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

Autor(es): Gonzalez-Quevedo A,Carriera R Fernandez,O'Farrill Z Lestayo,Luis I Suarez,Becquer R Mustelier,Luis Gonzalez R S


Resumo: Elevated cerebrospinal fluid (CSF) total protein (TP) concentration (mainly due to a dysfunctional blood-CSF barrier (B-CSFB)) with normal cell count is a hallmark for the diagnosis of Guillain-Barriota syndrome (GBS). This work presents the evaluation of B-CSFB dysfunction with respect to the course, severity, and clinical features of GBS. A sample of CSF was collected on admission from 68 patients of both genders (15 children and 53 adults) diagnosed with GBS. A follow-up CSF sample was obtained approximately 15 days after admission. TP concentration was determined in the CSF and 7.5% polycrylamide gel electrophoresis was employed for serum and CSF protein fractioning. A low percentage of prealbumin fraction was considered a test of impaired B-CSFB. Elevated TP concentration and lower prealbumin were observed in almost 70% of the patients on admission, but this percentage was lower (52.4%) during the first week from onset of symptoms. Both variables were directly associated with the time of evolution of the disease and also with a greater clinical severity. Follow-up CSF studies showed higher CSF TP and lower prealbumin percentages, while deceased patients did not display this response pattern in the follow-up CSF. B-CSFB dysfunction was present in only half of the patients with GBS during the first week from onset and it was directly associated with progression and clinical severity; nevertheless, a low B-CSFB dysfunction response during follow-up was associated with a lethal outcome, suggesting it could also serve a 'protective' effect during regeneration.


Imprenta: Neurology India, v. 57, n. 3, p. 288-294, 2009


Identificador do objeto digital: 10.4103/0028-3886.53282


Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Public health


Data de publicação: 2009