The discriminative value of CSF total protein (CSF-TP) in subtypes of Guillain–Barré syndrome has not been well documented in North-American patients. We reviewed 173 cases from a single institution, comprising the following clinical categories of neuropathy: 134 Sensorimotor (SM) GBS, 13 Motor (M) GBS, 8 Localized (L) GBS, and 18 Miller Fisher syndrome (MFS). We grouped the electrophysiological interpretation in primarily demyelinating, primarily axonal and normal / equivocal categories. Mean CSF-TP were substantially higher for SM and L-GBS, as well as cases classified as Acute-onset chronic inflammatory demyelinating polyneuropathy. They were lower for M-GBS and L-GBS. The most statistically significant correlation was found for elevated CSF-TP in GBS cases showing an electrophysiologic pattern classified as demyelinating (1.56 g/L) compared with axonal (0.68 g/L) or normal/ equivocal patterns (0.65 g/L). There was a correlation between CSF-TP and time interval between symptom onset and lumbar puncture. There was a weak correlation between CSF-TP and maximal overall-clinical severity grade, which was likely mostly determined by the electorphysiological pattern. Though CSF-TP is a sensitive test for GBS in the second week after onset, it may not be a reliable predictor of clinical severity. There is a robust association of CSF-TP elevation and a demyelinative electrophysiologic pattern and a suggestion that lower mean CSF-TP values can be expected in GBS-spectrum disorders thought to represent nodo-paranodopathies.
Guillain–Barre syndrome Cerebrospinal fluid protein Albuminocytologic dissociation Immune neuropathy
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Conflicts of interest
The authors of this manuscript have no conflicts of interest to disclose.
This study was approved by the Institutional Ethics (Medical Research) Committee.
van den Berg B et al (2014) Guillain-Barre syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol 10(8):469–482CrossRefGoogle Scholar
Fokke C et al (2014) Diagnosis of Guillain-Barre syndrome and validation of Brighton criteria. Brain 137(Pt 1):33–43CrossRefGoogle Scholar
Willison HJ, Jacobs BC, van Doorn PA (2016) Guillain-Barre syndrome. Lancet 388(10045):717–727CrossRefGoogle Scholar
Bourque PR, Brooks J, McCudden CR, Warman-Chardon J, Breiner A (2019) Age matters: impact of data-driven CSF protein upper reference limits in Guillain-Barré syndrome. Neurol Neuroimmunol Neuroinflamm 6:e576 (In press)CrossRefGoogle Scholar
Wakerley BR, Uncini A, Yuki N (2014) Guillain-Barre and Miller Fisher syndromes–new diagnostic classification. Nat Rev Neurol 10(9):537–544CrossRefGoogle Scholar
Van der Meche FG et al (2001) Diagnostic and classification criteria for the Guillain-Barre syndrome. Eur Neurol 45(3):133–139CrossRefGoogle Scholar
Rajabally YA et al (2015) Electrophysiological diagnosis of Guillain-Barre syndrome subtype: could a single study suffice? J Neurol Neurosurg Psychiatry 86(1):115–119CrossRefGoogle Scholar
Hughes RA et al (1978) Controlled trial prednisolone in acute polyneuropathy. Lancet 2(8093):750–753CrossRefGoogle Scholar
Group, P.E.S.G.-B.S.T (1997) Randomised trial of plasma exchange, intravenous immunoglobulin, and combined treatments in Guillain-Barre syndrome plasma exchange/sandoglobulin Guillain-Barre syndrome trial Group. Lancet 349(9047):225–230CrossRefGoogle Scholar
Wilkinson GN, Rogers CE (1973) Symbolic description of factorial models for analysis of variance. J R Stat Soc Series C (Appl Stat) 22(3):392–399Google Scholar
Fox J, Weisberg S (2018) An R companion to applied regression. Sage, Los AngelesGoogle Scholar
Berlit P, Rakicky J (1992) The Miller Fisher syndrome review of the literature. J Clin Neuroophthalmol 12(1):57–63PubMedGoogle Scholar
Lyu RK et al (1997) Guillain-Barre syndrome in Taiwan: a clinical study of 167 patients. J Neurol Neurosurg Psychiatry 63(4):494–500CrossRefGoogle Scholar
Wong AH et al (2015) Cytoalbuminologic dissociation in Asian patients with Guillain-Barre and Miller Fisher syndromes. J Peripher Nerv Syst 20(1):47–51CrossRefGoogle Scholar
Nishimoto Y et al (2004) Usefulness of anti-GQ1b IgG antibody testing in Fisher syndrome compared with cerebrospinal fluid examination. J Neuroimmunol 148(1–2):200–205CrossRefGoogle Scholar
Hegen H et al (2016) Upper reference limits for cerebrospinal fluid total protein and albumin quotient based on a large cohort of control patients: implications for increased clinical specificity. Clin Chem Lab Med 54(2):285–292CrossRefGoogle Scholar
McCudden CR et al (2017) Cerebrospinal fluid total protein reference intervals derived from 20 years of patient data. Clin Chem 63(12):1856–1865CrossRefGoogle Scholar
Ruts L, van Koningsveld R, van Doorn PA (2005) Distinguishing acute-onset CIDP from Guillain-Barre syndrome with treatment related fluctuations. Neurology 65(1):138–140CrossRefGoogle Scholar
Alessandro L et al (2018) Differences between acute-onset chronic inflammatory demyelinating polyneuropathy and acute inflammatory demyelinating polyneuropathy in adult patients. J Peripher Nerv Syst 23(3):154–158CrossRefGoogle Scholar
Dionne A, Nicolle MW, Hahn AF (2010) Clinical and electrophysiological parameters distinguishing acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy. Muscle Nerve 41(2):202–207PubMedGoogle Scholar