FREQUENCY AND CHARACTERISTICS OF DUAL PATHOLOGY IN PATIENTS WITH LESIONAL EPILEPSY

Citation
F. Cendes et al., FREQUENCY AND CHARACTERISTICS OF DUAL PATHOLOGY IN PATIENTS WITH LESIONAL EPILEPSY, Neurology, 45(11), 1995, pp. 2058-2064
Citations number
65
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
45
Issue
11
Year of publication
1995
Pages
2058 - 2064
Database
ISI
SICI code
0028-3878(1995)45:11<2058:FACODP>2.0.ZU;2-5
Abstract
We studied 167 patients who had identifiable lesions and temporal or e xtratemporal partial epilepsy. Pathology included neuronal migration d isorders (NMIDs) (48), low-grade tumors (52), vascular malformations ( 34), porencephalic cysts (16), and gliotic lesions as a result of cere bral insults early in life (17). MRI volumetric studies using thin (1. 5- or 3-mm) coronal images were performed in all patients and in 44 ag e-matched normal controls. An atrophic hippocampal formation (HF), ind icating dual pathology, was present in 25 patients (15%). Abnormal HF volumes were present in those with lesions involving temporal (17%) bu t also extratemporal (14%) areas. Age at onset and duration of epileps y did not influence the presence of HF atrophy. However, febrile seizu res in early childhood were more frequently, although not exclusively, found in patients with hippocampal atrophy. The frequency of hippocam pal atrophy in our patients with low-grade tumors (2%) and vascular le sions (9%) was low. Dual pathology was far more common in patients wit h NMDs (25%), porencephalic cysts (31%), and reactive gliosis (23.5%). Some structural lesions, such as NMDs, are more likely to be associat ed with hippocampal atrophy, independent of the distance of the lesion from the HF. In other types of lesions, such as vascular malformation s, dual pathology was found when the lesion was close to the HF. A com mon pathogenic mechanism during pre- or perinatal development may expl ain the occurrence of concomitant mesial temporal sclerosis and other structural lesions because of either (1) associated developmental abno rmalities or (2) predisposition to prolonged febrile convulsions. Furt her clarification of this issue would improve our understanding of the pathogenesis of mesial temporal sclerosis and lead to more efficient planning of surgical treatment for lesional epilepsy.