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Spinal Cord Reperfusion Injury: Case Report, Review of the Literature, and Future Treatment Strategies

A rare complication of cervical spine decompression is acute paralysis following the procedure. This neurologic deficit is thought to be due to reperfusion injury of a chronically ischemic spinal cord and is referred to as "white cord syndrome" given the pathognomonic finding of hyperinten...

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Detalles Bibliográficos
Autores principales: Wiginton, James G, Brazdzionis, James, Mohrdar, Cyrus, Sweiss, Raed, Lawandy, Shokry
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6764611/
https://www.ncbi.nlm.nih.gov/pubmed/31576271
http://dx.doi.org/10.7759/cureus.5279
Descripción
Sumario:A rare complication of cervical spine decompression is acute paralysis following the procedure. This neurologic deficit is thought to be due to reperfusion injury of a chronically ischemic spinal cord and is referred to as "white cord syndrome" given the pathognomonic finding of hyperintensity on T2-weighted MRI. Three prior cases have been reported. We present a case of transient quadriplegia following posterior cervical decompression. A 41-year-old male with cervical spondylotic myelopathy presented with bilateral progressive upper extremity weakness, hyperreflexia, and cervical spine MRI showing severe cord compression at C1 and partial hyperintense signal. Intraoperatively, after C1 bony decompression and without perceptible technical cause, the patient experienced a complete loss of both somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) with an eventual return to baseline prior to completing the operation. The patient awoke from surgery with acute quadriplegia without perceptible technical cause (intraoperative compression or evident anatomic compromise). An immediate postoperative MRI revealed a more pronounced hyperintensity in the central cervical cord on T2-weighted sequences. Treatment with increased mean arterial pressure (MAP) therapy and dexamethasone resulted in the patient regaining some movement over a period of hours and full strength over a period of months. The mechanism of acute weakness following cervical spine decompression in the absence of perceptible technical cause is not fully understood, but current theory suggests that a reperfusion injury is most likely the cause. It remains a diagnosis of exclusion. Familiarity with this potential postoperative complication can aid in appropriate postoperative therapy with early diagnosis and intervention leading to restored spinal cord function and excellent prognosis.