Abstract
Decompressive craniectomy (DC) is often required to manage rising intracranial pressure after traumatic brain injury (TBI). Syndrome of the trephine (SoT) is a reversible neurologic condition that often occurs following DC as a result of the unrepaired skull. The purpose of the present study is to characterize neurological impairment following TBI in rats with an unrepaired craniectomy versus rats with a closed cranium. Long Evans male rats received a controlled cortical impact (CCI) over the caudal forelimb area (CFA) of the motor cortex. Immediately after CCI, rats received either a hemi-craniectomy (TBI Open Skull Group) or an immediate acrylic cranioplasty restoring cranial anatomy (TBI Closed Skull Group). Motor performance was assessed on a skilled reaching task on post-CCI weeks 1—4, 8, 12, and 16. Three weeks after the CCI injury, the TBI Closed Skull Group demonstrated improved motor performance compared to TBI Open Skull Group. The TBI Closed Skull Group continued to perform better than the TBI Open Skull Group throughout weeks 4, 8, 12 and 16. The protracted recovery of CFA motor performance demonstrated in rats with unrepaired skulls following TBI suggests this model may be beneficial for testing new therapeutic approaches to prevent SoT.
Highlights
Decompressive craniectomy (DC) is often required to manage rising intracranial pressure after traumatic brain injury (TBI)
Syndrome of the trephine (SoT) is a poorly understood neurologic condition that occurs in patients with unrepaired cranial bone defects in conjunction with sinking skin flap syndrome
The symptoms of SoT are reversible once the cranial vault anatomy is restored either by replacing the cranial bone or using an implant to reconstruct the cranial defect weeks to months after the initial TBI3
Summary
Decompressive craniectomy (DC) is often required to manage rising intracranial pressure after traumatic brain injury (TBI). Syndrome of the trephine (SoT) is a reversible neurologic condition that often occurs following DC as a result of the unrepaired skull. After CCI, rats received either a hemicraniectomy (TBI Open Skull Group) or an immediate acrylic cranioplasty restoring cranial anatomy (TBI Closed Skull Group). Three weeks after the CCI injury, the TBI Closed Skull Group demonstrated improved motor performance compared to TBI Open Skull Group. The protracted recovery of CFA motor performance demonstrated in rats with unrepaired skulls following TBI suggests this model may be beneficial for testing new therapeutic approaches to prevent SoT. The symptoms of SoT are reversible once the cranial vault anatomy is restored either by replacing the cranial bone or using an implant to reconstruct the cranial defect weeks to months after the initial TBI3. Our hypothesis is that maintaining “normal” cranial vault anatomy is an important independent factor in determining TBI outcomes
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