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Background: Cerebral palsy with medically refractory spasticity and dystonia is a condition that often benefits from intrathecal baclofen pump therapy to treat these symptoms. In this case report, an intracranial baclofen catheter was placed in the prepontine space to improve withdrawal symptoms in a patient unable to undergo new lumbar catheter placement due to infection. Case Description: A 22-year-old female with past medical history of cerebral palsy presented with baclofen pump failure and was unable to undergo placement of a new lumbar baclofen catheter due to an infection in her lower back precluding safe and efficacious catheter placement. It was decided the patient would benefit from intrathecal baclofen administered in the prepontine space as a means to avoid a lumbar catheter and thus bypass this prior infection site. An endoscopic third ventriculostomy (ETV) was performed with the endoscope and the distal end of the baclofen pump catheter was fed through this ETV into the prepontine space. Placement in the prepontine space was confirmed by a follow-up head computed tomography. There was a significant improvement in autonomic symptoms and spasticity. By postoperative day 5, the patient was surgically and medically cleared for discharge. Conclusion: In cases of severe baclofen withdrawal due to dysfunctional pumps, immediate reversal is preferred but may not be feasible due to factors such as infection. This case report has demonstrated that prepontine catheter placement can be effective for the administration of baclofen to reverse withdrawal symptoms in these types of patients.

Although lipid peroxidation has long been associated with spinal cord injury (SCI), the specific role of lipid peroxidation-derived byproducts such as acrolein in mediating damage remains to be fully understood. Acrolein, an α-β unsaturated aldehyde, is highly reactive with proteins, DNA, and phospholipids and is considered as a second toxic messenger that disseminates and augments initial free radical events. Previously, we showed that acrolein increased following traumatic SCI and injection of acrolein induced tissue damage. Here, we demonstrate that microinjection of acrolein into the thoracic spinal cord of adult rats resulted in dose-dependent tissue damage and functional deficits. At 24 hours (acute) after the microinjection, tissue damage, motoneuron loss, and spinal cord swelling were observed on sections stained with cresyl violet. Luxol fast blue staining further showed that acrolein injection resulted in dose-dependent demyelination. At 8 weeks (chronic) after the microinjection, cord shrinkage, astrocyte activation, and macrophage infiltration were observed along with tissue damage, neuron loss, and demyelination. These pathological changes resulted in behavioral impairments as measured by both the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale and grid walking analysis. Electron microscopy further demonstrated that acrolein induced axonal degeneration, demyelination, and macrophage infiltration. These results, combined with our previous reports, strongly suggest that acrolein may play a critical causal role in the pathogenesis of SCI and that targeting acrolein could be an attractive strategy for repair after SCI.