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Eur Spine J. 2013 Sep;22(9):2057-61. doi: 10.1007/s00586-013-2829-y. Epub 2013 May 14.

Transient neurological deficit following midthoracic decompression for severe stenosis: a series of three cases.

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Hospital for Special Surgery, 535 East 70th Street, New York, NY, 10021, USA,



To report three cases of transient perioperative neurological deficit in the absence of direct cord insult following decompression of the severely stenotic thoracic spine.


The clinical and radiographic electronic medical records of three patients who underwent decompression for severe midthoracic stenosis with transient neurological deficits perioperatively were reviewed. The cases are presented with consideration of possible underlying mechanisms and multimodality intraoperative monitoring (IOM) findings.


Two patients had neurologic changes on IOM and Stagnara wake-up test, the remaining patient had absent motor and sensory potentials at baseline and throughout the case. IOM changes were observed immediately following decompression in the absence of direct cord insult or displacement. Postoperatively all patients experienced neurological motor deficits which presented as complete paralysis of the right lower extremity in two of the patients and the left lower extremity in one patient. The deficit was transient-improvement of motor strength occurred between 1 and 13 months of follow-up in all patients.


Decompression of a severely stenotic region of the thoracic spinal cord may lead to a complete yet transient motor deficit in the perioperative period in the absence of direct mechanical cord insult. Potential etiologies include ischemia-reperfusion injury, microthrombi, and altered perfusion due to internal recoil of spinal cord architecture following decompression. IOM may show conspicuous findings in such events, however, may not be relied upon when baseline potentials are sub-optimal. Recognition of this short-lived neurological deficit following decompression of the severely stenotic thoracic spine will improve preoperative patient counseling and merits further study for determination of the precise pathophysiology.

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