ALTERED PATTERNS OF CATECHOLAMINERGIC FIBERS IN FOCAL CORTICAL DYSPLASIA IN 2 PATIENTS WITH PARTIAL SEIZURES

Citation
S. Trottier et al., ALTERED PATTERNS OF CATECHOLAMINERGIC FIBERS IN FOCAL CORTICAL DYSPLASIA IN 2 PATIENTS WITH PARTIAL SEIZURES, Epilepsy research, 19(2), 1994, pp. 161-179
Citations number
47
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
09201211
Volume
19
Issue
2
Year of publication
1994
Pages
161 - 179
Database
ISI
SICI code
0920-1211(1994)19:2<161:APOCFI>2.0.ZU;2-Q
Abstract
We present the histologic study of two patients who underwent cerebral cortex resection for partial seizures linked with cortical dysplasia. The distinction of areas of seizure origin from areas of seizure prop agation was made according to stereoelectroencephalographic criteria. Samples of epileptogenic tissue were studied by using cytoarchitectoni c and immunohistochemical stainings. We mapped the catecholaminergic a fferents by employing antisera directed against tyrosine hydroxylase a nd dopamine-beta-hydroxylase enzymes. The epileptic activity was corre lated with the underlying patterns of cytoarchitectonic' and immunohis tochemical changes. The neuropathological features were focal and cons isted of large neurons dispersed through all but the first cortical la yer (associated in one case to giant glial cells), of variable disturb ance of lamination, of neuronal ectopia in the white matter and of mod erate proliferation of small glial cells. Areas of seizure onset coinc ided with that of dysplastic zones. Both laminar distribution and dens ity of catecholaminergic fibers were altered in the dysplastic cortice s (area of seizure onset) and there was an increase in the density of tyrosine hydroxylase-immunoreactive fibers in the surrounding areas of seizure propagation. Our results indicate that these developmental ep ileptogenic lesions were associated with abnormal neuronal circuitry. They provide evidence at the structural level of the increase in tyros ine hydroxylase activity previously reported in spiking areas of human epileptogenic cerebral cortex and they suggest that catecholamines ma y contribute toward limiting seizure activity propagation.