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Clinical and Research News
Psychosocial Interventions Beneficial in Schizophrenia
Psychiatric News
Volume 42 Number 23 page 22-22

Research is revealing the specific microcomponents of family and environmental stress that interact continually over time with a biologically compromised brain to produce schizophrenia.

That was the message psychiatrist William McFarlane, M.D., brought to APA's 2007 Institute on Psychiatric Services in New Orleans in October.

McFarlane described a large and growing body of research that has elucidated the specific nonbiological stressors that impact a compromised neurobiology—not just periodically in "large hits," but continually across childhood and adolescence, like a steady drizzle with a cascading effect toward psychosis. This burgeoning literature provides the theoretical foundation for the efficacy of psychosocial interventions, especially multifamily psychoeducational groups whose purpose and function McFarlane also described at the meeting.

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William McFarlane, M.D., was presented the APA/American Psychiatric Foundation Alexander Gralnick Award for Research in Schizophrenia at APA's fall institute. With him are Paul Burke (left), executive director of the foundation, and Thomas McGlashan, M.D., chair of the Gralnick award committee. 

Credit: Ellen Dallager

McFarlane is a professor of psychiatry at the University of Vermont and director of the Center for Psychiatric Research at Maine Medical Center and Spring Harbor Hospital. He delivered his lecture, "Biosocial Treatment of Schizophrenia," after being awarded the APA/American Psychiatric Foundation 2007 Alexander Gralnick Award for Research in Schizophrenia.

He stressed that a decade's worth of research on microcomponents of environmental stress affirms the genetic nature of schizophrenia and does nothing to revive long-discredited theories blaming families or" schizophrenogenic" mothers. Time and again research has shown that family and environmental stressors—encompassing very subtle interactions common to many families—work only in tandem with biological determinants to produce psychosis.

"Patients' symptoms seem to elicit certain kinds of rejecting or anxious responses, which in themselves elicit more symptoms," McFarlane said. "Who do you blame? It's really a no-fault situation—the family is doing something, but they are only responding to the disorder. The negativity is reciprocal.

"These young people may deteriorate very slowly in function, which can make family members anxious, angry, or depressed. And in many of the families that have had a history of schizophrenia or psychotic disorders, the anxiety level can begin to rise to astronomical levels. It can be extremely scary if they have some idea of what this might mean."

McFarlane is also director of the National Program Office of the Robert Wood Johnson (RWJ) Foundation for its Early Detection and Intervention for the Prevention of Psychosis Program and the Portland Early Identification and Referral (PIER) Program. The PIER program is the model for a fivesite program dedicated to prevention of schizophrenia that has been awarded a grant of $14.8 million from RWJ.

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McFarlane said the theoretical justification for psychosocial treatment of schizophrenia is founded on the late George Engel's" biopsychosocial" model of disease progression now well known among contemporary psychiatrists. But the most recent research on schizophrenia has revealed an important nuance: where once environmental influences were considered to be intermittent, occurring in large discrete" hits" on the biological mechanism, it now appears that some of these influences are continuous, dynamic, and interactive.

"There are big hits but also microhits that evoke changes at the biological and social levels in interaction with each other over time," he said. "The best way to conceive of this is as a kind of helix interacting systematically between those two elements."

He cited a model first put forward by Barbara Cornblatt, Ph.D., of Albert Einstein College of Medicine, in which insults to the brain occurring in utero lead to a chain of events beginning with cognitive deficits, affective symptoms, social isolation, and school failure.

"At some point in the progression of negative symptoms and disability, we have the superimposition of positive symptoms and the emergence of a diagnosis," McFarlane said. "Our conception is that these social and environmental factors are operating continuously."

And they are operating on a biologically based sensitivity to sensory stimulation, prolonged stress and strenuous demands, rapid change, complexity, social disruption, illicit drugs and alcohol, and negative emotional experience.

McFarlane also showed a brief computer video, produced by Paul Thompson, M.D., Judith Rappoport, M.D., and colleagues, showing the loss of cortical volume between the ages of 14 and 19 in children who go on to develop schizophrenia. That progressive loss of cortical volume would seem to present a hopeless case for schizophrenia, without a genetic cure.

"But Rappoport and Thompson themselves said that even though the progression of this process is genetically controlled, the initiation of it is not," McFarlane said. "Can we stop that progression? I don't know, but the biosocial model suggests we should look at the interaction between those social triggers and the biological process."

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Of all the biologically determined psychosocial sensitivities believed to precipitate psychosis, the most subtle are negative emotional experiences.

But paradoxically it is this factor— especially high family" expressed emotion"—for which there is the most accumulated data. High expressed emotion refers to the rejection, criticism, and anxious overinvolvement that patients are liable to elicit from parents and other family members.

One of the most conclusive studies documenting the role of high exppressed emotion in the risk for schizophrenia is a 2004 study by Pekka Tienari, Ph.D., and colleagues published in the March 2004 British Journal of Psychiatry.

In that study, a Finnish national sample of adoptees whose birth mothers had a schizophrenia-spectrum disorder was compared blindly with adoptees without this genetic risk. Adoptive rearing was assessed using family rating scales that looked at expressed emotion and other family relating patterns, based upon extended family observations at initial assessment. Adoptees were independently rediagnosed after a median interval of 12 years.

Tienari and colleagues found that family ratings were a significant predictor of schizophrenia-spectrum disorders in adoptees at high genetic risk of schizophrenia, but not in those at low genetic risk. They concluded that adoptees at high genetic risk are significantly more sensitive to adverse versus "healthy" rearing patterns than are adoptees at low genetic risk.

McFarlane emphasized that study rules out the possibility of family relating patterns having any effect on schizophrenia in the absence of a genetic risk. "But the only group that has a high risk are those that have a genetic risk and family dysfunction," he said. "Both are necessary, but neither alone is sufficient."

He added that Tienari's families were drawn from a random sample, so they could not be said to represent unusually dysfunctional families.

McFarlane also described his own work elucidating components of expressed emotion—warmth, protectiveness, rejection, and fusion—in the early and late prodromal phases. And he described a theoretical model of social performance deficits combined with perceptual distortions and pervasive anxiety eliciting criticism and anxiety from family members in the early prodrome; this in turn results in withdrawal, feelings of" oddness," and further functional deterioration.

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The work of Tienari, McFarlane, and others has laid the groundwork for psychosocial interventions, especially the use of multifamily psychoeducational groups. These groups are designed to empower family members with information about the disease and the kind of social interactions that can exacerbate symptoms in the affected family member.

In highly structured sessions, multifamily groups are taught specific strategies for lowering anxiety, conflict, and expressed emotion. These strategies are expressed with such simple, nonclinical tags as "go slow," "give 'em space," "set limits,"" keep it simple," "lower expectations," and" solve problems step by step."

McFarlane said a substantial body of literature has established the efficacy of such groups on measures such as improved family-member well-being, increased patient participation in rehabilitation, substantially increased employment rates, decreased psychiatric symptoms, improved social functioning, and decreased family distress.

"One of the interesting things about family psychoeducation is that a lot of clinical goals are achievable without the patient's participation," McFarlane said. "They have to give consent, but if they decide not to show up for the group, the family can be taught to alter the psychosocial environment to serve their needs even when the patient is not there."

An asbstract of "Genotype-Environment Interaction in Schizophrenia-Spectrum Disorder" is posted at<http://bjp.rcpsych.org/cgi/content/abstract/184/3/216>.

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William McFarlane, M.D., was presented the APA/American Psychiatric Foundation Alexander Gralnick Award for Research in Schizophrenia at APA's fall institute. With him are Paul Burke (left), executive director of the foundation, and Thomas McGlashan, M.D., chair of the Gralnick award committee. 

Credit: Ellen Dallager

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