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  • Title: [Morphological and functional neuro-imaging of surgical partial epilepsies in adults].
    Author: Mauguière F, Ryvlin P.
    Journal: Rev Neurol (Paris); 1996; 152(8-9):501-16. PubMed ID: 8991172.
    Abstract:
    This article reviews literature on morphological and functional neuro-imaging data in refractory partial epilepsies of adults including Magnetic Resonance Imaging (MRI); Single Photon Emission Computerised Tomography (SPECT) and Positron Emission Tomography (PET). Except for MRI, which is of unquestionable utility in the diagnosis of epileptogenic lesions, most of these investigations are justified only in the context of pre-operative evaluation of candidates to functional neurosurgery. In terms of interpretation the key issue is that of the relation between the images and the epileptogenic process itself. The specific utility of available techniques is as follows: MRI, in its present state of development, reveals a morphological abnormality in more than 80% of the cases previously considered as cryptogenic on the basis of X ray Computerised Tomography. However, hippocampal atrophy, which has a questionable relation with temporal lobe seizures, represents two thirds of abnormal images. Functional MRI and MR spectroscopy represent potential alternatives respectively to Wada test and interictal SPECT or PET. Ictal blood flow studies during video-EEG monitoring represent the major application of SPECT; showing a focal increase of blood flow in more than 90% of cases. Interictal SPECT is less informative, but necessary for interpreting ictal images. 18F-Deoxyglucose (FDG) PET shows a focal interictal hypometabolism in nearly 90% of patients with refractory temporal lobe epilepsy. The incidence of interictal hypometabolism is less, though more than 50%, in the other types of partial epilepsies. For diagnostic purpose PET studies of benzodiazepine (BZD)-receptors with 11C-Flumazenil are more widely used than those of opiate or mucarinic receptors. The reduced density of BZD receptors is likely to reflect neuronal loss, whereas interictal glucose hypometabolism reflects both the lesional process and secondary deactivation of perilesional areas due to anatomical or functional deafferentation.
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