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

Abstract

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.

Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome) following dengue fever

“…This fact can be explained because, unlike other arboviruses 2 , this virus rarely affects the central nervous system. The pathophysiology of these neurological complications can be explained by the occurrence of cerebral edema, cerebral hemorrhage, hyponatremia, liver failure associated with portasystemic encephalopathy, cerebral anoxia, microcapillary hemorrhage and/or the release of toxic products, which can occur separately or together 9 .…”

An unusual case of recurrent Guillain-Barré syndrome with normal cerebrospinal fluid protein levels: a case report

“…Study done by Gonzalez-Quevedo et al revealed raised CSF total proteins correlated with the degree of inflammation at the nerve roots and higher level of CSF proteins were related to clinical severity [12]. Corston et al studied amino acids in CSF of GBS patients quantitatively as well as qualitatively.…”

Relationship Between Cerebrospinal Fluid Protein Levels and Electrophysiologic Abnormalities in Guillain–Barré Syndrome

“…Within the first week of symptoms, normal CSF protein levels can be expected in anywhere from 33%-52% of patients. 9,11 Likewise, early on in the disease course, the well-described electrophysiologic abnormalities of prolonged distal latencies, slowed conduction velocities, abnormal F-waves, and temporal dispersion and/or conduction block are not typically present in their entirety. [12][13][14] Although the precise reason for the characteristic cytoalbuminologic dissociation described in GBS is not completely understood, it is likely due to early nerve root involvement.…”

“…14 With the premise that AIDP is a predominantly humorally mediated disease process, the CSF protein levels of patients with GBS can be used as a marker of BNB dysfunction. 7,9,10 Our retrospective review demonstrates that the degree of CSF protein elevation correlates with the number of electrophysiologic abnormalities on nerve conduction studies (NCSs) in patients with GBS.…”

“…7,8 Directly measuring the integrity of the blood-brain and BNB is challenging; however, elevated CSF protein concentration can be used as a surrogate marker in patients with GBS as it has been associated with increased permeability of the this barrier. 9 The destruction or malfunction of the BNB is considered to be one of the initiating pathologic disease processes in AIDP. In fact, sera from patients with GBS affect the permeability of the BNB, supporting the involvement of humoral factors causing BNB derangement in the acute stage.…”