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Mitochondrial “Hypermetabolic” Neurons in Paediatric Epileptic Foci

Published online by Cambridge University Press:  02 December 2014

Harvey B. Sarnat ,
Laura Flores-Sarnat ,
Walter Hader  and
Luis Bello-Espinosa
Harvey B. Sarnat*
Affiliation:
Department of Paediatrics, University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada Department of Pathology and Laboratory Medicine (Neuropathology), University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada Department of Clinical Neurosciences (Neurology), University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada
Laura Flores-Sarnat
Affiliation:
Department of Paediatrics, University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada Department of Clinical Neurosciences (Neurology), University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada
Walter Hader
Affiliation:
Department of Neurosurgery, University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada
Luis Bello-Espinosa
Affiliation:
Department of Paediatrics, University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada Department of Clinical Neurosciences (Neurology), University of Calgary Faculty of Medicine and Alberta Children's Hospital, Calgary, Alberta, Canada
*
Alberta Children's Hospital, 2888 Shaganappi Trail NW, Calgary, Alberta T3B 6A8, Canada
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Abstract

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Background:

Repetitively discharging neurons in epileptic foci have a high energy requirement that might be demonstrated histochemically as increased mitochondrial enzymatic activity in brain resections for epilepsy in children.

Materials and Methods:

Frozen sections were studied histochemically of 10 brain resections from 7 epileptic children, 2 months to 17 years of age. None had mitochondrial disease. Three patients had tuberous sclerosis (TS) or hemimegalencephy (HME). Tissues included hippocampus and neocortex. Oxidative enzymes were studied for respiratory chain complexes I, II, IV, using the muscle biopsy protocol. In addition, immunoreactivities of α-B-crystallin and transmission electron microscopy (EM) were performed.

Results:

Oxidative activities were variable in adjacent neurons within a field: a minority were intense, adjacent to neurons with weaker mitochondrial activity exhibiting poor contrast of the soma because of similar oxidative activity in surrounding neuropil. Endothelium of vessels uniformly exhibits strong activity. Alpha-B-crystallin reactivity was strong at these foci. EM confirmed an abundance of neuronal mitochondria with normal cristae. In TS and HME, many dysplastic neurons showed intense activity; balloon cells had sparse activity.

Conclusions:

Histochemistry of mitochondrial oxidative enzymes reveals scattered and clustered neurons with stronger activities than others at epileptic foci. Such intensely staining neurons may be functionally “hypermetabolic” but they do not signify mitochondrial disease. Individual intensely stained neurons might be epileptogenic, but do not denote an epileptogenic field in the same manner as α-B-crystallin, which also was strongly reactive in these foci.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 38 , Issue 6 , November 2011 , pp. 909 - 917
Copyright
Copyright © The Canadian Journal of Neurological 2011

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