N-acetylaspartate in the motor and sensory cortices following functional recovery after surgery for cervical spondylotic myelopathy.

Abstract

OBJECTIVE Cervical spondylotic myelopathy (CSM) is the most common cause of reversible spinal cord dysfunction in people over the age of 55 years. Following surgery for symptomatic CSM, patients demonstrate motor improvement early in the postoperative course, whereas sensory improvement can lag behind. The authors of the present study hypothesized that changes in the concentration of N-acetylaspartate (NAA) in the motor and sensory cortices in the brain would emulate the time course of neurological recovery following decompression surgery for CSM. Their aim was to compare and contrast how metabolite levels in the motor and sensory cortices change after surgery to reverse downstream spinal cord compression. METHODS Twenty-four patients with CSM and 8 control subjects were studied using proton MR spectroscopy (1H-MRS) images acquired on a 3.0-T Siemens MRI unit. The 1H-MRS data (TE 135 msec, TR 2000 msec) were acquired to measure absolute levels of NAA from the motor and sensory cortices in the cerebral hemisphere contralateral to the side of greater deficit at baseline in each subject. Data were also acquired at 6 weeks and 6 months following surgery. Control subjects were also evaluated at 6 weeks and 6 months following baseline data acquisition. Neurological function was measured in each subject at all time points using the Neck Disability Index (NDI), modified Japanese Orthopaedic Association (mJOA) questionnaire, and the American Spinal Injury Association (ASIA) neurological classification. RESULTS In the motor cortex of patients, NAA levels decreased significantly (p < 0.05) at 6 weeks and 6 months postsurgery compared with baseline levels. In the sensory cortex of patients, NAA levels decreased significantly (p < 0.05) only at 6 months after surgery compared with baseline and 6-week levels. No significant changes in NAA were found in control subjects. Clinical scores demonstrated significant (p < 0.05) motor recovery by 6 weeks, whereas sensory improvements (p < 0.05) appeared at only 6 months. CONCLUSIONS Findings suggest that metabolite changes in both the motor and sensory cortices mimic the time course of functional motor and sensory recovery in patients with CSM. The temporal course of neurological recovery may be influenced by metabolic changes in respective cortical regions.