Send to

Choose Destination
Acta Neurochir (Wien). 2009 Nov;151(11):1419-25. doi: 10.1007/s00701-009-0400-8. Epub 2009 Jun 5.

Modification of glucose metabolism in radiation-induced brain injury areas using cervical spinal cord stimulation.

Author information

Department of Radiation Oncology & Research Unit, Dr Negrín University Hospital, 35020 Las Palmas, Canary Islands, Spain.



Radiation-induced brain injury (RBI) is an insidious side-effect of radiotherapy mediated by vascular alterations, inflammation and ischaemia. In previous studies we had shown potential increases in loco-regional blood flow and glucose metabolism in brain tumours by using electrical cervical spinal cord stimulation (SCS). In this preliminary report we demonstrate the effect of cervical SCS on RBI-tissue metabolism, as assessed using [(18)F]fluorodeoxyglucose-positron emission tomography (FDG-PET).


SCS devices were inserted in eight patients with diagnosis of potential RBI in previously irradiated areas. While the SCS device was deactivated, each patient underwent an initial FDG-PET study to evaluate the clinical status. A second FDG-PET study was performed later the same day while the SCS device was activated in order to evaluate the effect of cervical SCS on glucose metabolism.


Basal glucose metabolism in RBI areas was 31% lower than peri-RBI areas (p = 0.009) and 32% lower than healthy contra-lateral areas (p = 0.020). There was a significant increase in glucose uptake during SCS in both the RBI (p = 0.005) and the peri-RBI (p = 0.004) areas, with measured increases of 38 and 42%, respectively. The estimated potential maximal residual activity of the first FDG dose's contribution to the activity on the second scan was <or=14.3 +/- 4.6%.


In this study using PET, SCS increased glucose metabolism in RBI and peri-RBI areas. These results warrant further clinical investigation to elucidate more fully the clinical usefulness of SCS in these patients.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center