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Postoperative Transient Neurologic Dysfunction: A Proposal for Pathophysiology.

Ji Hoon Phi1, Seung Jin Lee2, Hyun Seung Kang3

  • 1Division of Pediatric Neurosurgery, Seoul National University Children's Hospital, Seoul National University College of Medicine, Seoul, Korea.

Journal of Clinical Neurology (Seoul, Korea)
|July 5, 2018
PubMed
Summary

Postoperative transient neurologic dysfunction in moyamoya disease patients can mimic stroke or seizures but is fully reversible. This study suggests it may stem from transient cortical depression, offering new insights into neurosurgical patient recovery.

Keywords:
cortical spreading depressionencephalo-duro-arterio-synangiosismigrainemoyamoya diseasepostoperativetransient neurologic dysfunction

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Area of Science:

  • Neurosurgery
  • Neurology
  • Neuroscience

Background:

  • Sudden neurological deterioration is common in neurosurgical patients.
  • The cause is often unclear, excluding structural changes, ischemia, or seizures.
  • Postoperative transient neurologic dysfunction requires further pathophysiological understanding.

Purpose of the Study:

  • To investigate the pathophysiology of postoperative transient neurologic dysfunction.
  • To offer new insights into the mechanisms behind this condition.
  • To analyze cases of prolonged, reversible neurologic deficits after surgery.

Main Methods:

  • Studied 8 patients with moyamoya disease undergoing encephalo-duro-arterio-synangiosis.
  • Performed brain imaging (MRI, SPECT) and electroencephalography (EEG) during and after symptom resolution.
  • Evaluated patients with prolonged, reversible focal neurologic dysfunction of unknown origin.

Main Results:

  • Symptoms included dysarthria, hemiparesis, or hemiparesthesia developing 12 hours to 8 days post-surgery.
  • Symptoms lasted 12 to 17 days, with no significant interval changes on structural imaging.
  • Perfusion imaging showed increased cerebral blood flow, and EEG revealed slowing in the symptomatic hemisphere.

Conclusions:

  • Transient neurologic dysfunction can occur post-neurosurgery, lasting longer than typical transient ischemic attacks or seizures.
  • The condition eventually resolves spontaneously without specific treatment.
  • Proposed mechanism involves transient cortical depression, possibly triggered by mechanical stimulation, akin to migraine aura.