STUDY DESIGN: A retrospective study was conducted to investigate patients in whom segmental motor paralysis developed after expansive open-door laminoplasty for cervical myelopathy. OBJECTIVE: To propose the involvement of the spinal cord as a possible mechanism in the development of segmental motor paralysis. SUMMARY OF BACKGROUND DATA: Segmental motor paralysis is seen occasionally in patients who undergo expansive open-door laminoplasty for cervical myelopathy, and has long been attributed to nerve root lesions caused by either traumatic surgical techniques or a tethering effect induced by excessive posterior shift of the spinal cord after decompression. Involvement of spinal cord pathology is not suggested in the English literature. METHODS: The study group consisted of 15 patients (11 men and 4 women) in whom postoperative segmental motor paralysis developed after expansive open-door laminoplasty during a minimum follow-up of 2 years. Their average age at the time of surgery was 56 years. Characteristics of the paralysis, clinical symptoms, recovery rates calculated using pre- and postoperative Japanese Orthopedic Association scores, and radiographic findings including pre- and postoperative magnetic resonance images were analyzed retrospectively and compared with those of 126 patients without segmental paralysis who underwent expansive open-door laminoplasty. RESULTS: The paralysis occurred mainly, but not only, at C5, and eight patients had multilevel involvements predominantly in the hinge side, whereas two patients had paralysis on both sides. The paralysis had developed after an average of 4.6 days. Of the 15 patients, 14 reported severe numbness or dysesthesia in their hands before surgery, and their average recovery rate for upper extremity sensory disturbance was lower than for those without paralysis. Postoperative magnetic resonance imaging showed the presence of a T2 high-signal intensity zone in the spinal cord of all the patients. The level of such abnormal signal areas corresponded to the level of paralyzed segments in 10 of the 15 patients. Paralysis resolved completely in 11 patients. CONCLUSIONS: Delayed onset of paralysis, dysesthesiain the upper extremities, and the presence of T2 high-signal intensity zones suggest that a certain impairment in the gray matter of the spinal cord may play an important role in the development of postoperative segmental motor paralysis.
STUDY DESIGN: A retrospective study was conducted to investigate patients in whom segmental motor paralysis developed after expansive open-door laminoplasty for cervical myelopathy. OBJECTIVE: To propose the involvement of the spinal cord as a possible mechanism in the development of segmental motor paralysis. SUMMARY OF BACKGROUND DATA: Segmental motor paralysis is seen occasionally in patients who undergo expansive open-door laminoplasty for cervical myelopathy, and has long been attributed to nerve root lesions caused by either traumatic surgical techniques or a tethering effect induced by excessive posterior shift of the spinal cord after decompression. Involvement of spinal cord pathology is not suggested in the English literature. METHODS: The study group consisted of 15 patients (11 men and 4 women) in whom postoperative segmental motor paralysis developed after expansive open-door laminoplasty during a minimum follow-up of 2 years. Their average age at the time of surgery was 56 years. Characteristics of the paralysis, clinical symptoms, recovery rates calculated using pre- and postoperative Japanese Orthopedic Association scores, and radiographic findings including pre- and postoperative magnetic resonance images were analyzed retrospectively and compared with those of 126 patients without segmental paralysis who underwent expansive open-door laminoplasty. RESULTS: The paralysis occurred mainly, but not only, at C5, and eight patients had multilevel involvements predominantly in the hinge side, whereas two patients had paralysis on both sides. The paralysis had developed after an average of 4.6 days. Of the 15 patients, 14 reported severe numbness or dysesthesia in their hands before surgery, and their average recovery rate for upper extremity sensory disturbance was lower than for those without paralysis. Postoperative magnetic resonance imaging showed the presence of a T2 high-signal intensity zone in the spinal cord of all the patients. The level of such abnormal signal areas corresponded to the level of paralyzed segments in 10 of the 15 patients. Paralysis resolved completely in 11 patients. CONCLUSIONS: Delayed onset of paralysis, dysesthesiain the upper extremities, and the presence of T2 high-signal intensity zones suggest that a certain impairment in the gray matter of the spinal cord may play an important role in the development of postoperative segmental motor paralysis.