The aim of this study was to prospectively assess the regional changes of glucose metabolism of the cervical spinal cord in patients with degenerative cervical spine stenosis and symptomatic cervical myelopathy after decompressive surgery using 18 F-FDG PET. Methods: Twenty patients with symptomatic degenerative monosegmental cervical stenosis with neuroradiologic signs of spinal cord compression underwent decompressive surgery. The clinical course using a functional status score (Japanese Orthopedic Association [JOA] score), 18 F-FDG uptake, and MR imaging were assessed before and at follow-up 12 mo after surgery. Pre-and postoperative changes of 18 F-FDG PET were correlated to the patients' clinical outcome. Results: Ten patients demonstrated preoperatively a focally increased 18 F-FDG uptake at the level of the stenosis. At follow-up, the uptake declined significantly (P 5 0.008), and a significant improvement of JOA scores (P , 0.001) could be observed. The remaining 10 patients were characterized preoperatively by an inconspicuous glucose uptake at the level of cord compression in combination with a poststenotic decrease of 18 F-FDG uptake. At follow-up, both JOA scores and 18 F-FDG uptake changed insignificantly. Conclusion: Focal glucose hypermetabolism at the level of cervical spinal cord compression may predict an improved outcome after surgical decompression. Thus, this finding on 18 F-FDG PET suggests a functional damage in a reversible phase of cervical myelopathy. Compr ession of the cervical spinal cord due to degenerative cervical spine stenosis induces a progressive dysfunction of the myelon with subsequent neurologic deficits (i.e., cervical myelopathy) (1,2). MR imaging offers an exact morphologic visualization of the stenosis and the cord compression. However, there is no clear correlation between radiologic signs and clinical aspects of cervical myelopathy (3-6). Patients with severe stenosis and hyperintense signal alterations on T2-weighted MR images can lack any symptoms, and the degree of spinal cord compression correlates neither with the neurologic deficits nor with the recovery after surgical decompression (3-6). Therefore, mechanical compression of the cervical spinal cord alone seems not to be the essential factor for the development of myelopathy. Other factors such as a compression-induced neuroinflammation have been recently discussed (7-9).Given the limitations of conventional MR imaging in prediction of clinical outcome in patients with cervical myelopathy, 18 F-FDG PET has been used for metabolic assessment of the healthy, noncompressed cervical spinal cord (10-14) as well of the affected spinal cord (13). In a previous publication (15), we reported preliminary results of this prospective study on 18 F-FDG uptake in 20 patients with compression of the cervical spinal cord due to degenerative cervical spine stenosis and cervical myelopathy. In the present work, we report the final results including pre-and postoperative data of MR imaging and 18 F-FDG PET as well as the clinical...