Navegando por Palavras-chave "gliosis"

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    Characterization of reactive astrocytes in the chronic phase of the pilocarpine model of epilepsy
    (Blackwell Publishing Inc, 2002-01-01) Garzillo, Cibele Larrosa [UNIFESP]; Mello, Luiz Eugenio Araujo de Moraes [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Purpose: Astrogliosis is a prominent finding in human temporal lobe epilepsy. Work in animal models of temporal lobe epilepsy, however, have mostly concentrated on the acute phases of the studied models or have failed to demonstrate reactive gliosis during the chronic phases of such models.Methods: Here we used the pilocarpine model of chronic seizures and Cajal's gold sublimate technique for the staining reactive astrocytes to study this issue.Results: for half of the animals (nine of 17) subject to pilocarpine-induced status epilepticus (SE), when assessed 60 days later, variable levels of reactive astrocytes were seen in many thalamic, hippocampal, amygdalar, and neocortical areas. for the remaining half of the animals, however (eight of 17), despite a similar SE induction, as well as for controls, we could not detect stained reactive astrocytes.Conclusions: We hypothesize that these results might underlie possible differences in the frequency of recurrent spontaneous seizures.
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    Long-term outcome after temporal lobe epilepsy surgery in 434 consecutive adult patients Clinical article
    (Amer Assoc Neurological Surgeons, 2009-06-01) Elsharkawy, Alaa Eldin; Alabbasi, Abdel Hamid; Pannek, Heinz; Oppel, Falk; Schulz, Reinhard; Hoppe, Mathias; Hamad, Ana Paula [UNIFESP]; Nayel, Mohamed; Issa, Ahmed; Ebner, Alois; Bethel Epilepsy Ctr; Cairo Univ; Universidade Federal de São Paulo (UNIFESP); Krankenhaus Mara
    Object. the aim of this study was to evaluate the long-term efficacy of temporal lobe epilepsy (TLE) Surgery and potential risk factors for seizure recurrence after surgery.Methods. This retrospective study included 434 consecutive adult patients who underwent TLE surgery at Bethel Epilepsy Centre between 1991 and 2002.Results. Hippocampal sclerosis was found in 62% of patients, gliosis in 17.3%, tumors in 20%, and focal cortical dysplasia (FCD) in 6.9%. Based on a Kaplan-Meier analysis, the probability of Engel Class I outcome for the patients overall was 76.2% (95% CI 71-81%) at 6 months, 72.3% (95% CI 68-76%) at 2 years, 71.1% (95% CI 67-75%) at 5 years, 70.8% (95% CI 65-75%) at 10 years, and 69.4% (95% CI 64-74%) at 16 years postoperatively. the likelihood of remaining seizure free after 2 years of freedom from seizures was 90% (95% CI 82-98%) for 16 years. Seizure relapse Occurred in all subgroups. Patients with FCD had the highest risk of recurrence (hazard ratio 2.15, 95% CI 0.849-5.545). Predictors of remission were the presence of hippocampal atrophy on preoperative MR imaging and a family history of epilepsy. Predictors of relapse were the presence of bilateral interictal sharp waves and versive seizures. Six-month follow-up electroencephalography predicted relapse in patients with FCD. Short epilepsy duration was predictive of seizure remission in patients with tumors and gliosis; 28.1% of patients were able to discontinue antiepileptic medications without an increased risk of seizure recurrence (hazard ratio 1.05, 95% CI 0.933-1.20).Conclusions. These findings highlight the role of etiology in prediction of long-term Outcome after TLE surgery. (DOI: 10.3171/2008.6.JNS17613)
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    Sleep deprivation does not affect indices of necrosis or apoptosis in rat brain
    (Taylor & Francis Ltd, 2002-02-01) Hipólide, Débora Cristina [UNIFESP]; D'Almeida, Vania [UNIFESP]; Raymond, Roger; Tufik, Sergio [UNIFESP]; Nobrega, J. N.; Ctr Addict & Mental Hlth; Universidade Federal de São Paulo (UNIFESP)
    Recent indications of oxidative stress in hypothalamus of sleep deprived rats prompted us to address the possibility that sleep deprivation may induce pathological cell loss changes in brain. Indices of necrosis and apoptosis were quantified after 96 h of sleep deprivation induced by the classical platform technique in rats. Binding of the peripheral-type benzodiazepine ligand [H-3] PK 11195 to reactive astrocytes, a reliable and sensitive index of necrotic changes, was not altered in any of 14 brain regions examined. Likewise, no changes were found in mRNA levels of the apoptosis-related genes bcl-2 and bax in any of 24 brain regions examined. This was corroborated by quantitative TUNEL analyses in hypothalamus, amygdala, and cortex, which also revealed no effects in sleep deprived animals. These results are consistent with other recent evidence that sleep deprivation does not induce necrotic or apoptotic cell loss in brain. This suggests that recent findings of oxidative stress in sleep deprived brains do not result in cell loss. the possibility that sleep deprivation may result in functional deficits, or that structural changes may emerge after repeated episodes of sleep deprivation, remains to be addressed.