Many children with mental health problems are either not being seen, or are being seen by professionals who have not been trained in the principles of development and childhood psychopathology, said Thomas F. Anders, M.D. He told 

, "We believe that the care that many of these kids are getting today is inadequate." 

The Surgeon General's Report on Children's Mental Health and a number of studies suggest that the prevalence of children's mental health problems is increasing as stressors in society continue to increase. Meanwhile, the number of well-trained providers is decreasing, leading to a major crisis in providing services.

"These problems don't go away by themselves, and without treatment, they get worse," Anders said. "The enormous need that our society has for providing emotionally secure and physically safe environments for kids is huge, and our mental health professionals need to be a big part of that."

The U.S. Bureau of Health Professions projects that at current recruitment levels, the nation will have only two-thirds of child and adolescent psychiatrists needed to meet the demand by 2020--8,312 child psychiatrists versus a need for 12,624.

A "severe maldistribution" of practicing child psychiatrists further exacerbates the problem. While Massachusetts has 17.5 child and adolescent psychiatrists per 100,000 youths, West Virginia has only 1.3, and the national average is 7.5.

The workforce shortage issue has two complementary threads, according to Anders, president-elect of the American Academy of Child and Adolescent Psychiatry (AACAP) and co-chair of  its steering committee on work force issues.

The first one relates to the need for changes in the training of child and adolescent psychiatrists. The current track is a five-year program: three years of adult psychiatry followed by two years of child psychiatry.

"What happens as a result of that kind of training track is that a number of people who initially express their interest in child psychiatry really get ground down before they finish," said Anders, also a professor of psychiatry at the University of California, Davis, Medical Center. As many as 50% of students who are initially interested in child psychiatry lose that interest by the time they complete their adult training. Beginning this year, AACAP's goal is to increase recruitment into residency programs by 10% a year for the next decade. The training takes too long, and residents accrue too much debt, Anders said. As a point of contrast, pediatric residents do not take three years of internal medicine before they begin their pediatric training. They're trained primarily with children from the beginning, he said, adding that AACAP would like to see students trained in more integrated programs that offer experiences with children beginning on day one. Instead of doing a PG-1 year in internal medicine and adult neurology, students interested in child psychiatry would do a PG-1 in pediatrics and child neurology. They would have early exposure to children that would stay with them during their five years of training.

And although it's a long shot, Anders said, it would be nice to reduce the total amount of time it takes to get board certification as a child psychiatrist.

The second thread, he continued, relates to getting more appropriate reimbursements for child psychiatrists, which would help make the profession more attractive. Most insurers reimburse the services of child psychiatrists in about the same way as they do adult services.

A 50-minute session may work for an adult patient, but it is insufficient for doing an evaluation on a child. "You've got to see the family, you've got to talk to the teachers, you've got to see the kid in action in several different settings," he said. Consequently, child psychiatrists need to advocate for better reimbursement for the services they provide, including the ancillary services that are necessary to evaluate the child and provide treatment.

Few child psychiatrists can afford to live off the reimbursement rates that managed care companies are providing, so many of them are choosing to provide services only to patients who can pay out-of-pocket, Anders said. Consequently, rural populations, which tend to be poorer, get underserved, as do inner-city populations.

People in child psychiatry are not very interested in living in rural areas, Glenn J. Kashurba, M.D., told 

. "Generally speaking, child psychiatrists don't get out of the city."

Kashurba is the only child psychiatrist in a four-county area of rural Pennsylvania that is roughly the size of Massachusetts and home to about half a million people, he said. He evaluates 500 to 1,000 children a year.

He works at six different sites: an outpatient facility; an intermediate unit for special education services, where he established an autism assessment program; a partial-hospitalization facility; a residential treatment center; a small outpatient private practice that includes legal work; and a maximum-security prison for juvenile offenders.

After 15 years of working in the area, Kashurba said that he has given up on the idea of recruiting another child psychiatrist. "They just don't come here," he said. And with a dearth of child psychiatrists, "What ends up happening is that kids need services and they end up seeing somebody other than a child psychiatrist for those services."

That, he said, places additional stress on the system by forcing adult psychiatrists, pediatricians and family physicians to spend time practicing outside of areas where they feel comfortable.

Kashurba is co-chair of AACAP's workgroup on consumer issues. The group puts together the "Facts for Families" portion of the academy's Web site  and strives to make the role of child and adolescent psychiatrists more visible within the general and mental health care systems.

"You have to be very creative in what you do," he said. "You have to have good working relationships with the psychologists, the pediatricians, the family doc."

Having been in the Somerset, Pa., area for so long, Kashurba has established those relationships. When he first moved there, he set up an inpatient psychiatric facility for adults and adolescents at the local hospital. He was able to work closely with other physicians, allowing him to gain their trust.

When he left the hospital to devote his practice to child and adolescent psychiatry, doctors felt comfortable calling him for advice about managing their young patients' medications, he said.

It took about five years to establish a good working relationship with school personnel, who speak a different language from physicians, he said. Another obstacle was the negative experiences that the school staff had when sending children to Pittsburgh for psychiatric evaluations before his arrival.

But even that has become less of an option as the entire western half of the state has seen a decline in the availability of child psychiatric services, he said. "Even sending a kid into Pittsburgh for an evaluation has become so much harder."

When Kashurba first began conducting autism evaluations, he saw a number of significantly autistic 8- and 9-year-old children who had never seen a child psychiatrist. Instead, they had basically traveled two and a half hours into Pittsburgh just to see a social worker, he said.

Now that his program has cleared the backlog of older patients, Kashurba is able to assess children for autism at ages 3 and 4.

The region Kashurba serves includes the town of Shanksville, site of the Flight 93 crash on Sept. 11, 2001. Kashurba volunteered his services to meet with victims' families at the crash site. "Had I not gone, there wouldn't have been anyone there working with the families who had been trained at all with children."

Kashurba has written two books on the subject--

Courage After the Crash: Flight 93 Aftermath and Quiet Courage

The long-term effects of Sept. 11 on children in the four-county area were minimal, Kashurba said, although there was an intensification of pre-existing difficulties at the time of the attacks. 

A series of tornadoes that hit the region in 1998 provoked a much stronger reaction. The tornadoes were completely unexpected in the mountain region. The first one killed a 13-year-old girl. The next night, a stepfather and child died as a result of tornado damage to their home. And two days after the first storm, two more tornadoes struck, damaging 400 buildings as people sat in their basements listening to the radio for updates.

"That was actually a more traumatic thing for our kids long-term than Flight 93," Kashurba said. 

The Child Healthcare Crisis Relief Act would help address some of these issues. The legislation, currently being considered in the U.S. House and Senate, would provide scholarships and loan forgiveness as incentives for people to train as children's mental health care professionals--not only as psychiatrists, but as psychologists, social workers and counselors in school settings, and as psychiatric nurses.

The bill was introduced last year in the House by Reps. Patrick Kennedy (D-R.I.) and Ileana Ros-Lehtinen (R-Fla.) and in the Senate by Sens. Jeff Bingaman (D-N.M.) and Susan Collins (R-Maine). As of January, the legislation had 44 co-sponsors in the House and five co-sponsors in the Senate.

"This is one of the key bills that would increase access to treatment for children and adolescents with mental illnesses," Nuala S. Moore, AACAP's assistant director of government affairs, told 

. "We hope to see action in 2004 on the bill."

The goal, Moore said, is to increase bipartisan support in both chambers of the U.S. Congress and have it attached to the reauthorization bill for the Substance Abuse and Mental Health Services Administration (SAMHSA). However, SAMHSA reauthorization bills have a tendency to get delayed, and it appears unlikely that the 108th Congress will take action before it adjourns at the end of this year.

But Moore said she is optimistic that the Crisis Relief Act can get passed as awareness grows about the work force shortages. Work force issues are sure to be part of the Senate's SAMHSA subcommittee hearings on children's mental health issues this year, and the topic received attention last year from the Senate Governmental Affairs Committee during hearings on the Keeping Families Together Act, which would try to put an end to families relinquishing custody of their children in order for them to receive mental health services.

The Crisis Relief Act would allow for changes in the residency training sequence and provide more appropriate reimbursements from Medicare for that training, Anders said. As it stands now, Medicare will reimburse hospitals only for the full cost of residents through their first specialty. While a hospital is fully reimbursed for residents in adult psychiatry training, it receives only 50% reimbursement for the additional two-year residency in child and adolescent psychiatry.

The bill would increase the Medicare reimbursement to 100% of the costs for a residency in child psychiatry, making it more lucrative for hospitals to have these residency programs, stated Anders. 

The number of child psychiatry training programs in the United States dropped from 120 to 113 between 1990 and 2003.  

Articles

Many children today are receiving inadequate mental health care due to a decrease in the number of well-trained providers, while the prevalence of children's mental health problems is increasing. Legislation is pending in the U.S. House and Senate to address these issues.

Child Psychiatry Faces Workforce Shortage

On Jan. 6, the state of Arkansas executed Charles Singleton by lethal injection. His death went unnoticed by the national media, but it will be remembered and discussed in the years ahead by medical ethicists and everyone else interested in the intersections of human rights, psychiatry and law. Singleton by all accounts had become psychotic during the 24 years he spent on death row and would have been incompetent to be executed had he not been taking psychiatric medications. Richard Dieter, executive director of the Death Penalty Information Center in Washington, D.C., believes that Singleton is the first prisoner to be executed after being declared incompetent to be executed under the guidelines formulated by the U.S. Supreme Court in the case of 

The late Justice Thurgood Marshall, a lifelong opponent of capital punishment, wrote the majority opinion in 

, holding that the Eighth Amendment's prohibition of cruel and unusual punishment prevents the state from executing an insane prisoner. However, in what proved to be the crucial concurring opinion, the late Justice Lewis F. Powell Jr. emphasized that the state had a valid interest in imposing the death penalty on Ford and that the issue was not whether Ford could be executed, "but, when his execution may take place." And then in an ominous footnote Powell explained, "My point is only that if petitioner [Ford] is cured of his disease the state is free to execute him."

Powell's "cure to execute" footnote raised serious ethical questions for psychiatrists. The state might have a legal interest in curing and executing condemned prisoners, but psychiatrists thought it would be medically unethical to participate in that process. However, psychiatrists also recognized that it would be unethical to withhold treatment and allow a profoundly psychotic death row inmate to suffer and deteriorate. Ethical guidelines were established by the American Medical Association and the American Psychiatric Association, which recognized that an ethically responsible psychiatrist would have to steer an uncharted course between these pitfalls 

(Code of Medical Ethics, H-140.950 Physician Participation in Capital Punishment).

The Supreme Court's decision in Ford did not deal with the question of whether the state, in its efforts to cure death row inmates, could force antipsychotic medications on them. That issue was soon presented to the court in 

, 498 US 1075 (1990). The APA, in its amicus brief, emphasized the ethical quandaries for psychiatrists and urged the Supreme Court to commute Perry's death penalty to life imprisonment without possibility of parole. This would allow Perry to receive appropriate care without his psychiatrists having to worry that they would be facilitating his execution. The Supreme Court eventually sent the case back to Louisiana and has never resolved the question of whether a state can involuntarily treat, cure and execute a death row prisoner.

The Louisiana Supreme Court, however, had no difficulty deciding the answer to that question. In the case of 

, 610 So2d 746 (La 1992), the court gave great weight to the ethical objections of organized psychiatry and found compelling reasons within its own constitution not to force treatment on a condemned man so that he could be executed. The South Carolina Supreme Court soon followed the Louisiana precedent, and the state of Maryland passed legislation adopting the commutation approach the APA had urged on the U.S. Supreme Court in 

That is where the law seemed to stand until 1999 when the Arkansas Supreme Court broke with the precedents of its sister states and found a rationale for the treatment and execution of Charles Singleton, 338 Ark 135 (1999). Four years later, overruling its own three-judge panel, the Eighth Circuit Federal Court of Appeals issued an opinion supporting the state Supreme Court's decision in 

, 124 SCt 74 (2003). Chief Judge Roger Wollman, writing for the majority in a sharply divided 6-5 decision, ruled that neither the Eighth Amendment nor other procedural protections prohibited the execution of a death row inmate who "regained competency through appropriate medical care." The most startling line of the judge's decision was: "eligibility for execution is the only unwanted consequence of the medication."

Singleton's execution seemed to follow the scenario of Justice Powell's ominous footnote, but the real world of law and psychiatry is far more complicated. The ethical questions raised by the Singleton case, as we shall see, have more to do with physician-assisted suicide than with physician participation in capital punishment.

During his 24 years on death row, Singleton had been treated often for his psychiatric disorder. At times, he voluntarily took his medication 

(Appellant's Brief to the Eighth Circuit 2000 WL 33983423: 2000)

. For instance, in a 1995 hearing, Singleton stated that he was then voluntarily taking antipsychotic medication. Two years later, in 1997, he ceased taking the medication voluntarily. At that time his psychiatrist diagnosed him as psychotic, delusional and suffering from paranoid schizophrenia. He referred Singleton to the Medication Review Panel, which ordered involuntary treatment under the guidelines established by the Supreme Court in 

, 494 US 210 (1990). Harper provided for involuntary treatment when a prisoner is dangerous to self or others, and "the treatment is in the inmate's medical interest." Harper does not deal with the issue of restoration to competency to be executed. It was clear that Singleton had become competent to be executed under the regimen of depot injections ordered under 

According to the Arkansas Supreme Court, (99 SW2d 768,769):

The primary legal issue presented in this case was whether the State may mandatorily administer antipsychotic medication to a condemned prisoner [under Harper guidelines] when a collateral effect of that medication is to render him competent to understand the nature and reason for his execution.

The Arkansas Supreme Court ruled that it "must look to the intent of the state in its decision to involuntarily medicate appellant" and concluded that "the intent of the state was not to make him competent to be executed" but to treat him under 

How the state Supreme Court could identify the intention of the state of Arkansas baffled many who commented on the decision. As one reviewing judge noted respectfully, the state had been trying to execute Singleton for 20 years, which might indicate they had other intentions.

Singleton's lawyer Jeff Rosenzweig, who spoke to me by phone, has argued that treatment under 

for a death row inmate might be constitutionally permissible during a stay of execution. However, once an execution date has been set, continuing involuntary treatment is not in the inmate's medical interest and other constitutional limitations on the state's power apply. He made those arguments to the Eighth Circuit Federal Court of Appeals. Wollman, in the previously mentioned 6-5 decision, rejected Rosenzweig's argument; however, he did not rely on the Arkansas Supreme Court's intent of the state rationale. The judge reviewed the major constitutional cases dealing with the state's power to impose involuntary treatment. Wollman ignored the fact that none of those decisions dealt with capital punishment and that the Sell decision in his own court (about restoring competency to stand trial) had said that forced treatment for the death penalty raised different questions, 282 F3d 560 (2002). He reviewed the involuntary treatment decisions only for the standards they established for the medical appropriateness of forced treatment. Wollman observed that antipsychotic medication controlled Singleton's symptoms, that there were no untoward side effects, that there was no less intrusive treatment, that Singleton does not dispute that medication "is in his medical interest during the pendency of a stay of execution" and that it has restored his competency. These observations led Wollman to conclude that Singleton's treatment was medically appropriate and "the best medical interests of the prisoner must be determined without regard to whether there is a pending date of execution." Wollman then reformulated Powell's ominous footnote:

A state does not violate the Eighth Amendment as interpreted by Ford when it executes a prisoner who becomes incompetent ... but who subsequently regained competency through appropriate medical care.

Like the Arkansas Supreme Court, Wollman's opinion ignored the basic moral-legal question: Is it wrong--cruel and unusual, or excessive punishment--to restore a condemned madman to sanity so he can be executed by the state? Wollman also ignored the ethical questions raised by organized medicine and psychiatry that his dissenting colleagues addressed.

The Eighth Circuit opinion and the execution of Singleton have to be considered defeats for those who championed the ethical guidelines against psychiatric participation in capital punishment. But as noted, the case is more complicated than those guidelines imagined. At some point Singleton gave up his fight against the death penalty and asked his lawyer not to attempt further appeals. His lawyer reported that judges who conducted the hearings were very concerned that Singleton have informed consent, and he was told more than once in open court that if he took medication voluntarily it might lead to his execution. Nonetheless, at some point Singleton decided to take antipsychotic medication voluntarily because it controlled his symptoms. His lawyer confirmed that he was in fact taking the medication voluntarily in the weeks leading up to his execution. Furthermore, the governor of Arkansas indicated that if Singleton himself requested clemency he would consider granting it. But Singleton did not. According to his lawyer, he had become resigned to his fate.

Given these additional facts, one confronts a different set of ethical questions. Does a psychiatrist who is treating a death row inmate in Singleton's circumstances have an ethical duty to withhold a medical treatment that mitigates suffering and that the patient has decided to accept? One can perhaps imagine a psychiatrist determining that the patient/inmate is incompetent to make such a decision because he fails to appreciate that the treatment will bring about his execution. But a psychiatrist who attempted to make such difficult clinical and ethical determinations would (in my view) be considering the issues that have arisen in physician-assisted suicide and would get little help from organized psychiatry's guidelines on participation in capital punishment, which do not take into account the possibility that the inmate is consenting to treatment because he is resigned to his fate 

(Code of Medical Ethics, H-140.950 Physician Participation in Capital Punishment)

. It is important to emphasize that had Singleton continued to refuse medication and allowed his lawyer to attempt further appeals, there may well have been a different ruling.

Although the Singleton case is a defeat, in my experience, organized psychiatry's ethical opposition to participation in the death penalty has played an important role in modifying the law and the practice of capital punishment.

In January, the state of Arkansas executed Charles Singleton, a man known to be suffering from mental illness. That state's supreme court ruled that treating Singleton, even though it would cause him to be competent to be executed, was not cruel or unusual punishment nor unethical. Dr. Stone discusses the ramifications for other death penalty cases.

Condemned Prisoner Treated and Executed

I'm learning to bend the first notes
on the "Black Magic Woman" solo
when I ask my teacher, "What guitar
did Santana play at Woodstock?"
He just keeps strumming and lifts
his eyes to the poster over his head,
the same one I've stared at every
Wednesday for the past eight years,
the same star-burst Les Paul Classic
that hangs from my shoulders.
My throat constricts with the nausea
I remember from medical school
when I couldn't see the obvious--
sharp splinters of blood in a patient's nail bed
or a hemorrhage in an optic disc,
clear to those who knew how to look,
my patients risking their lives
while they watch me practice their songs.

Blind Spots

Depression and dementia are common in older people and their association is very complex. Major and minor depression occur often in patients with dementia and can be associated with deterioration in cognitive functioning. Many clinicians have difficulty determining whether dementia, depression or both are the underlying disease for their patients' apathy, psychomotor retardation, concentration deficit and short-term memory impairment. Moreover, depression in dementia brings additional disability to patients who are demented and their caregivers, and a previous history of depression may be associated with an increased risk for the subsequent development of a dementing illness.

In this article, we review the literature to address the interaction between depression and dementia and provide clinicians with information to improve the care of their patients who are demented.

The aging of the U.S. population has been accompanied by a dramatic rise in the prevalence of both depression and dementia. Among community-dwelling older adults, 3% to 11% have dementia (Boustani et al., 2003) and 2% to 14% have depression (Beekman et al., 1999). In long-term care settings, 44% to 53% of the residents have dementia (Magaziner et al., 2000) and 9% to 30% have depression (Parmelee et al., 1989; Payne et al., 2002; Rovner et al., 1991; Watson et al., 2003). 

Depending on the threshold used to define depression, the different scales and methods implemented to measure depressive symptoms, and various clinical settings, numerous studies in dementia estimate that depression occurs in 30% to 50% of patients (Olin et al., 2002). Approximately 24% of community-dwelling older adults with dementia (Lyketsos et al., 2000), 24% of residents in assisted living with dementia and 27% of those in nursing homes suffer from depression (Gruber-Baldini et al., 2003). 

Dementia leads to a high burden of suffering for patients, their families and for the entire society, with an annual cost of approximately $100 billion (Boustani et al., 2003). Furthermore, depression is independently related to poor outcomes, including greater medical morbidity, increased health care services use, functional decline and death (Charney et al., 2003). Having both dementia and depression increases the risk of mortality and disability and leads to higher health care utilization and costs (Kopetz et al., 2000; Lyketsos et al., 1999, 1997).

Does depression increase the risk for the future development of dementia? History of depression in early, mid- or late life has been associated with an increased risk for the future development of dementia. In a meta-analysis of seven case-controlled and six prospective cohort studies, Jorm (2001) found that history of depression approximately doubled the risk of developing dementia. More recently, a retrospective cohort study found a significant association between dementia and a history of depression symptoms that first reported within one year or more than 25 years before the onset of dementia (Green et al., 2003). Another longitudinal study found that 43% to 89% of elderly patients with depression who presented with cognitive impairment developed dementia within the following three to eight years (Table 1) (Schweitzer et al., 2002). 

Numerous hypotheses have been suggested to explain the previous association between depression and the increased risk for developing dementia. These hypotheses included that: 1) pharmacological treatment of depression might be a risk factor for dementia; 2) depression and dementia share common risk factors such as cerebrovascular disease; 3) depression is an early stage of dementia; 4) depression occurs as a reaction to the early cognitive decline of dementia; 5) depression hastens the clinical manifestation of dementia; and 6) depression-related glucocorticoid effects lead to hippocampal injuries and damage (Green et al., 2003; Jorm, 2001; Wilson et al., 2003). Nevertheless, recent data suggest that the association of depressive symptoms with Alzheimer's disease (AD) and cognitive impairment appears to be independent of cortical plaques and tangles and, therefore, depression may be a risk factor for dementia more than being early sign of its symptoms (Wilson et al., 2003).

The diagnosis of depression in dementia is not an easy task. Although the majority of patients with dementia do not develop major depression (Olin et al., 2002), more than half suffer from one or more depressive symptoms such as anxiousness, sadness, irritability, agitation or psychomotor retardation, sleep problems, diminished social activity, or loss of interest (Gruber-Baldini et al., 2003). There is an overlap between dementia and depressive symptoms and behaviors, and it is difficult to determine whether the dementing illness or depression is the underlying pathology. Although apathy is often associated with depression, approximately 60% of patients with dementia with apathy have no depression and 44% of patients with dementia with depression have no apathy (Lyketsos et al., 2001). 

Diminished social activity, loss of interest and apathy may be responses to a cognitive deficit, or they may be manifestations of major depression. Moreover, memory problems in early stages of dementia might compromise patients' self-report of depressive symptoms. Language and communication difficulties in later stages of dementia might change the expression of depressive symptoms. These atypical presentations often lead to lower rates of clinician recognition and diagnosis of depression (Gallo and Rabins, 1999).

 criteria to diagnose major depression among patients with dementia, 14% of the sample met the criteria for major depression based on patient interviews, and 50% met the diagnostic criteria on the basis of caregiver interviews (Mackenzie et al., 1989). This discrepancy might be due to the inability of the caregivers to distinguish between depressive symptoms and apathy, or to the caregivers' own depression.

Adding to the complexity of depression diagnosis in dementia, 60% to 70% of depressive symptoms in community-dwelling patients with dementia disappear within six months and 85% recur within one year (Lee and Lyketsos, 2003). Furthermore, patients with dementia might suffer from depressive disorders that are not related to dementia per se, such as adjustment disorder with depressed mood, recurrence of early and midlife major and minor depression, late-onset depression, and vascular depression (Lee and Lyketsos, 2003).

Due to the previous complexity and the absence of consensus on how to diagnose depression in patients who are demented, a panel of 21 experts in dementia and depression were assembled by the National Institute of Mental Health and suggested specific criteria for diagnosing depression in AD (Table 2) (Olin et al., 2002).

In addition to decreasing functional and cognitive status, depression in dementia interacts with other behavioral and psychological symptoms (such as agitation, delusions and hallucinations, and wandering). In one clinical trial, improvement in depressive symptoms among community-dwelling patients with AD with major depression was associated with a decrease in the behavioral and psychological symptoms (Lyketsos et al., 2003).

Various cross-sectional studies conducted in long-term care have found that depression in dementia was associated with higher prevalence of wandering and verbal agitation (Dwyer and Byrne, 2000; Gruber-Baldini et al., 2003). Nursing home residents with dementia who manifested physical or verbal aggression had an approximately threefold increase in the prevalence of depression than those without such behaviors (Lyketsos et al., 1999; Menon et al., 2001). Finally, in a study of 303 community-dwelling patients with AD, the presence of depression was associated with an almost twofold increase in the risk of delusions (Bassiony et al., 2002).

The goal of antidepressant treatment for depressive symptoms in dementia is to alleviate depressive suffering, improve cognitive performance and decrease the contribution of depression to the other health outcomes of dementia, such as behavioral and psychological symptoms and caregiver burden.

Pharmacological interventions, electroconvulsive therapy, and caregiver or care-recipient-based behavioral interventions are currently available for clinicians to manage depression among older adults. There is concern, however, that some of the antidepressants (such as the tricyclic antidepressants) and ECT might exacerbate the cognitive impairment of patients with dementia with depression. Furthermore, few data are available to confirm the efficacy of the previous interventions among this selected group of vulnerable older adults.

Two reviews of the literature have identified nine randomized, placebo-controlled trials that evaluated the efficacy of pharmacological interventions in reducing depression among patients with dementia (Bains et al., 2002; Olin et al., 2002). Five trials evaluated selective serotonin reuptake inhibitors (sertraline [Zoloft], fluoxetine [Prozac] and citalopram [Celexa]), three evaluated TCAs (clomipramine [Anafranil], imipramine [Tofranil] and maprotiline [Ludiomil]), and one trial evaluated moclobemide (Aurorix), a monoamine oxidase inhibitor not approved in the United States (Fuchs et al., 1993; Olin et al., 2002). These trials suggested that citalopram, sertraline, clomipramine, maprotiline and moclobemide might help in the management of depression in patients with dementia. The findings from the Olin et al. (2002) study are summarized in Table 3.

However, patients enrolled in these trials were selected from both long-term care and community settings and had a spectrum of depressive disorders that ranged from major depression to mild depressive symptoms. Not surprisingly, the impact of medications was greater when treating major depression. None of the previous trials demonstrated any positive effects of antidepressants on cognition. Citalopram and sertraline appeared to be helpful in reducing the other behavioral and psychological symptoms related to dementia, and sertraline had some positive effect on the functional deficit of dementia.

In addition to pharmacological interventions, randomized, controlled trials also show that exercise and behavioral management reduce depressive symptoms in community-dwelling patients with dementia (Teri et al., 2003, 1997). More recently, Brodaty et al. (2003) conducted a 12-week, randomized, controlled trial in 11 Australian nursing homes. They found no efficacy differences among psychogeriatric case management, general practitioners with psychogeriatric consultation and standard care in managing 86 residents with dementia with depression, psychosis or both.

Due to the aging of the U.S. population, coexisting depression and dementia present a significant public health problem. Depending on the severity of dementia, using both caregiver and care-recipient-based depression screening instruments will help increase the recognition of depression in dementia. Treating depression adequately in mid- or late life may decrease the risk of the future development of dementia. Verbal agitation and physical aggression might be symptoms of depression among patients with severe dementia. Sertraline and citalopram improve major depression in those with dementia but their efficacy in milder depression is uncertain. Finally, behavioral interventions decrease depressive symptoms in community-dwelling patients with mild-to-moderate dementia. For clinicians treating patients with dementia, the most important message is to routinely assess for depression and to treat it, because successful treatment can improve many dementia-related outcomes.

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 Magaziner J, German P, Zimmerman SI et al. (2000), The prevalence of dementia in a statewide sample of new nursing home admissions aged 65 and older: diagnosis by expert panel. Epidemiology of Dementia in Nursing Homes Research Group. Gerontologist 40(6):663-672.
 

 Menon AS, Gruber-Baldini AL, Hebel JR et al. (2001), Relationship between aggressive behaviors and depression among nursing home residents with dementia. Int J Geriatr Psychiatry 16(2):139-146.
 

 Olin JT, Katz IR, Meyers BS et al. (2002), Provisional diagnostic criteria for depression of Alzheimer disease: rationale and background. [Published erratum Am J Geriatr Psychiatry 10(3):264.] Am J Geriatr Psychiatry 10(2):129-141.
 

 Parmelee PA, Katz IR, Lawton MP (1989), Depression among institutionalized aged: assessment and prevalence estimation. J Gerontol 44(1):M22-M29. 
 

 Payne JL, Sheppard JM, Steinberg M et al. (2002), Incidence, prevalence, and outcomes of depression in residents of a long-term care facility with dementia. J Geriatr Psychiatry 17(3):247-253. 
 

 Rovner BW, German PS, Brant LJ et al. (1991), Depression and mortality in nursing homes. [Published erratum JAMA 265(20):2672.] JAMA 265(8):993-996 [see comment].
 

 Schweitzer I, Tuckwell V, O'Brien J, Ames D (2002), Is late onset depression a prodrome to dementia? Int J Geriatr Psychiatry 17(11):997-1005.
 

 Teri L, Gibbons LE, McCurry SM et al. (2003), Exercise plus behavioral management in patients with Alzheimer disease: a randomized controlled trial. JAMA 290(15):2015-2022.
 

 Teri L, Logsdon RG, Uomoto J, McCurry SM (1997), Behavioral treatment of depression in dementia patients: a controlled clinical trial. J Gerontol B Psychol Sci Soc Sci 52(4):P159-P166.
 

 Watson LC, Garrett JM, Sloane PD et al. (2003), Depression in assisted living: results from a four-state study. Am J Geriatr Psychiatry 11(5):534-542.
 

 Wilson RS, Schneider JA, Bienias JL et al. (2003), Depressive symptoms, clinical AD, and cortical plaques and tangles in older persons. Neurology 61(8):1102-1107.

Depression and dementia or Alzheimer's disease often go together. The presence of dementia may also increase the odds of depression. What can clinicians do to treat these two often comorbid conditions?

The Interface of Depression and Dementia

Cognitive deficits are increasingly being recognized as a central feature of schizophrenia. Some impairments are present before the hallmark positive symptoms of the illness emerge (Cornblatt et al., 1999; Davidson et al., 1999), and moderate-to-severe impairments across many cognitive domains are detectable at the time of the first episode (Bilder et al., 2000; Saykin et al., 1994). Cognitive deficits appear to be largely consistent in severity across changes in clinical state (Harvey et al., 1990) and appear stable from emergence of the first episode until after middle age (Rund, 1998). These findings suggest that cognitive deficits are not simply a consequence of the symptoms of the illness or its treatment. Throughout the course of the illness, positive symptoms fluctuate depending on the overall pattern of treatment response of the patient, while cognitive deficits are typically reported to manifest minimal improvement and to be the best predictors of impairments in functional skills (Green, 1996). Studies of cognitive deficits in schizophrenia have moved from descriptive to predictive since their link to functional outcome has been well-replicated (Green et al., 2000). Thus, cognitive deficits are now recognized as an important treatment goal.

With the aging of the baby boomer generation, a large number of patients with schizophrenia are now reaching late life. Yet, many studies of the course of schizophrenia have failed to include truly elderly patients. This may lead to misperceptions regarding the characteristics of cognitive impairments in later life, if the course of the illness is inferred from studies with truncated age ranges. In addition, many studies of possible age effects on cognition are cross-sectional, such that they compare the functioning of elderly patients to a younger cohort. This methodology is certainly more feasible and is often useful in generating hypotheses for longitudinal designs. However, conclusions from any cross-sectional studies about the course of any illness must be viewed with caution. An additional consideration involves overall lifetime outcome of the illness, often indexed by the residential status of older patients with schizophrenia. Those patients with substantial functional deficits would be expected to be more impaired than ambulatory patients, who have often had a much more variable course. In this review, we will discuss age-related changes in cognitive functioning in schizophrenia. 

A number of cross-sectional studies have been employed to compare cognitive functioning in older to younger patients with schizophrenia. Heaton et al. (1994) found that the cognitive profiles and levels of impairment in older ambulatory patients with schizophrenia were consistent with the impairments seen in younger patients. Both younger and older patients had prominent deficits in learning and memory, executive functioning, and attention, compared to control subjects. They even performed more poorly than patients with Alzheimer's disease (AD) on most domains. Although there were no age-associated differences in performance, the level of impairment was quite severe. Similar results were reported for scores on the Mattis Dementia Rating Scale (MDRS) (a global index of cognitive functioning) across the age range (Eyler Zorrilla et al., 2000). In this study, older ambulatory patients with schizophrenia were found to have no age-corrected greater impairments than younger patients. These cross-sectional studies suggest that cognitive impairments are stable from mid-life to later years, although the age range of these samples did not include a large number of truly elderly patients.

Although Heaton et al. (1994) and Eyler Zorrilla et al. (2000) found no age-related differences in cognition, it is important to examine additional cohorts, such as those patients with more chronic schizophrenia. While efforts at deinstitutionalization and community integration persist, a substantial number of patients with schizophrenia remain in psychiatric hospitals or other full-care residences, such as nursing homes, into late life. Since these patients have had a very different course of illness during most of their lives, compared to ambulatory patients, other characteristics may differ as well. Evans et al. (1999) found that institutionalized patients performed more poorly on the MDRS than ambulatory patients. Similarly, Harvey et al. (1998) found substantial differences between acutely and chronically ill patients using a neuropsychological battery designed for the assessment of older individuals. Other groups have also found more severe cognitive impairments in patients residing innursing homes compared to ambulatory patients (Auslander et al., 2001; Bartels et al., 1997).

Davidson et al. (1995) found age-related differences on the Mini-Mental State Examination (MMSE) in a sample of poor-outcome patients ranging from ages 25 to 95. Patients between ages 85 and 95 received an average score of only 9.6 (even when patients with scores of zero were excluded), a significant difference from the average score of 16 for patients between ages 65 and 75. These levels of impairment are consistent with the results of other studies of demographically similar patients in the United States (Arnold et al., 1995), the United Kingdom (Harvey et al., 1997a) and Japan (Seno et al., 1998). Bowie et al. (2002) found that age was associated with differences in cognition even for patients who had MMSE scores 18. This may have limited the ability to detect potential impairments in lower-functioning patients. 

In a longitudinal study of older ambulatory patients, Heaton et al. (2001) found no evidence of change over an average of 60 months on a comprehensive neuropsychological battery. However, only 22 of the 142 patients were over age 65 at entry into the study. Another longitudinal study reported that older patients had selectively greater impairments in abstraction abilities than younger patients, with no increased age-related differences in other aspects of cognitive functioning (Fucetola et al., 2000). Further, Granholm et al. (2000) reported that older patients had a reduced ability to process complex information, as shown by increased utilization of information-processing resources while performing an attentional task. There is some evidence of age-related changes in the ability to perform complex and resource-demanding tasks even in ambulatory patients.

In a study of hospitalized patients with chronic schizophrenia (age>65) with MMSE scores >17, 30% declined over a 30-month period (Harvey et al., 1999b). The best two predictors of cognitive decline were lower education and greater severity of positive symptoms at baseline. A follow-up study of geriatric patients with schizophrenia who entered the study while hospitalized and who were reassessed after they were discharged to nursing homes also demonstrated cognitive decline over an average of 2.5 years (Harvey et al., 1999a). 

Additional support for age-related cognitive decline comes from a study of chronically institutionalized patients ranging in age from 25 to 85 who were followed for six years and compared to healthy individuals and patients with AD (Friedman et al., 2001). This study found that the patients with schizophrenia had an age-associated risk of cognitive decline not found in the patients with AD or the healthy controls. The oldest patients with schizophrenia (ages 75 to 80 at baseline) dropped by six MMSE points in six years, while those under the age of 65 did not change in their functioning over the follow-up period. Furthermore, patients with AD declined by 12 or more MMSE points, regardless of age at entry into the study. This suggests that chronicity alone is not a sufficient determinant of cognitive decline until patients cross a certain age threshold. Later studies have indicated that newly incident medical conditions predict risk for cognitive decline (Friedman et al., 2002) and have sug-gested more recently that declines in cognitive functioning over time in poor-outcome patients predict the course of functional decline as well (Harvey and Davidson, 2002).

While a number of studies on cognition in older patients with schizophrenia have been published in the past decade, the specific effect of aging remains unclear. It appears that cognitive decline with aging in schizophrenia is multi-determined. While the decline does not appear to occur at all in younger patients, even those with a chronic course of illness, it is also not likely to be a pattern found in all older individuals with schizophrenia. 

It appears that certain risk factors-possibly a chronic course of illness, less education, higher levels of positive symptoms and poor baseline cognitive functioning-are associated with the age-related cognitive decline observed in some patients. Ambulatory patients may also decline in late life on particularly complex tasks. However, the timing and severity of the decline may differ from poor-outcome patients. 

Complicating the identification of those at risk for cognitive decline are the different research designs employed by various groups of researchers. This leads to the difficulty of parsing out the effects on cognition of life-long institutionalization, chronic psychosis, long-term antipsychotic medication administration and other factors. The Figure illustrates that longitudinal studies of chronically ill patients universally find global cognitive decline, while the only cross-sectional studies that failed to find age-related differences in cognition assessed only one specific domain and excluded low-functioning patients. In addition, a longitudinal study that failed to observe cognitive decline was of somewhat younger ambulatory patients. Since expected declines in cognition for healthy individuals only become substantial after age 65, it stands to reason that examination of patients with schizophrenia who are younger than 65 may be insufficient to detect decline.

Future longitudinal studies will assist in determining why cognitive decline occurs in late life for some patients with schizophrenia, but not for others. Consequently, treatment strategies for those at highest risk for decline may be developed in the near future. In turn, functional outcome, by way of improving or at least preserving cognitive functions, may be improved for the large number of elderly patients with schizophrenia.

 Arnold SE, Gur RE, Shapiro RM et al. (1995), Prospective clinicopathologic studies of schizophrenia: accrual and assessment of patients. Am J Psychiatry 152(5):731-737.
 

 Auslander LA, Lindamer LL, Delapena J et al. (2001), A comparison of community-dwelling olderschizophrenia patients by residential status.Acta Psychiatr Scand 103(5):380-386.
 

 Bartels SJ, Mueser KT, Miles KM (1997), A comparative study of elderly patients with schizophrenia and bipolar disorder in nursing homes and the community. Schizophr Res 27(2-3):181-190.
 

 Bilder RM, Goldman RS, Robinson D et al. (2000), Neuropsychology of first-episode schizophrenia: initial characterization and clinical correlates. Am J Psychiatry 157(4):549-559.
 

 Bowie CR, Harvey PD, Moriarty PJ et al. (2002), Cognitive assessment of geriatric schizophrenic patients with severe impairment. Arch Clin Neuropsychol 17(7):611-623.
 

 Cornblatt B, Obuchowski M, Roberts S et al. (1999), Cognitive and behavioral precursors of schizophrenia. Dev Psychopathol 11(3):487-508.
 

 Davidson M, Harvey PD, Powchik P et al. (1995), Severity of symptoms in chronically institutionalized geriatric schizophrenic patients. Am J Psychiatry 152(2):197-207.
 

 Davidson M, Reichenberg A, Rabinowitz J et al.(1999), Behavioral and intellectual markers for schizophrenia in apparently healthy male adolescents. Am J Psychiatry 156(9):1328-1335 [see comments].
 

 Evans JD, Negron AE, Palmer BW et al. (1999), Cognitive deficits and psychopathology in institutionalized versus community-dwelling elderly schizophrenia patients. J Geriatr Psychiatry Neurol 12(1):11-15.
 

 Eyler Zorrilla LT, Heaton RK, McAdams LA et al. (2000), Cross-sectional study of older outpatients with schizophrenia and healthy comparison subjects: no differences in age-related cognitive decline. Am J Psychiatry 157(8):1324-1326.
 

 Friedman JI, Harvey PD, Coleman T et al. (2001), Six-year follow-up study of cognitive and functional status across the lifespan in schizophrenia: a comparison with Alzheimer's disease and normal aging. Am J Psychiatry 158(9):1441-1448.
 

 Friedman JI, Harvey PD, McGurk SR et al. (2002), Correlates of change in functional status of institutionalized geriatric schizophrenic patients: focus on medical comorbidity. Am J Psychiatry 159(8):1388-1394.
 

 Fucetola R, Seidman LJ, Kremen WS et al. (2000), Age and neuropsychologic function in schizophrenia: a decline in executive abilities beyond that observed in healthy volunteers. Biol Psychiatry 48(2):137-146.
 

 Granholm E, Morris S, Asarnow RF et al. (2000), Accelerated age-related decline in processing resources in schizophrenia: evidence from pupillary responses recorded during the span of apprehension task. J Int Neuropsychol Soc 6(1):30-43.
 

 Green MF (1996), What are the functional consequences of neurocognitive deficits in schizophrenia? Am J Psychiatry 153(3):321-330 [see comment].
 

 Green MF, Kern RS, Braff DL, Mintz J (2000), Neurocognitive deficits and functional outcome in schizophrenia: are we measuring the "right stuff"? Schizophr Bull 26(1):119-136.
 

 Harvey PD, Davidson M (2002), Schizophrenia: course over the lifetime. In: Neuropsychopharmacology: Fifth Generation of Progress, Davis KL, Charney D, Coyle JT, Nemeroff C, eds. Philadelphia: Lippincott Williams & Wilkins.
 

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 Harvey PD, Howanitz E, Parrella M et al. (1998), Symptoms, cognitive functioning, and adaptive skills in geriatric patients with lifelong schizophrenia: a comparison across treatment sites. Am J Psychiatry 155(8):1080-1086.
 

 Harvey PD, Leff J, Trieman N et al. (1997a), Cognitive impairment in geriatric chronic schizophrenic patients: a cross-national study in New York and London. Int J Ger Psychiatry 12(10):1001-1007.
 

 Harvey PD, Lombardi J, Leibman M et al. (1997b), Verbal fluency deficits in geriatric and nongeriatric chronic schizophrenic patients. J Neuropsychiatry Clin Neurosci 9(4):584-590.
 

 Harvey PD, Parrella M, White L et al. (1999a), Convergence of cognitive and adaptive decline in late-life schizophrenia. Schizophr Res 35(1):77-84.
 

 Harvey PD, Silverman JM, Mohs RC et al. (1999b), Cognitive decline in late-life schizophrenia: a longitudinal study of geriatric chronically hospitalized patients. Biol Psychiatry 45(1):32-40.
 

 Heaton RK, Gladsjo JA, Palmer BW et al. (2001), Stability and course of neuropsychological deficits in schizophrenia. Arch Gen Psychiatry 58(1):24-32.
 

 Heaton RK, Paulsen JS, McAdams LA et al. (1994), Neuropsychological deficits in schizophrenics. Relationship to age, chronicity, and dementia. Arch Gen Psychiatry 51(6):469-476.
 

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 Saykin AJ, Shtasel DL, Gur RE et al. (1994), Neuropsychological deficits in neuroleptic naive patients with first-episode schizophrenia. ArchGen Psychiatry 51(2):124-131.
 

 Seno H, Shibata M, Fujimoto A et al. (1998), Evaluation of Mini Mental State Examination and Brief Psychiatric Rating Scale on aged schizophrenic patients. Psychiatry Clin Neurosci 52(6):567-570.

Recent studies have shown that patients with schizophrenia experience a greater decline in cognitive abilities with age. Given the large baby boomer population, how will this influence treatment for aging patients with schizophrenia?

The Effects of Age on Cognitive Deficits in Schizophrenia

The occurrence of eating disorders in men remains relatively rare but consistent. This is true despite recent research suggesting that male cases are far more numerous than had been previously thought. This brief article will comment on recent research findings in this area and describe their relevance to assessment and treatment.

Two studies support the notion that eating disorders are more common than had previously been thought (Health Canada, 2003; Woodside et al., 2001). Woodside et al. (2001) reported on the results of a 10,000-person community epidemiologic study. Combining full- and partial-syndrome eating disorder cases for both men and women, the investigators showed an overall rate of three female cases for every one male case-a far cry from the typical 10:1 or 20:1 ratio found in most treatment settings. However, this study assessed only limited Axis II parameters and, as 

 diagnoses were generated from the data, the prevalence of binge-eating disorder could not be assessed.

More recently, Health Canada (2003) released preliminary results from a national, face-to-face mental health survey of over 30,000 people performed in 2001 and 2002. This survey assessed for full-syndrome eating disorders and reported a ratio of male to female cases of approximately 1:5. This was somewhat higher than the findings from Woodside et al. (2001) but showed many more cases than might otherwise have been thought. The somewhat higher ratio in the Health Canada survey is almost certainly related to only full-syndrome cases that the Woodside et al. survey was too small to allow for.

Studies continue to show that the nature of the illness, when it occurs in men, is essentially indistinguishable from women. In Woodside et al. (2001), the sample of male eating disorder cases in the community was compared to female eating disorder cases in the same sample and a sample of 3,769 unaffected males. There were no significant differences in any variables relating to illness severity. As mentioned, both full- and partial-syndrome cases were included. Previous research showed that partial-syndrome cases did not differ from full-syndrome cases on most eating disorder variables; there was an excess of partial-syndrome cases of bulimia nervosa in males compared to females. This may have been an artifact of the small sample size in the study. 

Other studies have examined differences in personality between men and women with eating disorders (Fassino et al., 2001; Woodside et al., submitted for publication). These studies demonstrated that men with eating disorders had lower scores on the Temperament and Character Inventory (TCI) for Harm Avoidance, Reward Dependence and Cooperativeness. Our study also showed lower perfectionism in male cases. 

There is an extreme scarcity of literature regarding differential response to treatment in men with eating disorders compared to women. The literature that does exist suggests that men and women receive similar benefit from treatment for their eating disorder (Woodside and Kaplan, 1994). This is an area that deserves much more attention. 

We are thus left with a confusing situation: Men appear to suffer from eating disorders with a higher frequency than would be thought, based on data obtained from clinical settings, despite having a similar illness and similar responses to treatment. What could explain these findings and what impact might such explanations have for practicing clinicians? 

Why are fewer affected men identified in formal treatment settings? One possible explanation is that men simply do not see themselves as being at risk, and therefore dismiss or ignore symptoms that might be indicative of an illness requiring treatment. For example, a young woman who is overeating and vomiting would be quite likely to self-identify as having bulimia nervosa, due to the large amount of public attention that has been paid to these conditions. A young man with similar symptoms might simply think that his eating habits are bad or that he drinks too much, not paying too much attention otherwise. Friends-both male and female-might also have a lower index of suspicion for a formal eating disorder and attribute symptoms to other causes.

A young man who is losing weight might be identified as having a drug problem or AIDS, rather than suffering from anorexia nervosa. Again, neither male nor female friends might make the connection between the outward symptom and the presence of an illness, simply because of the societal expectation that individuals with eating disorders are all female.

The relevant message for clinicians is to be aware that men are at risk for eating disorders and to include a history of eating-related behaviors in their exams. This is particularly important in the identification of bulimia nervosa, which may have no outward symptoms.

Men may also be worried about assumptions about sexual orientation. There is a long controversy about the extent to which homosexual men might be over-represented among those males with eating disorders. To date, all the research done on this question has been in clinical samples and may be biased. Studies from these clinical populations have cited high rates of homosexual orientation (Herzog et al., 1984). Unfortunately, information on sexual orientation was not available for the Woodward et al. (2001) study. We are attempting to discover whether this information is available for the Health Canada (2003) study. Thus, there is no definitive answer to the question of sexual orientation and eating disorders.

One idea that has been raised to explain these findings is that homosexual men may be less reluctant to self-identify as suffering from an eating disorder because of the different focus on weight and shape in the homosexual male community. They may also simply be more willing to access treatment once they have identified their behaviors as troublesome. For the clinician, the most important issue to remember is to reassure heterosexual male patients that the diagnosis of an eating disorder does not require any specific sexual orientation and that no assumptions will be made about sexual orientation, one way or the other.

Men may be unwilling to enter treatment programs that are mainly for women. There is a fairly good awareness among both men and women about the extent to which eating disorders are a problem for women, which includes the idea that all available treatment programs are for women only. Alternately, men may experience a general reduction in help-seeking behaviors that is independent of diagnosis. I am unaware of any treatment programs specifically for men, aside from an occasional support group. Unfortunately, the lack of male-specific treatment programs reinforces the idea that treatment is only for women.

I am equally unaware of significant programs that exclude men. The reduced focus on treatment of men is usually related to the small number of men presenting for treatment--so a circular arrangement occurs. While there is little formal research on treatment outcome for men, most senior clinicians will indicate that the outcome appears to be similar for both men and women. I tell prospective male patients that the usual role a male patient ends up taking in a treatment group is that of a brother--someone the female patients trust and feel close to, but with whom there are clear boundaries. In my treatment programs, men are included in all aspects of the program when admitted. In fact, our female patients have told us that they appreciated having a male peer's input on issues pertaining to relationships, appearance and so forth.

For the clinician, the most important messages for male patients are that the treatment is the same for men and women and that men are generally welcomed, both by the treatment team and by other members of the treatment group. It is worth reassuring a male patient that he is likely to be accepted by the group and will find a comfortable place there.

Are there any differences in the treatment a male patient should receive? Generally, the answer to this question is no. Men respond to the same types of interventions as do women, to the best of our knowledge. There is sometimes a perception that men who are affected have more severe illness. This is probably due to the fact that when large numbers of male patients are compared to female patients, there are no significant differences.

Clinicians will of course be aware that men and women are socialized differently in Western culture, and while the overall process of eating disorder cognitions is the same, the precise content may be slightly different. For example, men are more involved in competitive sports and thus will talk more about their concerns about athletic prowess. 

It is important to remember that while rates of sexual abuse are lower in men than in women, that about 10% of men with an eating disorder reported a history of sexual abuse (Woodside et al., 2001). As is the case with women, such an occurrence may be an important factor in the etiology of the eating disorder.

The occurrence of eating disorders in men appears to be more common in the community than had previously been thought. There are a number of factors that may keep men out of treatment, ranging from lack of self-identification to perceived stigma. Once in treatment, men appear to respond in much the same way as do women.

 Fassino S, Abbate-Daga G, Leombruni P et al. (2001), Temperament and character in Italian men with anorexia nervosa: a controlled study with the temperament and character inventory. J Nerv Ment Dis 189(11):788-794.
 

 Health Canada (2003), Canadian Community Health Survey. Ottawa, Ontario: Statistics Canada.
 

 Herzog DB, Norman DK, Gordon C, Pepose M (1984), Sexual conflict and eating disorders in 27 males. Am J Psychiatry 141(8):989-990.
 

 Woodside DB, Bulik CM, Thornton L et al. (submitted for publication), Personality in men with eating disorders. J Psychosom Res.
 

 Woodside DB, Garfinkel PE, Lin E et al. (2001), Comparisons of men with full or partial eating disorders, men without eating disorders, and women with eating disorders in the community. Am J Psychiatry 158(4):570-574. 
 

 Woodside DB, Kaplan AS (1994), Day hospital treatment in males with eating disorders-response and comparison to females. J Psychosom Res 38(5):471-475.

Recent research has shown a higher incidence of men with eating disorders than previously thought. How do men with eating disorders differ from women in terms of assessment and treatment? What are the differences in risk factors and possible comorbidities, if any?

Psychiatric Times Vol 21 No 3

Child Psychiatry Faces Workforce Shortage

Condemned Prisoner Treated and Executed

Blind Spots

The Interface of Depression and Dementia

The Effects of Age on Cognitive Deficits in Schizophrenia

Assessing and Treating Men With Eating Disorders

The Complex Interaction of Cognitive Issues

The Impact of Antipsychotics on Cognitive Functioning in Schizophrenia

Suicide Ideation in the Elderly

Is ECT an Ethical Treatment?