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Michael R. Trimble

Researcher at UCL Institute of Neurology

Publications -  291
Citations -  21027

Michael R. Trimble is an academic researcher from UCL Institute of Neurology. The author has contributed to research in topics: Epilepsy & Tourette syndrome. The author has an hindex of 73, co-authored 289 publications receiving 19726 citations. Previous affiliations of Michael R. Trimble include University College London & Queen's University.

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The precuneus: a review of its functional anatomy and behavioural correlates.

TL;DR: A useful conceptual framework is provided for matching the functional imaging findings with the specific role(s) played by this structure in the higher-order cognitive functions in which it has been implicated, and activation patterns appear to converge with anatomical and connectivity data in providing preliminary evidence for a functional subdivision within the precuneus.
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The subgenual anterior cingulate cortex in mood disorders.

TL;DR: It is demonstrated that the mean gray matter volume of this anterior cingulate cortex (sgACC) cortex is abnormally reduced in subjects with major depressive disorder (MDD) and bipolar disorder, irrespective of mood state.
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The psychiatric comorbidity of epilepsy

TL;DR: A non‐systematic review of the literature allows us to draw some useful, although not definite, conclusions about the prevalence of psychiatric disorders in epilepsy.
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Activity in ventromedial prefrontal cortex covaries with sympathetic skin conductance level: a physiological account of a “default mode” of brain function

TL;DR: The findings point to a dissociation between neural systems controlling basal sympathetic tone (SCL) and transient skin conductance responses (SCRs), indicating that activity within VMPFC and OFC reflects a dynamic between exteroceptive and interoceptive deployment of attention.
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Brain activity relating to the contingent negative variation: an fMRI investigation.

TL;DR: Findings provide a likely functional neuroanatomical substrate for the CNV and demonstrate modulation of components of this neural circuitry by peripheral autonomic arousal, and suggest a mechanistic model whereby thalamocortical interactions regulate CNV amplitude.