Brain barrier dysfunction in Cuban Epidemic Optic Neuropathy

Background and purpose: There are practically no references to cerebrospinal fluid(CSF) studies in tropical or nutritional neuropathies. In the present paper we present the results of CSF studies in patients with Cuban Epidemic Optic Neuropathy (CEON) during epidemic and endemic periods, with an ap...

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Bibliographic Details
Published in:	European journal of neurology Vol. 15; no. 6; pp. 613 - 618
Main Authors:	González-Quevedo Monteagudo, A., Fernández Carriera, R., Santiesteban Freixas, R., Alfaro Capdegelle, I., Lara Rodríguez, R., Vicente Valdés, I., Santiago Luis González, R.
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-06-2008
Subjects:	Adult Aged blood brain barrier Blood-Brain Barrier - pathology cerebrospinal fluid Cuba - epidemiology Disease Outbreaks epidemic neuropathy Female Humans Immunoglobulin G - blood Immunoglobulin G - cerebrospinal fluid Male Middle Aged nutritional neuropathy Optic Nerve Diseases - cerebrospinal fluid Optic Nerve Diseases - epidemiology Optic Nerve Diseases - pathology optic neuropathy Time Cuba
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Summary:	Background and purpose: There are practically no references to cerebrospinal fluid(CSF) studies in tropical or nutritional neuropathies. In the present paper we present the results of CSF studies in patients with Cuban Epidemic Optic Neuropathy (CEON) during epidemic and endemic periods, with an appraisal as to the contribution of brain barriers′ function in the pathophysiology of this disease. Methods: Two hundred and five patients with CEON were studied during the epidemic period (1992–1993) and 12 patients outside the outbreak (1995–1997). CSF protein determination and electrophoresis were carried out, as well as serum and CSF albumin and immunoglobulin G (IgG) quantitation for calculating IgG and Qalb indexes, in order to evaluate intrathecal IgG synthesis and the permeability of the blood–CSF barrier (B‐CSF B). Results: One fourth of the patients had increased permeability of the B‐CSF B, but damage was more frequent between 16 and 60 days from onset of disease, disappearing after 120 days. B‐CSF B dysfunction was more prevalent in patients with severe neurological impairment, although it was not related to the severity of ophthalmological damage. The group of patients studied outside of the outbreak (endemic period) showed similar results. Discussion: The possible association of increased permeability of the B‐CSF B with oxidative stress, which lies on the basis of this epidemic outbreak, is discussed.
Bibliography:	istex:AD4C440F63394DC3C0BA2137CDCD9C98A63BAE74 ArticleID:ENE2136 ark:/67375/WNG-5NZ4BK68-G ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1351-5101 1468-1331 1471-0552
DOI:	10.1111/j.1468-1331.2008.02136.x