We hypothesized that in patients with intracerebral tumours a subcortical metabolical shift may be present when the underlying pathology can, itself, be the epileptogenic focus. We also assumed that by studying the alterations in glucose metabolism beyond the tumour's borders we could identify a modulator area.
Sixty-seven patients with supratentorial brain tumour associated epilepsy were investigated interictally, in normoglycaemic conditions, by using [18F]fluorodeoxyglucose positron emission tomography (FDG PET). The studies were analysed semiquantitatively by calculating standardized uptake values and asymmetry indices. Normal subjects and patients with non-epileptic brain lesions were used as controls.
Compared to normal controls frontal and temporal tumours showed significant changes in thalamic FDG uptake, which reflected hypometabolism of the affected side. It was noted in occipito-medial cortex in temporal tumours and in lentiform nucleus in frontal tumours as well. Comparison to lesional brains only proved that there was significant hypometabolism in lentiform nucleus in temporal tumours.
The quantified values obviously reflect biological changes. The observed subcortical hypometabolism is most likely secondary to underlying pathology. Although seizures in tumorous patients do not originate from subcortical structures their influence on cortical sites of seizure initiation could be explained by defective subcortical regulation of cortical excitability.