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Original Article

Effect of conduction block in classification and

prognosis of Guillain‑Barre syndrome

Yu‑Chen Wang, Guo‑Dong Feng, Jing Wang, Xue‑Dong Liu, Gang Zhao
Department of Neurology, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, Shaanxi, China.

ABSTRA CT
Aim: The aim was to investigate the electro‑physiological characteristics in disease progression of Guillain‑Barre syndrome (GBS) and
observe the effect of conduction block (CB) in classification and severity of the disease. Methods: Two hundred and ninety‑four patients
with GBS were divided into acute inflammatory demyelinating poly‑neuropathy (AIDP) group, acute motor axonal neuropathy (AMAN)
group and equivocal group according to their electro‑physiological results and then reclassificated after electro‑physiological review.
All of the patients were followed for 6 months since their attacks. Results: Bad prognosis is more pronounced in AMAN group than
in AIDP group (P < 0.05). Most of the patients classificated as AIDP transformed into AMAN when CB occurred in the early phase
of the disease. There is a positive relationship between CB in the early phase of the disease and severity of illness (P < 0.05),
but CB showed no correlation with prognosis of the patients (P > 0.05). Conclusion: CB in the early phase of GBS indicates the
probability of AIDP transforming into AMAN; it suggests that patients with CB in the early phase of the disease might be in serious
conditions in a certain extent.

Key words: Clinical features, Guillain‑Barre syndrome, nerve conduction block, nerve electrophysiology

INTRODUCTION of the GBS patients have a good prognosis, but some
may have a bad prognosis clinically. As the disease
Gillan-Barre syndrome (GBS), which is also progresses, some of the AIDP patients may turn into
known as acute inflammatory demyelinating AMAN; some patients without obvious curative effect
polyradiculoneuropathy, is an autoimmune disease may progress into chronic inflammatory demyelinating
in which the typical clinical symptoms are rapidly polyneuropathy; and some patients may transform
progressing symmetrical weakness, areflexia and into relapsing GBS. Neural electro-physiological
cerebrospinal fluid (CSF) protein levels elevated without examination, an irreplaceable auxiliary examination
accompanying pleocytosis. It usually affects spinal for diagnosis of GBS, can provide an important basis
nerve roots especially the anterior roots, ganglions and for the diagnosis and classification of the disease. In
peripheral nerves, sometimes affects the cranial nerves. this study, the clinical data of 338 GBS patients who
were hospitalized during the period of August 2008 to
According to its clinical manifestation, laboratory February 2013 were analyzed retrospectively.
examinations and electro-physiological characteristics,
GBS can be classified as acute inflammatory METHODS
demyelinating poly-neuropathy (AIDP), acute motor
axonal neuropathy (AMAN), acute motor sensory axonal Patients
neuropathy, Miller-Fisher syndrome (MFS), acute This study retrospectively includes 338 GBS patients
[1]
autonomic neuropathy, and acute sensory neuropathy. who were hospitalized during the period of August 2008
GBS is single-phase process and self-limiting, so most to February 2013. All the cases were diagnosed under the
diagnosis and treatment guidelines of GBS published in
Access this article online 2010 by Chinese medicine association. Excluding 20 cases
Quick Response Code: without neural electro-physiological examination and
Website: 24 patients who were diagnosed with MFS, 294 cases
www.nnjournal.net
were included in this study eventually, with 186 male
DOI: patients (63.3%) and 108 female patients (36.7%). Patient’s
10.4103/2347-8659.139718 ages ranged from 4 to 82 years (mean 40.4 ± 18.3 years),
and the average hospital stay was 18.8 days. There

Corresponding Author: Dr. Yu‑Chen Wang, Department of Neurology, Xijing Hospital, The Fourth Military Medical University,
No. 169 Changle West Road, Xi’an 710032, Shaanxi, China. E‑mail: xianhhwangyc@hotmail.com

Neuroimmunol Neuroinflammation | Volume 1 | Issue 2 | September 2014 77