Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Little is known about how ischemia affects hemodynamic responses to neural activation in the brain. We compare the effects of a motor activation task and a cerebral vasodilating agent, acetazolamide (ACZ), on regional cerebral blood flow (rCBF) in primary sensorimotor cortex (PSM) in six patients with major cerebral artery steno-occlusive lesions without paresis of the upper extremities. Quantitative rCBF was measured in all patients using H2(15)O autoradiographic method and positron emission tomography. The CBF was determined at rest, during a bimanual motor activation task, and 10 minutes after ACZ administration. With bimanual motor activation, rCBF increased significantly in both PSM compared with at rest (P < 0.01 on lesion side, and P < 0.02 on contralateral side). However, rCBF did not increase after ACZ injection in the PSM on the lesion side, whereas rCBF increased significantly in the contralateral PSM after ACZ injection compared with the level at rest. This result suggests that despite a decreased hemodynamic reserve, there is a nearly normal flow response to neural activation, indicating that the mechanism of vasodilation responsible for perfusion change is different for acetazolamide and neural activation. The relations among neural activation, hemodynamic status, and cerebral metabolism in the ischemic stroke patients are discussed.
J Cereb Blood Flow Metab 1998 Sep
PMID:Neural activation of the brain with hemodynamic insufficiency. 974 99

Cortical atrophy as demonstrated by measurement of cortical thickness (CT) is a hallmark of various neurodegenerative diseases. In the wake of an acute ischemic stroke, brain architecture undergoes dynamic changes that can be tracked by structural and functional magnetic resonance imaging studies as soon as 3 months after stroke. In this study, we measured changes of CT in cortical areas connected to subcortical stroke lesions in 12 patients with upper extremity paresis combining white-matter tractography and semi-automatic measurement of CT using the Freesurfer software. Three months after stroke, a significant decrease in CT of -2.6% (median, upper/lower boundary of 95% confidence interval -4.1%/-1.1%) was detected in areas connected to ischemic lesions, whereas CT in unconnected cortical areas remained largely unchanged. A cluster of significant cortical thinning was detected in the superior frontal gyrus of the stroke hemisphere using a surface-based general linear model correcting for multiple comparisons. There was no significant correlation of changes in CT with clinical outcome parameters. Our results show a specific impact of subcortical lesions on distant, yet connected cortical areas explainable by secondary neuro-axonal degeneration of distant areas.
J Cereb Blood Flow Metab 2015 Sep
PMID:Structural plasticity of remote cortical brain regions is determined by connectivity to the primary lesion in subcortical stroke. 2592 Sep 57