Current Psychiatry

I compliment Dr. Nasrallah for his courage and candor, which represents a deep commitment to the mentally ill and our society. He has articulated what many in our professional community strongly believe but don’t dare say publicly. I believe his message merits a broader dissemination, especially to policy makers. Thought leaders such as Dr. Nasrallah can make a difference by launching an educational campaign and start a new kind of advocacy movement.

Although I agree that patients with schizophrenia have suffered a great deal, a deinstitutionalized mental health system has limited means to care for patients with other psychiatric disorders. Increasingly, we see inpatients with multiple psychiatric morbidities along with Axis III issues. Traumatic psychopathologies, substance use disorders, and personality disorders constitute an incomplete list of conditions that cripple our patients who need longer and better care than they receive in the current therapeutic climate.

Substance use disorders are present in approximately 66% to 75% of admissions. Patients need care under 1 roof for substance use disorders and other co-occurring disorders concurrently rather than sequentially. After acute detoxification, patients are discharged from the hospital hoping to be accepted in a recovery program. However, by the time an inpatient substance abuse rehabilitation bed is available, the patient often has returned to chemicals or maladaptive behaviors, which leads to missed opportunities and unintended complications, namely treatment failure and resistance.

The eternal optimism that fueled the deinstitutionalization movement continues to nibble at inpatient and outpatient infrastructure. Over the years, fiscal forces have sliced mental health into 3 artificial compartments: mental health, addiction, and mental retardation and developmental disorders. Additionally, parity issues continue to block equal care. Managed care is leading to mechanical care—the patient is barely in the hospital and he is out. The ability to engage in thorough diagnostic assessment is limited by pressure to discharge patients.

Aftercare planning assumes unlimited access to care and the same optimism and zeal as deinstitutionalization advocates possessed. We tend to be oblivious to real issues such as uninsured or underinsured status and unmet basic needs. It is not surprising that nearly two-thirds of discharged patients do not return for their first follow-up appointment. If a discharged patient acts out, he is put in jail as if he is guilty of being mentally ill—a case of double discrimination.

Society supports expanding our jails and prisons more than state psychiatric hospitals. Is this a case of being “penny wise and pound foolish” and further stigmatizing mental illness? I agree that labels such as “dual diagnosis” are euphemisms. I also submit that categorizations such as “seriously ill” or “severe and persistent mental illness” could minimize the suffering of others who might benefit from what “asylum” treatment settings used to offer.

Diagnostic principles expect us to identify associated disorders, so-called comorbidities. The attributes of the correctional system—for example, understaffing—and outpatient infrastructure—such as provider musical chairs—do not maximize the diagnostic rigor needed to properly diagnose psychiatric illnesses and perform subsequent re-evaluations. Even in state hospitals inpatient days are shrinking, which in turn takes away the time clinicians need to perform a comprehensive diagnostic assessment—a prerequisite for good treatment planning.

One envies stalwarts such as Kraepelin and Bleuler whose genius we remember because they came of age with the “asylums.” These guys had the time but not many tools. Now we have many more tools, but we do not have time. However, I hope that common sense will prevail, and our society will advocate for a continuum of care that recognizes a legitimate role of “asylum” as outpatient health care.

Rudra Prakash, MD, DFAPA,
Clinical professor of psychiatry,
Vanderbilt University,
Staff psychiatrist,
Middle Tennessee Mental Health Institute,
Nashville, TN

I compliment Dr. Nasrallah for his courage and candor, which represents a deep commitment to the mentally ill and our society. He has articulated what many in our professional community strongly believe but don’t dare say publicly. I believe his message merits a broader dissemination, especially to policy makers. Thought leaders such as Dr. Nasrallah can make a difference by launching an educational campaign and start a new kind of advocacy movement.

Although I agree that patients with schizophrenia have suffered a great deal, a deinstitutionalized mental health system has limited means to care for patients with other psychiatric disorders. Increasingly, we see inpatients with multiple psychiatric morbidities along with Axis III issues. Traumatic psychopathologies, substance use disorders, and personality disorders constitute an incomplete list of conditions that cripple our patients who need longer and better care than they receive in the current therapeutic climate.

Substance use disorders are present in approximately 66% to 75% of admissions. Patients need care under 1 roof for substance use disorders and other co-occurring disorders concurrently rather than sequentially. After acute detoxification, patients are discharged from the hospital hoping to be accepted in a recovery program. However, by the time an inpatient substance abuse rehabilitation bed is available, the patient often has returned to chemicals or maladaptive behaviors, which leads to missed opportunities and unintended complications, namely treatment failure and resistance.

The eternal optimism that fueled the deinstitutionalization movement continues to nibble at inpatient and outpatient infrastructure. Over the years, fiscal forces have sliced mental health into 3 artificial compartments: mental health, addiction, and mental retardation and developmental disorders. Additionally, parity issues continue to block equal care. Managed care is leading to mechanical care—the patient is barely in the hospital and he is out. The ability to engage in thorough diagnostic assessment is limited by pressure to discharge patients.

Aftercare planning assumes unlimited access to care and the same optimism and zeal as deinstitutionalization advocates possessed. We tend to be oblivious to real issues such as uninsured or underinsured status and unmet basic needs. It is not surprising that nearly two-thirds of discharged patients do not return for their first follow-up appointment. If a discharged patient acts out, he is put in jail as if he is guilty of being mentally ill—a case of double discrimination.

Society supports expanding our jails and prisons more than state psychiatric hospitals. Is this a case of being “penny wise and pound foolish” and further stigmatizing mental illness? I agree that labels such as “dual diagnosis” are euphemisms. I also submit that categorizations such as “seriously ill” or “severe and persistent mental illness” could minimize the suffering of others who might benefit from what “asylum” treatment settings used to offer.

Diagnostic principles expect us to identify associated disorders, so-called comorbidities. The attributes of the correctional system—for example, understaffing—and outpatient infrastructure—such as provider musical chairs—do not maximize the diagnostic rigor needed to properly diagnose psychiatric illnesses and perform subsequent re-evaluations. Even in state hospitals inpatient days are shrinking, which in turn takes away the time clinicians need to perform a comprehensive diagnostic assessment—a prerequisite for good treatment planning.

One envies stalwarts such as Kraepelin and Bleuler whose genius we remember because they came of age with the “asylums.” These guys had the time but not many tools. Now we have many more tools, but we do not have time. However, I hope that common sense will prevail, and our society will advocate for a continuum of care that recognizes a legitimate role of “asylum” as outpatient health care.

Rudra Prakash, MD, DFAPA,
Clinical professor of psychiatry,
Vanderbilt University,
Staff psychiatrist,
Middle Tennessee Mental Health Institute,
Nashville, TN

I compliment Dr. Nasrallah for his courage and candor, which represents a deep commitment to the mentally ill and our society. He has articulated what many in our professional community strongly believe but don’t dare say publicly. I believe his message merits a broader dissemination, especially to policy makers. Thought leaders such as Dr. Nasrallah can make a difference by launching an educational campaign and start a new kind of advocacy movement.

Although I agree that patients with schizophrenia have suffered a great deal, a deinstitutionalized mental health system has limited means to care for patients with other psychiatric disorders. Increasingly, we see inpatients with multiple psychiatric morbidities along with Axis III issues. Traumatic psychopathologies, substance use disorders, and personality disorders constitute an incomplete list of conditions that cripple our patients who need longer and better care than they receive in the current therapeutic climate.

Substance use disorders are present in approximately 66% to 75% of admissions. Patients need care under 1 roof for substance use disorders and other co-occurring disorders concurrently rather than sequentially. After acute detoxification, patients are discharged from the hospital hoping to be accepted in a recovery program. However, by the time an inpatient substance abuse rehabilitation bed is available, the patient often has returned to chemicals or maladaptive behaviors, which leads to missed opportunities and unintended complications, namely treatment failure and resistance.

The eternal optimism that fueled the deinstitutionalization movement continues to nibble at inpatient and outpatient infrastructure. Over the years, fiscal forces have sliced mental health into 3 artificial compartments: mental health, addiction, and mental retardation and developmental disorders. Additionally, parity issues continue to block equal care. Managed care is leading to mechanical care—the patient is barely in the hospital and he is out. The ability to engage in thorough diagnostic assessment is limited by pressure to discharge patients.

Aftercare planning assumes unlimited access to care and the same optimism and zeal as deinstitutionalization advocates possessed. We tend to be oblivious to real issues such as uninsured or underinsured status and unmet basic needs. It is not surprising that nearly two-thirds of discharged patients do not return for their first follow-up appointment. If a discharged patient acts out, he is put in jail as if he is guilty of being mentally ill—a case of double discrimination.

Society supports expanding our jails and prisons more than state psychiatric hospitals. Is this a case of being “penny wise and pound foolish” and further stigmatizing mental illness? I agree that labels such as “dual diagnosis” are euphemisms. I also submit that categorizations such as “seriously ill” or “severe and persistent mental illness” could minimize the suffering of others who might benefit from what “asylum” treatment settings used to offer.

Diagnostic principles expect us to identify associated disorders, so-called comorbidities. The attributes of the correctional system—for example, understaffing—and outpatient infrastructure—such as provider musical chairs—do not maximize the diagnostic rigor needed to properly diagnose psychiatric illnesses and perform subsequent re-evaluations. Even in state hospitals inpatient days are shrinking, which in turn takes away the time clinicians need to perform a comprehensive diagnostic assessment—a prerequisite for good treatment planning.

One envies stalwarts such as Kraepelin and Bleuler whose genius we remember because they came of age with the “asylums.” These guys had the time but not many tools. Now we have many more tools, but we do not have time. However, I hope that common sense will prevail, and our society will advocate for a continuum of care that recognizes a legitimate role of “asylum” as outpatient health care.

Rudra Prakash, MD, DFAPA,
Clinical professor of psychiatry,
Vanderbilt University,
Staff psychiatrist,
Middle Tennessee Mental Health Institute,
Nashville, TN

I appreciate Dr. Nasrallah’s courage in giving voice to an opinion that many of us share but often are reluctant to express because the notion of asylum-based care is not politically correct.

This article was timely for me because I am reading The Lives They Left Behind: Suitcases from a State Hospital Attic, by Darby Penney and Peter Stastny. This book reviews the history of Willard Psychiatric Center in New York, which was the main employer in my hometown and where my mother and sister worked as psychiatric nurses before it closed in 1995.

Although Willard had warts— which I believe were related to its underfunded physical plant and difficulty attracting well-trained staff— it was a respite for many patients who could not live independently.

The book focuses on reconstructing the lives of long-term Willard patients from their belongings found in the hospital’s attic. What troubles me about the book is its nihilistic view of historic and modern psychiatry—a Szaszian view that there is a continuum of normal human responses to stress that includes delusions and hallucinations. According to this view, we have pathologized and medicalized normal behavior and poisoned people in an effort to help or isolate them. The authors liken patients’ meaningful work in kitchens, workshops, and on the farm to slave labor.

Living near Willard for most of my youth, it seemed to me that the benefits of purposeful work far exceeded what I see from the often-redundant arts and crafts recreational programs in today’s day programs and inpatient units. I was impressed with the ripe old age achieved by most of the patients profiled in this book, a luxury that I cannot imagine for many of my current patients. Too many of my patients cannot obtain safe housing or make routine primary care appointments.

This book provides proof of a strong antipsychiatry movement. Politicians seem comfortable under-funding mental health services by using the same misinformation to justify budget decisions.

Rory P. Houghtalen, MD,
Medical director,
Education and adult mental health,
ambulatory services,
Unity Behavioral Health,
Rochester, NY

I appreciate Dr. Nasrallah’s courage in giving voice to an opinion that many of us share but often are reluctant to express because the notion of asylum-based care is not politically correct.

This article was timely for me because I am reading The Lives They Left Behind: Suitcases from a State Hospital Attic, by Darby Penney and Peter Stastny. This book reviews the history of Willard Psychiatric Center in New York, which was the main employer in my hometown and where my mother and sister worked as psychiatric nurses before it closed in 1995.

Although Willard had warts— which I believe were related to its underfunded physical plant and difficulty attracting well-trained staff— it was a respite for many patients who could not live independently.

The book focuses on reconstructing the lives of long-term Willard patients from their belongings found in the hospital’s attic. What troubles me about the book is its nihilistic view of historic and modern psychiatry—a Szaszian view that there is a continuum of normal human responses to stress that includes delusions and hallucinations. According to this view, we have pathologized and medicalized normal behavior and poisoned people in an effort to help or isolate them. The authors liken patients’ meaningful work in kitchens, workshops, and on the farm to slave labor.

Living near Willard for most of my youth, it seemed to me that the benefits of purposeful work far exceeded what I see from the often-redundant arts and crafts recreational programs in today’s day programs and inpatient units. I was impressed with the ripe old age achieved by most of the patients profiled in this book, a luxury that I cannot imagine for many of my current patients. Too many of my patients cannot obtain safe housing or make routine primary care appointments.

This book provides proof of a strong antipsychiatry movement. Politicians seem comfortable under-funding mental health services by using the same misinformation to justify budget decisions.

Rory P. Houghtalen, MD,
Medical director,
Education and adult mental health,
ambulatory services,
Unity Behavioral Health,
Rochester, NY

I appreciate Dr. Nasrallah’s courage in giving voice to an opinion that many of us share but often are reluctant to express because the notion of asylum-based care is not politically correct.

This article was timely for me because I am reading The Lives They Left Behind: Suitcases from a State Hospital Attic, by Darby Penney and Peter Stastny. This book reviews the history of Willard Psychiatric Center in New York, which was the main employer in my hometown and where my mother and sister worked as psychiatric nurses before it closed in 1995.

Although Willard had warts— which I believe were related to its underfunded physical plant and difficulty attracting well-trained staff— it was a respite for many patients who could not live independently.

The book focuses on reconstructing the lives of long-term Willard patients from their belongings found in the hospital’s attic. What troubles me about the book is its nihilistic view of historic and modern psychiatry—a Szaszian view that there is a continuum of normal human responses to stress that includes delusions and hallucinations. According to this view, we have pathologized and medicalized normal behavior and poisoned people in an effort to help or isolate them. The authors liken patients’ meaningful work in kitchens, workshops, and on the farm to slave labor.

Living near Willard for most of my youth, it seemed to me that the benefits of purposeful work far exceeded what I see from the often-redundant arts and crafts recreational programs in today’s day programs and inpatient units. I was impressed with the ripe old age achieved by most of the patients profiled in this book, a luxury that I cannot imagine for many of my current patients. Too many of my patients cannot obtain safe housing or make routine primary care appointments.

This book provides proof of a strong antipsychiatry movement. Politicians seem comfortable under-funding mental health services by using the same misinformation to justify budget decisions.

Rory P. Houghtalen, MD,
Medical director,
Education and adult mental health,
ambulatory services,
Unity Behavioral Health,
Rochester, NY

Dr. Nasrallah’s viewpoint in “Bring back the asylums?” is bold, enlightening, contemporary, and precise. Highlighting deinstitutionalization’s consequences should raise awareness of this situation among Current Psychiatry readers.

Labeling patients as “clients” or “consumers” has always irritated me. We spend time and energy educating the public that psychiatric disorders are illnesses like diabetes or heart disease. Yet we perpetuate the stigma by acting as if something is wrong with the word “patient” by calling these individuals “consumers.”

Deinstitutionalization has had a tragic impact on the mentally ill. In 2002 the public was outraged when The New York Times reported that mentally ill patients were living in nursing homes in New York City. I thought that placing mentally ill individuals in locked nursing homes that were owned and operated by a major campaign contributor to the New York governor was one of the kindest methods in the state to treat mentally ill persons.

In 1999, a class-action suit was brought against New York City because mentally ill individuals were routinely released from prison in dangerous neighborhoods in the middle of the night with 2 subway tokens and $1.50 in cash. The case was settled out of court and the city pledged to provide services for inmates after their release.¹

I recently left a position at a state hospital and now work in a county jail. The transition has been enlightening. I suggest that everyone view the 2005 PBS Frontline documentary “The New Asylums.” The question posed in this program is “Have America’s jails and prisons become its new asylums?” It won’t take you long to realize that the answer is a sickening “Yes.”

It seems the United States has regressed to placing the mentally ill in cages. In 1825 the reverend Louis Dwight was shocked by what he saw when he took Bibles to inmates. He organized the Boston Prison Discipline Society, which encouraged the Massachusetts legislature to appoint a committee that ultimately recommended that all mentally ill inmates in jails and prison be transferred to Massachusetts General Hospital and legislated that confining these persons in the state’s jails was illegal. In 1833 the State Lunatic Asylum at Worcester opened, and more than half of the 164 patients came from jails.¹

Dorothea Dix followed with her campaign in 1842 when she taught a Sunday school class at the East Cambridge Jail. She found many mentally ill patients were housed in jails or wandered the streets. Dix visited 300 county jails and 18 prisons in 6 years. She exposed the horrendous conditions she witnessed and chided politicians for their lack of attention to the mentally ill. She is recognized for establishing 32 mental hospitals. By 1880 1,2

Today, the history of caring for the mentally ill has come full circle. Dorothea Dix would be disheartened to know that mentally ill individuals are again being locked away in jails or left to wander the streets.

What can a mental health professional do to improve care of mentally ill patients in jails or prisons? First, we must educate ourselves and be aware of what is happening in our field. Then we must educate the public and be involved in our professional organizations that have the resources and influence to initiate change. Contact your representatives, senators, governors, and your state’s department of corrections to begin to reverse the horrendous treatment of our most vulnerable citizens.

Virginia Singer, LPN
Las Vegas, NV

Dr. Nasrallah’s viewpoint in “Bring back the asylums?” is bold, enlightening, contemporary, and precise. Highlighting deinstitutionalization’s consequences should raise awareness of this situation among Current Psychiatry readers.

Labeling patients as “clients” or “consumers” has always irritated me. We spend time and energy educating the public that psychiatric disorders are illnesses like diabetes or heart disease. Yet we perpetuate the stigma by acting as if something is wrong with the word “patient” by calling these individuals “consumers.”

Deinstitutionalization has had a tragic impact on the mentally ill. In 2002 the public was outraged when The New York Times reported that mentally ill patients were living in nursing homes in New York City. I thought that placing mentally ill individuals in locked nursing homes that were owned and operated by a major campaign contributor to the New York governor was one of the kindest methods in the state to treat mentally ill persons.

In 1999, a class-action suit was brought against New York City because mentally ill individuals were routinely released from prison in dangerous neighborhoods in the middle of the night with 2 subway tokens and $1.50 in cash. The case was settled out of court and the city pledged to provide services for inmates after their release.¹

I recently left a position at a state hospital and now work in a county jail. The transition has been enlightening. I suggest that everyone view the 2005 PBS Frontline documentary “The New Asylums.” The question posed in this program is “Have America’s jails and prisons become its new asylums?” It won’t take you long to realize that the answer is a sickening “Yes.”

It seems the United States has regressed to placing the mentally ill in cages. In 1825 the reverend Louis Dwight was shocked by what he saw when he took Bibles to inmates. He organized the Boston Prison Discipline Society, which encouraged the Massachusetts legislature to appoint a committee that ultimately recommended that all mentally ill inmates in jails and prison be transferred to Massachusetts General Hospital and legislated that confining these persons in the state’s jails was illegal. In 1833 the State Lunatic Asylum at Worcester opened, and more than half of the 164 patients came from jails.¹

Dorothea Dix followed with her campaign in 1842 when she taught a Sunday school class at the East Cambridge Jail. She found many mentally ill patients were housed in jails or wandered the streets. Dix visited 300 county jails and 18 prisons in 6 years. She exposed the horrendous conditions she witnessed and chided politicians for their lack of attention to the mentally ill. She is recognized for establishing 32 mental hospitals. By 1880 1,2

Today, the history of caring for the mentally ill has come full circle. Dorothea Dix would be disheartened to know that mentally ill individuals are again being locked away in jails or left to wander the streets.

What can a mental health professional do to improve care of mentally ill patients in jails or prisons? First, we must educate ourselves and be aware of what is happening in our field. Then we must educate the public and be involved in our professional organizations that have the resources and influence to initiate change. Contact your representatives, senators, governors, and your state’s department of corrections to begin to reverse the horrendous treatment of our most vulnerable citizens.

Virginia Singer, LPN
Las Vegas, NV

Dr. Nasrallah’s viewpoint in “Bring back the asylums?” is bold, enlightening, contemporary, and precise. Highlighting deinstitutionalization’s consequences should raise awareness of this situation among Current Psychiatry readers.

Labeling patients as “clients” or “consumers” has always irritated me. We spend time and energy educating the public that psychiatric disorders are illnesses like diabetes or heart disease. Yet we perpetuate the stigma by acting as if something is wrong with the word “patient” by calling these individuals “consumers.”

Deinstitutionalization has had a tragic impact on the mentally ill. In 2002 the public was outraged when The New York Times reported that mentally ill patients were living in nursing homes in New York City. I thought that placing mentally ill individuals in locked nursing homes that were owned and operated by a major campaign contributor to the New York governor was one of the kindest methods in the state to treat mentally ill persons.

In 1999, a class-action suit was brought against New York City because mentally ill individuals were routinely released from prison in dangerous neighborhoods in the middle of the night with 2 subway tokens and $1.50 in cash. The case was settled out of court and the city pledged to provide services for inmates after their release.¹

I recently left a position at a state hospital and now work in a county jail. The transition has been enlightening. I suggest that everyone view the 2005 PBS Frontline documentary “The New Asylums.” The question posed in this program is “Have America’s jails and prisons become its new asylums?” It won’t take you long to realize that the answer is a sickening “Yes.”

It seems the United States has regressed to placing the mentally ill in cages. In 1825 the reverend Louis Dwight was shocked by what he saw when he took Bibles to inmates. He organized the Boston Prison Discipline Society, which encouraged the Massachusetts legislature to appoint a committee that ultimately recommended that all mentally ill inmates in jails and prison be transferred to Massachusetts General Hospital and legislated that confining these persons in the state’s jails was illegal. In 1833 the State Lunatic Asylum at Worcester opened, and more than half of the 164 patients came from jails.¹

Dorothea Dix followed with her campaign in 1842 when she taught a Sunday school class at the East Cambridge Jail. She found many mentally ill patients were housed in jails or wandered the streets. Dix visited 300 county jails and 18 prisons in 6 years. She exposed the horrendous conditions she witnessed and chided politicians for their lack of attention to the mentally ill. She is recognized for establishing 32 mental hospitals. By 1880 1,2

Today, the history of caring for the mentally ill has come full circle. Dorothea Dix would be disheartened to know that mentally ill individuals are again being locked away in jails or left to wander the streets.

What can a mental health professional do to improve care of mentally ill patients in jails or prisons? First, we must educate ourselves and be aware of what is happening in our field. Then we must educate the public and be involved in our professional organizations that have the resources and influence to initiate change. Contact your representatives, senators, governors, and your state’s department of corrections to begin to reverse the horrendous treatment of our most vulnerable citizens.

Virginia Singer, LPN
Las Vegas, NV

It is refreshing to see Dr. Nasrallah challenge the notion that deinstitutionalization benefits our patients. Discharge planning for our schizophrenic patients is the biggest obstacle my colleagues and I face.

We all have similar stories of managing an acute psychotic episode only to have the patient return within a few weeks after not taking prescribed medication or suffering the wraths of homelessness and poverty. Most of our schizophrenic patients lack necessary psychosocial and occupational necessities that would give them the best hope for recovery.

In an institution compliance is addressed, shelter is provided, and patients can hold a job, which gives them self-confidence and allows them to contribute economically to society. Also in an institution we can address patients’ comorbid substance use, which would increase the efficacy of our biologically based therapies. If we do not stand up for our patients they will continue to be victimized on the streets and many eventually will be institutionalized in the correctional system.

The dictionary defines asylum as “a place of retreat and security.” Shouldn’t psychiatrists fight for security in our patients’ insecure lives?

Jesse Rhoads, DO
Resident
Ohio State University, Columbus

It is refreshing to see Dr. Nasrallah challenge the notion that deinstitutionalization benefits our patients. Discharge planning for our schizophrenic patients is the biggest obstacle my colleagues and I face.

We all have similar stories of managing an acute psychotic episode only to have the patient return within a few weeks after not taking prescribed medication or suffering the wraths of homelessness and poverty. Most of our schizophrenic patients lack necessary psychosocial and occupational necessities that would give them the best hope for recovery.

In an institution compliance is addressed, shelter is provided, and patients can hold a job, which gives them self-confidence and allows them to contribute economically to society. Also in an institution we can address patients’ comorbid substance use, which would increase the efficacy of our biologically based therapies. If we do not stand up for our patients they will continue to be victimized on the streets and many eventually will be institutionalized in the correctional system.

The dictionary defines asylum as “a place of retreat and security.” Shouldn’t psychiatrists fight for security in our patients’ insecure lives?

Jesse Rhoads, DO
Resident
Ohio State University, Columbus

It is refreshing to see Dr. Nasrallah challenge the notion that deinstitutionalization benefits our patients. Discharge planning for our schizophrenic patients is the biggest obstacle my colleagues and I face.

We all have similar stories of managing an acute psychotic episode only to have the patient return within a few weeks after not taking prescribed medication or suffering the wraths of homelessness and poverty. Most of our schizophrenic patients lack necessary psychosocial and occupational necessities that would give them the best hope for recovery.

In an institution compliance is addressed, shelter is provided, and patients can hold a job, which gives them self-confidence and allows them to contribute economically to society. Also in an institution we can address patients’ comorbid substance use, which would increase the efficacy of our biologically based therapies. If we do not stand up for our patients they will continue to be victimized on the streets and many eventually will be institutionalized in the correctional system.

The dictionary defines asylum as “a place of retreat and security.” Shouldn’t psychiatrists fight for security in our patients’ insecure lives?

Jesse Rhoads, DO
Resident
Ohio State University, Columbus

Dr. Nasrallah’s observations are accurate for the vast number of patients with schizophrenia who are no longer housed in asylums. However, I hope that the solution is not to move backward.

Psychosocial treatments such as Assertive Community Treatment (ACT) are effective for alleviating the concerns Dr. Nasrallah raises, such as homelessness and poverty. ACT programs—which provide comprehensive, community-based psychiatric treatment, rehabilitation, and support for persons with serious and persistent mental illness—are associated with high patient satisfaction and lower costs. Some in the psychiatric community are not familiar with these evolving forms of therapy or are reluctant to embrace them. Likewise, clients do not know that these programs can make their lives better.

Instead of moving backward, let’s move forward to what professional ethics and research demands of us.

Walter Rush, MD
St. Paul, MN

Dr. Nasrallah’s observations are accurate for the vast number of patients with schizophrenia who are no longer housed in asylums. However, I hope that the solution is not to move backward.

Psychosocial treatments such as Assertive Community Treatment (ACT) are effective for alleviating the concerns Dr. Nasrallah raises, such as homelessness and poverty. ACT programs—which provide comprehensive, community-based psychiatric treatment, rehabilitation, and support for persons with serious and persistent mental illness—are associated with high patient satisfaction and lower costs. Some in the psychiatric community are not familiar with these evolving forms of therapy or are reluctant to embrace them. Likewise, clients do not know that these programs can make their lives better.

Instead of moving backward, let’s move forward to what professional ethics and research demands of us.

Walter Rush, MD
St. Paul, MN

Dr. Nasrallah’s observations are accurate for the vast number of patients with schizophrenia who are no longer housed in asylums. However, I hope that the solution is not to move backward.

Psychosocial treatments such as Assertive Community Treatment (ACT) are effective for alleviating the concerns Dr. Nasrallah raises, such as homelessness and poverty. ACT programs—which provide comprehensive, community-based psychiatric treatment, rehabilitation, and support for persons with serious and persistent mental illness—are associated with high patient satisfaction and lower costs. Some in the psychiatric community are not familiar with these evolving forms of therapy or are reluctant to embrace them. Likewise, clients do not know that these programs can make their lives better.

Instead of moving backward, let’s move forward to what professional ethics and research demands of us.

Walter Rush, MD
St. Paul, MN

I commend Dr. Henry Nasrallah for his editorial “Bring back the asylums?” (From the Editor, Current Psychiatry, March 2008, p. 19-20). I trained and worked at a large state hospital that was closely affiliated with the University of Michigan, whose residents and staff worked with our staff of general physicians. We had an excellent staff of psychiatrists—most of them board-certified—and psychiatric residents. We were routinely approved by the Joint Commission on Accreditation of Healthcare Organizations as well as the Council for Medical Education.

I lived on the hospital grounds, and people would ask if I was frightened to live there. My reply was no. It was scarier in Ann Arbor where the “druggies” and psychotics wandered the streets without treatment or supervision, much as it is now unless these individuals are in jail or prison.

At one time, this state hospital compared its operating costs with a nearby state prison and found the prison’s funding was 4 times greater than the hospital’s.

Joseph J. Tiziani, MD
Horseshoe Bay, TX

I commend Dr. Henry Nasrallah for his editorial “Bring back the asylums?” (From the Editor, Current Psychiatry, March 2008, p. 19-20). I trained and worked at a large state hospital that was closely affiliated with the University of Michigan, whose residents and staff worked with our staff of general physicians. We had an excellent staff of psychiatrists—most of them board-certified—and psychiatric residents. We were routinely approved by the Joint Commission on Accreditation of Healthcare Organizations as well as the Council for Medical Education.

I lived on the hospital grounds, and people would ask if I was frightened to live there. My reply was no. It was scarier in Ann Arbor where the “druggies” and psychotics wandered the streets without treatment or supervision, much as it is now unless these individuals are in jail or prison.

At one time, this state hospital compared its operating costs with a nearby state prison and found the prison’s funding was 4 times greater than the hospital’s.

Joseph J. Tiziani, MD
Horseshoe Bay, TX

I commend Dr. Henry Nasrallah for his editorial “Bring back the asylums?” (From the Editor, Current Psychiatry, March 2008, p. 19-20). I trained and worked at a large state hospital that was closely affiliated with the University of Michigan, whose residents and staff worked with our staff of general physicians. We had an excellent staff of psychiatrists—most of them board-certified—and psychiatric residents. We were routinely approved by the Joint Commission on Accreditation of Healthcare Organizations as well as the Council for Medical Education.

I lived on the hospital grounds, and people would ask if I was frightened to live there. My reply was no. It was scarier in Ann Arbor where the “druggies” and psychotics wandered the streets without treatment or supervision, much as it is now unless these individuals are in jail or prison.

At one time, this state hospital compared its operating costs with a nearby state prison and found the prison’s funding was 4 times greater than the hospital’s.

Joseph J. Tiziani, MD
Horseshoe Bay, TX

A widespread and enduring notion about schizophrenia is that it is a hopeless brain disease associated with progressive clinical, cognitive, social, and vocational deterioration. After all, community mental health centers are replete with profoundly disabled persons who carry a schizophrenia diagnosis. Most have no friends, spouses, or significant others and have not been employed for years. So can one argue that persons with schizophrenia ever recover?

How you define “recovery,” as discussed in this issue (page 40), certainly influences how you would answer that question. As a long-time schizophrenia researcher who has treated thousands of patients and conducted dozens of research projects into schizophrenia, I respond with a “definite maybe.”

Odds of recovery: 1 in 5?

The severity and outcome of any illness—including schizophrenia—falls into a bell-shaped curve, from very mild to very severe. Observations can be misleading, however. Kraepelin, for example, based his deteriorative description of schizophrenia on severely ill, long-term hospitalized patients. This biased sample did not include patients who remained in the community with their families, doing well enough not to need hospitalization.

The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) schizophrenia study¹ provides a good example of schizophrenia’s heterogeneity. At enrollment, the 1,460 outpatients ranged from no symptoms to severely ill. Schizophrenia outcome is similarly distributed.

The landmark Iowa 500 study² in the 1970s was one of the most thorough examinations of long-term schizophrenia outcomes, including recovery. With funding from the National Institute of Mental Health, researchers tracked down and interviewed hundreds of persons admitted 30 to 40 years earlier to the Iowa State Psychopathic Hospital and who met rigorous Research Diagnostic Criteria for schizophrenia. They found that:

Table

Expert consensus proposed criteria for schizophrenia remission

• 20% had recovered completely and resumed normal life
• 80% remained ill, with variable degrees of severity.

The best prognosis was for paranoid schizophrenia and the worst for non-paranoid schizophrenia; hebephrenia (“disorganized”) and undifferentiated schizophrenia had similarly poor outcomes.

A major confound for recovery from schizophrenia is that patients with psychotic bipolar disorder sometimes are misdiagnosed as having schizophrenia. Patients with bipolar disorder can achieve remission for a while, only to relapse again. If mis-diagnosed, they may be reported as “recovered” schizophrenia cases when they cycle out of a severe bipolar episode.

Treatment adherence: A key to recovery

Features associated with better outcome and possible recovery in schizophrenia include female gender, sudden onset of psychosis, paranoid subtype, high IQ, minimal negative symptoms, presence of an affective component, having a supportive family, good insight, continuity of care, and—very important—optimal treatment adherence.

Discontinuing treatment in schizophrenia leads to psychotic relapses and a lower probability of recovering. Therefore, I find it puzzling that injectable, long-acting antipsychotics are used infrequently in the United States, despite the high rate of treatment discontinuation in schizophrenia. In Europe, the rate of use of injectable antipsychotics is 3 times higher.

I have obtained extremely good outcomes—including recovery in patients who were regarded as hopelessly deteriorated—with long-acting injectable second-generation antipsychotics (SGAs) and dramatic functional recovery after giving patients injectable SGA treatment continuously for 2 years or more. My experience with depot first-generation antipsychotics (FGAs) was that they helped prevent relapse but did not help patients return to functioning. A possible explanation is that SGAs have been found to induce neurotropic factors and stimulate neurogenesis, whereas FGAs may lead to a decline in neurotropic factors and apoptotic loss of brain tissue.³

A useful remission measure

To measure clinically meaningful improvement (remission), I recommend criteria developed by schizophrenia experts (Table).⁴ These research criteria define remission based on core items in the Positive and Negative Syndrome Scale (PANSS). If symptoms remain in remission >6 months, social and vocational rehabilitation is more likely to restore a patient’s functional capacity. That functional improvement—not just symptomatic remission—would constitute true recovery.

Recovery is possible but appears to occur in a minority of patients.² Many patients can achieve remission, which enables them to gradually regain various degrees of functioning. Just as a stroke patient may need rehabilitation to learn to talk and walk again, individuals with schizophrenia can reclaim their lives with a balanced regimen of effective antipsychotic medication, coupled with personalized social, cognitive, and vocational rehabilitation.

A widespread and enduring notion about schizophrenia is that it is a hopeless brain disease associated with progressive clinical, cognitive, social, and vocational deterioration. After all, community mental health centers are replete with profoundly disabled persons who carry a schizophrenia diagnosis. Most have no friends, spouses, or significant others and have not been employed for years. So can one argue that persons with schizophrenia ever recover?

How you define “recovery,” as discussed in this issue (page 40), certainly influences how you would answer that question. As a long-time schizophrenia researcher who has treated thousands of patients and conducted dozens of research projects into schizophrenia, I respond with a “definite maybe.”

Odds of recovery: 1 in 5?

The severity and outcome of any illness—including schizophrenia—falls into a bell-shaped curve, from very mild to very severe. Observations can be misleading, however. Kraepelin, for example, based his deteriorative description of schizophrenia on severely ill, long-term hospitalized patients. This biased sample did not include patients who remained in the community with their families, doing well enough not to need hospitalization.

The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) schizophrenia study¹ provides a good example of schizophrenia’s heterogeneity. At enrollment, the 1,460 outpatients ranged from no symptoms to severely ill. Schizophrenia outcome is similarly distributed.

The landmark Iowa 500 study² in the 1970s was one of the most thorough examinations of long-term schizophrenia outcomes, including recovery. With funding from the National Institute of Mental Health, researchers tracked down and interviewed hundreds of persons admitted 30 to 40 years earlier to the Iowa State Psychopathic Hospital and who met rigorous Research Diagnostic Criteria for schizophrenia. They found that:

Table

Expert consensus proposed criteria for schizophrenia remission

• 20% had recovered completely and resumed normal life
• 80% remained ill, with variable degrees of severity.

The best prognosis was for paranoid schizophrenia and the worst for non-paranoid schizophrenia; hebephrenia (“disorganized”) and undifferentiated schizophrenia had similarly poor outcomes.

A major confound for recovery from schizophrenia is that patients with psychotic bipolar disorder sometimes are misdiagnosed as having schizophrenia. Patients with bipolar disorder can achieve remission for a while, only to relapse again. If mis-diagnosed, they may be reported as “recovered” schizophrenia cases when they cycle out of a severe bipolar episode.

Treatment adherence: A key to recovery

Features associated with better outcome and possible recovery in schizophrenia include female gender, sudden onset of psychosis, paranoid subtype, high IQ, minimal negative symptoms, presence of an affective component, having a supportive family, good insight, continuity of care, and—very important—optimal treatment adherence.

Discontinuing treatment in schizophrenia leads to psychotic relapses and a lower probability of recovering. Therefore, I find it puzzling that injectable, long-acting antipsychotics are used infrequently in the United States, despite the high rate of treatment discontinuation in schizophrenia. In Europe, the rate of use of injectable antipsychotics is 3 times higher.

I have obtained extremely good outcomes—including recovery in patients who were regarded as hopelessly deteriorated—with long-acting injectable second-generation antipsychotics (SGAs) and dramatic functional recovery after giving patients injectable SGA treatment continuously for 2 years or more. My experience with depot first-generation antipsychotics (FGAs) was that they helped prevent relapse but did not help patients return to functioning. A possible explanation is that SGAs have been found to induce neurotropic factors and stimulate neurogenesis, whereas FGAs may lead to a decline in neurotropic factors and apoptotic loss of brain tissue.³

A useful remission measure

To measure clinically meaningful improvement (remission), I recommend criteria developed by schizophrenia experts (Table).⁴ These research criteria define remission based on core items in the Positive and Negative Syndrome Scale (PANSS). If symptoms remain in remission >6 months, social and vocational rehabilitation is more likely to restore a patient’s functional capacity. That functional improvement—not just symptomatic remission—would constitute true recovery.

Recovery is possible but appears to occur in a minority of patients.² Many patients can achieve remission, which enables them to gradually regain various degrees of functioning. Just as a stroke patient may need rehabilitation to learn to talk and walk again, individuals with schizophrenia can reclaim their lives with a balanced regimen of effective antipsychotic medication, coupled with personalized social, cognitive, and vocational rehabilitation.

A widespread and enduring notion about schizophrenia is that it is a hopeless brain disease associated with progressive clinical, cognitive, social, and vocational deterioration. After all, community mental health centers are replete with profoundly disabled persons who carry a schizophrenia diagnosis. Most have no friends, spouses, or significant others and have not been employed for years. So can one argue that persons with schizophrenia ever recover?

How you define “recovery,” as discussed in this issue (page 40), certainly influences how you would answer that question. As a long-time schizophrenia researcher who has treated thousands of patients and conducted dozens of research projects into schizophrenia, I respond with a “definite maybe.”

Odds of recovery: 1 in 5?

The severity and outcome of any illness—including schizophrenia—falls into a bell-shaped curve, from very mild to very severe. Observations can be misleading, however. Kraepelin, for example, based his deteriorative description of schizophrenia on severely ill, long-term hospitalized patients. This biased sample did not include patients who remained in the community with their families, doing well enough not to need hospitalization.

The Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) schizophrenia study¹ provides a good example of schizophrenia’s heterogeneity. At enrollment, the 1,460 outpatients ranged from no symptoms to severely ill. Schizophrenia outcome is similarly distributed.

The landmark Iowa 500 study² in the 1970s was one of the most thorough examinations of long-term schizophrenia outcomes, including recovery. With funding from the National Institute of Mental Health, researchers tracked down and interviewed hundreds of persons admitted 30 to 40 years earlier to the Iowa State Psychopathic Hospital and who met rigorous Research Diagnostic Criteria for schizophrenia. They found that:

Table

Expert consensus proposed criteria for schizophrenia remission

• 20% had recovered completely and resumed normal life
• 80% remained ill, with variable degrees of severity.

The best prognosis was for paranoid schizophrenia and the worst for non-paranoid schizophrenia; hebephrenia (“disorganized”) and undifferentiated schizophrenia had similarly poor outcomes.

A major confound for recovery from schizophrenia is that patients with psychotic bipolar disorder sometimes are misdiagnosed as having schizophrenia. Patients with bipolar disorder can achieve remission for a while, only to relapse again. If mis-diagnosed, they may be reported as “recovered” schizophrenia cases when they cycle out of a severe bipolar episode.

Treatment adherence: A key to recovery

Features associated with better outcome and possible recovery in schizophrenia include female gender, sudden onset of psychosis, paranoid subtype, high IQ, minimal negative symptoms, presence of an affective component, having a supportive family, good insight, continuity of care, and—very important—optimal treatment adherence.

Discontinuing treatment in schizophrenia leads to psychotic relapses and a lower probability of recovering. Therefore, I find it puzzling that injectable, long-acting antipsychotics are used infrequently in the United States, despite the high rate of treatment discontinuation in schizophrenia. In Europe, the rate of use of injectable antipsychotics is 3 times higher.

I have obtained extremely good outcomes—including recovery in patients who were regarded as hopelessly deteriorated—with long-acting injectable second-generation antipsychotics (SGAs) and dramatic functional recovery after giving patients injectable SGA treatment continuously for 2 years or more. My experience with depot first-generation antipsychotics (FGAs) was that they helped prevent relapse but did not help patients return to functioning. A possible explanation is that SGAs have been found to induce neurotropic factors and stimulate neurogenesis, whereas FGAs may lead to a decline in neurotropic factors and apoptotic loss of brain tissue.³

A useful remission measure

To measure clinically meaningful improvement (remission), I recommend criteria developed by schizophrenia experts (Table).⁴ These research criteria define remission based on core items in the Positive and Negative Syndrome Scale (PANSS). If symptoms remain in remission >6 months, social and vocational rehabilitation is more likely to restore a patient’s functional capacity. That functional improvement—not just symptomatic remission—would constitute true recovery.

Recovery is possible but appears to occur in a minority of patients.² Many patients can achieve remission, which enables them to gradually regain various degrees of functioning. Just as a stroke patient may need rehabilitation to learn to talk and walk again, individuals with schizophrenia can reclaim their lives with a balanced regimen of effective antipsychotic medication, coupled with personalized social, cognitive, and vocational rehabilitation.

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Characteristics of stories told by patients with pseudologia fantastica

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

• Sertraline • Zoloft
  

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

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Characteristics of stories told by patients with pseudologia fantastica

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

• Sertraline • Zoloft
  

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

CASE: A tragic tale

Reverend R, a 62-year-old Methodist minister, is admitted to a general surgical service for abdominal pain secondary to a recurring bowel obstruction. While there, he learns that his pregnant 24-year-old fiancée was struck and killed by a drunk driver as she was driving to visit him. Her medical team was not able to save her child. The surgical service requests a psychiatric consultation for Reverend R to assist him with grieving.

Our team interviews Reverend R 3 days after his fiancée’s death. We did not have access to his psychiatric records before our evaluation, but his chart indicates Reverend R had been hospitalized for nearly 3 months after being transferred from another hospital. He has a history of colon cancer and cerebral palsy and has struggled with depression since college. He had 1 psychiatric hospitalization 26 years earlier and no history of suicide attempts. He has responded to pharmacotherapy and is taking sertraline, 100 mg daily.

Reverend R expresses grief, stating he has lost the love of his life. With prompting, he provides a few details about his fiancée but does not say much about the accident. He says he feels guilty and frustrated that he can’t attend his fiancée’s funeral because “I have a nasogastric tube.” He claims he has cried excessively in the last few days, repeatedly stating, “I soaked 4 towels.” He is profusely apologetic for expressing his grief, as if doing so was inappropriate.

Reverend R acknowledges feeling sad but denies pervasively depressed mood or anhedonia, excessive guilt, or feelings of hopelessness, helplessness, or worthlessness. His affect ranges from mildly dysphoric to jovial and witty. His thought form and content are logical, linear, and goal-oriented. He denies having preoccupations, obsessions, delusions, or hallucinations. Attention and concentration are intact without evidence of waxing and waning. Cognition and memory also are intact. His Folstein Mini-Mental State Exam (MMSE) score is 29/30. Insight and judgment are assessed to be good, and intellect is above average.

We end our interview by asking Reverend R for permission to contact his psychiatrist for additional information. He stops making eye contact, begins to stammer, and tells us he is acutely short of breath. We seek out his nurse to check him, and within a few minutes his shortness of breath resolves without intervention.

The authors’ observations

Reverend R’s presentation does not suggest that his fiancée died 3 days ago. Without prompting, he says little about her or the accident, but he provides a great deal of information about himself. He clearly enjoys our attention, several times enthusiastically asking, “What else would you like to know about me?” At times he focuses on irrelevant topics.

He does not appear depressed and, although Reverend R’s voice breaks at times, we do not observe tears. His intermittent jovial, witty manner is inappropriate, but he is oriented and his MMSE provides no evidence of delirium. He does not elaborate on his frustration at being unable to attend the funeral and seems satisfied with the possibility of watching a video of the service.

Reverend R does not meet DSM-IV-TR criteria for major depressive disorder. We feel his emotions and conduct are unusual in response to the stress and therefore, based on what we have learned so far, we believe he best meets criteria for an adjustment disorder.

HISTORY: A series of traumas

During our initial interview, Reverend R explains that his life has been characterized by a series of traumatic events (Table 1). He had been sexually assaulted twice: by an uncle during childhood and by a male nurse while hospitalized for depression 26 years ago. The nurse had HIV, but the Reverend tested negative.

The day before our visit was not only the Reverend’s birthday but also was to be his wedding day. The Reverend had met his fiancée, a nurse, at the nursing home where he lives. At times, she took him on outings for dinner and other activities.

We ask the Reverend precisely why he needed 24-hour care and why he had been in the nursing home for 15 years. He is not able to provide a reasonable explanation.

Table 1

Reverend R’s life story: A series of traumatic events

The authors’ observations

Reverend R talks almost incessantly about the atrocities he suffered throughout his life. Times of happiness and success are the exception.

We begin to doubt the veracity of certain details of his story. We question the plausibility of a young nurse having an intimate relationship with and becoming pregnant by a 62-year-old nursing home patient who was an ordained minister. Reverend R’s claim of being the nursing home’s public relations director and performing sermons there seems unlikely. His stories are inconsistent; whenever we question him, he creates a reply that he is convinced seems believable. A collateral history is imperative for us to establish a diagnosis.

FOLLOW-UP: His story starts to fray

At a follow-up visit the next day, the Reverend states that he has been sad and at times he will “fall apart” in response to his fiancée’s death. He says that a video of the memorial service his fiancée’s father gave him had been “hard to watch.” We ask if he has the video; he says that he sent it back to the nursing home.

The authors’ observations

It seems strange that Reverend R is concerned that talking with us could compromise his return to the nursing home. His questions and behavior are paranoid; we did not observe this type of behavior during our initial interview.

We investigate Reverend R’s claims. A hospital dismissal summary from 13 years ago documents that Reverend R had been caught pulling out his NG tube. Additionally, he was observed drinking out of the sink when he was advised to take nothing by mouth.

Within days of that hospitalization, he presented to our outpatient gastrointestinal clinic for a second opinion regarding his abdominal pain. His father demanded that the Reverend be admitted. When told that hospitalization was not warranted, Reverend R and his father became angry and abruptly left the office.

Our hospital’s nursing staff is a vital source of information because they observed Reverend R often during his 3-month stay. They are suspicious of his history because they noticed discrepancies, such as Reverend R telling one nurse his fiancée died on a Thursday and another she died on a Friday. He spoke of people visiting him, but the staff never saw any visitors.

The nursing staff reports that at times he would use profanity and was quite hostile. A member of our team saw him yelling at a female chaplain. In our initial interview he told our team that the chaplain had reprimanded him for having premarital relations with his fiancée.

We find no evidence of an accident that resulted in the death of a 24-year-old pregnant female. Obviously, there was never a funeral or visits from the fictitious fiancée’s father. The sexual assault by the male nurse while hospitalized is possible but not probable, given the other falsehoods Reverend R told.

The seminary Reverend R told us he attended exists, but we are not able to determine if he was educated there. He told some staff members he had obtained a Master’s degree and others a PhD.

Reverend R refuses to sign a release of information form for the nursing home. We speak with the nurse who worked with Reverend R’s psychiatrist, who confirms that the patient’s diagnosis was depression. She tells us that the Reverend said he relocated to that area to live closer to a man with whom he had a romantic relationship. Reverend R confided to her that his father never approved of the relationship, but his mother accepted it.

DIAGNOSIS: A rarely seen symptom

Reverend R meets the DSM-IV-TR criteria for factitious disorder (Table 2).¹ The presentation of a patient with this disorder may include:

• fabrication of subjective complaints
  
• self-inflicted conditions
  
• exaggeration or exacerbation of pre-existing conditions
  
• any combination of these.
  

Differential diagnosis for pseudologia fantastica includes dementia, delusional disorder, antisocial personality disorder, borderline personality disorder, factitious disorder, malingering, hypochondriasis, substance abuse/dependence, and schizophrenia/schizophreniform disorder.³

Table 2

DSM-IV-TR criteria for factitious disorder*

Characteristics of stories told by patients with pseudologia fantastica

Confronting patients such as Reverend R likely is not the best approach. Showing them respect and empathy is important. Creating a safe, supportive environment in which they can express themselves will encourage them to consider ongoing psychiatric care.^3,6

OUTCOME: Return to nursing home

Approximately 1 week after our follow-up visit, Reverend R was discharged to the nursing home where he had resided prior to the hospitalization. Several attempts to contact him to obtain additional information and collateral history were unsuccessful, but clearly we had enough information to refute the reason we were asked to evaluate him.

Related resources

• Epstein LA, Stern TA. Factitious illness: a 3-step consultation-liaison approach. Current Psychiatry 2007;6(4):54-58.
  
• Birch CD, Kelln BRC, Aquino EPB. A review and case report of pseudologia fantastica. Journal of Forensic Psychiatry and Psychology 2006;17(2):299-320.
  

• Sertraline • Zoloft
  

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

From alcohol to opioids, most addictive substances can induce sleep disturbances that persist despite abstinence and may increase the risk for relapse. Nearly all FDA-approved hypnotics are Schedule IV controlled substances that—although safe and effective for most populations—are prone to abuse by patients with substance use disorders.

You’re not alone if you hesitate to prescribe hypnotics to these patients; a study of 311 addiction medicine physicians found that they prescribed sleep-promoting medication to only 30% of their alcohol-dependent patients with insomnia.¹

This article presents evidence on how alcohol and other substances disturb sleep in patients with addictions. We discuss the usefulness of hypnotics, off-label sedatives, and cognitive-behavioral therapy (CBT). Our goal is to help you reduce your patients’ risk of relapse by addressing their sleep complaints.

Workup: 3 principles

Insomnia is multifactorial. Don’t assume that substance abuse is the only cause of prominent insomnia complaints. Insomnia in patients with substance use disorders may be a manifestation of protracted withdrawal or a primary sleep disorder. Evaluate your patient’s:

• other illnesses (psychiatric, medical, and other sleep disorders)
  
• sleep-impairing medications (such as activating antidepressants and theophylline)
  
• inadequate sleep hygiene
  
• dysfunctional beliefs about sleep.
  

Insomnia is a clinical diagnosis that does not require an overnight sleep laboratory study (polysomnography [PSG]). Diagnose insomnia when a patient meets DSM-IV-TR criteria (has difficulty falling asleep or staying asleep or feels that sleep is not refreshing for at least 1 month; and the sleep problem impairs daytime functioning and/or causes clinically significant distress). In addition, consider:

• PSG if you suspect other sleep disorders, particularly obstructive sleep apnea (OSA) and periodic limb movement disorder (PLMD)
  
• an overnight sleep study for treatment-resistant insomnia, when you have adequately treated other causes.
  

Sleep logs are useful. Ask patients to keep a sleep log for 2 weeks during early recovery, after acute withdrawal subsides. These diaries help assess sleep patterns over time, document improvement with abstinence, and engage the patient in treatment. The National Sleep Foundation can provide examples (see Related Resources).

Alcohol and sleep disturbances

Insomnia is extremely common in active drinkers and in those who are in treatment after having stopped drinking. Across 7 studies of 1,577 alcohol-dependent patients undergoing treatment, more than one-half reported insomnia symptoms (mean 58%, range 36% to 91%),^2,3 substantially higher than the rate in the general population (33%). Nicotine, marijuana, cocaine and other stimulants, and opioids also can disrupt sleep (Table 1).

Which came first? Sleep problems may be a pathway by which problematic substance use develops. In 1 study, sleep problems reported by mothers in boys ages 3 to 5 predicted onset of alcohol and drug use by ages 12 to 14.⁴ This relationship was not mediated by attention problems, anxiety/depression, or aggression. Thus, insomnia may increase the risk for early substance use.

In an epidemiologic study of >10,000 adults, the incidence of new alcohol use disorders after 1 year in those without psychiatric disorders at baseline was twice as high in persons with persistent insomnia as in those without insomnia.⁵

Patients with sleep disturbances may use alcohol to self-medicate,⁶ and tolerance to alcohol’s sedating effects develops quickly. As patients consume larger quantities with greater frequency to produce sleep, the risk for dependence may increase.

Comorbid sleep disorders. Alcohol-dependent patients with difficulty falling asleep may have abnormal circadian rhythms, as suggested by delayed onset of nocturnal melatonin secretion.⁷ They also may have low homeostatic sleep drive, another factor required to promote sleep.⁸

Habitual alcohol consumption before bedtime (1 to 3 standard drinks) is associated with mild sleep-disordered breathing (SDB) in men but not in women.⁹ SDB also may be more prevalent in alcohol-dependent men age >60.¹⁰

Consuming >2 drinks/day has been associated with restless legs and increased periodic limb movements during sleep. Twice as many women reporting high alcohol use were diagnosed with PLMD, compared with women reporting normal alcohol consumption.^10-11 Recovering alcohol-dependent patients have significantly more periodic limb movements associated with arousals (PLMA) from sleep than controls. Moreover, PLMA can predict 80% of abstainers and 44% of relapsers after 6 months of abstinence.¹²

Table 1

Sleep disruptions caused by substances of abuse

Multifaceted treatment

A thorough history is essential to evaluate sleep and guide treatment decisions. Refer patients to an accredited sleep disorders center if their history shows:

• loud snoring
  
• cessation of breathing
  
• frequent kicking during sleep
  
• excessive daytime sleepiness.
  

Chronic insomnia. Patients who report chronic insomnia and behaviors incompatible with sleep may be good candidates for cognitive-behavioral therapy for insomnia (CBT-I). Patient education can change maladaptive behaviors, such as staying in bed for long periods of time to compensate for sleep loss, using the bed for activities other than sleep, or worrying excessively about sleep (Box 1).¹³

Pharmacotherapy may be preferred:

• for patients with unstable physical or mental illness
  
• when CBT-I could exacerbate a comorbid condition (such as restricting sleep in a patient with bipolar disorder)
  
• for patients with low motivation for behavior change
  
• when trained CBT-I providers or resources to pay for CBT-I are limited.
  

Box 1

In older adults with insomnia but no history of addiction, CBT-I was more effective than placebo and as effective as a hypnotic alone (temazepam, 7.5 and 30 mg qhs) and a hypnotic/CBT-I combination in reducing nighttime wakefulness, increasing total sleep time, and increasing sleep efficiency. After 2 years, patients treated with CBT-I alone were most likely to maintain these initial treatment gains.¹⁵

Limited data exist on CBT-I’s effectiveness in patients with addiction. In 2 studies, alcohol-dependent patients reported improved sleep.^16,17 CBT-I also improved measures of anxiety and depression, fatigue, and some quality-of-life items.¹⁶

Box 2

In general, most physicians who specialize in treating addictions would not recommend these drug classes as first choice in postwithdrawal, substance-dependent patients complaining of chronic insomnia. Nevertheless, you are likely to encounter patients with a history of substance abuse/dependence who are taking legally prescribed benzodiazepine receptor agonists for insomnia, and they may be very reluctant to discontinue these medications.

Weigh and discuss with the patient the risks and benefits of taking vs discontinuing the hypnotic, as well as alternatives. Because chronic hypnotic use may interfere with addiction recovery, it is important to discuss the patient’s recovery plan.

If you decide to prescribe a hypnotic with abuse liability, the newer alpha-1-selective benzodiazepine receptor agonists are preferable—as they would be for non-addicted patients—because they are less likely to disrupt sleep architecture. They are also less likely than the long-acting benzodiazepines (such as flurazepam) to accumulate over time and result in daytime impairment.

Patient contracts. A written agreement can be useful whenever you prescribe a controlled substance for a patient with an addiction history. Include these issues:

• frequency of clinic visits for monitoring response and refills, requests for early refills, and telephone refills
  
• obtaining prescriptions from only one prescriber and one pharmacy
  
• abstinence from other abused substances
  
• urine drug screens and pill counts
  
• authorization for you to share information with other care providers or significant others
  
• an addiction recovery plan for other abused substances
  
• consequences of nonadherence.
  

Table 2

FDA-approved benzodiazepine receptor agonists for insomnia*

Off-label sedatives for insomnia

Like ramelteon, sedating agents that do not have abuse liability are first-choice medications for patients with addiction and co-occurring insomnia (Table 3):

• The most studied are gabapentin and trazodone.
  
• Quetiapine and mirtazapine may be considered as second-choice options.
  

In 2 open-label pilot studies of alcohol-dependent patients with insomnia:

• gabapentin (mean dose 953 mg) significantly improved sleep quality over 4 to 6 weeks²⁰
  
• both gabapentin (mean 888 mg qhs) and trazodone (mean 105 mg qhs) significantly improved Sleep Problems Questionnaire scores, but patients receiving gabapentin were less likely than those taking trazodone to feel tired upon awakening.²¹
  

Although gabapentin and the anticonvulsant pregabalin increase slow-wave sleep in healthy control subjects, evidence of a similar effect is lacking in alcohol-dependent patients.

Trazodone is the most commonly prescribed antidepressant for insomnia because of its sedating effect and low abuse potential. Trazodone was associated with greater sleep improvements vs placebo as measured via PSG in a randomized, double-blind trial of alcohol-dependent patients with insomnia.²³ In a second study, sleep outcomes were better with trazodone vs placebo over 12 weeks in alcohol-dependent patients, although patients in the trazodone group drank more heavily.²⁴

Other sedating antidepressants such as mirtazapine and doxepin have not been studied in patients with substance use disorders.

Quetiapine is a second-generation antipsychotic with sedating properties. When quetiapine, 25 to 200 mg/d, was given to alcohol-dependent veterans with sleep complaints, they remained abstinent more days and had fewer hospitalizations than veterans not receiving quetiapine.²⁵ Both groups had high rates of psychiatric comorbidity, and 90% had posttraumatic stress disorder. Improved abstinence was thought to result from improved sleep, but no sleep measures were included to test this hypothesis.

A recently published, randomized controlled pilot study reported significantly reduced drinking and craving in severely alcohol-dependent patients receiving quetiapine vs placebo, although sleep data were not included.²⁶

Other options. Tricyclic antidepressants carry risks of cardiotoxicity and other side effects but can be useful when other options have not worked or patients have comorbidities such as neuropathic pain or migraine headaches. Combinations of agents also may be considered for treatment-resistant insomnia.

Nonprescription remedies such as antihistamines, valerian root extract (from the herb Valeriana officinalis), and melatonin are commonly used for sleep, although data are limited in substance-abusing patients.

Table 3

Noncontrolled sedating agents for treating insomnia
in patients with a history of substance abuse

• American Academy of Sleep Medicine. www.sleepeducation.com.
  
• National Sleep Foundation. Sleep logs for downloading. www.sleepfoundation.org.
  
• Restless Legs Syndrome Foundation. www.rls.org.
  
• Brower KJ. Insomnia, alcoholism and relapse. Sleep Med Rev 2003;7:523-39.
  

• Amitriptyline • Elavil, Endep
  
• Doxepin • Sinequan
  
• Estazolam • ProSom
  
• Eszopiclone • Lunesta
  
• Flurazepam • Dalmane
  
• Gabapentin • Neurontin
  
• Methamphetamine • Desoxyn
  
• Methylphenidate • Concerta, Ritalin, others
  
• Mirtazapine • Remeron
  
• Nefazodone • Serzone
  
• Nortriptyline • Pamelor
  
• Pregabalin • Lyrica
  
• Quazepam • Doral
  
• Quetiapine • Seroquel
  
• Ramelteon • Rozerem
  
• Temazepam • Restoril
  
• Theophylline • Theo-24, others
  
• Trazodone • Desyrel
  
• Triazolam • Halcion
  
• Zaleplon • Sonata
  
• Zolpidem • Ambien, Ambien CR
  

Dr. Conroy and Dr. Arnedt report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Brower is a consultant to Pfizer.

Acknowledgment

This work was supported by an NIH grant to Dr. Brower (2K24 AA00304).

From alcohol to opioids, most addictive substances can induce sleep disturbances that persist despite abstinence and may increase the risk for relapse. Nearly all FDA-approved hypnotics are Schedule IV controlled substances that—although safe and effective for most populations—are prone to abuse by patients with substance use disorders.

You’re not alone if you hesitate to prescribe hypnotics to these patients; a study of 311 addiction medicine physicians found that they prescribed sleep-promoting medication to only 30% of their alcohol-dependent patients with insomnia.¹

This article presents evidence on how alcohol and other substances disturb sleep in patients with addictions. We discuss the usefulness of hypnotics, off-label sedatives, and cognitive-behavioral therapy (CBT). Our goal is to help you reduce your patients’ risk of relapse by addressing their sleep complaints.

Workup: 3 principles

Insomnia is multifactorial. Don’t assume that substance abuse is the only cause of prominent insomnia complaints. Insomnia in patients with substance use disorders may be a manifestation of protracted withdrawal or a primary sleep disorder. Evaluate your patient’s:

• other illnesses (psychiatric, medical, and other sleep disorders)
  
• sleep-impairing medications (such as activating antidepressants and theophylline)
  
• inadequate sleep hygiene
  
• dysfunctional beliefs about sleep.
  

Insomnia is a clinical diagnosis that does not require an overnight sleep laboratory study (polysomnography [PSG]). Diagnose insomnia when a patient meets DSM-IV-TR criteria (has difficulty falling asleep or staying asleep or feels that sleep is not refreshing for at least 1 month; and the sleep problem impairs daytime functioning and/or causes clinically significant distress). In addition, consider:

• PSG if you suspect other sleep disorders, particularly obstructive sleep apnea (OSA) and periodic limb movement disorder (PLMD)
  
• an overnight sleep study for treatment-resistant insomnia, when you have adequately treated other causes.
  

Sleep logs are useful. Ask patients to keep a sleep log for 2 weeks during early recovery, after acute withdrawal subsides. These diaries help assess sleep patterns over time, document improvement with abstinence, and engage the patient in treatment. The National Sleep Foundation can provide examples (see Related Resources).

Alcohol and sleep disturbances

Insomnia is extremely common in active drinkers and in those who are in treatment after having stopped drinking. Across 7 studies of 1,577 alcohol-dependent patients undergoing treatment, more than one-half reported insomnia symptoms (mean 58%, range 36% to 91%),^2,3 substantially higher than the rate in the general population (33%). Nicotine, marijuana, cocaine and other stimulants, and opioids also can disrupt sleep (Table 1).

Which came first? Sleep problems may be a pathway by which problematic substance use develops. In 1 study, sleep problems reported by mothers in boys ages 3 to 5 predicted onset of alcohol and drug use by ages 12 to 14.⁴ This relationship was not mediated by attention problems, anxiety/depression, or aggression. Thus, insomnia may increase the risk for early substance use.

In an epidemiologic study of >10,000 adults, the incidence of new alcohol use disorders after 1 year in those without psychiatric disorders at baseline was twice as high in persons with persistent insomnia as in those without insomnia.⁵

Patients with sleep disturbances may use alcohol to self-medicate,⁶ and tolerance to alcohol’s sedating effects develops quickly. As patients consume larger quantities with greater frequency to produce sleep, the risk for dependence may increase.

Comorbid sleep disorders. Alcohol-dependent patients with difficulty falling asleep may have abnormal circadian rhythms, as suggested by delayed onset of nocturnal melatonin secretion.⁷ They also may have low homeostatic sleep drive, another factor required to promote sleep.⁸

Habitual alcohol consumption before bedtime (1 to 3 standard drinks) is associated with mild sleep-disordered breathing (SDB) in men but not in women.⁹ SDB also may be more prevalent in alcohol-dependent men age >60.¹⁰

Consuming >2 drinks/day has been associated with restless legs and increased periodic limb movements during sleep. Twice as many women reporting high alcohol use were diagnosed with PLMD, compared with women reporting normal alcohol consumption.^10-11 Recovering alcohol-dependent patients have significantly more periodic limb movements associated with arousals (PLMA) from sleep than controls. Moreover, PLMA can predict 80% of abstainers and 44% of relapsers after 6 months of abstinence.¹²

Table 1

Sleep disruptions caused by substances of abuse

Multifaceted treatment

A thorough history is essential to evaluate sleep and guide treatment decisions. Refer patients to an accredited sleep disorders center if their history shows:

• loud snoring
  
• cessation of breathing
  
• frequent kicking during sleep
  
• excessive daytime sleepiness.
  

Chronic insomnia. Patients who report chronic insomnia and behaviors incompatible with sleep may be good candidates for cognitive-behavioral therapy for insomnia (CBT-I). Patient education can change maladaptive behaviors, such as staying in bed for long periods of time to compensate for sleep loss, using the bed for activities other than sleep, or worrying excessively about sleep (Box 1).¹³

Pharmacotherapy may be preferred:

• for patients with unstable physical or mental illness
  
• when CBT-I could exacerbate a comorbid condition (such as restricting sleep in a patient with bipolar disorder)
  
• for patients with low motivation for behavior change
  
• when trained CBT-I providers or resources to pay for CBT-I are limited.
  

Box 1

In older adults with insomnia but no history of addiction, CBT-I was more effective than placebo and as effective as a hypnotic alone (temazepam, 7.5 and 30 mg qhs) and a hypnotic/CBT-I combination in reducing nighttime wakefulness, increasing total sleep time, and increasing sleep efficiency. After 2 years, patients treated with CBT-I alone were most likely to maintain these initial treatment gains.¹⁵

Limited data exist on CBT-I’s effectiveness in patients with addiction. In 2 studies, alcohol-dependent patients reported improved sleep.^16,17 CBT-I also improved measures of anxiety and depression, fatigue, and some quality-of-life items.¹⁶

Box 2

In general, most physicians who specialize in treating addictions would not recommend these drug classes as first choice in postwithdrawal, substance-dependent patients complaining of chronic insomnia. Nevertheless, you are likely to encounter patients with a history of substance abuse/dependence who are taking legally prescribed benzodiazepine receptor agonists for insomnia, and they may be very reluctant to discontinue these medications.

Weigh and discuss with the patient the risks and benefits of taking vs discontinuing the hypnotic, as well as alternatives. Because chronic hypnotic use may interfere with addiction recovery, it is important to discuss the patient’s recovery plan.

If you decide to prescribe a hypnotic with abuse liability, the newer alpha-1-selective benzodiazepine receptor agonists are preferable—as they would be for non-addicted patients—because they are less likely to disrupt sleep architecture. They are also less likely than the long-acting benzodiazepines (such as flurazepam) to accumulate over time and result in daytime impairment.

Patient contracts. A written agreement can be useful whenever you prescribe a controlled substance for a patient with an addiction history. Include these issues:

• frequency of clinic visits for monitoring response and refills, requests for early refills, and telephone refills
  
• obtaining prescriptions from only one prescriber and one pharmacy
  
• abstinence from other abused substances
  
• urine drug screens and pill counts
  
• authorization for you to share information with other care providers or significant others
  
• an addiction recovery plan for other abused substances
  
• consequences of nonadherence.
  

Table 2

FDA-approved benzodiazepine receptor agonists for insomnia*

Off-label sedatives for insomnia

Like ramelteon, sedating agents that do not have abuse liability are first-choice medications for patients with addiction and co-occurring insomnia (Table 3):

• The most studied are gabapentin and trazodone.
  
• Quetiapine and mirtazapine may be considered as second-choice options.
  

In 2 open-label pilot studies of alcohol-dependent patients with insomnia:

• gabapentin (mean dose 953 mg) significantly improved sleep quality over 4 to 6 weeks²⁰
  
• both gabapentin (mean 888 mg qhs) and trazodone (mean 105 mg qhs) significantly improved Sleep Problems Questionnaire scores, but patients receiving gabapentin were less likely than those taking trazodone to feel tired upon awakening.²¹
  

Although gabapentin and the anticonvulsant pregabalin increase slow-wave sleep in healthy control subjects, evidence of a similar effect is lacking in alcohol-dependent patients.

Trazodone is the most commonly prescribed antidepressant for insomnia because of its sedating effect and low abuse potential. Trazodone was associated with greater sleep improvements vs placebo as measured via PSG in a randomized, double-blind trial of alcohol-dependent patients with insomnia.²³ In a second study, sleep outcomes were better with trazodone vs placebo over 12 weeks in alcohol-dependent patients, although patients in the trazodone group drank more heavily.²⁴

Other sedating antidepressants such as mirtazapine and doxepin have not been studied in patients with substance use disorders.

Quetiapine is a second-generation antipsychotic with sedating properties. When quetiapine, 25 to 200 mg/d, was given to alcohol-dependent veterans with sleep complaints, they remained abstinent more days and had fewer hospitalizations than veterans not receiving quetiapine.²⁵ Both groups had high rates of psychiatric comorbidity, and 90% had posttraumatic stress disorder. Improved abstinence was thought to result from improved sleep, but no sleep measures were included to test this hypothesis.

A recently published, randomized controlled pilot study reported significantly reduced drinking and craving in severely alcohol-dependent patients receiving quetiapine vs placebo, although sleep data were not included.²⁶

Other options. Tricyclic antidepressants carry risks of cardiotoxicity and other side effects but can be useful when other options have not worked or patients have comorbidities such as neuropathic pain or migraine headaches. Combinations of agents also may be considered for treatment-resistant insomnia.

Nonprescription remedies such as antihistamines, valerian root extract (from the herb Valeriana officinalis), and melatonin are commonly used for sleep, although data are limited in substance-abusing patients.

Table 3

Noncontrolled sedating agents for treating insomnia
in patients with a history of substance abuse

• American Academy of Sleep Medicine. www.sleepeducation.com.
  
• National Sleep Foundation. Sleep logs for downloading. www.sleepfoundation.org.
  
• Restless Legs Syndrome Foundation. www.rls.org.
  
• Brower KJ. Insomnia, alcoholism and relapse. Sleep Med Rev 2003;7:523-39.
  

• Amitriptyline • Elavil, Endep
  
• Doxepin • Sinequan
  
• Estazolam • ProSom
  
• Eszopiclone • Lunesta
  
• Flurazepam • Dalmane
  
• Gabapentin • Neurontin
  
• Methamphetamine • Desoxyn
  
• Methylphenidate • Concerta, Ritalin, others
  
• Mirtazapine • Remeron
  
• Nefazodone • Serzone
  
• Nortriptyline • Pamelor
  
• Pregabalin • Lyrica
  
• Quazepam • Doral
  
• Quetiapine • Seroquel
  
• Ramelteon • Rozerem
  
• Temazepam • Restoril
  
• Theophylline • Theo-24, others
  
• Trazodone • Desyrel
  
• Triazolam • Halcion
  
• Zaleplon • Sonata
  
• Zolpidem • Ambien, Ambien CR
  

Dr. Conroy and Dr. Arnedt report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Brower is a consultant to Pfizer.

Acknowledgment

This work was supported by an NIH grant to Dr. Brower (2K24 AA00304).

From alcohol to opioids, most addictive substances can induce sleep disturbances that persist despite abstinence and may increase the risk for relapse. Nearly all FDA-approved hypnotics are Schedule IV controlled substances that—although safe and effective for most populations—are prone to abuse by patients with substance use disorders.

You’re not alone if you hesitate to prescribe hypnotics to these patients; a study of 311 addiction medicine physicians found that they prescribed sleep-promoting medication to only 30% of their alcohol-dependent patients with insomnia.¹

This article presents evidence on how alcohol and other substances disturb sleep in patients with addictions. We discuss the usefulness of hypnotics, off-label sedatives, and cognitive-behavioral therapy (CBT). Our goal is to help you reduce your patients’ risk of relapse by addressing their sleep complaints.

Workup: 3 principles

Insomnia is multifactorial. Don’t assume that substance abuse is the only cause of prominent insomnia complaints. Insomnia in patients with substance use disorders may be a manifestation of protracted withdrawal or a primary sleep disorder. Evaluate your patient’s:

• other illnesses (psychiatric, medical, and other sleep disorders)
  
• sleep-impairing medications (such as activating antidepressants and theophylline)
  
• inadequate sleep hygiene
  
• dysfunctional beliefs about sleep.
  

Insomnia is a clinical diagnosis that does not require an overnight sleep laboratory study (polysomnography [PSG]). Diagnose insomnia when a patient meets DSM-IV-TR criteria (has difficulty falling asleep or staying asleep or feels that sleep is not refreshing for at least 1 month; and the sleep problem impairs daytime functioning and/or causes clinically significant distress). In addition, consider:

• PSG if you suspect other sleep disorders, particularly obstructive sleep apnea (OSA) and periodic limb movement disorder (PLMD)
  
• an overnight sleep study for treatment-resistant insomnia, when you have adequately treated other causes.
  

Sleep logs are useful. Ask patients to keep a sleep log for 2 weeks during early recovery, after acute withdrawal subsides. These diaries help assess sleep patterns over time, document improvement with abstinence, and engage the patient in treatment. The National Sleep Foundation can provide examples (see Related Resources).

Alcohol and sleep disturbances

Insomnia is extremely common in active drinkers and in those who are in treatment after having stopped drinking. Across 7 studies of 1,577 alcohol-dependent patients undergoing treatment, more than one-half reported insomnia symptoms (mean 58%, range 36% to 91%),^2,3 substantially higher than the rate in the general population (33%). Nicotine, marijuana, cocaine and other stimulants, and opioids also can disrupt sleep (Table 1).

Which came first? Sleep problems may be a pathway by which problematic substance use develops. In 1 study, sleep problems reported by mothers in boys ages 3 to 5 predicted onset of alcohol and drug use by ages 12 to 14.⁴ This relationship was not mediated by attention problems, anxiety/depression, or aggression. Thus, insomnia may increase the risk for early substance use.

In an epidemiologic study of >10,000 adults, the incidence of new alcohol use disorders after 1 year in those without psychiatric disorders at baseline was twice as high in persons with persistent insomnia as in those without insomnia.⁵

Patients with sleep disturbances may use alcohol to self-medicate,⁶ and tolerance to alcohol’s sedating effects develops quickly. As patients consume larger quantities with greater frequency to produce sleep, the risk for dependence may increase.

Comorbid sleep disorders. Alcohol-dependent patients with difficulty falling asleep may have abnormal circadian rhythms, as suggested by delayed onset of nocturnal melatonin secretion.⁷ They also may have low homeostatic sleep drive, another factor required to promote sleep.⁸

Habitual alcohol consumption before bedtime (1 to 3 standard drinks) is associated with mild sleep-disordered breathing (SDB) in men but not in women.⁹ SDB also may be more prevalent in alcohol-dependent men age >60.¹⁰

Consuming >2 drinks/day has been associated with restless legs and increased periodic limb movements during sleep. Twice as many women reporting high alcohol use were diagnosed with PLMD, compared with women reporting normal alcohol consumption.^10-11 Recovering alcohol-dependent patients have significantly more periodic limb movements associated with arousals (PLMA) from sleep than controls. Moreover, PLMA can predict 80% of abstainers and 44% of relapsers after 6 months of abstinence.¹²

Table 1

Sleep disruptions caused by substances of abuse

Multifaceted treatment

A thorough history is essential to evaluate sleep and guide treatment decisions. Refer patients to an accredited sleep disorders center if their history shows:

• loud snoring
  
• cessation of breathing
  
• frequent kicking during sleep
  
• excessive daytime sleepiness.
  

Chronic insomnia. Patients who report chronic insomnia and behaviors incompatible with sleep may be good candidates for cognitive-behavioral therapy for insomnia (CBT-I). Patient education can change maladaptive behaviors, such as staying in bed for long periods of time to compensate for sleep loss, using the bed for activities other than sleep, or worrying excessively about sleep (Box 1).¹³

Pharmacotherapy may be preferred:

• for patients with unstable physical or mental illness
  
• when CBT-I could exacerbate a comorbid condition (such as restricting sleep in a patient with bipolar disorder)
  
• for patients with low motivation for behavior change
  
• when trained CBT-I providers or resources to pay for CBT-I are limited.
  

Box 1

In older adults with insomnia but no history of addiction, CBT-I was more effective than placebo and as effective as a hypnotic alone (temazepam, 7.5 and 30 mg qhs) and a hypnotic/CBT-I combination in reducing nighttime wakefulness, increasing total sleep time, and increasing sleep efficiency. After 2 years, patients treated with CBT-I alone were most likely to maintain these initial treatment gains.¹⁵

Limited data exist on CBT-I’s effectiveness in patients with addiction. In 2 studies, alcohol-dependent patients reported improved sleep.^16,17 CBT-I also improved measures of anxiety and depression, fatigue, and some quality-of-life items.¹⁶

Box 2

In general, most physicians who specialize in treating addictions would not recommend these drug classes as first choice in postwithdrawal, substance-dependent patients complaining of chronic insomnia. Nevertheless, you are likely to encounter patients with a history of substance abuse/dependence who are taking legally prescribed benzodiazepine receptor agonists for insomnia, and they may be very reluctant to discontinue these medications.

Weigh and discuss with the patient the risks and benefits of taking vs discontinuing the hypnotic, as well as alternatives. Because chronic hypnotic use may interfere with addiction recovery, it is important to discuss the patient’s recovery plan.

If you decide to prescribe a hypnotic with abuse liability, the newer alpha-1-selective benzodiazepine receptor agonists are preferable—as they would be for non-addicted patients—because they are less likely to disrupt sleep architecture. They are also less likely than the long-acting benzodiazepines (such as flurazepam) to accumulate over time and result in daytime impairment.

Patient contracts. A written agreement can be useful whenever you prescribe a controlled substance for a patient with an addiction history. Include these issues:

• frequency of clinic visits for monitoring response and refills, requests for early refills, and telephone refills
  
• obtaining prescriptions from only one prescriber and one pharmacy
  
• abstinence from other abused substances
  
• urine drug screens and pill counts
  
• authorization for you to share information with other care providers or significant others
  
• an addiction recovery plan for other abused substances
  
• consequences of nonadherence.
  

Table 2

FDA-approved benzodiazepine receptor agonists for insomnia*

Off-label sedatives for insomnia

Like ramelteon, sedating agents that do not have abuse liability are first-choice medications for patients with addiction and co-occurring insomnia (Table 3):

• The most studied are gabapentin and trazodone.
  
• Quetiapine and mirtazapine may be considered as second-choice options.
  

In 2 open-label pilot studies of alcohol-dependent patients with insomnia:

• gabapentin (mean dose 953 mg) significantly improved sleep quality over 4 to 6 weeks²⁰
  
• both gabapentin (mean 888 mg qhs) and trazodone (mean 105 mg qhs) significantly improved Sleep Problems Questionnaire scores, but patients receiving gabapentin were less likely than those taking trazodone to feel tired upon awakening.²¹
  

Although gabapentin and the anticonvulsant pregabalin increase slow-wave sleep in healthy control subjects, evidence of a similar effect is lacking in alcohol-dependent patients.

Trazodone is the most commonly prescribed antidepressant for insomnia because of its sedating effect and low abuse potential. Trazodone was associated with greater sleep improvements vs placebo as measured via PSG in a randomized, double-blind trial of alcohol-dependent patients with insomnia.²³ In a second study, sleep outcomes were better with trazodone vs placebo over 12 weeks in alcohol-dependent patients, although patients in the trazodone group drank more heavily.²⁴

Other sedating antidepressants such as mirtazapine and doxepin have not been studied in patients with substance use disorders.

Quetiapine is a second-generation antipsychotic with sedating properties. When quetiapine, 25 to 200 mg/d, was given to alcohol-dependent veterans with sleep complaints, they remained abstinent more days and had fewer hospitalizations than veterans not receiving quetiapine.²⁵ Both groups had high rates of psychiatric comorbidity, and 90% had posttraumatic stress disorder. Improved abstinence was thought to result from improved sleep, but no sleep measures were included to test this hypothesis.

A recently published, randomized controlled pilot study reported significantly reduced drinking and craving in severely alcohol-dependent patients receiving quetiapine vs placebo, although sleep data were not included.²⁶

Other options. Tricyclic antidepressants carry risks of cardiotoxicity and other side effects but can be useful when other options have not worked or patients have comorbidities such as neuropathic pain or migraine headaches. Combinations of agents also may be considered for treatment-resistant insomnia.

Nonprescription remedies such as antihistamines, valerian root extract (from the herb Valeriana officinalis), and melatonin are commonly used for sleep, although data are limited in substance-abusing patients.

Table 3

Noncontrolled sedating agents for treating insomnia
in patients with a history of substance abuse

• American Academy of Sleep Medicine. www.sleepeducation.com.
  
• National Sleep Foundation. Sleep logs for downloading. www.sleepfoundation.org.
  
• Restless Legs Syndrome Foundation. www.rls.org.
  
• Brower KJ. Insomnia, alcoholism and relapse. Sleep Med Rev 2003;7:523-39.
  

• Amitriptyline • Elavil, Endep
  
• Doxepin • Sinequan
  
• Estazolam • ProSom
  
• Eszopiclone • Lunesta
  
• Flurazepam • Dalmane
  
• Gabapentin • Neurontin
  
• Methamphetamine • Desoxyn
  
• Methylphenidate • Concerta, Ritalin, others
  
• Mirtazapine • Remeron
  
• Nefazodone • Serzone
  
• Nortriptyline • Pamelor
  
• Pregabalin • Lyrica
  
• Quazepam • Doral
  
• Quetiapine • Seroquel
  
• Ramelteon • Rozerem
  
• Temazepam • Restoril
  
• Theophylline • Theo-24, others
  
• Trazodone • Desyrel
  
• Triazolam • Halcion
  
• Zaleplon • Sonata
  
• Zolpidem • Ambien, Ambien CR
  

Dr. Conroy and Dr. Arnedt report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products. Dr. Brower is a consultant to Pfizer.

Acknowledgment

This work was supported by an NIH grant to Dr. Brower (2K24 AA00304).

Whether you encounter postpartum depression (PPD) in a patient you have been treating or in one referred by her obstetrician, early, aggressive treatment is essential. Although PPD shares some symptoms with major depressive disorder (MDD)—and may be a subtype of that disorder—it also has distinguishing characteristics, such as timing of symptom onset (Box 1).^1,2 Two screening tools facilitate diagnosis (Box 2).^2-4

Women with PPD usually respond to pharmacotherapy, but antidepressants’ potential effects on a nursing mother’s newborn are important to consider.

HPA axis dysregulation

Although the precise cause of PPD remains unclear, a better understanding is emerging of the complicated interplay of estrogen and progesterone with the hypothalamic-pituitary-adrenal (HPA) axis and other neuroregulatory systems associated with depressive illness. Two lines of evidence implicate hormonal dysregulation:

• Despite normal reproductive hormone levels, women with PPD may have an abnormal response to changes in these levels.⁵
  
• Abnormalities in HPA axis activity appear to be associated with reproductive endocrine-related mood disorders in vulnerable women, particularly during the transition from childbirth to the immediate postpartum period.
  

• high estrogen and progesterone levels
  
• a hyperactive HPA axis (normal during pregnancy)
  
• high plasma cortisol level, stimulated in part by high levels of estrogen and progesterone.^7,8
  

A hallmark feature of the HPA axis in depression is altered response to stress and inability to maintain regulation:

• In MDD, HPA axis hyperactivity is one of the most robust biological findings.¹¹ In general, women with MDD exhibit high baseline cortisol and an exaggerated response to the dexamethasone/corticotropin releasing hormone test.
  
• In contrast, women with PPD experience a more blunted ACTH response to CRH, which may reflect a hyporeactive HPA axis.⁹
  

It has been hypothesized that both increased cortisol and decreased cortisol (observed under conditions of sustained elevated gonadal steroid levels or withdrawal of gonadal steroids) may result in insufficient glucocorticoid signaling.¹³ Impaired glucocorticoid signaling may be the “final common pathway” leading to psychiatric disturbance in MDD and PPD.

Understanding the characteristics of HPA axis reactivity in women with PPD could improve early identification and, theoretically, prevention or immediate treatment for at-risk women. In addition to HPA axis dysregulation, disturbances in other endocrine systems may play a role in PPD. Women with antenatal total and free thyroxine concentrations in the lower euthyroid range may be at increased risk of developing postpartum depressive symptoms.¹⁴

Box 2

Risks with or without treatment

PPD has potentially serious adverse consequences and needs to be aggressively treated. Ethical and practical challenges have hindered PPD research, however, and evidence to guide treatment is limited.¹⁵

Approximately 70% of mothers in the United States breast-feed their infants at least for the first 3 months.¹⁶ With any patient with PPD who is breast-feeding, carefully discuss the risk of antidepressant side effects for the mother and child.¹⁷

Also discuss potential risks and benefits of treatment vs no treatment.¹⁷ Potential risks of untreated depression include:

• impaired mother/child bonding because of ongoing maternal depressive illness
  
• impaired cognitive, emotional, and social development in the child.¹⁸
  

• educate the patient about potential antidepressant side effects for mother and baby
  
• avoid communicating “mixed messages” to the patient about the risk and benefits of treatment
  
• ensure the health of mother and baby.¹⁷
  

Antidepressants. In general, women with PPD respond well to antidepressant therapy. They may be hesitant to take any medication while breast-feeding because of possible harmful effects to their babies, but most studies examining antidepressant use by lactating women found low rates of adverse events in infants exposed to antidepressants (Table).^19-24 Potential adverse effects include:

• sedation
  
• changes in sleep or feeding
  
• irritability.¹⁷
  

SSRIs. Few adverse events have been reported with sertraline, paroxetine, and fluvoxamine during lactation.²⁰ However, paroxetine may be associated with increased risk of cardiac abnormalities in infants exposed during the first trimester of pregnancy.²⁶ Two agents in this class may be less desirable:

• fluoxetine, because it has a long half-life
  
• citalopram, because of potentially high breast milk concentration.²⁰
  

Other antidepressants. Venlafaxine and duloxetine are not recommended because of limited data about use of these agents during lactation. Bupropion poses a small increased risk of seizures in newborns but is not absolutely contraindicated.²⁴ Trazodone also has limited data, but in clinical practice it has been used safely at low doses for many years.²⁰

Psychotherapeutic techniques—including individual or group therapy—also can effectively reduce depressive symptoms in women with PPD.²⁷

Table

Antidepressants for postpartum depression

Clinician resource

• Cuijpers P, Brännmark JG, van Straten A. Psychological treatment of postpartum depression: a meta-analysis. J Clin Psychol 2008;64(1):103-18.
  

• American Psychiatric Association. Postpartum depression. www.healthyminds.org/postpartumdepression.cfm.
  

• Amitriptyline • Elavil, Endep
  
• Bupropion • Wellbutrin
  
• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Desipramine • Norpramin
  
• Doxepin • Sinequan
  
• Duloxetine • Cymbalta
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Imipramine • Tofranil
  
• Mirtazapine • Remeron
  
• Nortriptyline • Aventyl
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, GlaxoSmithKline, and The Foundation of Hope.

Dr. Payne receives research/grant support from AstraZeneca, Novartis, Stanley Medical Research Institute, and Wyeth Pharmaceuticals.

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

Whether you encounter postpartum depression (PPD) in a patient you have been treating or in one referred by her obstetrician, early, aggressive treatment is essential. Although PPD shares some symptoms with major depressive disorder (MDD)—and may be a subtype of that disorder—it also has distinguishing characteristics, such as timing of symptom onset (Box 1).^1,2 Two screening tools facilitate diagnosis (Box 2).^2-4

Women with PPD usually respond to pharmacotherapy, but antidepressants’ potential effects on a nursing mother’s newborn are important to consider.

HPA axis dysregulation

Although the precise cause of PPD remains unclear, a better understanding is emerging of the complicated interplay of estrogen and progesterone with the hypothalamic-pituitary-adrenal (HPA) axis and other neuroregulatory systems associated with depressive illness. Two lines of evidence implicate hormonal dysregulation:

• Despite normal reproductive hormone levels, women with PPD may have an abnormal response to changes in these levels.⁵
  
• Abnormalities in HPA axis activity appear to be associated with reproductive endocrine-related mood disorders in vulnerable women, particularly during the transition from childbirth to the immediate postpartum period.
  

• high estrogen and progesterone levels
  
• a hyperactive HPA axis (normal during pregnancy)
  
• high plasma cortisol level, stimulated in part by high levels of estrogen and progesterone.^7,8
  

A hallmark feature of the HPA axis in depression is altered response to stress and inability to maintain regulation:

• In MDD, HPA axis hyperactivity is one of the most robust biological findings.¹¹ In general, women with MDD exhibit high baseline cortisol and an exaggerated response to the dexamethasone/corticotropin releasing hormone test.
  
• In contrast, women with PPD experience a more blunted ACTH response to CRH, which may reflect a hyporeactive HPA axis.⁹
  

It has been hypothesized that both increased cortisol and decreased cortisol (observed under conditions of sustained elevated gonadal steroid levels or withdrawal of gonadal steroids) may result in insufficient glucocorticoid signaling.¹³ Impaired glucocorticoid signaling may be the “final common pathway” leading to psychiatric disturbance in MDD and PPD.

Understanding the characteristics of HPA axis reactivity in women with PPD could improve early identification and, theoretically, prevention or immediate treatment for at-risk women. In addition to HPA axis dysregulation, disturbances in other endocrine systems may play a role in PPD. Women with antenatal total and free thyroxine concentrations in the lower euthyroid range may be at increased risk of developing postpartum depressive symptoms.¹⁴

Box 2

Risks with or without treatment

PPD has potentially serious adverse consequences and needs to be aggressively treated. Ethical and practical challenges have hindered PPD research, however, and evidence to guide treatment is limited.¹⁵

Approximately 70% of mothers in the United States breast-feed their infants at least for the first 3 months.¹⁶ With any patient with PPD who is breast-feeding, carefully discuss the risk of antidepressant side effects for the mother and child.¹⁷

Also discuss potential risks and benefits of treatment vs no treatment.¹⁷ Potential risks of untreated depression include:

• impaired mother/child bonding because of ongoing maternal depressive illness
  
• impaired cognitive, emotional, and social development in the child.¹⁸
  

• educate the patient about potential antidepressant side effects for mother and baby
  
• avoid communicating “mixed messages” to the patient about the risk and benefits of treatment
  
• ensure the health of mother and baby.¹⁷
  

Antidepressants. In general, women with PPD respond well to antidepressant therapy. They may be hesitant to take any medication while breast-feeding because of possible harmful effects to their babies, but most studies examining antidepressant use by lactating women found low rates of adverse events in infants exposed to antidepressants (Table).^19-24 Potential adverse effects include:

• sedation
  
• changes in sleep or feeding
  
• irritability.¹⁷
  

SSRIs. Few adverse events have been reported with sertraline, paroxetine, and fluvoxamine during lactation.²⁰ However, paroxetine may be associated with increased risk of cardiac abnormalities in infants exposed during the first trimester of pregnancy.²⁶ Two agents in this class may be less desirable:

• fluoxetine, because it has a long half-life
  
• citalopram, because of potentially high breast milk concentration.²⁰
  

Other antidepressants. Venlafaxine and duloxetine are not recommended because of limited data about use of these agents during lactation. Bupropion poses a small increased risk of seizures in newborns but is not absolutely contraindicated.²⁴ Trazodone also has limited data, but in clinical practice it has been used safely at low doses for many years.²⁰

Psychotherapeutic techniques—including individual or group therapy—also can effectively reduce depressive symptoms in women with PPD.²⁷

Table

Antidepressants for postpartum depression

Clinician resource

• Cuijpers P, Brännmark JG, van Straten A. Psychological treatment of postpartum depression: a meta-analysis. J Clin Psychol 2008;64(1):103-18.
  

• American Psychiatric Association. Postpartum depression. www.healthyminds.org/postpartumdepression.cfm.
  

• Amitriptyline • Elavil, Endep
  
• Bupropion • Wellbutrin
  
• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Desipramine • Norpramin
  
• Doxepin • Sinequan
  
• Duloxetine • Cymbalta
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Imipramine • Tofranil
  
• Mirtazapine • Remeron
  
• Nortriptyline • Aventyl
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, GlaxoSmithKline, and The Foundation of Hope.

Dr. Payne receives research/grant support from AstraZeneca, Novartis, Stanley Medical Research Institute, and Wyeth Pharmaceuticals.

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

Whether you encounter postpartum depression (PPD) in a patient you have been treating or in one referred by her obstetrician, early, aggressive treatment is essential. Although PPD shares some symptoms with major depressive disorder (MDD)—and may be a subtype of that disorder—it also has distinguishing characteristics, such as timing of symptom onset (Box 1).^1,2 Two screening tools facilitate diagnosis (Box 2).^2-4

Women with PPD usually respond to pharmacotherapy, but antidepressants’ potential effects on a nursing mother’s newborn are important to consider.

HPA axis dysregulation

Although the precise cause of PPD remains unclear, a better understanding is emerging of the complicated interplay of estrogen and progesterone with the hypothalamic-pituitary-adrenal (HPA) axis and other neuroregulatory systems associated with depressive illness. Two lines of evidence implicate hormonal dysregulation:

• Despite normal reproductive hormone levels, women with PPD may have an abnormal response to changes in these levels.⁵
  
• Abnormalities in HPA axis activity appear to be associated with reproductive endocrine-related mood disorders in vulnerable women, particularly during the transition from childbirth to the immediate postpartum period.
  

• high estrogen and progesterone levels
  
• a hyperactive HPA axis (normal during pregnancy)
  
• high plasma cortisol level, stimulated in part by high levels of estrogen and progesterone.^7,8
  

A hallmark feature of the HPA axis in depression is altered response to stress and inability to maintain regulation:

• In MDD, HPA axis hyperactivity is one of the most robust biological findings.¹¹ In general, women with MDD exhibit high baseline cortisol and an exaggerated response to the dexamethasone/corticotropin releasing hormone test.
  
• In contrast, women with PPD experience a more blunted ACTH response to CRH, which may reflect a hyporeactive HPA axis.⁹
  

It has been hypothesized that both increased cortisol and decreased cortisol (observed under conditions of sustained elevated gonadal steroid levels or withdrawal of gonadal steroids) may result in insufficient glucocorticoid signaling.¹³ Impaired glucocorticoid signaling may be the “final common pathway” leading to psychiatric disturbance in MDD and PPD.

Understanding the characteristics of HPA axis reactivity in women with PPD could improve early identification and, theoretically, prevention or immediate treatment for at-risk women. In addition to HPA axis dysregulation, disturbances in other endocrine systems may play a role in PPD. Women with antenatal total and free thyroxine concentrations in the lower euthyroid range may be at increased risk of developing postpartum depressive symptoms.¹⁴

Box 2

Risks with or without treatment

PPD has potentially serious adverse consequences and needs to be aggressively treated. Ethical and practical challenges have hindered PPD research, however, and evidence to guide treatment is limited.¹⁵

Approximately 70% of mothers in the United States breast-feed their infants at least for the first 3 months.¹⁶ With any patient with PPD who is breast-feeding, carefully discuss the risk of antidepressant side effects for the mother and child.¹⁷

Also discuss potential risks and benefits of treatment vs no treatment.¹⁷ Potential risks of untreated depression include:

• impaired mother/child bonding because of ongoing maternal depressive illness
  
• impaired cognitive, emotional, and social development in the child.¹⁸
  

• educate the patient about potential antidepressant side effects for mother and baby
  
• avoid communicating “mixed messages” to the patient about the risk and benefits of treatment
  
• ensure the health of mother and baby.¹⁷
  

Antidepressants. In general, women with PPD respond well to antidepressant therapy. They may be hesitant to take any medication while breast-feeding because of possible harmful effects to their babies, but most studies examining antidepressant use by lactating women found low rates of adverse events in infants exposed to antidepressants (Table).^19-24 Potential adverse effects include:

• sedation
  
• changes in sleep or feeding
  
• irritability.¹⁷
  

SSRIs. Few adverse events have been reported with sertraline, paroxetine, and fluvoxamine during lactation.²⁰ However, paroxetine may be associated with increased risk of cardiac abnormalities in infants exposed during the first trimester of pregnancy.²⁶ Two agents in this class may be less desirable:

• fluoxetine, because it has a long half-life
  
• citalopram, because of potentially high breast milk concentration.²⁰
  

Other antidepressants. Venlafaxine and duloxetine are not recommended because of limited data about use of these agents during lactation. Bupropion poses a small increased risk of seizures in newborns but is not absolutely contraindicated.²⁴ Trazodone also has limited data, but in clinical practice it has been used safely at low doses for many years.²⁰

Psychotherapeutic techniques—including individual or group therapy—also can effectively reduce depressive symptoms in women with PPD.²⁷

Table

Antidepressants for postpartum depression

Clinician resource

• Cuijpers P, Brännmark JG, van Straten A. Psychological treatment of postpartum depression: a meta-analysis. J Clin Psychol 2008;64(1):103-18.
  

• American Psychiatric Association. Postpartum depression. www.healthyminds.org/postpartumdepression.cfm.
  

• Amitriptyline • Elavil, Endep
  
• Bupropion • Wellbutrin
  
• Citalopram • Celexa
  
• Clomipramine • Anafranil
  
• Desipramine • Norpramin
  
• Doxepin • Sinequan
  
• Duloxetine • Cymbalta
  
• Escitalopram • Lexapro
  
• Fluoxetine • Prozac
  
• Fluvoxamine • Luvox
  
• Imipramine • Tofranil
  
• Mirtazapine • Remeron
  
• Nortriptyline • Aventyl
  
• Paroxetine • Paxil
  
• Sertraline • Zoloft
  
• Sertraline • Zoloft
  
• Venlafaxine • Effexor
  

Dr. Meltzer-Brody receives research/grant support from AstraZeneca, GlaxoSmithKline, and The Foundation of Hope.

Dr. Payne receives research/grant support from AstraZeneca, Novartis, Stanley Medical Research Institute, and Wyeth Pharmaceuticals.

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