WHITE-MATTER NEURONAL HETEROTOPIA IN TEMPORAL-LOBE EPILEPSY - A MORPHOMETRIC AND IMMUNOHISTOCHEMICAL STUDY

Citation
Ja. Emery et al., WHITE-MATTER NEURONAL HETEROTOPIA IN TEMPORAL-LOBE EPILEPSY - A MORPHOMETRIC AND IMMUNOHISTOCHEMICAL STUDY, Journal of neuropathology and experimental neurology, 56(12), 1997, pp. 1276-1282
Citations number
31
ISSN journal
00223069
Volume
56
Issue
12
Year of publication
1997
Pages
1276 - 1282
Database
ISI
SICI code
0022-3069(1997)56:12<1276:WNHITE>2.0.ZU;2-S
Abstract
A frequent abnormality in temporal lobes (TL) resected for pharmacores istant epilepsy is the presence of heterotopic neurons within white ma tter (WM). We compared heterotopic neuron density in 22 TLs surgically resected from epilepsy patients with TLs from 22 non-neurologic cases obtained at autopsies. Neuronal density was assessed on LFB-PAS-stain ed and parallel sections immunoreacted for microtubule-associated-prot ein-2 (MAP-2). The white matter area was outlined by an image analysis system. Neurons, identified by morphologic features, were counted wit hin the marked area. Results are expressed as mean +/- SD neurons/mm(2 ). LFB/PAS sections: Epilepsy cases 4.11 +/- 1.86, Autopsy (normal) 2. 35 +/- 0.96; MAP-2 sections: Epilepsy cases 4.08 +/- 1.22, autopsy (no rmal) 1.68 +/- 0.92 (significant at 0.05 level by Wilcoxon's Rank Sums test). The lower number of MAP-2-immunopositive neurons in the contro l group as compared with the histologically identified group is most l ikely the result of antigen degradation resulting from an increased po stmortem interval, These results indicate that normal TLWM contains a heterotopic population of neurons, and that this neuronal density is s ignificantly higher in epilepsy patients. It is felt that this increas ed neuronal density is an epiphenomenon rather than the cause of seizu res, and may be the result of decreased white matter either secondary to disruption of myelination. or loss of neurons as part of mesial tem poral sclerosis.