Reversible monoparesis following decompressive hemicraniectomy for traumatic brain injury

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Object

The “syndrome of the trephined” is an uncommon and poorly understood disorder of delayed neurological deficit following craniectomy. From the authors' extensive experience with decompressive hemicraniectomy for traumatic brain injury (TBI), they have encountered a number of patients who developed delayed motor deficits, also called “motor trephine syndrome,” and reversal of the weakness following cranioplasty repair. The authors set out to study motor function systematically in this patient population to define the incidence, contributing factors, and outcome of patients with motor trephine syndrome.

Methods

The authors evaluated patient demographics, injury characteristics, detailed motor examinations, and CT scans in 38 patients with long-term follow-up after decompressive hemicraniectomy for TBI.

Results

Ten patients (26%) experienced delayed contralateral upper-extremity weakness, beginning 4.9 ± 0.4 months (mean ± standard error) after decompressive hemicraniectomy. Motor deficits improved markedly within 72 hours of cranioplasty repair, and all patients recovered full motor function. The CT perfusion scans, performed in 2 patients, demonstrated improvements in cerebral blood flow commensurate with resolution of cerebrospinal fluid flow disturbances on CT scanning and return of motor strength. Comparisons between 10 patients with and 20 patients (53%) without delayed motor deficits identified 3 factors—ipsilateral contusions, abnormal cerebrospinal fluid circulation, and longer intervals to cranioplasty repair—to be strongly associated with delayed, reversible monoparesis following decompressive hemicraniectomy.

Conclusions

Delayed, reversible monoparesis, also called motor trephine syndrome, is common following decompressive hemicraniectomy for TBI. The results of this study suggest that close follow-up of motor strength with early cranioplasty repair may prevent delayed motor complications of decompressive hemicraniectomy.

Abbreviations used in this paper: CBF = cerebral blood flow; CBV = cerebral blood volume; CSF = cerebrospinal fluid; EDH = epidural hematoma; GCS = Glasgow Coma Scale; MTT = mean transit time; SDH = subdural hematoma; SE = standard error; TBI = traumatic brain injury; VP = ventriculoperitoneal.

Article Information

Address correspondence to: Shirley I. Stiver, M.D., Ph.D., Department of Neurosurgery, University of California, San Francisco, 1001 Potrero Avenue, Room 101, San Francisco, California 94110-0899. email: sstiver@neurosurg.ucsf.edu.

© AANS, except where prohibited by US copyright law.

Headings

Figures

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    Schematic of patient groups and selection criteria.

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    Axial CT scans obtained without contrast material in 2 representative cases (Patients A and B) at the time of injury (panels a and d), following decompressive hemicraniectomy (panels b and e), and prior to cranioplasty (panels c and f). Initial CT scans showed evidence of SDHs (arrows) with mass effect and midline shift. Following decompressive hemicraniectomy and evacuation of the SDH, there is evidence of blossoming of ipsilateral contusions (arrows) in the frontal lobe of Patient A (panel b) and in the temporal lobe of Patient B (panel e) (arrowheads in both panels indicate Jackson–Pratt drains). The CT scans obtained immediately prior to cranioplasty in Patient A (panel c) and 1 month prior to cranioplasty in Patient B (panel f) demonstrate areas of hypoattenuation consistent with leakage of CSF and edema in the parenchyma underlying the skull defect (arrows).

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    Serial perfusion CT studies obtained in Patient A before and after cranioplasty repair. Axial CT scans obtained without contrast addition (NCT) and perfusion maps of MTT, CBF, and CBV obtained at the level of the foramen of Monro are shown. Studies obtained immediately before cranioplasty (a), showing hypoattenuation in the right frontal lobe. The CBF is reduced in the area of the hypoattenuation as well as in adjacent brain tissue. Studies performed at 48 hours (b) and 5 days (c) after cranioplasty repair demonstrate resolution of the hypoattenuation, together with focal improvements in MTT and CBF in that area (this is especially well demonstrated when comparing rows a and c, which contain scans obtained at exactly the same level). This time course was consistent with edema and CSF leakage into the parenchyma, progressively improving over time following cranioplasty. During this interval, motor strength in the patient's contralateral upper extremity improved markedly.

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    Serial perfusion CT studies obtained in Patient B, before and after cranioplasty repair. Axial CT scans obtained without contrast addition and perfusion maps of MTT, CBF, and CBV obtained at the level of the foramen of Monro are shown. a: This perfusion CT study was performed 1 month prior to cranioplasty, and it demonstrates enlargement of the ventricular system, together with hypoattenuation consistent with a combination of encephalomalacia, CSF leakage, and edema. The CBF is reduced not only in the hypoattenuated area of CSF and edema, but throughout the hemisphere ipsilateral to the decompression. b: A perfusion CT study performed 24 hours after insertion of a VP shunt shows response in the size of the ventricles and hypoattenuated areas of CSF underlying the craniectomy defect, but no or only slight improvement in CBF. c: Studies repeated 1 month later, immediately before cranioplasty repair, continue to show abnormal hypoattenuation and impaired CBF ipsilateral to the hemicraniectomy. Motor strength was Grade 4/5 in the contralateral grip at the time of shunt insertion. At 1 month after VP shunt insertion, the patient's grip had deteriorated to Grade 3/5, and she no longer had antigravity strength in finger extension. d: Follow-up CT scans obtained 24 hours after cranioplasty repair showing reduction in the size of the ventricles and in the hypoattenuated areas of CSF and edema. Perfusion studies demonstrate significant improvement in CBF, CBV, and MTT throughout the hemisphere ipsilateral to the cranioplasty. Improvements in brain perfusion within 24 hours of skull repair coincided with the return of grip strength to Grade 4/5 and antigravity finger extension.

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