encephalomyelitis/seizures

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Acute disseminated encephalomyelitis (ADEM) presenting with seizures secondary to anti-tetanus toxin vaccination.

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Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease of the central nervous system (CNS) that is known to occur spontaneously in association with specific and non-specific viral illnesses and after vaccination against various pathogens. Although it is often a

Lack of correlation of central nervous system inflammation and neuropathology with the development of seizures following acute virus infection.

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Infection of C57BL/6 mice by the intracerebral route with the Daniels (DA) strain of Theiler's murine encephalomyelitis virus (TMEV) resulted in acute behavioral seizures in approximately 50% of the mice. By titration, the viral dose correlated with the percentage of mice developing seizures;

Evaluating an etiologically relevant platform for therapy development for temporal lobe epilepsy: effects of carbamazepine and valproic acid on acute seizures and chronic behavioral comorbidities in the Theiler's murine encephalomyelitis virus mouse model.

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Central nervous system infections can underlie the development of epilepsy, and Theiler's murine encephalomyelitis virus (TMEV) infection in C57BL/6J mice provides a novel model of infection-induced epilepsy. Approximately 50-65% of infected mice develop acute, handling-induced seizures during the

Cannabidiol reduces seizures following CNS infection with Theiler's murine encephalomyelitis virus.

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Identifikohuni Regjistrohu

C57BL/6J mice infected with Theiler's murine encephalomyelitis virus (TMEV) develop acute behavioral seizures in the first week of infection and later develop chronic epilepsy. The TMEV model provides a useful platform to test novel antiseizure therapeutics. The present study was

Acute epileptic seizures in myelin oligodendrocyte glycoprotein encephalomyelitis and neuromyelitis optica spectrum disorder: A comparative cohort study.

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BACKGROUND Little is known about the incidence and characteristics of acute epileptic seizures in myelin oligodendrocyte glycoprotein encephalomyelitis (MOG-EM) and neuromyelitis optica spectrum disorder (NMOSD). In this study, we compared the incidence and characteristics of acute epileptic

Suppression of clinical weakness in experimental autoimmune encephalomyelitis associated with weight changes, and post-decapitation convulsions after intracisternal-ventricular administration of 6-hydroxydopamine.

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Selective depletion of central nervous system norepinephrine (NE) by the neurotoxin 6-hydroxydopamine (6-OHDA) in rats subsequently inoculated with myelin basic protein (MBP) and complete Freund's adjuvant (CFA) produced experimental autoimmune encephalomyelitis (EAE) without the usual expected

Experimental epilepsy: electrically and chemically induced convulsions modulate experimental allergic encephalomyelitis and other immune inflammatory reactions in the rat.

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Male Wistar rats were exposed to electroconvulsive shock (ECS) and pentylentetrazol (PTZ) for a period of 38 consecutive days; 21 days before and 17 days after immunization with guinea pig spinal cord in complete Freund's adjuvant (CFA) ECS and PTZ completely prevented the appearance of paralysis

Severity of experimental allergic encephalomyelitis in rats depends upon the temporal contiguity between limbic seizures and inoculation.

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Limbic seizures (forepaw clonus) were induced in Lewis rats by subcutaneous injections of lithium (3 mEq/kg) followed 24 h later by a muscarinic agent. Either 7 days before, 7 days after, or on the day of seizures, rats were inoculated with a spinal cord preparation. Other groups received these

Metallothionein reduces central nervous system inflammation, neurodegeneration, and cell death following kainic acid-induced epileptic seizures.

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We examined metallothionein (MT)-induced neuroprotection during kainic acid (KA)-induced excitotoxicity by studying transgenic mice with MT-I overexpression (TgMT mice). KA induces epileptic seizures and hippocampal excitotoxicity, followed by inflammation and delayed brain damage. We show for the

[A case of acute disseminated encephalomyelitis with convulsion, gait disturbance, facial palsy and multifocal CT lesions].

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Yield of emergent neuroimaging among children presenting with a first complex febrile seizure.

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OBJECTIVE The objective of this study was to assess the risk of intracranial pathology requiring immediate intervention among children presenting with their first complex febrile seizure (CFS). METHODS This is a retrospective cohort review of patients 6 to 60 months of age evaluated in a pediatric

The immune response to picornavirus infection and the effect of immune manipulation on acute seizures.

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Identifikohuni Regjistrohu

Viral infection of the central nervous system can result in encephalitis. About 20% of individuals who develop viral encephalitis go on to develop epilepsy. We have established an experimental model where virus infection of mice with Theiler's murine encephalomyelitis virus (TMEV) leads to acute

A young woman with seizures, visual impairment, and paralysis.

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Anti-MOG encephalomyelitis is a recently described demyelinating, autoimmune disease of the central nervous system, identified by antibodies against myelin oligodendrocyte glycoprotein (MOG).A previously healthy 20-year-old woman was admitted to hospital

Once initiated, viral encephalitis-induced seizures are consistent no matter the treatment or lack of interleukin-6.

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Identifikohuni Regjistrohu

Theiler's murine encephalomyelitis virus infection of C57BL/6 mice results in acute behavioral seizures in 50% of the mice. Treatment of infected mice with minocycline or infection of interleukin (IL)-6-deficient chimeric mice results in a significant decrease in the number of mice developing

Early predictors of epilepsy and subsequent relapse in children with acute disseminated encephalomyelitis.

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Identifikohuni Regjistrohu

To identify predictors of epilepsy and clinical relapses in children presenting with acute disseminated encephalomyelitis (ADEM).Children presenting with ADEM between 2005 and 2017 and tested clinically for MOG-Ab were identified from three tertiary

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