Upper extremity palsy following cervical decompression surgery results from a transient spinal cord lesion

• Published in: Spine (Philadelphia, Pa. 1976) Vol. 32; no. 6; p. E197
• Main Authors: Hasegawa, Kazuhiro, Homma, Takao, Chiba, Yoshikazu
• Format: Journal Article
• Language: English
• Published: United States 15.03.2007
• Subjects: Age Factors; Aged; Cervical Vertebrae - surgery; Decompression, Surgical - adverse effects; Female; Follow-Up Studies; Humans; Incidence; Japan - epidemiology; Logistic Models; Magnetic Resonance Imaging; Male; Myelography; Odds Ratio; Paralysis - epidemiology; Paralysis - etiology; Paralysis - physiopathology; Predictive Value of Tests; Reperfusion Injury - epidemiology; Reperfusion Injury - etiology; Reperfusion Injury - physiopathology; Retrospective Studies; Risk Assessment; Risk Factors; Severity of Illness Index; Spinal Cord Compression - diagnosis; Spinal Cord Compression - pathology; Spinal Cord Compression - surgery; Spinal Cord Injuries - complications; Spinal Cord Injuries - epidemiology; Spinal Cord Injuries - etiology; Spinal Fusion; Time Factors; Tomography, X-Ray Computed; Treatment Outcome; Upper Extremity - physiopathology; Japan
• ISSN: 1528-1159
• DOI: 10.1097/01.brs.0000257576.84646.49

Retrospective analysis. To test the hypothesis that spinal cord lesions cause postoperative upper extremity palsy. Postoperative paresis, so-called C5 palsy, of the upper extremities is a common complication of cervical surgery. Although there are several hypotheses regarding the etiology of C5 palsy, convincing evidence with a sufficient study population, statistical analysis, and clear radiographic images illustrating the nerve root impediment has not been presented. We hypothesized that the palsy is caused by spinal cord damage following the surgical decompression performed for chronic compressive cervical disorders. The study population comprised 857 patients with chronic cervical cord compressive lesions who underwent decompression surgery. Anterior decompression and fusion was performed in 424 cases, laminoplasty in 345 cases, and laminectomy in 88 cases. Neurologic characteristics of patients with postoperative upper extremity palsy were investigated. Relationships between the palsy, and patient sex, age, diagnosis, procedure, area of decompression, and preoperative Japanese Orthopaedic Association score were evaluated with a risk factor analysis. Radiographic examinations were performed for all palsy cases. Postoperative upper extremity palsy occurred in 49 cases (5.7%). The common features of the palsy cases were solely chronic compressive spinal cord disorders and decompression surgery to the cord. There was no difference in the incidence of palsy among the procedures. Cervical segments beyond C5 were often disturbed with frequent multiple segment involvement. There was a tendency for spontaneous improvement of the palsy. Age, decompression area (anterior procedure), and diagnosis (ossification of the posterior longitudinal ligament) are the highest risk factors of the palsy. The results of the present study support our hypothesis that the etiology of the palsy is a transient disturbance of the spinal cord following a decompression procedure. It appears to be caused by reperfusion after decompression of a chronic compressive lesion of the cervical cord. We recommend that physicians inform patients and surgeons of the potential risk of a spinal cord deficit after cervical decompression surgery.