First-episode schizophrenia. A window of opportunity for optimizing care and outcomes.

Department of Psychiatry, Medical College of Georgia, Augusta 30912, USA.
Postgraduate Medicine (Impact Factor: 1.7). 10/2006; Spec No:5-19.
Source: PubMed


The pernicious course of schizophrenia has spurred efforts to identify and effectively treat this condition as early as possible. This assertive therapeutic stance is supported by epidemiologic data suggesting a substantial time lag between onset of illness and therapeutic intervention, and by neurobiologic data suggesting that brain changes present in first-episode psychosis are comparable to those in chronic schizophrenia. The proposal that atypical antipsychotic medications may prevent illness deterioration and/or be a restorative intervention is an appealing, but as yet unproven, hypothesis. Major challenges to maximizing treatment outcomes in first-episode schizophrenia include optimizing timing and effectiveness of pharmacologic interventions, service coordination, and access to care. We present data on the onset and presentation of first-episode schizophrenia and emerging findings about the neurobiology of first episodes, review nonpharmacologic and pharmacologic management, and summarize clinical research data on use of atypical antipsychotics in first-episode patients.

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    • "The study of first-episode psychosis (FEP) is particularly advantageous in understanding the neurobiology of schizophrenia in part because of the opportunity to minimize the potential impact of confounds, such as illness duration, medication effects, and the psychiatric and medical comorbidities that are associated with chronicity of illness (Buckley and Evans 2006). Only a few studies have reported the decreased serum or plasma BDNF levels in first-episode patients with schizophrenia (Buckley et al. 2007; Rizos et al. 2008). "
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    ABSTRACT: There is much interest, derived from current neurochemical, genetic, and therapeutic research, in the role of brain neurotrophins in schizophrenia. Neurotrophins play key roles in neuronal development and differentiation (i.e., promoting dendritogenesis and synaptogenesis), and in orchestrating the neuronal response to stress/noxious stimuli. Additionally, neurotrophins are modulators across monominergic (dopamine and serotonin), gabaergic and cholinergic systems. These roles focus on important areas of the etiopathophysiology of schizophrenia. Clinical studies show reductions in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NFG) in schizophrenic patients as compared to normal control subjects, as well as differences in patients receiving first-generation antipsychotics (FGAs) or second-generation antipsychotics (SGAs). We now report on BDNF levels in subjects with first-episode psychosis in comparison with normal healthy controls. Compared to normal controls (N=14; 290.5+/-38.81 pg/ml), first-episode psychotic patients showed significant reduction (N=15; 135+/-21.77 pg/ml; P=0.001; f=12.873) in plasma BDNF. Additionally, plasma BDNF levels showed a significant negative correlation (N=13' r=0.584, P=0.0362) only with positive symptom scores at base line and no significant correlations were found with any of the cognitive performance test battery or motor function test scores. Low BDNF levels at the onset of psychosis suggest that it may contribute to the pathogenesis of schizophrenia and/or perhaps could be a helpful neurobiological marker for possible early treatment intervention.
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