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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

1
Department of Radiation Oncology & Research Unit, Dr Negrín University Hospital, 35020 Las Palmas, Canary Islands, Spain. bernardinoclavo@terra.es

Abstract

PURPOSE:

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).

METHODS:

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.

RESULTS:

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%.

CONCLUSIONS:

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.

PMID:
19499176
DOI:
10.1007/s00701-009-0400-8
[Indexed for MEDLINE]

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