Mj. Fulham et al., DECREASED CEREBRAL GLUCOSE-METABOLISM IN PATIENTS WITH BRAIN-TUMORS -AN EFFECT OF CORTICOSTEROIDS, Journal of neurosurgery, 83(4), 1995, pp. 657-664
The authors measured cerebral glucose metabolism (CMR(glc)) using [F-1
8]fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) in pa
tients with brain tumors to evaluate the effect of exogenous corticost
eroids (in this instance, dexamethasone) on glucose metabolism. Fifty-
six FDG-PET studies obtained in 45 patients with unilateral supratento
rial brain tumors were analyzed. Patients with brain tumors were divid
ed into three groups: 1) patients with cushingoid symptoms, who had be
en treated with combinations of radiotherapy and chemotherapy taking o
ral dexamethasone; 2) patients not taking dexamethasone but treated wi
th radiotherapy; and 3) patients not taking dexamethasone who had not
been treated with radiotherapy. Serial FDG-PET scans were obtained in
eight of the cushingoid patients. Glucose metabolism was measured in t
he contralateral cerebral and ipsilateral cerebellar hemispheres in pa
tients and compared to measurements taken from 19 normal volunteers. T
he authors found that in the cushingoid brain tumor patients there was
a marked reduction in CMR(glc) compared to normal volunteers and othe
r brain tumor patients (Kruskal-Wallis test; p 0.001). In the majority
of patients who had serial FDG-PET scans, there was a decline in gluc
ose metabolism over time and in one patient, in whom dexamethasone was
reduced in dosage, there was a subsequent increase in CMR The authors
conclude that there is a generalized reduction in CMR in brain tumor
patients taking dexamethasone compared to other brain tumor patients a
nd normal volunteers, and that this effect is independent of radiother
apy, concurrent anticonvulsant medication: acid transhemispheric funct
ional disconnection (transhemispheric diaschisis).