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Motor trephine syndrome: a mechanistic hypothesis
Shirley I Stiver1, Max Wintermark, Geoffrey T Manley
1Department of Neurosurgery, University of California San Francisco, San Francisco General Hospital, 1001 Potrero Avenue, Room 101, San Francisco, CA 94110-0899, USA. sstiver@neurosurg.ucsf.edu
Acta Neurochirurgica. Supplement
|April 25, 2009
Summary
Motor trephine syndrome, a delayed monoparesis after decompressive hemicraniectomy for traumatic brain injury, is linked to contusions and delayed cranioplasty. This condition rapidly reverses after bone replacement.
Area of Science:
- Neurosurgery
- Neurology
- Traumatic Brain Injury Research
Background:
- Motor trephine syndrome is a delayed, reversible contralateral monoparesis following decompressive hemicraniectomy for traumatic brain injury (TBI).
- Understanding the causal factors of this syndrome is crucial for neurotrauma patient management.
Purpose of the Study:
- To identify the etiological factors contributing to the development of motor trephine syndrome in TBI patients.
Main Methods:
- Retrospective review of clinical records and imaging studies for TBI patients who underwent decompressive hemicraniectomy and subsequent cranioplasty.
- Detailed analysis of motor function recovery from injury up to 6 months post-cranioplasty.
Main Results:
- Contusion blossoming, cerebrospinal fluid (CSF) circulation dysfunction, and prolonged intervals to cranioplasty repair were significantly associated with motor trephine syndrome.
- Hypothesized mechanism involves decompensated CSF flow, leading to parenchymal edema and reduced cerebral blood flow (CBF).
Conclusions:
- Pre-existing contusions, large hemispheric decompressions, and delayed cranioplasty facilitate CSF and edema transparenchymal flow.
- "Motor trephine syndrome" demonstrates rapid and complete reversibility following cranioplasty repair.
- Restoration of the bone flap normalizes CSF/edema dynamics and CBF, correlating with motor function improvement.
