Delayed Neurologic Deficit after Thoracolumbar Kyphosis Correction: One Case Report

Study design: Case Report. Objective: To present one case suffering from delayed neurologic deficit after kyphosis deformity correction and analyze its potential etiological factors, how to identify and treat it. Summary of background data: Tardive neurologic deficits occur much less than acute ones after corrections of spinal deformities. Currently some risk factors, such as postoperative hypotension, deformity severity, and intraoperative haemorrhage are considered to be related with its occurrence and worsening though the true mechanisms are not clear. Extrinsic cord compression should be excluded by radiographic examinations before conservative treatments, such as improving blood perfusion, eliminating cord edema, suppressing local inflammation; promoting neurite outgrowth can be applied. If these don’t lead to functional recovery of spinal cord, emergency operation returning the cord to its former kyphotic position can also be considered. Methods: This 44 year-old female patient demonstrated thoracolumbar kyphosis of 136.9° combined with incompetence of spinal cord before operation, and underwent posterior vertebra column resection with the kyphotic correction of 68.8°. No neurologic dysfunction was found during operation. Results: Neurologic deficit appeared on the sixth day after operation, showing motion disability and sensation weakening of both lower extremities. Imaging examinations failed to reveal mechanical compression, such as haematoma or displaced implant. After use of glucocorticoid, gamma globulin, monosialotetrahexosylganglioside, alprostadil and rehabilitation therapies, her myodynamia of both lower extremities recovered greatly, especially muscles extensor, however, her sensation didn’t ameliorate. Conclusions: Delayed-onset neurologic deficit is rarely seen. Detailed history collection and meticulous physical examination are strongly recommended. Early identification and correct treatments can avert incomplete spinal cord from permanent damage.