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From the Department of Neurology and Neurosurgery, McGill University, and the Montreal Neurological Institute and Hospital, Montreal, Quebec, Canada.
Address correspondence and reprint requests to Dr. Douglas L. Arnold, Montreal Neurological Hospital and Institute, 3801 University Street, Montreal, Quebec, Canada, H3A 2B4.
Cortical developmental malformations are best diagnosed by MRI and are often the cause of refractory epilepsy. Little is known about the metabolic cell function on MR spectroscopy of these types of brain anomaly. We studied 23 patients with cortical developmental malformations and refractory epilepsy using proton MR spectroscopic imaging. Mean age was 28 years (range, 9 to 47 years). The lesions examined were focal cortical dysplasia (n = 5), heterotopia (four band, six periventricular, two subcortical), polymicrogyria(n = 3), tuberous sclerosis (n = 2), and polymicrogyria and periventricular nodular heterotopia (n = 1). We measured the relative signal intensity of N-acetylaspartate/creatine (NAA/Cr) in the lesion, in the perilesional region, and in the region remote from the visible lesion. The values were compared with those from similar brain regions of 25 normal control subjects. The mean NAA/Cr z score values for the 23 patients were as follows: lesion, -2.20 ± 0.32 (mean ± SE), n = 21; perilesional region, -1.01 ± 0.38, n = 15; and distant region, -0.03 ± 0.34, n = 18 (p < 0.0002). Despite the presence of a large number of neurons, heterotopia showed a relative decrease of NAA in some patients, suggesting that the neurons present were dysfunctional. The maximal NAA/Cr decrease, indicating metabolic dysfunction, colocalized to the structural malformation as defined by MRI and extended to normal-appearing regions adjacent to the visible lesion.
Supported by a grant from the MRC Canada. Dr. Li is recipient of a fellowship from the Savoy Foundation for Research in Epilepsy of Canada.
Received May 19, 1997. Accepted in final form September 9, 1997.
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