CSF Findings in Relation to Clinical Characteristics, Subtype, and Disease Course in Patients With Guillain-Barré Syndrome.
Journal
Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060
Informations de publication
Date de publication:
06 06 2023
06 06 2023
Historique:
received:
15
07
2022
accepted:
27
02
2023
pmc-release:
06
06
2024
medline:
7
6
2023
pubmed:
20
4
2023
entrez:
19
04
2023
Statut:
ppublish
Résumé
To investigate CSF findings in relation to clinical and electrodiagnostic subtypes, severity, and outcome of Guillain-Barré syndrome (GBS) based on 1,500 patients in the International GBS Outcome Study. Albuminocytologic dissociation (ACD) was defined as an increased protein level (>0.45 g/L) in the absence of elevated white cell count (<50 cells/μL). We excluded 124 (8%) patients because of other diagnoses, protocol violation, or insufficient data. The CSF was examined in 1,231 patients (89%). In 846 (70%) patients, CSF examination showed ACD, which increased with time from weakness onset: ≤4 days 57%, >4 days 84%. High CSF protein levels were associated with a demyelinating subtype, proximal or global muscle weakness, and a reduced likelihood of being able to run at week 2 (odds ratio [OR] 0.42, 95% CI 0.25-0.70; ACD is a common finding in GBS, but normal protein levels do not exclude this diagnosis. High CSF protein level is associated with an early severe disease course and a demyelinating subtype. Elevated CSF cell count, rarely ≥50 cells/μL, is compatible with GBS after a thorough exclusion of alternative diagnoses. This study provides Class IV evidence that CSF ACD (defined by the Brighton Collaboration) is common in patients with GBS.
Sections du résumé
BACKGROUND AND OBJECTIVES
To investigate CSF findings in relation to clinical and electrodiagnostic subtypes, severity, and outcome of Guillain-Barré syndrome (GBS) based on 1,500 patients in the International GBS Outcome Study.
METHODS
Albuminocytologic dissociation (ACD) was defined as an increased protein level (>0.45 g/L) in the absence of elevated white cell count (<50 cells/μL). We excluded 124 (8%) patients because of other diagnoses, protocol violation, or insufficient data. The CSF was examined in 1,231 patients (89%).
RESULTS
In 846 (70%) patients, CSF examination showed ACD, which increased with time from weakness onset: ≤4 days 57%, >4 days 84%. High CSF protein levels were associated with a demyelinating subtype, proximal or global muscle weakness, and a reduced likelihood of being able to run at week 2 (odds ratio [OR] 0.42, 95% CI 0.25-0.70;
DISCUSSION
ACD is a common finding in GBS, but normal protein levels do not exclude this diagnosis. High CSF protein level is associated with an early severe disease course and a demyelinating subtype. Elevated CSF cell count, rarely ≥50 cells/μL, is compatible with GBS after a thorough exclusion of alternative diagnoses.
CLASSIFICATION OF EVIDENCE
This study provides Class IV evidence that CSF ACD (defined by the Brighton Collaboration) is common in patients with GBS.
Identifiants
pubmed: 37076309
pii: WNL.0000000000207282
doi: 10.1212/WNL.0000000000207282
pmc: PMC10256127
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2386-e2397Investigateurs
R A C Hughes
(RAC)
H P Hartung
(HP)
L C de Koning
(LC)
M Mandarakas
(M)
M van Woerkom
(M)
R C Reisin
(RC)
S W Reddel
(SW)
S T Hsieh
(ST)
J M Addington
(JM)
S Ajroud-Driss
(S)
L Alessandro
(L)
U A Badrising
(UA)
G Balloy
(G)
I R Bella
(IR)
T E Bertorini
(TE)
R Bhavaraju-Sanka
(R)
M Bianco
(M)
T H Brannagan
(TH)
K Brennan
(K)
C Briani
(C)
S Butterworth
(S)
C C Chao
(CC)
S Chen
(S)
K G Claeys
(KG)
M E Conti
(ME)
J S Cosgrove
(JS)
M C Dalakas
(MC)
M Derejko
(M)
M M Dimachkie
(MM)
A Echaniz-Laguna
(A)
C Fokke
(C)
T Fujioka
(T)
E A Fulgenzi
(EA)
T García Sobrino
(TG)
C J Gijsbers
(CJ)
J M Gilchrist
(JM)
J M Goldstein
(JM)
J Goodfellow
(J)
N A Goyal
(NA)
S Grisanti
(S)
L Gutmann
(L)
M Htut
(M)
K Jellema
(K)
I Jericó Pascual
(IJ)
M C Jimeno-Montero
(MC)
K Kaida
(K)
H Kerkhoff
(H)
M Khoshnoodi
(M)
L Kiers
(L)
M Kuwahara
(M)
J Y Kwan
(JY)
S S Ladha
(SS)
L Landschoff Lassen
(LL)
V Lawson
(V)
E Lee Pan
(EL)
M P T Lunn
(MPT)
H Manji
(H)
C Márquez Infante
(CM)
E Martinez Hernandez
(EM)
G Mataluni
(G)
M G Mattiazzi
(MG)
C J McDermott
(CJ)
G D Meekins
(GD)
G Morís de la Tassa
(G)
C Nascimbene
(C)
R J Nowak
(RJ)
P Orizaola
(P)
M Osei-Bonsu
(M)
A Pardal
(A)
E Pascual-Goñi
(E)
R M Pascuzzi
(RM)
V Prada
(V)
M Pulley
(M)
I Rojas-Marcos
(I)
S A Rudnicki
(SA)
G M Sachs
(GM)
L Santoro
(L)
A Savransky
(A)
L Schwindling
(L)
Y Sekiguchi
(Y)
C L Sommer
(CL)
C-Y Tan
(CY)
H Tankisi
(H)
P T Twydell
(PT)
P van Damme
(P)
T van der Ree
(T)
R van Koningsveld
(R)
J D Varrato
(JD)
V Vélez Santamaria
(VV)
C Walgaard
(C)
Y Yamagishi
(Y)
L Zhang
(L)
None Mm
L Zhou
(L)
Commentaires et corrections
Type : CommentIn
Type : ErratumIn
Informations de copyright
© 2023 American Academy of Neurology.
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