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lüll Brain imaging in idiopathic generalized epilepsies Duncan JSEpilepsia 2005[]; 46 Suppl 9 (ä): 108-11While it is generally accepted that there is no neuroimaging abnormality in idiopathic generalized epilepsy (IGE), image processing and quantitative magnetic resonance imaging (MRI) studies suggest that there may be subtle structural abnormalities. Magnetic resonance spectroscopy indicates neuronal dysfunction with differing abnormalities in the IGE subsyndromes, and high concentrations of glutamate and glutamine have been inferred in the frontal lobes, and low gamma-aminobutyric acid levels in the occipital lobe. Studies of cerebral blood distribution at the time of absences have given complex results. The general consensus is of an increase in the thalamus and broad decreases in the neocortex, reflecting a suppression of neuronal activity, but with some increases, that may indicate focal areas of activation. Positron emission tomography (PET) ligand studies with an opioid tracer have inferred neocortical release of endogenous opioids at the time of serial absences. In combination with neurophysiological methods, PET studies with specific ligands have the potential to clarify the functional anatomy and neurochemical circuits that underlie IGE.|*Magnetic Resonance Imaging[MESH]|*Magnetic Resonance Spectroscopy[MESH]|*Positron-Emission Tomography[MESH]|*Tomography, Emission-Computed, Single-Photon[MESH]|Brain Mapping[MESH]|Brain/diagnostic imaging/metabolism/*pathology[MESH]|Cerebrovascular Circulation/physiology[MESH]|Epilepsy, Generalized/*diagnosis/diagnostic imaging/metabolism[MESH]|Fluorodeoxyglucose F18[MESH]|Glucose/metabolism[MESH]|Humans[MESH]|Oxygen/blood[MESH]|Receptors, GABA-A/metabolism[MESH]|Receptors, Opioid/metabolism[MESH]|Technetium Tc 99m Exametazime[MESH] |