topiramate and Encephalitis

topiramate has been researched along with Encephalitis* in 4 studies

Reviews

1 review(s) available for topiramate and Encephalitis

ArticleYear
[Role of immunity in the pathophysiology of intractable epilepsy-postencephalitic epilepsy & immunity].
    No to hattatsu = Brain and development, 2014, Volume: 46, Issue:3

    Topics: Adolescent; Adult; Apoptosis; Autoantibodies; Blood-Brain Barrier; Child; Child, Preschool; Encephalitis; Epilepsy; Female; Fructose; Humans; Male; Matrix Metalloproteinase 9; Receptors, N-Methyl-D-Aspartate; Time Factors; Tissue Inhibitor of Metalloproteinase-1; Topiramate; Young Adult

2014

Other Studies

3 other study(ies) available for topiramate and Encephalitis

ArticleYear
Neuroprotective effects of various doses of topiramate against methylphenidate-induced oxidative stress and inflammation in isolated rat amygdala: the possible role of CREB/BDNF signaling pathway.
    Journal of neural transmission (Vienna, Austria : 1996), 2016, Volume: 123, Issue:12

    Methylphenidate (MPH) abuse damages brain cells. The neuroprotective effects of topiramate (TPM) have been reported previously, but its exact mechanism of action still remains unclear. This study investigated the in vivo role of various doses of TPM in the protection of rat amygdala cells against methylphenidate-induced oxidative stress and inflammation. Seventy adult male rats were divided into seven groups. Groups 1 and 2 received normal saline (0.7 ml/rat) and MPH (10 mg/kg), respectively, for 21 days. Groups 3, 4, 5, 6, and 7 were concurrently treated with MPH (10 mg/kg) and TPM (10, 30, 50, 70, and 100 mg/kg), respectively, for 21 days. elevated plus maze (EPM) was used to assess motor activity disturbances. In addition, oxidative, antioxidantand inflammatory factors and CREB, Ak1, CAMK4, MAPK3, PKA, BDNF, and c FOS gene levels were measured by RT-PCR, and also, CREB and BDNF protein levels were measured by WB in isolated amygdalae. MPH significantly disturbed motor activity and TPM (70 and 100 mg/kg) neutralized its effects. MPH significantly increased lipid peroxidation, mitochondrial GSSG levels and IL-1β and TNF-α level and CAMK4 gene expression in isolated amygdala cells. In contrast, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and CREB, BDNF Ak1, MAPK3, PKA, BDNF, and c FOS expression significantly decreased. The various doses of TPM attenuated these effects of MPH. It seems that TPM can be used as a neuroprotective agent and is a good candidate against MPH-induced neurodegeneration.

    Topics: Animals; Brain-Derived Neurotrophic Factor; Central Nervous System Stimulants; CREB-Binding Protein; Disease Models, Animal; Dose-Response Relationship, Drug; Encephalitis; Fructose; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Lipid Peroxidation; Male; Maze Learning; Methylphenidate; Mitochondria; Neuroprotective Agents; Oxidative Stress; Rats; Signal Transduction; Superoxide Dismutase; Topiramate

2016
Topiramate-valproate-induced encephalopathy in migraine.
    Headache, 2012, Volume: 52, Issue:8

    Topics: Adult; Analgesics; Drug Therapy, Combination; Encephalitis; Fructose; Humans; Male; Migraine Disorders; Topiramate; Valproic Acid

2012
Effect of topiramate, in combination with lidocaine, and phenobarbital, in acute encephalitis with refractory repetitive partial seizures.
    Brain & development, 2009, Volume: 31, Issue:8

    Acute encephalitis with refractory repetitive partial seizure (AERRPS) is a peculiar type of post-encephalitic/encephalopathic epilepsy. Here we report an analysis of AERRPS in a series of children and propose an effective treatment option for seizure control in these children.. We retrospectively reviewed cases of AERRPS treated in a pediatric intensive care unit, between February 2002 and June 2006. Clinical characteristics were systemically assessed. Burst suppression coma was induced by high-dose suppressive therapy; 24-h electroencephalogram (EEG) monitoring was performed on each patient. The goal of treatment was to achieve complete clinical seizure control or burst-suppression pattern on EEG, aiming for an interburst interval of >5s. Brain imaging was done for each patient.. There were nine patients (seven boys), aged 5-15 years. Clinical symptoms included fever (100%), upper respiratory symptoms (66.7%) and altered consciousness (66.7%). All patients received multiple high-dose suppressive drugs and were intubated with/without inotropic agents. Seizures in three patients were stopped after high-dose lidocaine infusion (6-8 mg/kg/h) in the acute stage and three patients were stopped after high dose phenobarbital (serum level 60-80 ug/mL) combined with high-dose oral topiramate (15-20 mg/kg/day). Follow-up for this study was 16-61 months. Two subjects died while seven developed epilepsy and/or neurologic deficits; none returned to baseline. All survivors were discharged and continued multiple antiepileptic medications.. Our data indicates that children with AERRPS have high mortality and morbidity rates. High-dose topiramate combined with high-dose lidocaine infusion or high-dose phenobarbital in the acute stage might be an effective treatment option for children with AERRPS.

    Topics: Acute Disease; Adolescent; Anticonvulsants; Child; Drug Therapy, Combination; Electroencephalography; Encephalitis; Epilepsies, Partial; Female; Fructose; Humans; Lidocaine; Magnetic Resonance Imaging; Male; Phenobarbital; Radiography; Severity of Illness Index; Syndrome; Topiramate; Treatment Outcome

2009