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Incomplete seizure reduction following resection of focal oligodendroglial hyperplasia

Published online by Cambridge University Press:  10 December 2015

J.A.E. Radic
Affiliation:
Division of Neurosurgery, Moffitt Cancer Center, University of South Florida, Tampa, FL, USA
H.C. Rutherford
Affiliation:
Division of Neurosurgery, Department of Anatomic Pathology, Moffitt Cancer Center, University of South Florida, Tampa, FL, USA
R.J.B. Macaulay
Affiliation:
Division of Neurosurgery, Department of Anatomic Pathology, Moffitt Cancer Center, University of South Florida, Tampa, FL, USA
R.M. Sadler
Affiliation:
Division of Neurology, Dalhousie University, Halifax, NS, Canada
T. Bardouille
Affiliation:
Biomedical Translational Imaging Centre, IWK Health Centre, Halifax, NS, Canada
A. Ross
Affiliation:
Division of Nuclear Medicine, Department of Diagnostic Radiology, Dalhousie University, Halifax, NS, Canada
D.B. Clarke
Affiliation:
Division of Neurosurgery, Moffitt Cancer Center, University of South Florida, Tampa, FL, USA
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Abstract

Type
Abstracts
Copyright
Copyright © The Canadian Journal of Neurological Sciences Inc. 2015 

The patient presented as a 39 year old right hand dominant female with medically refractory epilepsy. Pre-operative investigations, including MRI, electro- and magneto-encephalography, and fluorodeoxyglucose positron emission tomography (PET) were concordant with a lesion in the right inferomesial frontal lobe. Subdural electrode recordings demonstrated seizure onset in the right anterior inferior frontal lobe. The patient underwent surgical resection of the lesion.

Histopathology revealed an increased cell density of oligodendrocytes (3350.5 cells/mm2, compared to 1683.6 cells/mm2 in adjacent normal-appearing white matter, p<0.001). Myelination (luxol fast blue staining) was normal. Supernumerary cells were negative for IDH1R132H by immunohistochemistry, IDH1/2 wildtype by Sequenom, and negative for Ki-67, synaptophysin, and BRAF V600E. The overlying cortex was completely normal, with no gliosis, balloon cell, neuronal dysmorophology or calcification. The original neuropathologic diagnosis was oligodendroglial hamartoma, although a more descriptive diagnosis of focal oligodendroglial hyperplasia is preferred. The patient continues to have 1-2 nocturnal partial (focal with dyscognitive features) seizures per month, but has had no convulsive seizure since her surgery (4.5 year follow-up). Oligodendroglial hyperplasia is a poorly characterized subtype of microdysgenesis, and a rare cause of medically refractory epilepsy. Histologically, it is important that it is differentiated from oligodendroglioma. Because of the paucity of published cases, the clinical impact of surgical resection of oligodendroglial hyperplasia found within the seizure onset zone is uncertain.

Conflictsof Interest:

None.