'White cord syndrome', a rare but disastrous complication of transient paralysis after posterior cervical decompression for severe cervical spondylotic myelopathy and spinal stenosis: A case report.

Abstract

Transient paralysis following spinal decompression surgery is a rare but devastating postoperative complication. Spinal cord ischemia-reperfusion injury has been identified as one of the crucial pathogenic factors contributing to the sudden neurological deterioration associated with spinal decompression surgery. ‘White cord syndrome’ is a characteristic imaging manifestation of spinal cord ischemia-reperfusion injury, referring to high intramedullary signal changes in the sagittal T2-weighted MRI scan with unexplained neurological deficits following surgical decompression. The present study reported on the case of a 51-year old male patient who suffered from acute left limb hemiplegic paralysis following posterior cervical laminectomy decompression for severe cervical spondylotic myelopathy and spinal stenosis, which were caused by ossification of the posterior longitudinal ligament. The patient's neurological function gradually improved after the immediate administration of high-dose methylprednisolone therapy combined with mannitol and neurotrophic drugs. At the 2-month follow-up, the intensity of the spinal cord signal on MRI had almost returned to normal and the ‘white cord syndrome’ had disappeared. However, the patient complained of postoperative neck swelling pain caused by cerebrospinal fluid leakage; therefore, an additional cerebrospinal fluid leakage exploration and neoplasty were performed. At 2 weeks after the second surgery, the patient's neck swelling pain was relieved and the area of cerebrospinal fluid leakage was significantly reduced. Despite the low incidence rate, surgeons should be aware of this complication, particularly when treating chronic severe cervical spinal stenosis with anterior or posterior decompression. Once transient paralysis occurs, early diagnosis and interventions are essential to reverse the neurological deficit.