Cervical Spondylotic Myelopathy: Metabolite Changes in the Primary Motor Cortex after Surgery.
Purpose To characterize longitudinal metabolite alterations in the motor cortex of patients with cervical spondylotic myelopathy (CSM) by using proton magnetic resonance (MR) spectroscopy and to evaluate white matter integrity with diffusion-tensor imaging in patients who are recovering neurologic function after decompression surgery. Materials and Methods Informed written consent was obtained for all procedures and the study was approved by Western University's Health Sciences Research Ethics Board. Twenty-eight patients with CSM and 10 healthy control subjects were prospectively recruited and underwent two separate 3-T MR imaging examinations 6 months apart. Patients with CSM underwent surgery after the first examination. N-acetylaspartate (NAA), an indicator of neuronal mitochondrial function, normalized to creatine (Cr) levels were measured from the motor cortex contralateral to the greater functional deficit side in the patient group and on both sides in the control group. Fractional anisotropy and mean diffusivity were measured by means of diffusion-tensor imaging in the white matter adjacent to the motor and sensory cortices of the hand and the entire cerebral white matter. Clinical data were analyzed by using Student t tests. Results In patients with CSM, NAA normalized to Cr (NAA/Cr) levels were significantly lower 6 months after surgery (1.48 ± 0.08; P < .03) compared with preoperative levels (1.73 ± 0.09), despite significant improvement in clinical questionnaire scores. Fractional anisotropy and mean diffusivity were the same (P > .05) between the patient and control groups in all measured regions at all time points. Conclusion NAA/Cr levels decreased in the motor cortex in patients with CSM 6 months after successful surgery. Intact white matter integrity with decreased NAA/Cr levels suggests that mitochondrial metabolic dysfunction persists after surgery.©RSNA, 2016 Online supplemental material is available for this article.
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Izabela
I
Aleksanderek
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Stuart M K
SM
McGregor
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Todd K
TK
Stevens
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Sandy
S
Goncalves
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Robert
R
Bartha
From the Department of Medical Biophysics (I.A., S.G., R.B., N.D.) and Centre for Functional and Metabolic Mapping, Robarts Research Institute (I.A., T.K.S., S.G., R.B.), University of Western Ontario, London, Ontario, Canada; and Department of Clinical Neurologic Sciences, Division of Neurosurgery, University Hospital, London Health Sciences Centre, 339 Windermere Rd, London, Ontario, Canada N6A 5A5 (S.M.K.M., N.D.).
Neil
N
Duggal
D016880:Anisotropy; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D002574:Cervical Vertebrae / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000601:surgery; D003401:Creatine / Q000378:metabolism*; D019299:Decompression, Surgical; D056324:Diffusion Tensor Imaging; D005260:Female; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009044:Motor Cortex / Q000000981:diagnostic imaging / Q000378:metabolism*; D011184:Postoperative Period; D011446:Prospective Studies; D013118:Spinal Cord Diseases / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000601:surgery; D055009:Spondylosis / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000601:surgery
D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine