Clinical Application of Experimental Cortical Dysplasia in Rats

Tanaka, Tatsuya; Tsuda, Hiroshige; Hashizume, Kazuyoshi; Sakurai, Juro; Hodozuka, Akira; Nakai, Hirofumi

doi:10.1177/08830738050200041401

Cited by 2 publications

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References 19 publications

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“…A high proportion of children with these malformations present with epilepsy, which is often resistant to medical treatment. Several mechanisms underlying the pathogenesis of intractable epilepsies in cortical malformations have been proved: decreased number of inhibitory neurons [1][2][3], up-regulated expression of receptors for excitatory neurotransmitters on the dysmorphic neurons [4], aberrant innervation of the excitatory efferents to the surrounding area of dysplastic lesions [5], and alteration in the intrinsic membrane property of ectopic neurons [6]. These can explain the high epileptogenesity within and outside the malformed cortex.…”

Section: Introductionmentioning

confidence: 99%

Treatment of epilepsy in severely disabled children with bilateral brain malformations

Saito¹,

Sugai²,

Nakagawa³

et al. 2009

Journal of the Neurological Sciences

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Section: Introductionmentioning

confidence: 99%

Treatment of epilepsy in severely disabled children with bilateral brain malformations

Saito¹,

Sugai²,

Nakagawa³

et al. 2009

Journal of the Neurological Sciences

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Focal cortical dysplasia: pathophysiological approach

et al. 2006

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Clinical and experimental studies on focal cortical dysplasia ( FCD ) were carried out.For the experimental study, an experimental FCD model of rats was developed. Twenty Wistar rats at 0-2 days after birth were used for the study. Kainic acid ( KA ) solution was injected stereotaxically into medial and lateral sites of the sensori-motor cortex.Bipolar electrodes were inserted in 5 rats. Their behavior and EEG were recorded using a digital video-EEG monitoring system. After observation periods of 1, 2 and 6 months, rats were perfused for pathological study. FCD was observed adjacent to the site of KA 2 injection in all rats more than one month after the injection. EEG recording demonstrated focal spike discharges in and around the site of injection. However, clinical seizure was not observed. Pathological studies showed decrease in GABA-A receptors and increase in GABA-B receptors not only in the lesion but also in perilesional areas. Fifteen surgical cases of FCD with intractable epilepsy were subjected to the clinical study. Neuro-imaging studies including high-resolution MRI and SPECT were performed. Conventional EEG studies demonstrated focal EEG abnormalities with epileptic phenomena. At surgery, intraoperative electrocorticography ( ECoG ) was performed in order to localize epileptic foci under neuroleptoanalgesia.Thirteen patients showed epileptiform discharges on preresection ECoG. All foci in non-eloquent areas were resected. Pathological studies including immunohistochemical staining were performed, and characteristics of the FCD in relation to EEG findings were analyzed. Patients in whom total lesionectomy with complete focus resection was performed had favorable postoperative courses. Nine patients ( 64.3% ) have been seizure-free with reduced medication, and significant improvement was achieved in two patients ( 14.3% ). Electrophysiological examination revealed epileptogenecity not only in the lesions but also in perilesional areas. The immunohistochemical studies showed decrease in GABA-A receptors and increase in GABA-B receptors in both the lesions 3 and perilesional areas, but NMDA receptors were almost negative in both areas.Glutamate R-1 was decreased in both areas, but glutamate R-2 was increased in both areas. These findings support the results of electrophysiological study. In conclusion, not only the epileptic property of experimental focal cortical dysplasia but also perilesional epileptogenesis was demonstrated. These findings supported the results of surgery for patients with focal cortical dysplasia. In cases of FCD, total removal of the lesion and resection of the perilesional epileptic focus are needed for a good outcome.

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Clinical Application of Experimental Cortical Dysplasia in Rats

Cited by 2 publications

References 19 publications

Treatment of epilepsy in severely disabled children with bilateral brain malformations

Treatment of epilepsy in severely disabled children with bilateral brain malformations

Focal cortical dysplasia: pathophysiological approach

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