Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between 1934 and 1988, 34 patients with tumoural parietal lobe epilepsy were treated surgically at the Montreal Neurological Institute (MNI). Fifteen had right-sided and 16 left-sided resections. The remaining three patients had biopsies only. Follow-up ranging from 1 to 40 years (mean 12.3 years) was available for 28 patients. Seventy-five percent (21 out of 28) became seizure free or had rare seizures. Permanent post-operative sensory deficits were described in 12% of patients. An aura was described by 79%. 62% had somatosensory symptoms, contralateral to the epileptogenic region in all but one. Visual illusions (12%), aphasia (9%) and disturbances of body image (6%), were much less common at the beginning of the attacks. Intra-operative cortical stimulation reproduced the habitual aurae in 10 out of 25 (40%) of the patients. The clinical manifestations suggested different spread patterns: 21% had tonic posturing of the extremities, 82% focal clonic activity, 15% head deviation, 9% automatisms and 6% difficulty speaking. Eleven (32%) had Todd's paralysis and 18% postictal dysphasia. Almost half the patients had impaired two-point discrimination in contralateral fingers; two of these also had impaired stereognosis, but only one had astereognosis without coexisting primary cortical sensory deficit. Review of this, now historical, series shows that parietal lobe tumours can be resected with good control of previously intractable seizures. Such an approach is preferable to postponing resection until the lesion is shown to increase in volume.
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PMID:Tumoural parietal lobe epilepsy. Clinical manifestations and outcome in 34 patients treated between 1934 and 1988. 749 87

The case of a 15-year-old right-handed girl with developmental delay, mild retardation, astereognosis, and tactile discrimination impairment in the left arm, is reported. During sleep, right partial simple motor seizures with sialorrhea and saliva pooling were present, sometimes followed by secondary generalization. Absences and drop attacks were also observed. Electroencephalography revealed left centrotemporal spike waves spreading to the homologous contralateral region, generalized 3-Hz spike-and-wave complexes enhanced by hyperventilation, and generalized polyspike-and-wave discharges during drowsiness. Magnetic resonance imaging showed right perisylvian (opercular) malformation. Benign epilepsy of childhood with centrotemporal spikes (BECCTS) is a focal idiopathic epilepsy presumed to be of genetic origin. Although brain damage is not expected, structural lesions including opercular macrogyria have been reported. This coexistence has been considered mainly causal and only exceptionally causal. The Foix-Chavany-Marie syndrome or operculum syndrome is the result of bilateral opercular damage. In our child the right structural and the left functional lesions appeared mutually activated, yielding a transient opercular syndrome. The concomitance of BECCTS and developmental opercular dysplasia is suggestive of a common genetic substratum.
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PMID:Benign epilepsy of childhood with centrotemporal spikes and unilateral developmental opercular dysplasia. 792 39