Neurologic function was also evaluated by using the Medical Research Council (MRC) sum score of six bilateral muscle tissue in arms and legs, ranging from 0 (tetraparalytic) to 60 (normal strength)[14]. The short-term prognosis of ganglioside-associated GBS, as measured by the HFGS score and the MRC sum score at discharge, was poorer (4.30.5 vs 2.81.1; 17.312.9 vs 46.013.9, bothp<0.001). All the patients in the ganglioside+ group offered an axonal form of GBS, namely acute motor axonal neuropathy (AMAN). When compared with the AMAN patients in the ganglioside group, more severe functional deficits at nadir and poorer recovery after standard treatment were still prominent in ganglioside-associated GBS. Anti-GM1 and anti-GT1a antibodies were detectable in patients with AMAN while not in patients with the demyelinating subtype of GBS. The concentrations of these BAX antibodies in patients with AMAN were insignificantly different between the ganglioside+ and ganglioside groups. In sum, ganglioside-associated GBS may be a devastating side effect of intravenous use of gangliosides, which usually manifests a more severe clinical course and poorer end result. == Introduction == Guillain-Barr syndrome (GBS) is an immune-mediated disorder in the peripheral nervous system with inflammatory infiltration, Alosetron demyelination and/or axonal damage as the main pathological features[1]. Depending on the involvement of nerve fiber types (sensory, motor and autonomic) and the predominant nature of nerve injury (demyelination or axonal degeneration), GBS can be divided into acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor-sensory axonal neuropathy (AMSAN), Miller-Fisher syndrome (MFS) and some other relatively rare subtypes[1]. AIDP and AMAN are the major subtypes of GBS and they are distinct from each other in terms of immunopathogenesis, electrophysiological findings, pathological changes and responses to treatment, etc[2]. AMAN, a real motor axonal subtype of GBS, which was in the beginning recognized from GBS Alosetron patients in northern China[3], is usually more frequent in eastern Asia and Central and South America[2]. Immunohistochemical studies on AMAN revealed antibody-mediated damage to the motor axonal membrane suggestive of an immune response directed against the motor axolemma[3][4]. AMASN is usually another axonal Alosetron subtype of GBS in which axonal degeneration entails both motor and sensory nerves[1]. AMAN and AMASN are associated withCampylobacter jejunienteritis and antibodies against gangliosides[2]. High titers of anti-GM1 antibodies were found in patients who developed GBS following exogenous gangliosides injection[5][7], leading to the suspicion that exogenous gangliosides might be foreign to humans and may act as an immunogenic agent. The animal model of AMAN shares pathological features with human AMAN[8]. Despite reports on GBS following intravenous use of gangliosides in Europe several decades ago, which led to its withdrawal from European market[9], ganglioside as a nutritional agent has been hitherto widely used in China and ganglioside-associated GBS cases have been rarely documented. Therefore, it remains unknown whether the clinical Alosetron course and the outcome of ganglioside-associated GBS are distinguishable from non-ganglioside-associated sporadic GBS. In this study, we recognized patients who developed GBS after receiving intravenous gangliosides and compared them with those without Alosetron receiving gangliosides, aiming to depict a distinctive picture of ganglioside-associated GSB. == Materials and Methods == == Study subjects == This study was approved by the ethics committee of the First Hospital of Jilin University or college, Changchun, China. Written informed consent was obtained from all patients. All GBS patients who were admitted to Department of Neurology of the First Hospital of Jilin University or college in 2013 were enrolled. These patients fulfilled the diagnostic criteria for GBS[10]. The Department of Neurology of the First Hospital of Jilin University or college is the largest center for the diagnosis and treatment of neurological diseases in northeast China. Gangliosides as an exclusive component (monosialotetrahexosylganglioside sodium salt injection) or part of a compound (cattle encephalon glycoside and ignotin injection) have never been.