Page 225 - ILAE_Lectures_2015

clinical series indicate that 18FDG-PET does not appear to provide additional clinically
useful information in the majority of patients with frontal lobe epilepsy.

Malformations of cortical development

Glucose metabolism has been detected using 18FDG-PET in the layers of ectopic neurones in
band heterotopia154 and in heterotopic nodules and displaced grey matter155,156, implying
synaptic activity. Cognitive activation tasks using H215O PET, in patients with MCD have
shown that heterotopia and malformed cortex may participate in higher cerebral functions,
but also showed widespread atypical cortical organisation, indicating that there may be
extensive disorganisation of normal structure-function correlates in these patients, that would
have implications for the planning of any surgical resection157,158.

Conclusion

Studies with 18FDG-PET have defined the major cerebral metabolic associations and
consequences of epilepsy but the data are non-specific with regard to aetiology and
abnormalities are more widespread than the pathological lesions. The place of the
investigation is in the presurgical work up of patients with refractory partial seizures and
normal or non-definitive MRI scans, or if data are discordant, in order to generate a
hypothesis that may then be tested with intracranial EEG recordings. Activation studies with
H215O may determine the functional anatomy of cerebral processes in both healthy and
pathological brains; but these studies are now increasingly performed with functional MRI.

POSITRON EMISSION TOMOGRAPHY STUDIES OF SPECIFIC LIGANDS

Positron emission tomography may be used to demonstrate the binding of specific ligands,
for example, 11C-flumazenil (FMZ) to the central benzodiazepine-GABAA receptor complex
(cBZR), 11C-diprenorphine and 11C-carfentanil to opiate receptors and 11C-deprenyl to MAO-
B. The technique is costly and scarce, but gives quantitative data with superior spatial
resolution to SPECT.

Central benzodiazepine receptors

The most important inhibitory transmitter in the central nervous system, gamma amino-
butyric acid (GABA) acts at the GABAA-central benzodiazepine receptor complex.
Flumazenil is a specific, reversibly bound antagonist at the alpha subunit types 1,2,3 and 5 of
the cBZR and 11C-FMZ is a PET ligand that acts as a useful marker of the GABAA-cBZR
complex in vivo.

Comparative studies with 18FDG-PET scans have shown the area of reduced 11C-FMZ
binding to be more restricted than is the area of reduced glucose metabolism in TLE138,139,159-
161. Patients who were seizure free after neocortical resection had smaller non-resected cortex
with preoperative FMZ PET abnormalities. In contrast there were no significant correlations
between non-resected FDG PET abnormalities and outcome. This implied that abnormalities
of FMZ PET indicated epileptic tissue, whereas FDG PET abnormalities were not so
predictive140.

In patients with unilateral HS, reduction of cBZR binding was initially thought to be confined
to the sclerotic hippocampus162. A combination of voxel-based and partial volume corrected
regional analyses, however, detected extrahippocampal abnormalities of cBZR binding in
50% patients with HS, and identified bilateral hippocampal abnormalities of cBZR in one-