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Pathophysiology of transient neurological deficit in patients with chronic subdural hematoma: A systematic review

Jurre Blaauw1,2, Josje M van Zundert1, Heleen M den Hertog3

  • 1Department of Neurology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Acta Neurologica Scandinavica
|March 31, 2022
PubMed

Insights

Transient neurological deficits in chronic subdural hematoma (CSDH) have unclear causes. This review found proposed mechanisms like epileptic activity or blood flow obstruction, but the exact pathophysiology remains elusive, requiring further research.

Area of Science:

  • Neurology
  • Neurosurgery

Background:

  • Chronic subdural hematoma (CSDH) can present with transient neurological deficits (TNDs) that mimic transient ischemic attacks.
  • The prevalence of TNDs in CSDH ranges from 1% to 24%, with varying definitions impacting reported rates.

Purpose of the Study:

  • To systematically review and identify the proposed pathophysiological mechanisms underlying TNDs in patients with CSDH.

Main Methods:

  • A systematic literature search was conducted on Pubmed and Embase for articles on TND pathophysiology in CSDH.
  • Two independent reviewers selected studies and extracted data from 316 identified references, with 15 meeting inclusion criteria.

Main Results:

  • Multiple pathophysiological mechanisms for TND in CSDH were proposed.
  • Epileptic activity was suggested by three studies, while three others deemed it unlikely.
  • Blood flow obstruction due to the hematoma or swelling was suggested by five papers; six studies offered no definitive mechanism.

Conclusions:

  • The exact pathophysiology of TND in CSDH remains unclear despite various proposed mechanisms.
  • Future research should integrate brain MRI (with diffusion-weighted imaging) and EEG to elucidate TND pathophysiology.
  • Improved understanding may lead to optimized CSDH treatment strategies.

Keywords:
chronic subdural hematomapathophysiologysystematic reviewtransient neurological deficits

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