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The Journal of Neuroscience, July 1, 2001, 21(13):4789-4800

Neuronal Hypertrophy in the Neocortex of Patients with Temporal Lobe Epilepsy

Sarah Bothwell^{1, 4}, Gloria E. Meredith^{1, 2}, Jack Phillips⁴, Hugh Staunton⁴, Colin Doherty³, Elena Grigorenko⁵, Steven Glazier⁵, Sam A. Deadwyler⁵, Cormac A. O'Donovan⁵, and Michael Farrell⁴

¹ Department of Zoology, Trinity College, University of Dublin, Dublin 2, Ireland, ² Department of Basic Medical Science, University of Missouri-Kansas City, School of Medicine, Kansas City, Missouri 64108, ³ Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114, ⁴ Departments of Anatomy and Clinical Neurological Sciences, Royal College of Surgeons in Ireland, Dublin 2, Ireland, and ⁵ Departments of Neurology, Neurosurgery, and Physiology and Pharmacology, Bowman Gray School of Medicine, Winston-Salem, North Carolina 27157

The underlying cause of neocortical involvement in temporal lobe epilepsy (TLE) remains a fundamental and unanswered question. Magnetic resonance imaging has shown a significant loss in temporal lobe volume, and it has been proposed that neocortical circuits are disturbed functionally because neurons are lost. The present study used design-based stereology to estimate the volume and cell number of Brodmann's area 38, a region commonly resected in anterior temporal lobectomy. Studies were conducted on the neocortex of patients with or without hippocampal sclerosis (HS). Results provide the surprising finding that TLE patients have significant atrophy of neocortical gray matter but no loss of neurons. Neurons are also significantly larger, dendritic trees appear sparser, and spine density is noticeably reduced in TLE specimens compared with controls. The increase in neuronal density we found in TLE patients is therefore attributable to large neurons occupying a much smaller volume than in normal brain. Neurons in the underlying white matter are also increased in size but, in contrast to other reports, are not significantly elevated in number or density. Neuronal hypertrophy affects HS and non-HS brains similarly. The reduction in neuropil and its associated elements therefore appears to be a primary feature of TLE, which is not secondary to cell loss. In both gray and white matter, neuronal hypertrophy means more perikaryal surface area is exposed for synaptic contacts and emerges as a hallmark of this disease.

Key words: temporal lobe epilepsy; stereology; Brodmann's area 38; ectopia; cortical atrophy; neuronal hypertrophy; hippocampal sclerosis

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21134789-12$05.00/0

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