dc.contributorUniv Toronto
dc.contributorUniversidade de São Paulo (USP)
dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.creatorHamani, C.
dc.creatorEwerton, FIS
dc.creatorBonilha, S. M.
dc.creatorBallester, G.
dc.creatorMello, LEAM
dc.creatorLozano, A. M.
dc.date.accessioned2016-01-24T12:34:14Z
dc.date.accessioned2023-09-04T18:23:30Z
dc.date.available2016-01-24T12:34:14Z
dc.date.available2023-09-04T18:23:30Z
dc.date.created2016-01-24T12:34:14Z
dc.date.issued2004-01-01
dc.identifierNeurosurgery. Philadelphia: Lippincott Williams & Wilkins, v. 54, n. 1, p. 191-195, 2004.
dc.identifier0148-396X
dc.identifierhttp://repositorio.unifesp.br/handle/11600/27578
dc.identifier10.1227/01.NEU.0000097552.31763.AE
dc.identifierWOS:000187944300045
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8614043
dc.description.abstractOBJECTIVE: the thalamus is thought to play an important role in secondary generalization of seizures. the aim of the present study was to investigate the influence of anterior thalamic nucleus lesions and high-frequency stimulation in the pilocarpine. model of secondarily generalized seizures in rats.METHODS: Adult Wistar rats underwent unilateral (n = 7) or bilateral anterior nucleus thalamotomies (n = 10), or unilateral (n = 4) or bilateral (n = 9) anterior thalamic nucleus stimulation through implanted electrodes. Control animals (n = 9) received bilateral implants but no stimulation. Seven days after these procedures, animals were : provided pilocarpine (320 mg/kg intraperitoneally) to induce seizures and status epilepticus (SE). Electrographic recordings from hippocampal and cortical electrodes were evaluated, and ictal behavior was assessed.RESULTS: in the control group, 67% of the animals developed SE 15.3 +/- 8.8 minutes after. pilocarpine administration. Neither unilateral anterior nucleus lesions nor stimulation significantly reduced the propensity or latency for developing seizures and SE. Bilateral thalamic. stimulation did not prevent SE (observed in 56% of the animals), but it significantly prolonged. the latency to its development (48.4 +/- 17.7 min, P = 0.02). Strikingly, no animal with bilateral anterior nucleus thalamotomies developed seizures or SE with pilocarpine.CONCLUSION: Bilateral anterior thalamic nuclear complex stimulation and thalamotomies were protective against SE induced by pilocarpine.
dc.languageeng
dc.publisherLippincott Williams & Wilkins
dc.relationNeurosurgery
dc.rightsAcesso restrito
dc.subjectanterior nucleus
dc.subjectdeep brain stimulation
dc.subjectepilepsy
dc.subjectthalamotomy
dc.subjectthalamus
dc.titleBilateral anterior thalamic nucleus lesions and high-frequency stimulation are protective against pilocarpine-induced seizures and status epilepticus
dc.typeArtigo


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