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Objective: A follow-up study of patients with schizophrenia was conducted to examine change in striatal volumes and extrapyramidal symptoms after a change in medication. Method: Thirty seven patients with schizophrenia and 23 healthy volunteers were examined. Patients at baseline receiving typical antipsychotics (N=10) or risperidone but exhibiting limited response (N=13) were switched to treatment with olanzapine. Patients receiving risperidone and exhibiting a good response (N=14) continued treatment with risperidone. Caudate, putamen, and pallidal volumes were assessed with magnetic resonance imaging. The Extrapyramidal Symptoms Rating Scale was used to assess clinical signs and symptoms. Results: At baseline, basal ganglia volumes in patients treated with typical antipsychotics were greater than in healthy subjects (putamen: 7.0% larger; globus pallidus: 20.7% larger). After the switch to olanzapine, putamen and globus pallidus volumes decreased (9.8% and 10.7%, respectively) and did not differ from those of healthy subjects at the follow-up evaluation. Akathisia was also reduced. In the patients receiving risperidone at baseline, basal ganglia volumes did not differ between those exhibiting good and poor response, and no significant volume changes were observed in subjects with poor risperidone response after the switch to olanzapine treatment. Conclusions: Olanzapine reversed putamen and globus pallidus enlargement induced by typical antipsychotics but did not alter volumes in patients previously treated with risperidone. Changes in striatal volumes related to typical and atypical antipsychotics may represent an interactive effect between individual medications and unique patient characteristics.

Objective: The authors performed a longitudinal study of the effects on thalamic volume of switching from typical to atypical antipsychotic medications. Method: Magnetic resonance imaging scans were acquired from 10 subjects with chronic schizophrenia taking typical antipsychotics and 20 healthy volunteers. Subjects with schizophrenia were switched to olanzapine; both groups were rescanned. Results: At baseline, thalamic volumes in subjects with chronic schizophrenia were 5.8% greater than those of healthy volunteers. At follow-up, there was no significant difference between groups. Additional analysis revealed a significant positive correlation between baseline thalamic volume and dosage of typical antipsychotic medication. Higher dosages at baseline were correlated with larger reductions in volume after the switch to olanzapine. Conclusions: Antipsychotic medication effects may be a factor in the wide range of thalamic volume differences reported between subjects with schizophrenia and healthy volunteers. (Am J Psychiatry 2006; 163:2005-2007)

The Hierarchical Taxonomy of Psychopathology (HiTOP) is an empirical structuralmodel of psychological symptoms formulated to improve the reliability andvalidity of clinical assessment. Neurobiology can inform assessments of earlyrisk and intervention strategies, and the HiTOP model has greater potential tointerface with neurobiological measures than traditional categorical diagnosesgiven its enhanced reliability. However, one complication is that observedbiological correlates of clinical symptoms can reflect various factors, rangingfrom dispositional risk to consequences of psychopathology. In this paper, weargue that the HiTOP model provides an optimized framework for conductingresearch on the biological correlates of psychopathology from an ontogeneticperspective that distinguishes among indicators of liability, current symptoms,and consequences of illness. Through this approach, neurobiological research cancontribute more effectively to identifying individuals at high dispositionalrisk, indexing treatment-related gains, and monitoring the consequences ofmental illness, consistent with the aims of the HiTOP framework.

Objective: The basal ganglia may contribute to extrapyramidal movement disorders, affective disturbances, and cognitive deficits in schizophrenia. Basal ganglia volumes are putatively affected by antipsychotic medications. The purpose of this study was to determine the long-term effects of risperidone treatment in a cohort of first-episode patients with schizophrenia. Method: The subjects were 30 patients with first-episode schizophrenia, 12 patients chronically treated with typical antipsychotics, and 23 healthy comparison subjects. They were scanned by magnetic resonance imaging at baseline. The first-episode patients received 1 year of continuous risperidone treatment, after which they and the comparison subjects were rescanned. Caudate, putamen, and globus pallidus volumes were determined from coronal images. Results: The baseline caudate, putamen, and globus pallidus volumes were significantly larger in the chronically treated patients than in the untreated first-episode subjects and comparison subjects. These volumes did not differ between the first-episode patients and healthy comparison subjects. Basal ganglia volumes were unchanged after 1 year of exposure to risperidone in the first-episode subjects. Extrapyramidal movement disorders were present in the majority of chronically treated patients and more than one-third of the never-medicated first-episode patients at baseline. Conclusions: This group of first-episode patients did not exhibit abnormalities of basal ganglia volumes, nor were basal ganglia volumes affected by exposure to risperidone. Movement disorders were observed in both first-episode and chronically treated patients, suggesting effects of both illness and medications. (Am J Psychiatry 2001; 158:625-631)

Schizophrenia is associated with abnormalities in cortical thickness, including both thicker and thinner cortices than controls. Although less reliably than in patients, non‐psychotic relatives of schizophrenia patients have also demonstrated both thicker and thinner cortices than controls, suggesting an effect of familial or genetic liability. We investigated cortical thickness in 25 schizophrenia patients, 26 adult non‐psychotic first‐degree biological relatives, and 23 community controls using the automated program FreeSurfer. Contrary to hypotheses, we found relatives of schizophrenia patients had greater cortical thickness in all lobes compared to patients and controls; however, this finding was not as widespread when compared to controls. In contrast, schizophrenia patients only demonstrated a thinner right fusiform region than controls and relatives. Our finding of greater thickness in adult biological relatives could represent a maladaptive abnormality or alternatively, a compensatory mechanism. Previous literature suggests that the nature of abnormalities in relatives can vary by the age of relatives and change across the developmental period. Abnormalities in patients may depend on lifestyle factors and on current and previous anti‐psychotic medication use. Our results speak to the need to study various populations of patients and relatives across the lifespan to better understand different developmental periods and the impact of environmental factors. © 2015 Wiley Periodicals, Inc.

Schizophrenia has been reliably associated with impairments in backward masking performance, while bipolar disorder has less consistently been tied to such a deficit. To examine the genetic determinants of visual perception abnormalities in schizophrenia and bipolar disorder, this study evaluated the diagnostic specificity of backward masking performance deficits and whether masking deficits were associated with catechol‐O‐methyl transferase (COMT) genotype. A location‐based backward masking task, which equated participants on the perceptual intensity of stimuli, was completed by 41 schizophrenia outpatients, 28 bipolar outpatients, and 43 nonpsychiatric controls. COMT genotype data were available for 39 schizophrenia outpatients, 28 bipolar outpatients, and 20 nonpsychiatric controls. Schizophrenia patients demonstrated impaired backward masking performance compared to controls and bipolar patients. A group by COMT genotype interaction was detected with schizophrenia Met homozygotes performing more poorly than control and bipolar Met homozygotes, and worse than Val homozygote and heterozygote schizophrenia patients. This study provides novel evidence for differential effects of the COMT gene on neural systems underlying visual perception in schizophrenia and bipolar disorder. The COMT Met allele may be associated with deficits in schizophrenia that are unrelated to neural systems supporting sustained attention or working memory. © 2007 Wiley‐Liss, Inc.