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Prognostic Implications of Early Albuminocytological Dissociation in Guillain–Barré Syndrome

Published online by Cambridge University Press:  18 August 2022

Edwin Steven Vargas-Cañas
Affiliation:
Neuromuscular diseases Department, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
Javier Andrés Galnares-Olalde
Affiliation:
Neuromuscular diseases Department, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
Fausto León-Velasco
Affiliation:
Neurology Department, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
Miguel García-Grimshaw
Affiliation:
Neurology Department, Neurology Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico
Alonso Gutiérrez
Affiliation:
Neurology Department, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
Juan Carlos López-Hernández*
Affiliation:
Neuromuscular diseases Department, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, Mexico City, Mexico
*
Corresponding author: Juan Carlos López-Hernández, Insurgentes Sur 3877, LA Fama, Tlalpan, Mexico City, Mexico. Email: juanca9684@hotmail.com

Abstract:

Background:

Half of Guillain–Barré syndrome (GBS) present elevated cerebrospinal fluid (CSF) protein levels within 1 week since symptom onset and 80% within 2 weeks. Our objective was to determine the clinical and prognostic implication of albuminocytological dissociation in early GBS.

Methods:

An ambispective cohort study was conducted. Good outcome was considered if the patient was able to walk unaided (Guillain-Barré disability score [GDS] ≤ 2 points) at 3-month follow-up. Patients were classified into two groups: with and without albuminocytological dissociation; we compared clinical and paraclinic characteristics between the groups. We analyzed clinical and electrophysiological factors related to presenting early dissociation through a multivariate model.

Results:

We included 240 patients who fulfilled Asbury criteria for GBS. On further selection, only 94 patients fulfilled inclusion. Mean age was 45.94 ± 17.1 years and 67% were male. Median time from symptom onset to admission was 5 days (IQR 3–6). Regarding albuminocytological dissociation and electrophysiological variants, we found a significant difference: acute inflammatory demyelinating polyneuropathy (AIDP) [60.6% vs 26.2%, p = 0.002], acute motor axonal neuropathy (AMAN) [21.2% vs 49.1%, p = 0.009] and acute motor sensory axonal neuropathy (AMSAN) [12.1% vs 1.6%, p = 0.05]. We did not observe significant differences in recovery of independent walking in short term between both groups. The presence of conduction block in any variant (OR 3.21, 95% CI 1.12–9.16, p = 0.02) and absence of sural registration (OR 5.69, 95% CI 1.48–21.83, p = 0.011) were independent factors related to early dissociation.

Conclusions:

Early dissociation (<7 days) is not associated with any particular clinical feature or unfavorable outcome. It is more common to see in AIDP rather than axonal variants.

Résumé :

RÉSUMÉ :

Implications pronostiques de la dissociation albumino-cytologique précoce dans le cas du syndrome de Guillain-Barré.

Contexte :

La moitié des cas de syndrome de Guillain-Barré (SGB) présentent des taux élevés de protéines dans le liquide céphalo-rachidien (LCR) dans la semaine suivant l’apparition des symptômes et 80 % d’entre eux dans les deux semaines. Notre objectif est ici de déterminer l’implication clinique et pronostique de la dissociation albumino-cytologique à un stade précoce du SGB.

Méthodes :

Une étude de cohorte ambispective a ainsi été effectuée. Un résultat a été considéré « bon » dans la mesure où un patient était capable de marcher sans aide (GDS ≤ 2 points) lors d’un suivi effectué au bout de 3 mois. Les patients à l’étude ont été classés en deux groupes : avec et sans dissociation albumino-cytologique. Nous avons ensuite comparé entre elles les caractéristiques cliniques et paracliniques des deux groupes. Au moyen d’un modèle multivarié, nous avons en outre analysé les facteurs cliniques et électro-physiologiques liés à la présentation d’une dissociation précoce.

Résultats :

Nous avons inclus 240 patients qui remplissaient les critères d’Asbury pour le SGB. Après une nouvelle sélection, seuls 94 patients ont été inclus. L’âge moyen de ces derniers était de 45,94 ± 17,1 ans tandis que 67 % étaient des hommes. Le délai médian entre l’apparition des symptômes et l’admission était de 5 jours (EI 3-6). En ce qui concerne la dissociation albumino-cytologique et les variantes électro-physiologiques, nous avons constaté une différence notable : PDIA [60,6 % contre 26,2 %, p = 0,002], NAMA [21,2 % contre 49,1 %, p = 0,009] et NAAMS [12,1 % contre 1,6 %, p = 0,05]. Précisons que nous n’avons pas observé entre les deux groupes de différences significatives dans la récupération autonome à court terme de la marche. La présence d’un bloc de conduction nerveux dans n’importe quelle variante (RC 3,21 ; IC 95 % 1,12-9,16; p = 0,02) et l’absence d’enregistrement des triceps suraux (RC 5,69 ; IC 95 % 1,48-21,83 ; p = 0,011) étaient des facteurs indépendants liés à une dissociation précoce.

Conclusions :

La dissociation précoce (< 7 jours) n’est associée à aucune caractéristique clinique particulière ni à une issue défavorable. Elle est plus fréquente dans le cas de la PDIA que dans les autres variantes axonales.

Type
Original Article
Copyright
© The Author(s), 2022. Published by Cambridge University Press on behalf of Canadian Neurological Sciences Federation

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Footnotes

These authors contributed equally to this work.

References

Sejvar, JJ, Kohl, KS, Gidudu, J, et al. Guillain-Barré syndrome and Fisher syndrome: case definitions and guidelines for collection, analysis, and presentation of immunization safety data. Vaccine. 2011;29:599612. DOI 10.1016/j.vaccine.2010.06.003.CrossRefGoogle ScholarPubMed
Fokke, C, van den Berg, B, Drenthen, J, Walgaard, C, van Doorn, PA, Jacobs, BC. Diagnosis of Guillain-Barré syndrome and validation of Brighton criteria. Brain. 2014;137:3343. DOI 10.1093/brain/awt285.CrossRefGoogle ScholarPubMed
Brettschneider, J, Petzold, A, Süssmuth, S, Tumani, H. Cerebrospinal fluid biomarkers in Guillain-Barré syndrome--where do we stand? J Neurol. 2009;256:312. DOI 10.1007/s00415-009-0097-x.CrossRefGoogle ScholarPubMed
Wakerley BR, Uncini A, Yuki N, GBS Classification Group, GBS Classification Group. Guillain-Barré and Miller Fisher syndromes--new diagnostic classification. Nat Rev Neurol. 2014;10:537–44. DOI 10.1038/nrneurol.2014.138 Epub 2014 Jul 29. Erratum in: Nat Rev Neurol. 2014;10:612. PMID: 25072194.CrossRefGoogle Scholar
Berciano, J, Sedano, MJ, Pelayo-Negro, AL, et al. Proximal nerve lesions in early Guillain-Barré syndrome: implications for pathogenesis and disease classification. J Neurol. 2017;264:221–36. DOI 10.1007/s00415-016-8204-2.CrossRefGoogle ScholarPubMed
Walgaard, C, Lingsma, HF, Ruts, L, et al. Prediction of respiratory insufficiency in Guillain-Barré syndrome. Ann Neurol. 2010;67:781–7. DOI 10.1002/ana.21976.Google ScholarPubMed
Berciano, J, Orizaola, P, Gallardo, E, et al. Very early Guillain-Barré syndrome: a clinical-electrophysiological and ultrasonographic study. Clin Neurophysiol Pract. 2019;5:19. DOI 10.1016/j.cnp.2019.11.003.Google ScholarPubMed
Illes, Z, Blaabjerg, M. Cerebrospinal fluid findings in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathies. Handb Clin Neurol. 2017;146:125138. DOI 10.1016/B978-0-12-804279-3.00009-5.CrossRefGoogle ScholarPubMed
Doets, AY, Verboon, C, van den Berg, B,  et al. Regional variation of Guillain-Barré syndrome. Brain. 2018;141:28662877. DOI 10.1093/brain/awy232.CrossRefGoogle ScholarPubMed
Hughes, RA, Newsom-Davis, JM, Perkin, GD, Pierce, JM. Controlled trial prednisolone in acute polyneuropathy. Lancet 1978;2:750-3.CrossRefGoogle ScholarPubMed
Uncini, A, Kuwabara, S. The electrodiagnosis of Guillain-Barré syndrome subtypes: Where do we stand? Clin Neurophysiol. 2018;129:2586-2593. DOI 10.1016/j.clinph.2018.09.025.CrossRefGoogle ScholarPubMed
Wakerley, BR, Yuki, N. Mimics and chameleons in Guillain-Barré and Miller Fisher syndromes. Pract Neurol. 2015;15:90–9. DOI 10.1136/practneurol-2014-000937.CrossRefGoogle ScholarPubMed
Asbury, AK, Cornblath, DR. Assessment of current diagnostic criteria for Guillain-Barré syndrome. Ann Neurol. 1990;27:S21–4.CrossRefGoogle ScholarPubMed
Bourque, PR, Brooks, J, McCudden, CR, Warman-Chardon, J, Breiner, A. Age matters: Impact of data-driven CSF protein upper reference limits in Guillain-Barré syndrome. Neurol Neuroimmunol Neuroinflamm. 2019;6:e576. DOI 10.1212/NXI.0000000000000576.CrossRefGoogle ScholarPubMed
Breiner, A, Moher, D, Brooks, J, Cheng, W, Hegen, H, Deisenhammer, F, McCudden, CR, Bourque, PR. Adult CSF total protein upper reference limits should be age-partitioned and significantly higher than 0.45 g/L: a systematic review. J Neurol. 2019;266:616624. DOI 10.1007/s00415-018-09174-z.CrossRefGoogle ScholarPubMed
Sahin, S, Cinar, N, Karsidag, S. Are cerebrospinal fluid protein levels and plasma neutrophil/lymphocyte ratio associated with prognosis of Guillain Barré syndrome? Neurol Int. 2017;9:7032.CrossRefGoogle ScholarPubMed
Saba, K, Hossieny, ZS, Arnold, WD, et al. CSF protein level and short-term prognosis in Guillain-Barré syndrome. J Clin Neuromuscul Dis. 2019;21:118–9. DOI 10.1097/CND.0000000000000259.CrossRefGoogle ScholarPubMed
López-Hernández, JC, Colunga-Lozano, LE, Galnares-Olalde, JA, Vargas-Cañas, ES. Electrophysiological subtypes and associated prognosis factors of Mexican adults diagnosed with Guillain-Barré syndrome, a single center experience. J Clin Neurosci. 2021;86:85–6.CrossRefGoogle ScholarPubMed
Zaeem, Z, Siddiqi, ZA, Zochodne, DW. Autonomic involvement in Guillain-Barré syndrome: an update. Clin Auton Res. 2019;29:289–99.CrossRefGoogle ScholarPubMed
Michel-Chávez, A, Chiquete, E, Gulías-Herrero, A, Carrillo-Pérez, DL, Olivas-Martínez, A, Macías-Gallardo, J, Aceves-Buendía, J, Ruiz-Ruiz, E, Bliskunova, T, Portillo-Valle, J, Cobilt-Catana, R, Ortiz-Quezada, JA, Durán-Coyote, S, Rodríguez-Perea, E, Aguilar-Salas, E, Cantú-Brito, C, García-Ramos, G, Estañol, B. Predictors of mechanical ventilation in Guillain-Barré syndrome with axonal subtypes. Can J Neurol Sci. 2022:1–25. DOI 10.1017/cjn.2022.19. Epub ahead of print.Google ScholarPubMed
Fehmi, J, Scherer, SS, Willison, HJ, , Rinaldi S. Nodes, paranodes and neuropathies. J Neurol Neurosurg Psychiatry. 2018;89:6171.CrossRefGoogle ScholarPubMed
Bromberg, MB, Albers, JW. Patterns of sensory nerve conduction abnormalities in demyelinating and axonal peripheral nerve disorders. Muscle Nerve. 1993;16:262–6. DOI 10.1002/mus.880160304.CrossRefGoogle ScholarPubMed
Umapathi, T, Koh, JS, Cheng, YJ, Goh, EJH, Lim, CSJ. The utility of sural-sparing pattern in the electrodiagnosis of regional subtypes of Guillain-Barré Syndrome. Clin Neurophysiol Pract. 2020;5:43–5. DOI 10.1016/j.cnp.2019.12.002.CrossRefGoogle ScholarPubMed