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discharge. The response rate was 65.0%. Twenty-one literature, [10,11] thus suggesting a poor prognosis in more
percent of the patients had serous sequel which was the patients. The classification based on early stage GBS
same as those reported in the literature. The mortality electrophysiologic results only may lead to inaccurate
was 10.6% which was higher than previously reported. [6] judgment of the patients’ diagnosis and prognosis,
instead continuous electrophysiology recheck can
The most common subtypes of GBS are AIDP and reflect the change of patient’s condition without delay.
AMAN with only motor fiber damage. According to
the literature, in North America and Europe more Among the patients transforming from AIDP into
than 90% of the patients is classified as AIDP, but AMAN, CB occurred in 17 cases in the early onset
[4]
in China, the most common subtype is AMAN, and of the illness: 5 and 7 cases in AMAN and unclear
65% of the GBS are AMAN. In this study, most cases classification group, respectively. CB is a blockage in
[7]
among the 294 GBS patients were AIDP. Of these, a nerve that prevents impulses from being conducted
132 cases were classified as AIDP based on their first across a given segment although the nerve beyond is
electro-physiological examination. These findings are viable and is one of the important electro-physiological
in contrast with what previously reported. parameters of peripheral nerve functional status.
CB is one of the physiological results caused by
Because the classification based on early stage demyelination and is also the basic physiological
GBS electro-physiological results is inaccurate, mechanism of most clinical manifestations. [12] Most
electrophysiology testing was repeated after the illness studies of CB published before are on multifocal motor
developed and the percentage of AIDP and AMAN neuropathy and amyotrophic lateral sclerosis, peroneal
cases changed comparing to the early stage results. muscular atrophy and peripheral neuropathy caused by
[8]
We classified patients into AIDP and AMAN groups pressure. [13] Though conventional wisdom holds that
and unclear classification group which included the main cause of CB is demyelination and CB is the
patients whose electro-physiological testing were typical characteristics of demyelinating, recent studies
normal and those who did not meet the diagnostic demonstrated that demyelination is not the only reason
criteria of AIDP and AMAN. We found that during for CB. It can caused by demyelination, depolarization
disease progression electro-physiological results, on node of ranvier nearby axolemma, hyperpolarization
as well as the electro-physiological classification, and sodium channel damage. [14] The damage of nearby
changed. The percentage of AMAN patients after axolemma may cause CB, electro-physiological manifest
recheck increased significantly compared to the first as decreased amplitude, discretized waveform. If the
check (from 18% to 41%), which is the same as reported illness continues to progress, reversible CB will turn
literature, [8,9] and AIDP reduced from 44% to 31%. into irreversible CB, and axonal degeneration. This
We also found that AMAN had a worse prognosis might explain why some of the CB cases transformed
than AIDP, and this finding is consistent with the into AMAN in electro-physiological classification.

Table 2: All cases classifications and prognosis Our study demonstrated that CB not only occurred in
Prognosis AIDP AMAN Total AIDP patients, but also in AMAN and unclear classification
Good prognosis 59 27 86 patients. In recent years, other groups found that CB plays
Poor prognosis 12 19 31 an important role in axon damaged AMAN. [15,16] Kuwabara
Total 71 46 117 [17]
2
χ = 8.535, P = 0.003. AIDP: acute inflammatory demyelinating poly‑neuropathy; et al. thought that the possible cause of CB in AMAN
AMAN: acute motor axonal neuropathy was axonal degeneration. The bridge type union of GM-1
antibody-mediated inflammatory cells and axons, the
Table 3: Rechecked cases classifications and prognosis release of inflammatory mediators, local acidosis, damage
Prognosis AIDP AMAN Total on sodium ion channel of Axonal membrane and tight
Good prognosis 35 8 43 junction of axon myelin (some authors believe that this
Poor prognosis 6 9 15 is a different type of demyelination from AIDP) resulted
Total 41 17 58 in a further decline of the safety factors, eventually
χ = 9.197, P = 0.002. AIDP: acute inflammatory demyelinating poly‑neuropathy;
2
AMAN: acute motor axonal neuropathy leading to CB. [18]

Table 4: Relationship between different classifications nerve CB and the severity in 294 cases
Severity AIDP AMAN Unclear
With CB Without CB Total With CB Without CB Total With CB Without CB Total
Slight 6 18 24 2 17 19 2 24 26
Severe 50 28 78 20 42 62 32 53 85
Total 56 46 102 22 59 81 34 77 111
AIDP: acute inflammatory demyelinating poly‑neuropathy; AMAN: acute motor axonal neuropathy; CB: conduction block

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