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Abhilash K. Desai, MD, FAPA, Associate professor, Director Center for Healthy Brain Aging, Department of neurology and psychiatry, Division of geriatric psychiatry, Associate professor, Department of internal medicine, Division of geriatric medicine, St. Louis University School of Medicine, St. Louis, MO
Mehrzad Seraji, MD, Fellow, Department of neurology and psychiatry, Division of geriatric psychiatry, St. Louis University School of Medicine, St. Louis, MO
Maurice Redden, MD, Instructor, Department of neurology and psychiatry, Division of geriatric psychiatry, St. Louis University School of Medicine, St. Louis, MO
Ramasubba Tatini, MD, Private practice, St. Louis, MO
The number of older adults (age ≥65) who developed schizophrenia before age 45 is expected to double in the next 2 decades; the 1-year prevalence of schizophrenia among older adults is approximately 0.6%. This article reviews how positive, negative, and cognitive symptoms and social functioning change over decades and discusses strategies for reducing the impact of long-term antipsychotic use on neurologic and physical health. Although some patients experience schizophrenia onset later in life, in this article we focus on older adults who developed the illness before age 45.
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Leslie Citrome, MD, MPH, Professor of psychiatry, New York University School of Medicine, New York, NY, Director, Clinical Research and Evaluation Facility, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY
Researchers in Finland surprised psychiatrists this year by announcing that clozapine “seems to be associated with a substantially lower mortality than any other antipsychotic.” This finding also surprised the researchers, who expected their 11-year study to link long-term use of second-generation (“atypical”) antipsychotics with increased mortality in patients with schizophrenia. Instead they found longer lives in patients who used antipsychotics (and particularly clozapine), compared with no antipsychotic use.
This study’s findings do not change clozapine’s association with potentially fatal agranulocytosis as well as weight gain, metabolic abnormalities, and other adverse effects. Clozapine also is difficult to administer, and patients must be enrolled in FDA-mandated registries. These obstacles might discourage you from offering clozapine to patients who could benefit from it.
Why bother considering clozapine? Because recent data on decreased mortality, decreased suicidality, and control of aggressive behavior make clozapine a compelling choice for many patients. Careful attention to clozapine’s adverse effect profile is necessary, but you can manage these risks with appropriate monitoring.
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Listen to Dr. Citrome discuss discusses how to determine if clozapine is an appropriate choice for your patient
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Stabilizing glutamate transmission may benefit some patients with treatment-resistant schizophrenia.
John A. Gray, MD, PhD
Resident, department of psychiatry, postdoctoral fellow, department of cellular and molecular pharmacology, University of California, San Francisco
Samuel C. Risch, MD
Professor, department of psychiatry, University of California, San Francisco
Current antipsychotics are reasonably effective in treating positive symptoms, but they do less to improve the negative and cognitive symptoms that contribute to patients’ long-term poor functional capacity and quality of life. So what do psychiatrists do in clinical practice to mitigate antipsychotics’ limitations? We augment.Schizophrenia patients routinely are treated with polypharmacy—often with antidepressants or anticonvulsants—in attempts to improve negative symptoms, aggression, and impulsivity. Most adjuncts, however—including divalproex, antidepressants, and lithium—have shown very small, inconsistent, or no effects. The only agent with a recent meta-analysis supporting its use as augmentation in treatment-resistant schizophrenia is lamotrigine, an anticonvulsant approved for use in epilepsy.This article examines the evidence supporting off-label use of lamotrigine as an augmenting agent in schizophrenia and explains the rationale, based on lamotrigine’s probable mechanism of action as a stabilizer of glutamate neurotransmission.
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