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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...

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A Mouse Model for Vascular Cognitive Impairment and Dementia Based on Needle-guided Asymmetric Bilateral Common Carotid Artery Stenosis
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Altered callosal function in cerebral microangiopathy.

Matthias Wittstock1, Annette Grossmann, Erwin Kunesch

  • 1Human Cortical Physiology Laboratory, Department of Neurology, University of Rostock, Gehlsheimer Str. 20, 18147, Rostock, Germany. matthias.wittstock@med.uni-rostock.de

Journal of Neurology
|November 17, 2009
PubMed
Summary
This summary is machine-generated.

Cerebral microangiopathy (CMA) significantly impacts corpus callosum function, leading to callosal dysfunction and atrophy. This study shows CMA extent correlates with impaired bimanual tapping and ipsilateral silent period, suggesting CMA

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Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
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Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
07:47

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases

Published on: December 6, 2016

Area of Science:

  • Neuroscience
  • Neurology
  • Neuroimaging

Background:

  • Callosal dysfunction is a hallmark of central nervous system diseases.
  • Cerebral microangiopathy (CMA) may cause callosal pathway demyelination.
  • Understanding CMA's impact on the corpus callosum is crucial.

Purpose of the Study:

  • To investigate callosal function in relation to the extent of cerebral microangiopathy (CMA).
  • To correlate neurophysiological measures of callosal function with CMA severity and callosal atrophy.

Main Methods:

  • Bimanual tapping task and transcranial magnetic stimulation (TMS) to assess callosal function.
  • Analysis of ipsilateral silent period (iSP) and transcallosal conduction time (TCT).
  • Correlation of functional data with cerebral magnetic resonance imaging (cMRI) scores for CMA extent and callosal atrophy in 44 CMA patients and 10 controls.

Main Results:

  • Pathological iSP findings and disturbed bimanual tapping correlated significantly with higher CMA scores.
  • The extent of CMA was significantly correlated with the degree of callosal atrophy.
  • CMA significantly affects callosal pathways, likely through chronic demyelination.

Conclusions:

  • Cerebral microangiopathy considerably impacts corpus callosum pathways.
  • Callosal atrophy and dysfunction are linked to the extent of CMA.
  • Ipsilateral silent period (iSP) analysis can assess the clinical impact of CMA detected by cMRI.