Histopathological findings in chronic pharmacoresistant temporal epilepsy: a pathognomonic combination of lesions maintaining neuron injury?

ABSTRACT

Progression and pharmacoresistance of epileptic seizures is clinically not yet well predicted and comprehensible. This was a pathological study of surgical specimens of resected temporal lobe and hippocampus in chronic pharmacoresistant temporal epilepsy, in order to determine any lesions that might play a role in the onset or in the maintenance of this type of epilepsy, and any lesions that might result in as wide a variety of lesions as have been reported in the different studies in the literature. This was a prospective histopathological study of successive mesial temporal and extrahippocampal structures removed from patients suffering from refractory epilepsy. Serial cut sections of 1.5 - 2 mm were studied between October 1997 and December 2004 in the Epilepsy Centre of Damascus University. A retrospective review was done later. Sixty-six consecutive surgical specimens from 66 patients with refractory epilepsy lasting for 1 - 32 years [mean = 16.2 years] were received and studied. Our series included 33 males and 33 females [2 - 45 years; average 22 years]. Pathological study revealed some constant lesions observed in all cases signs of neuronal injury with cell lysis, apoptosis followed by neuronal loss, cortical dysplasia/ dysgenesis, hippocampal and temporal gliosis and focal degenerative cystic changes. Other observations were as follows neuroglial tumours and malformations [20 cases, 30%], subependymal cortical heterotopia [13 cases, 20%], gyral fusion [16 cases, 24%] with abnormal elongation of the sulcus in [6 cases 9%], inflammation [10 cases, 15%], vascular tumours/ malformations [5 cases, 7.5%], gliomas [5 cases, 7.5%], severe atrophy [2 cases, 3%], small meningeal nodule [1 case, 1.5%], and old haemorrhage [1 case, 1.5%].In this series, a large variety of lesions were found with constant signs of neuronal injury and loss. A presumable epileptogenic focus was found in many cases [58%], and the multiplicity and multifocality of lesions were well documented. A good understanding of the sequencing of the processes leading to cell injury might contribute in the prevention of progression of epileptic seizure in previously susceptible patients