Surgical treatment of limbic epilepsy associated with extrahippocampal lesions: the problem of dual pathology

Abstract

The authors present their review of 178 patients who underwent en bloc temporal lobectomies as surgical treatment for intractable epilepsy. Hippocampal cell density was quantitatively analyzed and the histology of the anterior temporal lobe was reviewed. Fifty-four patients (30.3%) had evidence of extrahippocampal lesions in addition to neuronal cell loss within the hippocampus (the dual pathology group). The pattern of cell loss was analyzed in the remaining 124 cases (69.7%) with no extrahippocampal pathology, and compared with that of the dual pathology group and a control group of four nonepileptic patients. Hippocampal cell loss was found in almost all epileptic patients compared to the control group. Severe cell loss greater than 30% of control values was found in 88.7% of patients without extrahippocampal lesions, but in only 51.8% of patients with dual pathology. The difference between these two groups was statistically significant (p less than 0.001). In the dual pathology group, lesions of different pathology had a significant relationship with the degree of hippocampal cell loss: all 12 patients with glioma had mild cell loss, whereas all 13 patients with heterotopia were associated with severe cell loss. Severity of hippocampal cell loss was also analyzed in relation to seizure history: a prior severe head injury was associated with severe cell loss. Other factors such as seizure duration, secondary generalization, or family history of seizures were not associated with hippocampal damage. Dual pathology may produce a combination of neocortical and temporolimbic epilepsies that warrants a precise definition of the true epileptogenic area prior to surgical treatment.

Behavioral, Psychotic, and Anxiety Disorders in Epilepsy: Etiology, Clinical Features, and Therapeutic Implications

“…Nevertheless, some authors hypothesized that patients with treatment-refractory epilepsy and Ammon's horn sclerosis are at reduced risk for psychosis (45,47,72). Patients with a history of febrile convulsions exhibit specific cell loss in the CA fields of the hippocampus (82,83). This great reduction in cells of these areas might provide some protection against overactivity of hippocampal neurons induced by interictal BEHA VIORA L, PSYCHO TIC, AND ANXIETY DISORDERS s7 epileptiform activity and related to development of delusions (45).…”

Failed epilepsy surgery for mesial temporal lobe sclerosis: a review of the pathophysiology

“…27,28,43 The presence of dual pathology in patients with MTS has been well described in the literature. Some authors have found a 15%-30% incidence of this type of dual pathology in their series of patients with TLE.…”

“…Some authors have found a 15%-30% incidence of this type of dual pathology in their series of patients with TLE. 27,41 In this situation both the dysplastic temporal neocortex and the sclerotic hippocampus can be epileptogenic. It appears that the contribution of the hippocampus to seizure generation corresponds to the degree of hippocampal pathology, whereas even mild forms of cortical dysplasia can be epileptogenic.…”

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

“…The occurrence of 'dual pathology' in patients with TLE was initially proposed by Rush and Morrell [7] and Lévesque et al [8]. Dual pathology does not merely indicate the anatomical coexistence of HS with an extrahippocampal lesion, but also pathophysiological mechanisms such as the kindling phenomenon and secondary hippocampal epileptogenesis [9,10,11,12].…”