herpes simplex/seizures

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Herpes simplex virus vectors overexpressing the glucose transporter gene protect against seizure-induced neuron loss.

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We have generated herpes simplex virus (HSV) vectors vIE1GT and v alpha 4GT bearing the GLUT-1 isoform of the rat brain glucose transporter (GT) under the control of the human cytomegalovirus ie1 and HSV alpha 4 promoters, respectively. We previously reported that such vectors enhance glucose uptake

Herpes simplex virus type 1 inoculation enhances hippocampal excitability and seizure susceptibility in mice.

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Herpes simplex virus type 1 (HSV-1) is the major pathogen related to epilepsy. However, little is known about the pathogenesis of HSV-1-associated epilepsy. Here, we report that corneal inoculation of mice with HSV-1 induces acute spontaneous behavioural and electrophysiological seizures and

Neurovirulence of two clonally related herpes simplex virus type 1 strains in a rabbit seizure model.

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Herpes simplex virus type 1 (HSV-1) strains vary widely with regard to neurovirulence, but their tropism for specific central nervous system structures and their ability to induce seizures are poorly defined. We have used the clonally related +GC and -GC strains of HSV-1 to define the

Reverse crossed cerebellar diaschisis in partial complex seizures related to herpes simplex encephalitis.

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Tc-99m HMPAO brain SPECT was performed in a patient who had partial complex seizures for 1 year after successful acyclovir treatment of biopsy-proven herpes simplex encephalitis 2 years earlier. In spite of antiepileptic medications, her seizures were intractable and occurred daily. Tc-99m HMPAO was

Central nervous system herpes simplex virus infection in afebrile children with seizures.

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Central nervous system herpes simplex virus infection is suspected in patients presenting with acute-onset seizures and lethargy. The potential neurologic sequelae from untreated herpes infection can prompt empirical acyclovir therapy, even in afebrile subjects. The objectives of this study were to

Risk of bacterial or herpes simplex virus meningitis/encephalitis in children with complex febrile seizures.

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OBJECTIVE To estimate the rates of bacterial meningitis and herpes simplex virus (HSV) encephalitis in children presenting with complex febrile seizures. METHODS Health records from 2002 to 2006 of all children 6 months to 6 years with a discharge diagnosis from the Hospital for Sick Children

Pathology of chronic herpes infection associated with seizure disorder: a report of two cases with tissue detection of herpes simplex virus 1 by the polymerase chain reaction.

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Although uncommon, the association of chronic encephalitis with epilepsy is well recognized. While a viral etiology has been suspected based on the morphology, to date no virus has been successfully cultured from the brain in patients with Rasmussen's encephalitis. We describe the pathologic

Simultaneous detection of herpes simplex virus 1 and 2 in the cerebrospinal fluid of a patient with seizures and encephalitis.

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We report a case of a 62-year-old female with seizures and encephalitis. Molecular testing of the patient's cerebrospinal fluid was positive for both herpes simplex virus 1 and 2 (HSV-1 and HSV-2). To our knowledge, this is the first report of simultaneous detection of HSV-1 and HSV-2 in

Presence of herpes simplex DNA in surgical tissue from human epileptic seizure foci detected by polymerase chain reaction: preliminary study.

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OBJECTIVE To determine whether herpes simplex virus causes monofocal epilepsy and to assess the presence of herpes simplex virus 1 (HSV-1) and HSV-2 in surgical specimens from patients with epilepsy by using polymerase chain reaction and Southern blot analysis. BACKGROUND Herpes simplex virus is a

Parechovirus-A3 encephalitis presenting with focal seizure mimicking herpes simplex virus infection.

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Febrile neonates and young infants presenting with seizure require immediate evaluation and treatment. Herein we experienced two young infants with parechovirus-A3 (PeV-A3) encephalitis, initially presented with focal seizure suspecting herpes simplex virus (HSV)

Valacyclovir treatment ameliorates the persistently increased pentylenetetrazol-induced seizure susceptibility in mice with herpes simplex virus type 1 infection.

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Herpes simplex virus type 1 (HSV-1) is an important pathogen related to epilepsy. We have shown previously that corneal inoculation of mice with HSV-1 causes acute spontaneous behavioral and electrophysiological seizures and increases hippocampal excitability and kainite-induced seizure

Viral risk factor for seizures: pathobiology of dynorphin in herpes simplex viral (HSV-1) seizures in an animal model.

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Up to 89% of patients with herpes simplex virus type-1 (HSV-1) encephalitis can have seizures. Possibly, viruses are environmental triggers for seizures in genetically vulnerable individuals. Inherited dynorphin promoter polymorphisms are associated with temporal lobe epilepsy and febrile seizures

Seizure, neuron loss, and mossy fiber sprouting in herpes simplex virus type 1-infected organotypic hippocampal cultures.

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OBJECTIVE Epileptic seizures are frequently seen after viral encephalitis. Herpes simplex virus type 1 (HSV-1) encephalitis is the most common cause of acquired epilepsy in humans. However, little information is available about the neuropathogenesis of HSV-1-associated seizures. We have developed an

Neuropathology of herpes simplex virus encephalitis in a rat seizure model.

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Herpes simplex virus type 1 (HSV-1) is the cause of a serious and often fatal encephalitis. Patients who survive herpes simplex encephalitis (HSE) experience behavioral abnormalities including profound cognitive dysfunctions. We have developed a rat model of acute HSE to investigate the cognitive

Seizures and epilepsy in herpes simplex virus encephalitis: current concepts and future directions of pathogenesis and management.

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Mortality related to herpes simplex virus encephalitis (HSE) dropped dramatically with the systematic initiation of antiviral treatment in encephalitic syndromes. Further efforts need to be taken to reduce long-term morbidity in the survivors. In this regard, the high rate of postencephalitic

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