Related Experiment Video
Updated: Jun 23, 2026
Measuring and Manipulating Functionally Specific Neural Pathways in the Human Motor System with Transcranial Magnetic Stimulation
Published on: February 23, 2020
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
Background:
In our neurotrauma practice, "motor trephine syndrome" was defined as a contralateral monoparesis that developed as a delayed and reversible complication in patients treated with decompressive hemicraniectomy for traumatic brain injury (TBI). The goal of this study was to define causal factors associated with this syndrome.
Methods:
We retrospectively reviewed clinical records and imaging studies of all patients undergoing decompressive hemicraniectomy followed by cranioplasty repair in our comprehensive database of TBI patients. Detailed analysis of motor function from the time of injury to 6 months following cranioplasty repair identified three patterns of motor recovery.
Results:
Blossoming of contusions, CSF circulation dysfunction, and longer times to cranioplasty repair were strongly associated with "motor trephine syndrome". We hypothesize that "motor trephine syndrome" arises from decompensated CSF flow with transgression of CSF fluid and edema into brain parenchyma, together with associated decrements in cerebral blood flow.
Conclusion:
Prior contusion injury, decreased skull resistance with large hemispheric decompressions, and longer intervals to cranioplasty repair facilitate transparenchymal flow of CSF and edema. "Motor trephine syndrome" is rapidly reversible following cranioplasty repair. CSF and edema fluid changes within the parenchyma and CBF normalize, coincident with improvements in the patient's motor function, upon replacement of the bone.
