Motor trephine syndrome: a mechanistic hypothesis.

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.