Frequency and characteristics of dual pathology in patients with lesional epilepsy

Abstract

We studied 167 patients who had identifiable lesions and temporal or extratemporal partial epilepsy. Pathology included neuronal migration disorders (NMDs) (48), low-grade tumors (52), vascular malformations (34), porencephalic cysts (16), and gliotic lesions as a result of cerebral 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 age-matched normal controls. An atrophic hippocampal formation (HF), indicating dual pathology, was present in 25 patients (15%). Abnormal HF volumes were present in those with lesions involving temporal (17%) but also extratemporal (14%) areas. Age at onset and duration of epilepsy did not influence the presence of HF atrophy. However, febrile seizures in early childhood were more frequently, although not exclusively, found in patients with hippocampal atrophy. The frequency of hippocampal atrophy in our patients with low-grade tumors (2%) and vascular lesions (9%) was low. Dual pathology was far more common in patients with NMDs (25%), porencephalic cysts (31%), and reactive gliosis (23.5%). Some structural lesions, such as NMDs, are more likely to be associated with hippocampal atrophy, independent of the distance of the lesion from the HF. In other types of lesions, such as vascular malformations, dual pathology was found when the lesion was close to the HF. A common pathogenic mechanism during pre- or perinatal development may explain the occurrence of concomitant mesial temporal sclerosis and other structural lesions because of either (1) associated developmental abnormalities or (2) predisposition to prolonged febrile convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

Congenital destructive hemispheric lesions and epilepsy: clinical features and relevance of associated hippocampal atrophy

“…We have detected HA by visual analysis in 70% of the patients in the group of cystic lesions and in 77,7% in the group of atrophic lesions. Although the frequency of HA in both groups was much higher than in the series of Cendes et al 5 , we found no significant difference between our two groups.…”

“…A previous study in patients with temporal and extratemporal lesional epilepsy of different etiologies, showed that cystic and atrophic lesions had associated HA in 31 and 23.5% of patients respectively, suggesting a vascular pathogenesis to HA in these cases 5 . We have detected HA by visual analysis in 70% of the patients in the group of cystic lesions and in 77,7% in the group of atrophic lesions.…”

“…These insults result either in cystic or atrophic lesions commonly within a particular vascular distribution. The advances in neuroimaging techniques, particularly magnetic resonance imaging (MRI), turned it possible to re-evaluate the spectrum of structural brain abnormalities associated with the more obvious lesion (cystic or atroph) [3][4][5][6][7] . A striking association has been found between these lesions and atrophy of medial temporal structures, suggesting that they share a common pathogenic mechanism in these cases [5][6][7] .…”

Coexistent pathology in chronic epilepsy patients with neoplasms

“…[7][8][9][10] In a subset of these tumors, which are generally low-grade glial or glioneuronal neoplasms, multiple pathologies, which potentially may contribute to the genesis of these seizures, are identifiable (dual pathology). [11][12][13][14][15][16] Among these, there is a well-established association of certain neoplasms with malformations of cortical development (cortical dysplasia), particularly dysembryoplastic neuroepithelial tumors and gangliogliomas. [17][18][19][20] The purpose of this study is to systematically review one institution's experience with neoplasms associated with identifiable coexistent pathology arising in the setting of chronic epilepsy.…”

Temporal lobe epilepsy associated with 'triple pathology' of hippocampal sclerosis, focal cortical dysplasia and cavernoma in the ipsilateral frontal lobe

“…Using chronic subdural electrode recording, an interictal electrocorticogram (ECoG) demonstrated that the medial temporal lobe lesion and the FCD lesion exhibited independent paroxysmal discharges, while an ictal ECoG demonstrated that the medial temporal lobe was the ictal onset zone. We postulated that the FCD lesion Introduction 'Dual pathology' in patients with temporal lobe epilepsy (TLE) refers to the coexistence of hippocampal sclerosis (HS) and extrahippocampal lesions such as focal cortical dysplasias (FCD), vascular malformations including cavernoma (CA), and primary benign brain tumors including ganglioglioma, dysembryoplastic neuroepithelial tumors, pleomorphic xanthoastrocytomas, and low grade astrocytomas [1,2,3]. We report herein a rare case of TLE with triple pathology of HS, and FCD and CA in the ipsilateral frontal lobe.…”