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Articles linked to this work by shared authors, journal, and citation graph.

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An appraisal of blood-cerebrospinal fluid barrier dysfunction during the course of Guillain Barré syndrome.

Neurology India·2009
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[Immunological study of cerebrospinal fluid using a human IgM antiserum produced in Cuba. A preliminary evaluation].

Revista de neurologia·2002
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[Folic acid deficiency and increased concentrations of formate in serum and cerebrospinal fluid of patients with epidemic optical neuropathy].

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[Amino acids as biochemical markers in epidemic and endemic optic neuropathies].

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[A retrospective study of patients with epidemic optic neuropathy in a health area].

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[The research and work of the Instituto de Neurología y Neurocirugía on epidemic neuropathy from the 1st workshop in 1994 up to the date of the 2nd workshop in 1998].

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Updated: Jul 6, 2026

An Acute Retinal Model for Evaluating Blood Retinal Barrier Breach and Potential Drugs for Treatment
09:33

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Published on: September 13, 2016

Brain barrier dysfunction in Cuban epidemic optic neuropathy.

A González-Quevedo Monteagudo1, R Fernández Carriera, R Santiesteban Freixas

  • 1Instituto de Neurología y Neurocirugía, Vedado, La Habana, Cuba. aglez@infomed.sld.cu

European Journal of Neurology
|April 16, 2008
PubMed
Summary

Cerebrospinal fluid (CSF) studies in Cuban Epidemic Optic Neuropathy (CEON) revealed increased blood-CSF barrier permeability in one-fourth of patients, particularly those with severe neurological impairment. This dysfunction, linked to oxidative stress, was transient and more common during the epidemic phase.

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Area of Science:

  • Neuroscience
  • Neurology
  • Immunology

Background:

  • Limited cerebrospinal fluid (CSF) research exists for tropical and nutritional neuropathies.
  • Cuban Epidemic Optic Neuropathy (CEON) serves as a model for studying neuro-inflammation and barrier function.

Purpose of the Study:

  • To investigate cerebrospinal fluid (CSF) alterations in patients with Cuban Epidemic Optic Neuropathy (CEON).
  • To assess the role of blood-brain barrier (B-CSF B) function in CEON pathophysiology during epidemic and endemic periods.

Main Methods:

  • Studied 205 CEON patients during an epidemic (1992-1993) and 12 during an endemic period (1995-1997).
  • Performed CSF protein analysis, electrophoresis, and quantified serum/CSF albumin and IgG.
  • Calculated IgG and Q(alb) indexes to evaluate intrathecal IgG synthesis and blood-CSF barrier (B-CSF B) permeability.

Main Results:

  • Increased blood-CSF barrier (B-CSF B) permeability was observed in 25% of patients.
  • B-CSF B dysfunction peaked between 16-60 days post-onset and resolved after 120 days.
  • Barrier dysfunction correlated with neurological severity but not ophthalmological damage; similar findings were noted in the endemic period.

Conclusions:

  • Transient blood-CSF barrier (B-CSF B) dysfunction is implicated in CEON pathophysiology.
  • The observed B-CSF B permeability increase may be associated with oxidative stress, a potential underlying mechanism for the epidemic outbreak.