 4 times that of the general population (3.6%), using the same methodology.10
If 12.5% of 1 million combat-exposed service members develop PTSD, 125,000 service members may be affected. This rough estimate—7 times the number of personnel officially reported as “wounded”—does not take into account the wide variability of combat exposure among deployed troops or the effects of combat stress interventions (which might decrease the rate). Nor does it consider the impact of multiple rotations and possible decreased combat simulation training in reserve troops (which might increase the rate).
During the Civil War, soldiers with pathologic reactions to combat were described as having “irritable heart” or “soldier’s heart.”9 Since then, every war has seen new names and descriptions for combinations of psychological and somatic symptoms resulting from war experiences.
Affected troops in World War I were said to have “shell shock,” whereas those in World War II and the Korean War had “combat fatigue.” Those fighting in the jungles of Vietnam had posttraumatic stress disorder (PTSD).
Along with evolving psychiatric nomenclature and diagnostic schema, each war—including those in Iraq and Afghanistan—has had unique symptom constellations.11 These differences relate to the contemporary state of scientific and medical knowledge, sociocultural factors, and popular press concerns. Some differences stem from actual or perceived weapon effects (such as chemical warfare or depleted uranium).
For example, World War I physicians at first considered “shell shock” to result from traumatic effects of high-explosive shells on the brain. This explanation proved inadequate when soldiers without direct concussive exposure expressed trauma-related symptoms.12
To develop, PTSD requires synergy between a severe stressor and a neurobiologic response. Because of genetic endowment or experience, not all persons are susceptible to the high levels of stress and associated hypothalamus-pituitary-adrenal axis activation required for the disorder to occur. Specific individual differences in coping, trauma history, and biology may predispose some individuals to PTSD.11
Mr. L’s story: Detached and irritable
As a combat infantryman, Mr. L was in seven fire fights, in which three of his buddies died. In responding to your questions, he admits feeling disconnected from his children and from his old friends who did not go to Iraq. He describes frequent arguments with his wife, though they had rarely argued previously. He denies psychiatric problems before his 12-month rotation in Iraq.
Being wounded in combat, surviving multiple life-threatening events, and experiencing combat of greater intensity and duration all increase the risk of developing PTSD. Mr. L’s multiple fire fights, loss of three friends, and other combat experiences place him at high risk for developing PTSD.
Typical combat experiences in Iraq and Afghanistan reported by Army and Marine troops are outlined in Table 3.7 Familiarizing yourself with these experiences can help you interview combat-exposed patients after you develop trust and rapport with them.
Table 3
Combat experiences reported by U.S. troops
after deployment in Iraq or Afghanistan
| Experience | Army groups | Marine group | |
|---|---|---|---|
| Afghanistan | Iraq | ||
| Being attacked or ambushed | 58% | 89% | 95% |
| Receiving incoming artillery, rocket or mortar fire | 84% | 86% | 92% |
| Being shot at or receiving small-arms fire | 66% | 93% | 97% |
| Shooting or directing fire at the enemy | 27% | 77% | 87% |
| Being responsible for death of an enemy combatant | 12% | 48% | 65% |
| Being responsible for death of a noncombatant | 1% | 14% | 28% |
| Seeing dead bodies or human remains | 39% | 95% | 94% |
| Seeing dead or seriously injured Americans | 30% | 65% | 75% |
| Knowing someone seriously injured or killed | 43% | 86% | 87% |
| Participating in demining operations | 16% | 38% | 34% |
| Seeing ill or injured women or children whom you were unable to help | 46% | 69% | 83% |
| Being wounded or injured | 5% | 14% | 9% |
| Being shot or hit, but protective gear saved you | * | 8% | 10% |
| Having a buddy who was near you shot or hit | * | 22% | 26% |
| Clearing or searching homes or buildings | 57% | 80% | 86% |
| Engaging in hand-to-hand combat | 3% | 22% | 9% |
| Saved the life of a soldier or civilian | 6% | 21% | 19% |
| * Question not included in this survey | |||
| Source: Adapted and reprinted with permission from Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004; 351:13-22. | |||
Workup of combat veterans
Military psychiatrists provide support and treatment during and immediately after combat, but they do not associate acute reactions with specific psychiatric diagnoses to avoid “pathologizing” brief reactions to combat. To provide appropriate treatment for returning troops, however, you will need to characterize clinically significant psychopathology by using DSM IV-TR criteria for acute stress disorder and PTSD.12
We recommend that you manage a returning service member according to usual clinical practice. This includes a thorough history and appropriate medical and laboratory workup. Because soldiers commonly minimize their symptoms and concerns—particularly if they fear full disclosure could jeopardize their military careers—consider including collateral history from the patient’s family and friends in your assessment.
Differential diagnosis of mental disorders in combat troops is broad. You will need to obtain a thorough substance abuse history, with particular attention to use of alcohol to self-medicate symptoms. It will be important to assess safety issues, including potential for suicide, homicide, and domestic violence.
Many soldiers report difficulties with re-entering family life. Marital and sexual problems may develop because of role changes that occurred during a long separation. Pre-existing marital problems may be exacerbated, and both military members and spouses may express concerns about infidelity. Separation and divorce rates may be high.
Mr. L’s story: Alcohol ‘helps me sleep’
When you ask Mr. L about his use of alcohol, he notes that he was cited for driving while intoxicated at age 28. “I used to have a problem with drinking, but after my ticket I didn’t drink ‘til I came back from Iraq,” he says. “Now it’s the only thing that calms me down and helps me sleep.”
Comorbid diagnoses associated with PTSD are the rule. Mr. L’s drinking to self-medicate his PTSD symptoms puts him at risk of redeveloping alcohol problems. Use current best practices for managing depression, anxiety disorders, and substance abuse (if present) to guide treatment.
Suicidal behavior has also been strongly associated with PTSD.13 Thus, address Mr. L’s access to firearms, and include suicide assessment and regular followup in any treatment plan.
Head injuries in iraq
The use of effective body armor has dramatically changed the types of wounds and injuries sustained in combat. Kevlar body armor has decreased the frequency of mortal chest and abdominal wounds, leading to an unprecedented proportion of head and neck wounds, including eye injuries. In the war in Iraq and Afghanistan, 22% of evacuated casualties have injuries to the head, neck, and face.14
At the same time, rapid treatment of open and closed head injuries—often fatal in past wars—has improved survival. As a result, the prevalence of traumatic brain injury in veteran populations is believed to be substantially higher now than in previous conflicts.15
Mr. L’s story: ‘I forget everything’
Mr. L reports that after he served 8 months in Iraq, his vehicle was destroyed by a roadside bomb. He lost consciousness and was hospitalized briefly before returning to duty and completing his tour.
“I’m having trouble concentrating at work, and it seems like I forget everything,” he says. “My boss has complained about mistakes I make when planning our construction jobs. Could that explosion be causing my problems?”
Mr. L’s loss of consciousness associated with a blast injury and his cognitive complaints suggest possible mild traumatic brain injury. Consider neuropsychological testing and brain imaging studies, along with possible referral to appropriate rehabilitation programs if needed.
Treatment resources
The Iraq War Clinician Guide16 delineates military approaches to prevention, as well as acute intervention and initial treatment after evacuation from a war zone. This guide also:
- outlines rationales for removing affected service members from combat and eventually returning them to duty or medically retiring them if severe symptoms continue to interfere with ability to function.
- describes the biopsychosocial approach used by the Walter Reed Army Medical Center Psychiatric Consultation Service to address the multifactorial needs of the traumatized amputee.
- National Center for PTSD: The War in Iraq. www.ncptsd.va.gov/topics/war.html
Comprehensive Web site designated by Congress to provide information for military veterans with PTSD. Clinician’s guide available, plus fact sheets for family and patients. - National Center for PTSD. Iraq War Clinician Guide (2nd ed). www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf
Detailed guide for treating the soldier in combat. Includes treatment options for PTSD and the veteran with amputation. - U.S. Army Center for Health Promotion and Preventive Medicine. Supporting Guidelines. www.pdhealth.mil/clinicians/support.asp
Collection of guidelines for PTSD, major depression, and medically unexplained symptoms following combat. - Military One Source. www.militaryonesource.com
Resource for active duty and reserve soldiers and family members. Portal for support services, policies, and education. Brief confidential counseling support for soldiers and family members. - Veterans Administration (VA)/Department of Defense (DOD) Clinical Practice Guideline for Management of PTSD, January 2004. www.oqp.med.va.gov/cpg/PTSD/PTSD_Base.htm
Includes list of clinical trials, medication dosing, and evidence basis for treatment with pharmacotherapy and psychotherapy. - American Psychiatric Association. Practice Guideline for the Treatment of Patients With Acute Stress Disorder and Posttraumatic Stress Disorder. http://www.psych.org/psych_pract/treatg/pg/PTSD-PG-PartsA-B-C-New.pdf
Background and guidelines for managing PTSD, including treatment recommendations, evidence basis, background, and areas for future research.
Disclosure
Drs. Lineberry, Bostwick, and Rundell previously served on active duty in the U.S. Air Force for 12, 5, and 23 years, respectively.
1. Benjamin M. How many have gone to war? Salon.com April 12, 2005. Available at: http://www.salon.com/news/feature/2005/04/12/troops_numbers/index_np.html. Accessed Dec. 13, 2005.
2. United States Government Accountability Office. Testimony before the Committee on Government Reform, House of Representatives. Reserve forces. Army National Guard’s role, organization, and equipment need to be reexamined. Oct. 20, 2005. Available at: http://www.gao.gov/new.items/d06170t.pdf. Accessed Oct. 26, 2005.
3. Wetzel K. Senators told of Guard struggles. Seattle Times Oct. 20, 2005. Available at: http://seattletimes.nwsource.com/html/local-news/2002571967_soldiers20m.html. Accessed Oct. 26, 2005.
4. Associated Press. Survey: 30% of returning Iraq vets suffer mental ills. USA Today July 28, 2005. Available at: http://www.usatoday.com/news/health/2005-07-28-iraq-vets-health_x.htm?csp=34. Accessed Oct. 26, 2005.
5. Zoroya G. One in four Iraq vets ailing on return. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-side_x.htm. Accessed Oct. 26, 2005.
6. Zoroya G. Troops screened as never before. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-stress-side_x.htm. Accessed Oct. 26, 2005.
7. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22.
8. Prigerson HG, Maciejewski PK, Rosenheck RA. Combat trauma: trauma with highest risk of delayed onset and unresolved posttraumatic stress disorder symptoms, unemployment, and abuse among men. J Nerv Ment Dis 2001;189:99-108.
9. Narrow WE, Rae DS, Robins LN, Regier DA. Revised prevalence estimates of mental disorders in the United States: using a clinical significance criterion to reconcile 2 surveys’ estimates. Arch Gen Psychiatry 2002;59:115-23.
10. Lieberman HR, Bathalon GP, Falco CN, et al. Severe decrements in cognition, function and mood induced by sleep loss, heat, dehydration, and under-nutrition during simulated combat. Biol Psychiatry 2005;57:422-9.
11. Nemeroff CB, Bremner JD, Foa EB, et al. Posttraumatic stress disorder: a state-of-the-science review. J Psychiatr Res (In press; Oct 2005 epub ahead of publication).
12. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington, DC: American Psychiatric Association; 2000.
13. Sareen J, Houlahan T, Cox BJ, Asmundson GJ. Anxiety disorders associated with suicidal ideation and suicide attempts in the national comorbidity survey. J Nerv Ment Dis 2005;193:450-4.
14. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysis of battlefield head and neck injuries in Iraq and Afghanistan. Otolarnygol Head Neck Surg 2005;133:497-504.
15. Okie S. Traumatic brain injury in the war zone. N Engl J Med 2005;352(20):2043-7.
16. Cozza SJ, Benedek DM, Bradley JC, et al. Topics specific to the psychiatric treatment of military personnel. In: Schnurr PP, Cozza SJ (eds). Iraq War clinician guide (2nd ed). Washington, DC: National Center for PTSD. Walter Reed Army Medical Center; 2004:4-20. Available at: http://www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf Accessed Oct. 26, 2005.
1. Benjamin M. How many have gone to war? Salon.com April 12, 2005. Available at: http://www.salon.com/news/feature/2005/04/12/troops_numbers/index_np.html. Accessed Dec. 13, 2005.
2. United States Government Accountability Office. Testimony before the Committee on Government Reform, House of Representatives. Reserve forces. Army National Guard’s role, organization, and equipment need to be reexamined. Oct. 20, 2005. Available at: http://www.gao.gov/new.items/d06170t.pdf. Accessed Oct. 26, 2005.
3. Wetzel K. Senators told of Guard struggles. Seattle Times Oct. 20, 2005. Available at: http://seattletimes.nwsource.com/html/local-news/2002571967_soldiers20m.html. Accessed Oct. 26, 2005.
4. Associated Press. Survey: 30% of returning Iraq vets suffer mental ills. USA Today July 28, 2005. Available at: http://www.usatoday.com/news/health/2005-07-28-iraq-vets-health_x.htm?csp=34. Accessed Oct. 26, 2005.
5. Zoroya G. One in four Iraq vets ailing on return. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-side_x.htm. Accessed Oct. 26, 2005.
6. Zoroya G. Troops screened as never before. USA Today Oct. 18, 2005. Available at: http://www.usatoday.com/news/world/iraq/2005-10-18-troops-stress-side_x.htm. Accessed Oct. 26, 2005.
7. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. N Engl J Med 2004;351:13-22.
8. Prigerson HG, Maciejewski PK, Rosenheck RA. Combat trauma: trauma with highest risk of delayed onset and unresolved posttraumatic stress disorder symptoms, unemployment, and abuse among men. J Nerv Ment Dis 2001;189:99-108.
9. Narrow WE, Rae DS, Robins LN, Regier DA. Revised prevalence estimates of mental disorders in the United States: using a clinical significance criterion to reconcile 2 surveys’ estimates. Arch Gen Psychiatry 2002;59:115-23.
10. Lieberman HR, Bathalon GP, Falco CN, et al. Severe decrements in cognition, function and mood induced by sleep loss, heat, dehydration, and under-nutrition during simulated combat. Biol Psychiatry 2005;57:422-9.
11. Nemeroff CB, Bremner JD, Foa EB, et al. Posttraumatic stress disorder: a state-of-the-science review. J Psychiatr Res (In press; Oct 2005 epub ahead of publication).
12. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed, text rev). Washington, DC: American Psychiatric Association; 2000.
13. Sareen J, Houlahan T, Cox BJ, Asmundson GJ. Anxiety disorders associated with suicidal ideation and suicide attempts in the national comorbidity survey. J Nerv Ment Dis 2005;193:450-4.
14. Xydakis MS, Fravell MD, Nasser KE, Casler JD. Analysis of battlefield head and neck injuries in Iraq and Afghanistan. Otolarnygol Head Neck Surg 2005;133:497-504.
15. Okie S. Traumatic brain injury in the war zone. N Engl J Med 2005;352(20):2043-7.
16. Cozza SJ, Benedek DM, Bradley JC, et al. Topics specific to the psychiatric treatment of military personnel. In: Schnurr PP, Cozza SJ (eds). Iraq War clinician guide (2nd ed). Washington, DC: National Center for PTSD. Walter Reed Army Medical Center; 2004:4-20. Available at: http://www.ncptsd.va.gov/war/iraq_clinician_guide_v2/iraq_clinician_guide_v2.pdf Accessed Oct. 26, 2005.
Discontinuation Symptoms: Never Say Never
In " Tips to manage and prevent discontinuation syndromes " ( Current Psychiatry , September 2005), Dr. Sriram Ramaswamy et al state, "no discontinuation symptoms have been reported with mirtazapine, bupropion, or duloxetine."
Discontinuation symptoms with mirtazapine and bupropion—though quite rare—have been described in case reports. 1 - 4 Also, a discontinuation syndrome was observed after duloxetine was abruptly stopped in placebo-controlled clinical trials; this is noted in the package insert.
James W. Jefferson, MDMadison Institute of Medicine, Inc.Clinical professor of psychiatryUniversity of Wisconsin Medical School, Madison
1. Benazzi F. Mirtazapine withdrawal symptoms [letter]. Can J Psychiatry 1998;43:525.-
2. Berigan TR. Mirtazapine-associated withdrawal symptoms: a case report [letter]. Prim Care Companion J Clin Psychiatry 2001;3:143.-
3. Berigan TR, Harazin JS. Bupropion-associated withdrawal symptoms: a case report. Prim Care Companion J Clin Psychiatry 1999;1:50-1.
3. Berigan TR. Bupropion-associated withdrawal symptoms revisited: a case report [letter]. Prim Care Companion J Clin Psychiatry 2002;4:78.-
In " Tips to manage and prevent discontinuation syndromes " ( Current Psychiatry , September 2005), Dr. Sriram Ramaswamy et al state, "no discontinuation symptoms have been reported with mirtazapine, bupropion, or duloxetine."
Discontinuation symptoms with mirtazapine and bupropion—though quite rare—have been described in case reports. 1 - 4 Also, a discontinuation syndrome was observed after duloxetine was abruptly stopped in placebo-controlled clinical trials; this is noted in the package insert.
James W. Jefferson, MDMadison Institute of Medicine, Inc.Clinical professor of psychiatryUniversity of Wisconsin Medical School, Madison
In " Tips to manage and prevent discontinuation syndromes " ( Current Psychiatry , September 2005), Dr. Sriram Ramaswamy et al state, "no discontinuation symptoms have been reported with mirtazapine, bupropion, or duloxetine."
Discontinuation symptoms with mirtazapine and bupropion—though quite rare—have been described in case reports. 1 - 4 Also, a discontinuation syndrome was observed after duloxetine was abruptly stopped in placebo-controlled clinical trials; this is noted in the package insert.
James W. Jefferson, MDMadison Institute of Medicine, Inc.Clinical professor of psychiatryUniversity of Wisconsin Medical School, Madison
1. Benazzi F. Mirtazapine withdrawal symptoms [letter]. Can J Psychiatry 1998;43:525.-
2. Berigan TR. Mirtazapine-associated withdrawal symptoms: a case report [letter]. Prim Care Companion J Clin Psychiatry 2001;3:143.-
3. Berigan TR, Harazin JS. Bupropion-associated withdrawal symptoms: a case report. Prim Care Companion J Clin Psychiatry 1999;1:50-1.
3. Berigan TR. Bupropion-associated withdrawal symptoms revisited: a case report [letter]. Prim Care Companion J Clin Psychiatry 2002;4:78.-
1. Benazzi F. Mirtazapine withdrawal symptoms [letter]. Can J Psychiatry 1998;43:525.-
2. Berigan TR. Mirtazapine-associated withdrawal symptoms: a case report [letter]. Prim Care Companion J Clin Psychiatry 2001;3:143.-
3. Berigan TR, Harazin JS. Bupropion-associated withdrawal symptoms: a case report. Prim Care Companion J Clin Psychiatry 1999;1:50-1.
3. Berigan TR. Bupropion-associated withdrawal symptoms revisited: a case report [letter]. Prim Care Companion J Clin Psychiatry 2002;4:78.-
Hope for 'meth' addiction?
" 'No energy, no hope,' and no clear diagnosis ," by Drs. Jaesu Han and Mary Ann Barnovitz ( Current Psychiatry , October 2005) offers an interesting and relevant description of one patient's struggle with chronic amphetamine use.
Dr. Han mentioned that no specific, well-established treatments exist for methamphetamine dependence. However, the matrix model—a comprehensive, vigorous, and well-studied approach—encompasses the treatments mentioned as well as other methods.
Developed to treat cocaine dependence in the 1980s, the matrix model is a 16-week program that comprises individual and group sessions, addresses relapse prevention, offers family psychoeducation, and promotes 12-step therapy. Matrix model therapy recognizes how a patient's methamphetamine dependence can affect his or her family—something a 12-step program alone cannot address. 1 - 3
Matrix model therapy is the only program with evidence of effectiveness for treating methamphetamine dependence and is supported by the U.S. Substance Abuse and Mental Health Services Administration.
Other methamphetamine dependence treatments are in the pipeline. Researchers are studying use of existing medications—such as gamma-vinyl GABA, modafinil, selegiline, bupropion, and odansetron—and developing monoclonal antibodies to methamphetamine. 1 , 3
Adegboyega Oyemade, MDChief resident, department of psychiatry,Albany Medical Center, Albany, NY
Minesh Patel, MDFellow in child and adolescent psychiatryNew York Medical CollegeWestchester Medical CenterValhalla, NY
1. Volkow ND. Methamphetamine abuse. Testimony before U.S. Senate Committee on Appropriations. Subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 21, 2005. Available at:http://www.drugabuse.gov/Testimony/4-21-05Testimony.html . Accessed Oct. 28, 2005.
2. Methamphetamine treatment: the matrix model. Addiction Messenger. Northwest Frontier Addiction Technology Transfer Center 2002;5(2):1-3.Available at: http://www.nfattc.org/AM_v5_Series_1.pdf . Accessed Oct. 31, 2005.
3. Sommerfield J. Beating an addiction to meth. Researchers zero in on brain effects, treatment approaches. MSNBC.com. Available at: http://msnbc.com/news/507186.asp . Accessed Oct. 31, 2005.
" 'No energy, no hope,' and no clear diagnosis ," by Drs. Jaesu Han and Mary Ann Barnovitz ( Current Psychiatry , October 2005) offers an interesting and relevant description of one patient's struggle with chronic amphetamine use.
Dr. Han mentioned that no specific, well-established treatments exist for methamphetamine dependence. However, the matrix model—a comprehensive, vigorous, and well-studied approach—encompasses the treatments mentioned as well as other methods.
Developed to treat cocaine dependence in the 1980s, the matrix model is a 16-week program that comprises individual and group sessions, addresses relapse prevention, offers family psychoeducation, and promotes 12-step therapy. Matrix model therapy recognizes how a patient's methamphetamine dependence can affect his or her family—something a 12-step program alone cannot address. 1 - 3
Matrix model therapy is the only program with evidence of effectiveness for treating methamphetamine dependence and is supported by the U.S. Substance Abuse and Mental Health Services Administration.
Other methamphetamine dependence treatments are in the pipeline. Researchers are studying use of existing medications—such as gamma-vinyl GABA, modafinil, selegiline, bupropion, and odansetron—and developing monoclonal antibodies to methamphetamine. 1 , 3
Adegboyega Oyemade, MDChief resident, department of psychiatry,Albany Medical Center, Albany, NY
Minesh Patel, MDFellow in child and adolescent psychiatryNew York Medical CollegeWestchester Medical CenterValhalla, NY
" 'No energy, no hope,' and no clear diagnosis ," by Drs. Jaesu Han and Mary Ann Barnovitz ( Current Psychiatry , October 2005) offers an interesting and relevant description of one patient's struggle with chronic amphetamine use.
Dr. Han mentioned that no specific, well-established treatments exist for methamphetamine dependence. However, the matrix model—a comprehensive, vigorous, and well-studied approach—encompasses the treatments mentioned as well as other methods.
Developed to treat cocaine dependence in the 1980s, the matrix model is a 16-week program that comprises individual and group sessions, addresses relapse prevention, offers family psychoeducation, and promotes 12-step therapy. Matrix model therapy recognizes how a patient's methamphetamine dependence can affect his or her family—something a 12-step program alone cannot address. 1 - 3
Matrix model therapy is the only program with evidence of effectiveness for treating methamphetamine dependence and is supported by the U.S. Substance Abuse and Mental Health Services Administration.
Other methamphetamine dependence treatments are in the pipeline. Researchers are studying use of existing medications—such as gamma-vinyl GABA, modafinil, selegiline, bupropion, and odansetron—and developing monoclonal antibodies to methamphetamine. 1 , 3
Adegboyega Oyemade, MDChief resident, department of psychiatry,Albany Medical Center, Albany, NY
Minesh Patel, MDFellow in child and adolescent psychiatryNew York Medical CollegeWestchester Medical CenterValhalla, NY
1. Volkow ND. Methamphetamine abuse. Testimony before U.S. Senate Committee on Appropriations. Subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 21, 2005. Available at:http://www.drugabuse.gov/Testimony/4-21-05Testimony.html . Accessed Oct. 28, 2005.
2. Methamphetamine treatment: the matrix model. Addiction Messenger. Northwest Frontier Addiction Technology Transfer Center 2002;5(2):1-3.Available at: http://www.nfattc.org/AM_v5_Series_1.pdf . Accessed Oct. 31, 2005.
3. Sommerfield J. Beating an addiction to meth. Researchers zero in on brain effects, treatment approaches. MSNBC.com. Available at: http://msnbc.com/news/507186.asp . Accessed Oct. 31, 2005.
1. Volkow ND. Methamphetamine abuse. Testimony before U.S. Senate Committee on Appropriations. Subcommittee on Labor, Health and Human Services, Education, and Related Agencies, April 21, 2005. Available at:http://www.drugabuse.gov/Testimony/4-21-05Testimony.html . Accessed Oct. 28, 2005.
2. Methamphetamine treatment: the matrix model. Addiction Messenger. Northwest Frontier Addiction Technology Transfer Center 2002;5(2):1-3.Available at: http://www.nfattc.org/AM_v5_Series_1.pdf . Accessed Oct. 31, 2005.
3. Sommerfield J. Beating an addiction to meth. Researchers zero in on brain effects, treatment approaches. MSNBC.com. Available at: http://msnbc.com/news/507186.asp . Accessed Oct. 31, 2005.
Blogs: Personal and professional
Text:
Once reserved for personal diaries, the Web log or “blog” has become a powerful cybertool for self-expression, news, and debate. Physicians are increasingly using blogs to communicate and stay abreast, and advances in search engine technology make blogs easy to find and easier to start.
This article reviews numerous uses for blogs, plus information on starting your own.
The birth of the blog
Blogs started as public online diaries that provided a forum for self-expression and support. Blogs are similar to personal home pages and newsletters, except that authors update the content more frequently—daily in many cases—and readers can post comments for public viewing. Blogs combine elements of individual and group psychotherapy with a public journal.
Patients and families, for example, use schizophrenia.com to list their favorite blogs or create their own. Moodswing.org lists blogs for persons with bipolar disorder and their families.
Medical professionals also have discovered the therapeutic benefits of blog writing. Crazy Tracy features a psychiatric nurse’s musings about her work and personal life. Physicians post their experiences with patients and their thoughts about health care on blogs such as Intueri.org and Shrinkette.
Although blogs are public, many if not most authors keep identifying information out of their author profiles. Posting your e-mail address on a blog, for example, may open the door to viruses, spamming, or identity theft.
Also, recounting a specific case on a blog could breach patient confidentiality. Instead, post abstract case information to protect the patient’s anonymity.
Blog evolution
Blogs are also becoming well entrenched in business. Most corporate Web sites include blogs for employees to make announcements about products and services. Compared with discussion forums such as Invision Power Board, a blog helps create a sense of community without the constraints of defined topic headings seen in a bulletin board.
Google’s 2003 purchase of Pyra Labs—which developed Blogger, the easy-to-use blog creation site—helped push blogs into the mainstream. Even the CIA is using enterprise-based blog software to collect, organize, and publish information on its Intranet. (See “Psyber Psychiatry. Web logs: Blogging into the future,” January 2003.)
Medical blogs. A growing number of blogs, such as PsychNotes, AATP Interactive, and CodeBlueBlog, disseminate medical news. Authors cull information from clinical journals and Web sites to discuss their opinions and draw attention to new findings. Many medical blogs link to others, using pieces of code from blogLinker or Blogroller, so finding medical blogs is easy.
Some search engines and directories allow users to search exclusively for blogs. Technorati, a well-known blog search engine, searches based on links to sites and keyword tags. The blog sites’ authors choose the keywords, such as “schizophrenia” or “psychiatry.” Keyword tags can be linked to Web sites offering other services, such as photo sharing and listing favorite Web sites.
Social tagging
Even search engines cannot keep up with the growing number of sites proliferating on the Web. Enter social tagging, through which users can share common interests by storing links to Web sites. Blog users can use social tagging to consolidate links to other blogs.
Social tagging sites such as del.icio.us, Furl, and Shadows allow users to store URLs of sites they want to save and share. After creating an account, the user adds URLs with keyword tags into a database. Users can search the database for sites of interest. Using the keyword “psychiatry” on del.icio.us, for example, I found the Virtual Hospital Emergency Services Handbook and other mental health references. Each site found under the keyword also lists the number of users who have added that site to their “favorites” list.
Flickr and Buzznet offer a similar service to help users find photos related to keywords; these photos can be linked to blogs.
Rollyo and Wink are similar to social tagging sites, but with a twist. After establishing an account, users create a specialized search using a keyword tag but specify which Web sites to search. This type of keyword search could be more productive than conventional Web searches if the user knows which sites may produce useful results.
Although the Internet continues to grow almost exponentially, social tagging helps create a sense of community and a shared knowledge base. At SuprGlu, users gather content from other social tagging sites where they have an account. Ning expands upon this process, providing a free online service for building social blogs and connecting blog users based on common interests. These sites and services help make the Internet a much smaller and more useful place.
Starting your own blog
Not long ago, bloggers needed special software to post links to other blogs and comments from readers. Also, archiving previous posts required some skill, as this process was not automated.
Today, blog creation sites take the technical difficulty out of creating and hosting blogs, allowing authors to use the Web browser to edit and then publish the blog. These services, however, may have limited ‘skins’ or templates to customize your site’s look, and your URL will be based on the host name, such as boredhousewife.blogspot.com. You can circumvent this problem by registering your own URL and purchasing blog creation software such as Movable Type.
Send questions about blogs or this column to Dr. Luo or e-mail to [email protected].
Disclosure:
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions he expresses in this column are his own and do not necessarily reflect those of Current Psychiatry.
Text:
Once reserved for personal diaries, the Web log or “blog” has become a powerful cybertool for self-expression, news, and debate. Physicians are increasingly using blogs to communicate and stay abreast, and advances in search engine technology make blogs easy to find and easier to start.
This article reviews numerous uses for blogs, plus information on starting your own.
The birth of the blog
Blogs started as public online diaries that provided a forum for self-expression and support. Blogs are similar to personal home pages and newsletters, except that authors update the content more frequently—daily in many cases—and readers can post comments for public viewing. Blogs combine elements of individual and group psychotherapy with a public journal.
Patients and families, for example, use schizophrenia.com to list their favorite blogs or create their own. Moodswing.org lists blogs for persons with bipolar disorder and their families.
Medical professionals also have discovered the therapeutic benefits of blog writing. Crazy Tracy features a psychiatric nurse’s musings about her work and personal life. Physicians post their experiences with patients and their thoughts about health care on blogs such as Intueri.org and Shrinkette.
Although blogs are public, many if not most authors keep identifying information out of their author profiles. Posting your e-mail address on a blog, for example, may open the door to viruses, spamming, or identity theft.
Also, recounting a specific case on a blog could breach patient confidentiality. Instead, post abstract case information to protect the patient’s anonymity.
Blog evolution
Blogs are also becoming well entrenched in business. Most corporate Web sites include blogs for employees to make announcements about products and services. Compared with discussion forums such as Invision Power Board, a blog helps create a sense of community without the constraints of defined topic headings seen in a bulletin board.
Google’s 2003 purchase of Pyra Labs—which developed Blogger, the easy-to-use blog creation site—helped push blogs into the mainstream. Even the CIA is using enterprise-based blog software to collect, organize, and publish information on its Intranet. (See “Psyber Psychiatry. Web logs: Blogging into the future,” January 2003.)
Medical blogs. A growing number of blogs, such as PsychNotes, AATP Interactive, and CodeBlueBlog, disseminate medical news. Authors cull information from clinical journals and Web sites to discuss their opinions and draw attention to new findings. Many medical blogs link to others, using pieces of code from blogLinker or Blogroller, so finding medical blogs is easy.
Some search engines and directories allow users to search exclusively for blogs. Technorati, a well-known blog search engine, searches based on links to sites and keyword tags. The blog sites’ authors choose the keywords, such as “schizophrenia” or “psychiatry.” Keyword tags can be linked to Web sites offering other services, such as photo sharing and listing favorite Web sites.
Social tagging
Even search engines cannot keep up with the growing number of sites proliferating on the Web. Enter social tagging, through which users can share common interests by storing links to Web sites. Blog users can use social tagging to consolidate links to other blogs.
Social tagging sites such as del.icio.us, Furl, and Shadows allow users to store URLs of sites they want to save and share. After creating an account, the user adds URLs with keyword tags into a database. Users can search the database for sites of interest. Using the keyword “psychiatry” on del.icio.us, for example, I found the Virtual Hospital Emergency Services Handbook and other mental health references. Each site found under the keyword also lists the number of users who have added that site to their “favorites” list.
Flickr and Buzznet offer a similar service to help users find photos related to keywords; these photos can be linked to blogs.
Rollyo and Wink are similar to social tagging sites, but with a twist. After establishing an account, users create a specialized search using a keyword tag but specify which Web sites to search. This type of keyword search could be more productive than conventional Web searches if the user knows which sites may produce useful results.
Although the Internet continues to grow almost exponentially, social tagging helps create a sense of community and a shared knowledge base. At SuprGlu, users gather content from other social tagging sites where they have an account. Ning expands upon this process, providing a free online service for building social blogs and connecting blog users based on common interests. These sites and services help make the Internet a much smaller and more useful place.
Starting your own blog
Not long ago, bloggers needed special software to post links to other blogs and comments from readers. Also, archiving previous posts required some skill, as this process was not automated.
Today, blog creation sites take the technical difficulty out of creating and hosting blogs, allowing authors to use the Web browser to edit and then publish the blog. These services, however, may have limited ‘skins’ or templates to customize your site’s look, and your URL will be based on the host name, such as boredhousewife.blogspot.com. You can circumvent this problem by registering your own URL and purchasing blog creation software such as Movable Type.
Send questions about blogs or this column to Dr. Luo or e-mail to [email protected].
Disclosure:
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions he expresses in this column are his own and do not necessarily reflect those of Current Psychiatry.
Text:
Once reserved for personal diaries, the Web log or “blog” has become a powerful cybertool for self-expression, news, and debate. Physicians are increasingly using blogs to communicate and stay abreast, and advances in search engine technology make blogs easy to find and easier to start.
This article reviews numerous uses for blogs, plus information on starting your own.
The birth of the blog
Blogs started as public online diaries that provided a forum for self-expression and support. Blogs are similar to personal home pages and newsletters, except that authors update the content more frequently—daily in many cases—and readers can post comments for public viewing. Blogs combine elements of individual and group psychotherapy with a public journal.
Patients and families, for example, use schizophrenia.com to list their favorite blogs or create their own. Moodswing.org lists blogs for persons with bipolar disorder and their families.
Medical professionals also have discovered the therapeutic benefits of blog writing. Crazy Tracy features a psychiatric nurse’s musings about her work and personal life. Physicians post their experiences with patients and their thoughts about health care on blogs such as Intueri.org and Shrinkette.
Although blogs are public, many if not most authors keep identifying information out of their author profiles. Posting your e-mail address on a blog, for example, may open the door to viruses, spamming, or identity theft.
Also, recounting a specific case on a blog could breach patient confidentiality. Instead, post abstract case information to protect the patient’s anonymity.
Blog evolution
Blogs are also becoming well entrenched in business. Most corporate Web sites include blogs for employees to make announcements about products and services. Compared with discussion forums such as Invision Power Board, a blog helps create a sense of community without the constraints of defined topic headings seen in a bulletin board.
Google’s 2003 purchase of Pyra Labs—which developed Blogger, the easy-to-use blog creation site—helped push blogs into the mainstream. Even the CIA is using enterprise-based blog software to collect, organize, and publish information on its Intranet. (See “Psyber Psychiatry. Web logs: Blogging into the future,” January 2003.)
Medical blogs. A growing number of blogs, such as PsychNotes, AATP Interactive, and CodeBlueBlog, disseminate medical news. Authors cull information from clinical journals and Web sites to discuss their opinions and draw attention to new findings. Many medical blogs link to others, using pieces of code from blogLinker or Blogroller, so finding medical blogs is easy.
Some search engines and directories allow users to search exclusively for blogs. Technorati, a well-known blog search engine, searches based on links to sites and keyword tags. The blog sites’ authors choose the keywords, such as “schizophrenia” or “psychiatry.” Keyword tags can be linked to Web sites offering other services, such as photo sharing and listing favorite Web sites.
Social tagging
Even search engines cannot keep up with the growing number of sites proliferating on the Web. Enter social tagging, through which users can share common interests by storing links to Web sites. Blog users can use social tagging to consolidate links to other blogs.
Social tagging sites such as del.icio.us, Furl, and Shadows allow users to store URLs of sites they want to save and share. After creating an account, the user adds URLs with keyword tags into a database. Users can search the database for sites of interest. Using the keyword “psychiatry” on del.icio.us, for example, I found the Virtual Hospital Emergency Services Handbook and other mental health references. Each site found under the keyword also lists the number of users who have added that site to their “favorites” list.
Flickr and Buzznet offer a similar service to help users find photos related to keywords; these photos can be linked to blogs.
Rollyo and Wink are similar to social tagging sites, but with a twist. After establishing an account, users create a specialized search using a keyword tag but specify which Web sites to search. This type of keyword search could be more productive than conventional Web searches if the user knows which sites may produce useful results.
Although the Internet continues to grow almost exponentially, social tagging helps create a sense of community and a shared knowledge base. At SuprGlu, users gather content from other social tagging sites where they have an account. Ning expands upon this process, providing a free online service for building social blogs and connecting blog users based on common interests. These sites and services help make the Internet a much smaller and more useful place.
Starting your own blog
Not long ago, bloggers needed special software to post links to other blogs and comments from readers. Also, archiving previous posts required some skill, as this process was not automated.
Today, blog creation sites take the technical difficulty out of creating and hosting blogs, allowing authors to use the Web browser to edit and then publish the blog. These services, however, may have limited ‘skins’ or templates to customize your site’s look, and your URL will be based on the host name, such as boredhousewife.blogspot.com. You can circumvent this problem by registering your own URL and purchasing blog creation software such as Movable Type.
Send questions about blogs or this column to Dr. Luo or e-mail to [email protected].
Disclosure:
Dr. Luo reports no financial relationship with any company whose products are mentioned in this article. The opinions he expresses in this column are his own and do not necessarily reflect those of Current Psychiatry.