Patterns of neurological deficits and recovery of postoperative C5 nerve palsy.

OBJECTIVE

Paresis of the C5 nerve is a well-recognized complication of cervical spine surgery. Numerous studies have investigated its incidence and possible causes, but the specific pattern and character of neurological deficits, time course, and relationship to preoperative cord signal changes remain incompletely understood.

METHODS

Records of patients undergoing cervical decompressive surgery for spondylosis, disc herniation, or ossification of the longitudinal ligament, including the C4-5 level, were reviewed from a 15-year period, identifying C5 palsy cases. Data collected included age, sex, diabetes and smoking statuses, body mass index, surgical levels, approach, presence of increased cord signal intensity, and modified Japanese Orthopaedic Association (mJOA) scores. Narrative descriptions of the patterns and findings on neurological examination were reviewed, and complications were noted. The minimum follow-up requirement for the study was 12 months.

RESULTS

Of 642 patients who underwent cervical decompressive surgery, 18 developed C5 palsy (2.8%). The incidence was significantly lower following anterior surgery (6 of 441 [1.4%]) compared with that following cervical laminectomy and fusion (12 of 201 [6.0%]) (p < 0.001). There were 10 men and 8 women whose mean age was 66.7 years (range 54-76 years). The mean preoperative mJOA score of 11.4 improved to 15.6 at the latest follow-up examination. There were no differences between those with and without C5 palsy with regard to sex, age, number of levels treated, or pre- or postoperative mJOA score. Fifteen patients with palsy (83%) had signal changes/myelomalacia on preoperative T2-weighted imaging, compared with 436 of 624 (70%) patients without palsy; however, looking specifically at the C4-5 level, signal change/myelomalacia was present in 12 of 18 (67%) patients with C5 palsy, significantly higher than in the 149 of 624 (24%) patients without palsy (p < 0.00003). Paresis was unilateral in 16 (89%) and bilateral in 2 (11%) patients. All had deltoid weakness, but 15 (83%) exhibited new biceps weakness, 8 (44%) had triceps weakness, and 2 (11%) had hand intrinsic muscle weakness. The mean time until onset of palsy was 4.6 days (range 2-14 days). Two patients (11%) complained of shoulder pain preceding weakness; 3 patients (17%) had sensory loss. Recovery to grade 4/5 deltoid strength occurred in 89% of the patients. No patient had intraoperative loss of somatosensory or motor evoked potentials or abnormal intraoperative C5 electromyography activity.

CONCLUSIONS

Postoperative C5 nerve root dysfunction appears in a delayed fashion, is predominantly a motor deficit, and weakness is frequently appreciated in the biceps and triceps muscles in addition to the deltoid muscle. Preoperative cord signal change/myelomalacia at C4-5 was a significant risk factor. No patient had a detectable deficit in the immediate postoperative period or changes in intraoperative neuromonitoring status. Neurological recovery to at least that of grade 4/5 occurred in nearly 90% of the patients.