gms | German Medical Science

Objective: The impact of glucose uptake using ¹⁸F-FDG PET regarding the functional recovery after decompressive surgery and the pathophysiologic role of compression induced local neuroinflammation of the spinal cord in patients with degenerative cervical spine stenosis and myelopathy was determined.

Method: 23 patients with degenerative cervical stenosis with both, clinical symptoms and neuroradiological signs (e.g., intramedullary hyperintensity on T2-weighted MRI) of spinal cord compression were included. 20 patients underwent decompressive surgery. Clinical course using a functional status score (JOA score), maximal standardized uptake values (SUV) of ¹⁸F-FDG uptake, and MRI were assessed before and 12 months after operation. Three patients refused surgery and the impact of a steroid medication alone to myelopathic symptoms and the changes of glucose uptake in PET were monitored.

Results: A complete decompression of the stenosis with a release of the cervical spinal cord were documented by postoperative MRIs in all surgical patients. PET imaging identified two pattern of disturbed glucose metabolism: One group (n=10) demonstrated preoperatively a focally increased ¹⁸F-FDG uptake at the level of the stenosis (SUV 2.3 ± 0.4). At follow-up, the uptake declined significantly (SUV 1.9 ± 0.5; P = 0.008) and these patients experienced a significant clinical recovery (pre- vs. postoperative JOA score: 9.5 ± 2.5 vs. 14.6 ± 1.7; P < 0.001).

The other group (n=10) was characterized preoperatively by an inconspicuous glucose uptake at the level of cord compression (SUV, 1.9 ± 0.2). At follow-up, the ¹⁸F-FDG uptake didn't change (SUV 1.8 ± 0.3; P = 0.031) and no relevant clinical improvement was observed (pre- vs. postoperative JOA score: 11.6 ± 2.5 vs. 12.2 ± 2.4; P = 0.081).

Dexamethasone medication in the three non-surgical patients led to transient clinical improvement and normalization of the locally increased ¹⁸F-FDG uptake in PET control.

Conclusions: Focal glucose hypermetabolism at the level of cord compression predicts an improved outcome after surgical decompression suggesting a functional damage in a reversible phase of myelopathy. In contrast, a lack of hypermetabolism predicts a poor recovery potential and suggests irreversible structural damage of the spinal cord. Focal hypermetabolism appears to occur temporarily and might reflect a compression-induced inflammatory response with intramedullary infiltration of glucose-consuming macrophages, which can be suppressed with steroids.