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Related Experiment Videos

Cortical blood flow changes during spreading depression in cats.

R D Piper1, G A Lambert, J W Duckworth

  • 1Institute of Neurological Sciences, Prince Henry Hospitals, University of New South Wales, Little Bay, Sydney, Australia.

The American Journal of Physiology
|July 1, 1991
PubMed
Summary

Cortical spreading depression (CSD) causes initial hyperemia, followed by prolonged oligemia and impaired cerebrovascular reactivity in cats. These changes may link CSD to human migraine with aura.

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Area of Science:

  • Neuroscience
  • Cerebrovascular Physiology
  • Migraine Pathophysiology

Background:

  • Cortical spreading depression (CSD) is a wave of neuronal and glial depolarization that spreads across the cerebral cortex.
  • CSD is implicated in the pathophysiology of migraine with aura and other neurological disorders.
  • Understanding the cerebrovascular changes associated with CSD is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the dynamic changes in cortical blood flow and cerebrovascular reactivity following CSD induction in an animal model.
  • To assess the impact of CSD on CO2 reactivity and vasomotor activity in the cerebral microcirculation.
  • To explore the potential relevance of observed cerebrovascular alterations to human migraine with aura.

Main Methods:

Related Experiment Videos

  • CSD was induced via superficial cortical pinprick in alpha-chloralose-urethan-anesthetized cats.
  • Laser-Doppler velocimetry (LDV) was employed to measure cortical blood flow (CBF).
  • Cerebrovascular reactivity was assessed using CO2 inhalation challenges and hypotension-induced autoregulation tests.

Main Results:

  • CSD induced a transient hyperemic phase with a peak increase in CBF of 215 +/- 48% lasting 2.7 +/- 0.4 min.
  • This was followed by a prolonged oligemic phase, with CBF reduced by 20 +/- 4% at 1 hour and 28 +/- 4% at 2 hours post-CSD.
  • CSD abolished CO2 reactivity for at least 10 hours, decreased spontaneous vasomotor activity, but preserved autoregulation to hypotension.

Conclusions:

  • CSD profoundly alters cortical blood flow dynamics, causing initial hyperemia followed by sustained oligemia.
  • The significant impairment of cerebrovascular reactivity post-CSD suggests a potential mechanism contributing to migraine aura symptoms.
  • These findings in a feline model highlight the critical role of cerebrovascular dysregulation in CSD and its link to migraine pathophysiology.