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Robin M. Murray

Researcher at King's College London

Publications -  1583
Citations -  128883

Robin M. Murray is an academic researcher from King's College London. The author has contributed to research in topics: Psychosis & Schizophrenia. The author has an hindex of 171, co-authored 1539 publications receiving 116362 citations. Previous affiliations of Robin M. Murray include University of Cambridge & National Institutes of Health.

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Temporal course of auditory hallucinations.

TL;DR: Functional magnetic resonance imaging supports the hypothesis that during hallucinations activation in cortical regions mediating the generation of inner speech may precede the engagement of areas implicated in the perception of auditory verbal material.
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Resting Hyperperfusion of the Hippocampus, Midbrain, and Basal Ganglia in People at High Risk for Psychosis

TL;DR: A high risk for psychosis was associated with increased resting activity in the hippocampus, midbrain, and basal ganglia, which is consistent with animal models that propose that psychotic symptoms may be generated when hippocampal hyperactivity drives hyperactivity in regions involved in subcortical dopamine signaling.
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Brain MRI abnormalities in schizophrenia: Same genes or same environment?

TL;DR: Using genetic model fitting on twin and sibling data, differential sources of covariation between schizophrenia and brain volumes are demonstrated, genetic in the case of whole brain volume and individual specific environment in the cases of lateral ventricles.
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Minor physical anomalies in psychoses: associations with clinical and putative aetiological variables

TL;DR: There was a weak association between the presence of MPAs and positive family history of a major psychiatric disorder, and those with MPAs required more frequent and longer psychiatric admissions, and showed impaired ability on a test sensitive to left parietal system function.
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No evidence for an association of affective disorders with high- or low-activity allele of catechol-o-methyltransferase gene

TL;DR: It is concluded that genetic variation that determines high and low activities of COMT does not have a major effect on the vulnerability to affective disorders in the sample of patients with bipolar disorder and unipolar depression.