Brain Advance Access originally published online on December 23, 2004
Brain 2005 128(2):321-337; doi:10.1093/brain/awh357
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Brain Vol. 128 No. 2 © Guarantors of Brain 2004; all rights reserved
Electroclinical, MRI and neuropathological study of 10 patients with nodular heterotopia, with surgical outcomes
1 Epilepsy Surgery Centre ‘C. Munari’, Departments of 2 Neuroradiology and 3 Pathology, Niguarda Hospital, Milan and 4 Division of Experimental Neurophysiology, National Neurological Institute ‘C. Besta’, Milano, Italy
Correspondence: Roberto Spreafico, MD, PhD, Divisione di Neurofisiologia Sperimentale e Neuroanatomia, Istituto Nazionale Neurologico ‘C. Besta’, Via Celoria 11, 20133 Milan, Italy E-mail: spreafico{at}istituto-besta.it
We present the results of a retrospective study on 10 patients operated on for intractable epilepsy associated with nodular heterotopia as identified by high resolution MRI. Seven patients had unilateral heterotopia, one patient had symmetric bilateral heterotopia and two patients had asymmetric bilateral heterotopia. By stereo-electroencephalogram (SEEG) (nine patients) interictal activity within nodules was similar in all cases, and ictal activity never started from nodules alone but from the overlying cortex or simultaneously in nodules and cortex. Excellent outcomes (Engel class Ia, 1987) were achieved in the seven patients with unilateral heterotopia, showing that surgery can be highly beneficial in such cases when the epileptogenic zone is carefully located prior to surgery by MRI and particularly SEEG. For the bilateral cases surgical outcomes were Engel IIa (one patient) or Engel IIIa (two patients). Histological/immunohistochemical studies of resected specimens showed that all nodules had similar microscopic organization, even though their extent and location varied markedly. The overlying cortex was dysplastic in nine patients, but of normal thickness. We suggest that nodule formation may be the result of a dual mechanism: (i) failure of a stop signal in the germinal periventricular region leading to cell overproduction; and (ii) early transformation of radial glial cells into astrocytes resulting in defective neuronal migration. The intrinsic interictal epileptiform activity of nodules may be due to an impaired intranodular GABAergic system.
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