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Functional magnetic resonance imaging responses in CADASIL.

Ikreet Cheema1, Aaron R Switzer1, Cheryl R McCreary2

  • 1Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.

Journal of the Neurological Sciences
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Summary

Blood oxygen-level dependent (BOLD) functional MRI responses are preserved in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) patients, unlike in cerebral amyloid angiopathy (CAA). This suggests preserved cortical blood flow regulation in CADASIL.

Keywords:
CADASILCerebral amyloid angiopathyFunctional MRI

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Area of Science:

  • Neuroimaging
  • Neurology
  • Vascular Biology

Background:

  • Cerebral amyloid angiopathy (CAA) shows reduced blood oxygen-level dependent (BOLD) functional MRI (fMRI) responses, indicating impaired vascular reactivity.
  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is another small vessel disease affecting the brain.

Purpose of the Study:

  • To investigate whether BOLD responses are reduced in CADASIL, similar to CAA.
  • To compare BOLD responses between CADASIL, CAA, and control groups.

Main Methods:

  • BOLD fMRI data were acquired during visual stimulation (checkerboard) and a motor task (finger-tapping).
  • BOLD response amplitudes in the visual and motor cortices were compared across 5 CADASIL, 18 CAA, and 18 control subjects.
  • Analyses controlled for age and hypertension.

Main Results:

  • BOLD responses to visual stimuli differed significantly between groups (p<0.001), but not for the motor task (p=0.47).
  • CADASIL patients exhibited a greater visual cortex BOLD response (3.95%) compared to both CAA patients (1.73%) and controls (2.88%).
  • Visual BOLD response was significantly higher in CADASIL than in CAA (p<0.001) and controls (p=0.04).

Conclusions:

  • BOLD amplitude responses were increased in the visual cortex and unchanged in the motor cortex of CADASIL patients.
  • Cortical blood flow regulation appears relatively preserved in CADASIL, contrasting with impaired occipital vascular reactivity in CAA.
  • Preserved reactivity in CADASIL may stem from primarily subcortical injury, with potential compensatory mechanisms for subcortical damage driving increased activation.