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64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

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Focal hypermetabolism in 18F-FDG PET indicates neuroinflammation and potential of postsurgical recovery in cervical myelopathy

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  • Frank W. Floeth - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Klinik für Wirbelsäule und Schmerz, St.-Vinzenz Krankenhaus, Düsseldorf
  • Karl-Josef Langen - Institut für Neurowissenschaften und Medizin, Forschungszentrum Jülich, Jülich
  • Norbert Galldiks - Institut für Neurowissenschaften und Medizin, Forschungszentrum Jülich, Jülich; Neurologische Klinik, Universität zu Köln, Köln
  • Sven Eicker - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Klinik für Neurochirurgie, Universitätsklinik Hamburg Eppendorf
  • Hans-Jakob Steiger - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf
  • Jörg Herdmann - Neurochirurgische Klinik, Heinrich-Heine-Universität, Düsseldorf; Klinik für Wirbelsäule und Schmerz, St.-Vinzenz Krankenhaus, Düsseldorf

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMO.02.02

doi: 10.3205/13dgnc011, urn:nbn:de:0183-13dgnc0110

Published: May 21, 2013

© 2013 Floeth et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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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.