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White cord syndrome following posterior decompression and fusion for severe OPLL and an acute traumatic cervical injury – A case report and review of literature

BACKGROUND: White cord syndrome (WCS) refers to the observation of intramedullary hyperintensity due to edema/ischemia and swelling on postoperative T2-weighted MRI sequences in the setting of unexplained neurological deficits after cervical spinal cord decompression. Pathophysiologically, WCS/reper...

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Detalles Bibliográficos
Autores principales: Dahapute, Aditya Anand, Balasubramanian, Sai Gautham, Annis, Prokopis
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Scientific Scholar 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699864/
https://www.ncbi.nlm.nih.gov/pubmed/36447894
http://dx.doi.org/10.25259/SNI_692_2022
Descripción
Sumario:BACKGROUND: White cord syndrome (WCS) refers to the observation of intramedullary hyperintensity due to edema/ischemia and swelling on postoperative T2-weighted MRI sequences in the setting of unexplained neurological deficits after cervical spinal cord decompression. Pathophysiologically, WCS/reperfusion injury (RPI) occurs due to oxygen derived free radicals as a result of acute reperfusion or direct trauma from blood flow itself. Intraoperative neurophysiologic monitoring (IONM) can give early warning and detect neurologic deficits. Here, we are presenting a case of a patient who had a chronic severe ossification of posterior longitudinal ligament (OPLL) of cervical cord, underwent decompressive surgery, and developed quadriplegia postoperatively without any perceptible iatrogenic cord trauma, documented by IONM and postoperative MRI with classical signs of WCS. CASE DESCRIPTION: A 63-year-old male presented with low velocity fall at home followed by quadriparesis. X-ray images on presentation showed C6 fracture and local kyphosis. MRI images showed that there is marked spinal canal stenosis from C2 down to C4 due to OPLL with intrinsic signal changes in the cord. On decompression, motor-evoked potential signals were not present below C4. Immediate postoperative MRI was done to rule out any compressive pathology. MRI showed T2 hyperintensity of the cord at C3 level with cord edema. No evidence of epidural hematoma or other compressive lesion was found and the diagnosis of WCS/RPI was established. CONCLUSION: WCS is essentially a diagnosis of exclusion. Very rarely, patients sustain severe/new neurological deficits postoperatively attributed to WCS. Unless, this is confirmed postoperatively with classical MRI signs of intramedullary hyperintensity, the diagnosis should not be invoked.