0000000000548178
AUTHOR
Helmut K. Wolf
An increase of hippocampal calretinin-immunoreactive neurons correlates with early febrile seizures in temporal lobe epilepsy
Numerous studies indicate that initial precipi- tating injuries (IPI) such as febrile seizures during early childhood may play a pivotal role in the pathogenesis of temporal lobe epilepsy (TLE) and Ammon's horn sclero- sis (AHS). Previous data demonstrate an increase of hori- zontally oriented neurons in molecular layers of hip- pocampal subfields, which are immunoreactive for calre- tinin (CR-ir) and resemble Cajal-Retzius-like cells. Cajal- Retzius cells are transiently expressed in the murine de- veloping hippocampus and are critically involved in neu- ronal pattern formation. Here we investigated a potential relationship between the distribution of horizontally ori- ented calretinin-imm…
Subregional Pathology of the Amygdala Complex and Entorhinal Region in Surgical Specimens From Patients With Pharmacoresistant Temporal Lobe Epilepsy
The hippocampus, amygdala complex, and entorhinal region represent anatomically linked limbic structures of the mesiotemporal lobe. Chronic seizures and mnestic deficits in patients with pharmacoresistant mesial temporal lobe epilepsy (TLE) appear to correlate with distinct patterns of histopathological alterations in these areas. The complex anatomical organization of the amygdala and entorhinal region, however, render a detailed neuropathological evaluation of surgical specimens difficult. In this study, we present a combined cytoarchitectonical, pigmentarchitectonical, myelinarchitectonical, and immunohistochemical reconstruction of the amygdala, entorhinal region, and hippocampus from s…
Evidence for developmental precursor lesions in epilepsy-associated glioneuronal tumors
The etiology and pathogenesis of epilepsy-associated local lesions remain largely unknown. Histopathologically, the most frequent lesions comprise gangliogliomas and glioneuronal malformations, i.e., hamartias or hamartomas, with a preferred location in the temporal lobe of young patients. A characteristic histopathological admixture of glial and neuronal elements, the focal appearance and the benign clinical behaviour suggest a malformative nature. So far, no molecular genetic alterations specifically involved in the pathogenesis of these glioneuronal lesions have been identified. However, immunohistochemical analysis revealed distinct distribution patterns of oncofetal antigens. The embry…
Neural antigens in oligodendrogliomas and dysembryoplastic neuroepithelial tumors
Oligodendrogliomas and dysembryoplastic neuroepithelial tumors (DNT) are frequently associated with epilepsies and share the presence of oligodendroglia-like cells with small round nuclei and optically empty perinuclear halos. The two entities may be difficult to discriminate in small surgical specimens and the origin and differentiation of the oligodendroglia-like cells has been controversial. To better characterize and distinguish the two entities we examined 25 oligodendrogliomas and 16 DNT immunohistochemically for the presence of the proliferation-associated Ki-67 antigen and the following neural antigens: the alpha 1 subunit of the GABAA receptor (GABAR), N-methyl-D-aspartate receptor…
The CD34 epitope is expressed in neoplastic and malformative lesions associated with chronic, focal epilepsies.
The etiology and pathogenesis of complex focal lesions associated with chronic, intractable epilepsy are largely unknown. Some data indicate that malformative changes of the central nervous system may preceed the development of gangliogliomas and other epilepsy-associated neoplasms. In the present immunhistochemical study, we have examined epilepsy-associated lesions for CD34, a stem cell marker transiently expressed during early neurulation. Surprisingly, most tissue samples from patients with chronic epilepsy (n = 262) revealed neural cells immunoreactive for CD34. Prominent immunoreactivity was detected in gangliogliomas (74%), low-grade astrocytomas (62%) and oligodendrogliomas (59%). O…