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Related Experiment Videos

The large striatocapsular infarct. A clinical and pathophysiological entity.

C Weiller1, E B Ringelstein, W Reiche

  • 1Department of Neurology, Klinikum Rheinisch-Westfaelische Technische Hochshule, Aachen, West Germany.

Archives of Neurology
|October 1, 1990
PubMed
Summary

Large striatocapsular infarctions stem from middle cerebral artery blockages, not small vessel disease. Persistent blockages cause decreased blood flow, leading to neurological deficits like aphasia or neglect.

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Area of Science:

  • Neurology
  • Vascular Neurology
  • Neuroimaging

Background:

  • Subcortical large striatocapsular infarctions are often misdiagnosed as lacunar infarcts.
  • Understanding the underlying vascular cause is crucial for accurate diagnosis and treatment.

Purpose of the Study:

  • To investigate the etiology of large striatocapsular infarctions.
  • To correlate infarct location and size with cerebral blood flow and neurological deficits.
  • To differentiate between large-vessel and small-vessel disease as causes.

Main Methods:

  • Studied 29 patients with large striatocapsular infarctions using MRI, CT, transcranial Doppler ultrasonography, selective carotid angiography, and SPECT.
  • Assessed cerebral blood flow, blood volume, and perfusion reserve.

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  • Correlated imaging findings with clinical presentation, including aphasia and neglect.

    • Main Results:

    • Infarctions involved territories of lenticulostriate, Heubner's, or anterior choroidal arteries, suggesting middle cerebral artery (MCA) origin.
    • Occlusive disease of the MCA (large-vessel disease) was identified as the cause, not small-vessel disease.
    • Persistent MCA occlusion correlated with decreased cortical blood flow and neuropsychological deficits (aphasia/neglect).
    • Rapid MCA recanalization or stenosis without decreased cortical blood flow was observed in patients without deficits.

    Conclusions:

    • Large striatocapsular infarctions result from MCA occlusive disease (large-vessel disease).
    • Neuropsychological deficits are linked to reduced cortical blood flow from persistent MCA occlusion.
    • Distinguishes infarct etiology from lacunar events, emphasizing MCA's role.