F. Mauguiere et P. Ryvlin, MORPHOLOGICAL AND FUNCTIONAL NEURO-IMAGIN G IN REFRACTORY PARTIAL EPILEPSIES OF ADULTS, Revue neurologique, 152(8-9), 1996, pp. 501-516
This article reviews literature on morphological and functional neuro-
imaging data in refractory partial epilepsies of adults including Magn
etic Resonance Imaging (MRI), Single Photon Emission Computerised Tomo
graphy (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 contex
t of pre-operative evaluation of candidates to functional neurosurgery
. In terms of interpretation the key issue is that of the relation bet
ween the images and the epileptogenic process itself. The specific uti
lity 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 ra
y Computerised Tomography. However, hippocampal atrophy, which has a q
uestionable relation with temporal lobe seizures, represents two third
s of abnormal images. Functional MRI and MR spectroscopy represent pot
ential alternatives respectively to Wada test and interictal SPECT or
PET. Ictal blood flow studies during video-LEG monitoring represent th
e major application of SPECT; showing a focal increase of blood flow i
n more than 90 % of cases. Interictal SPECT is less informative, but n
ecessary for interpreting ictal images. F-18-Deoxyglucose (FDG) PET sh
ows a focal interictal hypometabolism in nearly 90 % of patients with
refractory temporal lobe epilepsy. The incidence of interictal hypomet
abolism is less, though more than 50 %, in the other types of partial
epilepsies. For diagnostic purpose PET studies of benzodiazepine (BZD)
- receptors with C-11-Flumazenil are more widely used than those of op
iate or mucarinic receptors. The reduced density of BZD receptors is l
ikely to reflect neuronal loss, whereas interictal glucose hypometabol
ism reflects both the lesional process and secondary deactivation of p
erilesional areas due to anatomical or functional deafferentation.