Literature DB >> 8559385

Plasmapheresis in Rasmussen's encephalitis.

P I Andrews1, M A Dichter, S F Berkovic, M R Newton, J O McNamara.   

Abstract

Rasmussen's encephalitis (RE) is a progressive childhood disorder characterized by intractable focal seizures, hemiplegia, dementia, and inflammatory histopathology. The process is typically limited to one cerebral hemisphere. We report four patients with pathologically confirmed RE who were treated with repeated plasmapheresis. Three patients exhibited repeated, dramatic, transient responses to plasmapheresis, manifested by reduced seizure frequency and improved neurologic function. One patient exhibited marginal improvement after treatment with plasmapheresis. These observations indicate that circulating factors, likely autoantibodies, are pathogenic in at least some patients with RE and suggest that RE is an autoimmune disease. Plasmapheresis may be a useful adjunctive therapy in status epilepticus, and can also aid in assessment of residual function in the diseased hemisphere before surgical resection.

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Year:  1996        PMID: 8559385     DOI: 10.1212/wnl.46.1.242

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  18 in total

1.  Utility of Tc 99m HMPAO SPECT in the early diagnosis of Rasmussen's syndrome.

Authors:  F Paladin; G Capovilla; A Bonazza; R Mameli
Journal:  Ital J Neurol Sci       Date:  1998-08

Review 2.  Future prospects for the drug treatment of epilepsy.

Authors:  A Nicolson; J P Leach
Journal:  CNS Drugs       Date:  2001       Impact factor: 5.749

3.  Struggling with Rasmussen's syndrome.

Authors:  Eileen P G Vining
Journal:  Epilepsy Curr       Date:  2006 Jan-Feb       Impact factor: 7.500

4.  Humanized mouse model of Rasmussen's encephalitis supports the immune-mediated hypothesis.

Authors:  Hania Kebir; Lionel Carmant; François Fontaine; Kathie Béland; Ciprian M Bosoi; Nathalie T Sanon; Jorge I Alvarez; Sébastien Desgent; Camille L Pittet; David Hébert; Marie-Josée Langlois; Rose-Marie Rébillard; Dang K Nguyen; Cécile Cieuta-Walti; Gregory L Holmes; Howard P Goodkin; John R Mytinger; Mary B Connolly; Alexandre Prat; Elie Haddad
Journal:  J Clin Invest       Date:  2018-04-09       Impact factor: 14.808

Review 5.  Intravenous immunoglobulin in neurological disease: a specialist review.

Authors:  C M Wiles; P Brown; H Chapel; R Guerrini; R A C Hughes; T D Martin; P McCrone; J Newsom-Davis; J Palace; J H Rees; M R Rose; N Scolding; A D B Webster
Journal:  J Neurol Neurosurg Psychiatry       Date:  2002-04       Impact factor: 10.154

Review 6.  Rasmussen's encephalitis: clinical features, pathobiology, and treatment advances.

Authors:  Sophia Varadkar; Christian G Bien; Carol A Kruse; Frances E Jensen; Jan Bauer; Carlos A Pardo; Angela Vincent; Gary W Mathern; J Helen Cross
Journal:  Lancet Neurol       Date:  2014-02       Impact factor: 44.182

Review 7.  Immunity and Inflammation in Epilepsy.

Authors:  Annamaria Vezzani; Bethan Lang; Eleonora Aronica
Journal:  Cold Spring Harb Perspect Med       Date:  2015-12-18       Impact factor: 6.915

Review 8.  Immunomodulatory therapies in neurologic critical care.

Authors:  Logan M McDaneld; Jeremy D Fields; Dennis N Bourdette; Anish Bhardwaj
Journal:  Neurocrit Care       Date:  2009-09-23       Impact factor: 3.210

Review 9.  Encephalitis and epilepsy.

Authors:  Jan Bauer; Christian G Bien
Journal:  Semin Immunopathol       Date:  2009-09-11       Impact factor: 9.623

Review 10.  Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, anti-NMDA-NR1 antibodies, anti-NMDA-NR2A/B antibodies, anti-mGluR1 antibodies or anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren's syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor's expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy.

Authors:  Mia Levite
Journal:  J Neural Transm (Vienna)       Date:  2014-08-01       Impact factor: 3.575

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