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From the Istituto Nazionale Neurologico "C. Besta" (Drs. Spreafico, Battaglia, Arcelli, and Avanzini), Department of Experimental Neurophysiology and Epileptology, Milano, Italy; the Montreal Neurological Hospital and Institute (Drs. Andermann, Dubeau, Olivier, Villemure, Tampieri, and Avoli), Department of Neurology and Neurosurgery, McGill University, Montréal, Québec, Canada; and the Hospital Sao Lucas de UCRS (Dr. Palmini), Servi
o de Neurologia, Porto Allegre, Brazil.
Address correspondence and reprint requests to Dr. Roberto Spreafico, Department of Experimental Neurophysiology and Epileptology, Istituto Nazionale Neurologico "C. Besta," via Celoria 11-20133 Milano, Italy.
Human cortical dysplastic lesions are frequently associated with severe partial epilepsies. We report an immunocytochemical investigation on cortical tissue from three surgically treated patients, 20, 38, and 14 years old, with intractable epilepsy due to cortical dysplasia. The studies were performed using antibodies recognizing cytoskeletal proteins, calcium-binding proteins, and some subunits of glutamate receptors. The specimens from the three patients displayed common features: (1) focal cytoarchitectural abnormalities with an increased number of giant pyramidal neurons through all cortical layers except layer I; (2) large, round-shaped balloon cells mainly concentrated in the deepest part of the cortex and in the white matter;(3) a decrease of calcium binding protein immunopositive 
-aminobutyric acid (GABA)ergic neurons; and (4) abnormal baskets of parvalbumin-positive terminals around the excitatory (pyramidal and large, round-shaped) neurons. These data provide evidence that the epileptogenicity in these types of cortical dysplasia is due to an increase in excitatory neurons coupled with a decrease in GABAergic interneurons.
Supported by the Mariani Foundation for Pediatric Neurology, by the Italian Ministry of Health (grant ICS 030. 3RF95/223), and by Medical Research Council of Canada (grant MT-8109) and the Hospital for Sick Children Foundation (grant XG-056).
Received May 22, 1997. Accepted in final form September 2, 1997.
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