anti-GM1 Ganglioside Antibodies Research Articles

Mixed IgG and IgM anti-GM1 ganglioside antibody positive multifocal motor neuropathy with severe secondary axonal loss in a Filipino female

Approximately 40% of patients with multifocal motor neuropathy had anti-GM1 IgM antibodies, while only 1 out of 88 patients had anti-GM1 IgG antibodies. Unlike its predominantly demyelinating IgM counterpart, the anti-GM1 IgG antibody is often seen in the axonal variant of Guillain Barre syndrome. As it affects axons, it is also associated with worse prognosis. We report here a 58-year-old woman who was admitted for 3 months history of progressive asymmetric weakness, initially involving the right-hand extensors, eventually affecting the contralateral side and the lower extremities. The electrodiagnostic examination revealed multifocal pure motor demyelinating neuropathy with severe axonal loss. On nerve ultrasound, the axons were small in non-compressive areas. The extremely elevated anti-GM1 IgM titer (1:51,200, nv<1:800) was consistent with the diagnosis of MMN. Her anti-GM1 IgG antibodies (1: 12,800, nv<1:800) was also elevated. In conclusion, the presence of concomitant anti-GM IgG and anti-GM1 IgM may lead to an MMN with more severe axonal loss.

Emerging Infection, Vaccination, and Guillain-Barré Syndrome: A Review.

Guillain–Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system that typically develops within 4 weeks after infection. In addition to conventional infectious diseases with which we are familiar, emerging infectious diseases, such as Zika virus infection and coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), have also been suggested to be associated with GBS. GBS is mainly categorized into a demyelinating subtype known as acute inflammatory demyelinating polyneuropathy (AIDP) and an axonal subtype known as acute motor axonal neuropathy (AMAN). Most patients who develop GBS after Zika virus infection or COVID-19 have AIDP. The concept of molecular mimicry between pathogens and human peripheral nerve components was established through studies of AMAN with anti-ganglioside GM1 antibodies occurring after Campylobacter jejuni infection. Although such mimicry between specific pathogens and myelin or Schwann cell components has not been clearly demonstrated in AIDP, a similarity of Zika virus and SARS-CoV-2 proteins to human proteins has been suggested. With the development of global commerce and travel, emerging infectious diseases will continue to threaten public health. From this viewpoint, the development of vaccines and antiviral drugs is important to prepare for and control emerging infectious diseases. Although a decrease in the number of patients after the 2015–2016 Zika epidemic increased the difficulty in conducting phase 3 trials for Zika virus vaccines, the efficacy and safety of new vaccines have recently been demonstrated for COVID-19. In general, vaccines can decrease the risk of infectious disease by stimulating the immune system, and discussions regarding an increased risk of autoimmune disorders, such as GBS, have been ongoing for many years. However, the risk of GBS is not considered a legitimate reason to limit the administration of currently available vaccines, as only a trivial association or no association with GBS has been demonstrated.

Macrophages and Autoantibodies in Demyelinating Diseases.

Myelin phagocytosis by macrophages has been an essential feature of demyelinating diseases in the central and peripheral nervous systems, including Guillain–Barré syndrome (GBS), chronic inflammatory demyelinating polyneuropathy (CIDP), and multiple sclerosis (MS). The discovery of autoantibodies, including anti-ganglioside GM1 antibodies in the axonal form of GBS, anti-neurofascin 155 and anti-contactin 1 antibodies in typical and distal forms of CIDP, and anti-aquaporin 4 antibodies in neuromyelitis optica, contributed to the understanding of the disease process in a subpopulation of patients conventionally diagnosed with demyelinating diseases. However, patients with these antibodies are now considered to have independent disease entities, including acute motor axonal neuropathy, nodopathy or paranodopathy, and neuromyelitis optica spectrum disorder, because primary lesions in these diseases are distinct from those in conventional demyelinating diseases. Therefore, the mechanisms underlying demyelination caused by macrophages remain unclear. Electron microscopy studies revealed that macrophages destroy myelin as if they are the principal players in the demyelination process. Recent studies suggest that macrophages seem to select specific sites of myelinated fibers, including the nodes of Ranvier, paranodes, and internodes, for the initiation of demyelination in individual cases, indicating that specific components localized to these sites play an important role in the behavior of macrophages that initiate myelin phagocytosis. Along with the search for autoantibodies, the ultrastructural characterization of myelin phagocytosis by macrophages is a crucial step in understanding the pathophysiology of demyelinating diseases and for the future development of targeted therapies.

Characteristics, treatments, and prognosis of a critical illness polyneuromyopathy patient with positive anti-GM1 after severe traumatic brain injury: A case report.

To investigate the clinical features, treatment and prognosis of critical illness polyneuromyopathy (CIPNM) in patients with severe traumatic brain injury (sTBI) who had positive anti-ganglioside GM1 (anti-GM1) antibody IgG. A case of CIPNM with positive anti-GM1 antibody IgG was retrospectively analysed and followed-up for 30months. After 1week of treatment with large dose of short-term glucocorticoid and human immunoglobulin, the muscle strength of both lower extremities was restored to grade 1. Three months later, the muscle strength and muscle tension of the patient's limbs returned to normal except for grade 3 of bilateral dorsal extensor muscle strength. In addition, the patient can walk alone with a waddling gait. After 30months, there was no recurrence. The application of large dose of short-term glucocorticoid and human immunoglobulin to CIPNM that are positive for anti-GM1 antibodies may be an effective treatment.

Determining the Utility of the Guillain-Barré Syndrome Classification Criteria.

Background and PurposeSeveral variants of Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) exist, but their frequencies vary in different populations and do not always meet the inclusion criteria of the existing diagnostic criteria. However, the GBS classification criteria by Wakerley and colleagues recognize and define the clinical characteristics of each variant. We applied these criteria to a GBS and MFS cohort with the aim of determining their utility.MethodsConsecutive GBS and MFS patients presenting to our center between 2010 and 2020 were analyzed. The clinical characteristics, electrophysiological data, and antiganglioside antibody profiles of the patients were utilized in determining the clinical classification.ResultsThis study classified 132 patients with GBS and its related disorders according to the new classification criteria as follows: 64 (48.5%) as classic GBS, 2 (1.5%) as pharyngeal-cervical-brachial (PCB) variant, 7 (5.3%) as paraparetic GBS, 29 (22%) as classic MFS, 3 (2.3%) as acute ophthalmoparesis, 2 (1.5%) as acute ataxic neuropathy, 2 (1.5%) as Bickerstaff brainstem encephalitis (BBE), 17 (12.9%) as GBS/MFS overlap, 4 (3%) as GBS/BBE overlap, 1 (0.8%) as MFS/PCB overlap, and 1 (0.8%) as polyneuritis cranialis. The electrodiagnosis was demyelinating in 55% of classic GBS patients but unclassified in 79% of classic MFS patients. Anti-GM1, anti-GD1a, anti-GalNAc-GD1a, and anti-GD1b IgG ganglioside antibodies were more commonly detected in the axonal GBS subtype, whereas the anti-GQ1b and anti-GT1a IgG ganglioside antibodies were more common in classic MFS and its subtypes.ConclusionsMost of the patients in the present cohort met the criteria of either classic GBS or MFS, but variants were seen in one-third of patients. These findings support the need to recognize variants of both syndromes in order to achieve a more-complete case ascertainment in GBS.

Hepatitis E virus-associated Guillain-Barre syndrome: Revision of the literature.

IntroductionThe association between preceding infection of hepatitis E virus (HEV) and Guillain–Barre syndrome (GBS) has been found for more than a decade, while hepatitis E virus‐associated Guillain–Barre syndrome (HEV‐associated GBS) still remains poorly understood. Initially discovered in 2000, the association between GBS and HEV has been focused by neurologists increasingly. Five percent of patients with GBS had preceding acute HEV infection in the Netherlands and higher rate was found in Bangladesh (11%) where HEV is endemic.MethodAn extensive review of relevant literature was undertaken.ResultsHepatitis E virus infection may induce GBS via direct viral damage according to recent research findings. On the other hand, the presence of antiganglioside GM1 or GM2 antibodies in serum of some HEV‐associated GBS patients indicates that HEV infection may trigger GBS by activating autoimmune response to destroy myelin or axon mistakenly. Management of HEV‐associated GBS has no obvious difference from GBS. It mainly consists of supportive therapy and immunotherapy. Intravenous immunoglobulin (IVIG) or plasma exchange (PLEX) was used in most reported cases, which is the main strategy for clinical treatment of HEV‐associated GBS. Whether antiviral therapy could be additional strategy other than the routine therapy to shorten the length of disease course is one of the most urgent problems and requires further study.ConclusionsAn overview of possible pathogenesis will gain a first insight into why HEV, traditionally recognized as only hepatotropic, can induce many neurological disorders represented by GBS. Moreover, understanding of the underlying mechanisms may contribute to development of a novel therapeutic strategy. This review also summarizes management and clinical characteristics of HEV‐associated GBS, aiming to achieve early recognition and good recovery.

Anti-GM1 ganglioside antibodies modulate membrane-associated sphingomyelin metabolism by altering neutral sphingomyelinase activity

Previous studies have shown that patients with Guillain-Barré syndrome express autoantibodies against ganglioside GM1 (GM1), although its pathogenic significance for the development of the disease remains to be elucidated.nSMase2 is the best characterized neutral sphingomyelinase (nSMase) found in neuronal cells. Activation of this enzyme leads to ceramide production, which is a known second messenger of the cell-death program in neuronal cells.We have explored the effects of anti-GM1 antibodies on sphingomyelin metabolism of PC12 cells stably transfected with human trk cDNA (PCtrk cells) by determining their effects on nSMase2 activity. The data we present here strongly suggest that anti-GM1 caused a significant change in sphingomyelin content of the membrane fraction in PCtrk cells. Both nSMase2 activity and the level of nSMase2 protein were significantly decreased by anti-GM1 treatment of PCtrk cells, while acidic SMase activities remained unchanged.Our results indicate, for the first time, that anti-GM1 may produce profound impacts on lipid metabolism in neuronal cell membranes.

The Potential Misdiagnosis of Multifocal Motor Neuropathy as Amyotrophic Lateral Sclerosis—A Case Series

Multifocal motor neuropathy (MMN) is a rare neuropathy that is often treatable with immunomodulatory therapy if diagnosed early. However, accurate diagnosis is difficult due to a significant overlap of symptoms with other neurological conditions, such as amyotrophic lateral sclerosis (ALS). Evidence of immunoglobulin M (IgM) anti-ganglioside GM1 antibodies and electrodiagnostic findings of conduction block are useful diagnostic criteria for MMN but are not universal findings. This review explores the differential diagnosis of MMN and ALS and discusses three cases of MMN initially diagnosed as ALS, in which the correct diagnosis allowed effective treatment. These cases highlight the need for greater awareness of MMN among physicians.

Analysis of the clinical and electrophysiological characteristics of multifocal motor neuropathy

Ten patients diagnosed with multifocal motor neuropathy (MMN) were recruited in the Department of Neurology at Chinese PLA General Hospital from January 1, 2009 to August 31, 2015. The clinical and electrophysiological features were analyzed retrospectively. All patients complained of progressive asymmetric limb weakness, which was more severe in distal than in proximal. Five presented muscle atrophy. None had sensory disturbances. All suffered diminished or disappeared tendon reflex, whereas Babinski signs were negative. Multi-focal conduction block (CB) was confirmed by nerve conduction studies (NCS) in all patients and 7 showed spontaneous potentials in needle electrode electromyography. Abnormal sensory nerve conduction was seen in 3 patients. Laboratory test revealed anti-ganglioside GM1 antibody in cerebrospinal fluid (CSF) in 6 cases and elevated CSF protein in 7 cases. Limb weakness alleviated greatly in 9 cases after intravenous immunoglobulin (IVIg) treatment. But the other one reported poor response, who had long course of disease, serious limb weakness and obvious muscle atrophy. Motor nerve damage is the most important manifestation of MMN and sensory nerve damage may also appear. NCS is essential to the diagnosis of this disease, with CB as the characteristic electrophysiological feature. IVIg is an effective treatment.

Anti-GM1 ganglioside antibodies impair membrane and rafts glycolipids metabolism in PC12 cells

Anti-GM1 ganglioside antibodies impair membrane and rafts glycolipids metabolism in PC12 cells

Concentrations of antiganglioside M1 antibodies, neuron-specific enolase, and interleukin 10 as potential markers of autonomic nervous system impairment in celiac disease.

INTRODUCTION Celiac disease (CD) is an immune-mediated enteropathy related to permanent gluten intolerance, characterized by gastrointestinal symptoms as well as nongastrointestinal symptoms, including neurologic ones. The presence of neuron-specific enolase (NSE), interleukin 10 (IL-10), and antiganglioside M1 (anti-GM1) antibodies has been demonstrated for neurologic conditions as well as immune disorders with neurologic manifestations. OBJECTIVES The aim of the study was to determine the concentrations of IL-10, NSE, and anti-GM1 antibodies in the course of CD and their correlation with changes in electrogastrography (EGG) and with heart rate variability (HRV). PATIENTS AND METHODS The study included 68 participants: 34 patients with CD and 34 healthy individuals. We assessed the concentrations of IL-10 and NSE as well as the presence of anti-GM1 antibodies in serum. We investigated correlations between the concentrations of IL-10, NSE, and anti-GM1 antibodies and the results of EGG and HRV. RESULTS Patients with CD had a higher level of anti-GM1 antibodies than controls (1.38 ng/ml [0.98-2.03 ng/ml] vs 0.81 ng/ml [0.35-1.15 ng/ml]). Median IL-10 concentrations in patients with CD differed significantly from those in controls (7 pg/ml [4.33-11.48 pg/ml] vs 4.27 pg/ml [2.44-7 pg/ml]; P = 0.010). In HRV analysis, a positive correlation between IL-10 concentrations and very low frequency spectrum was observed (r = 0.63; P = 0.003). There was no correlation between the concentrations of IL-10, NSE, or anti-GM1 antibodies and EGG parameters. CONCLUSIONS Chronic inflammation in the course of CD may lead to autonomic nervous system impairment and development of neurologic disorders. Therefore, anti-GM1 antibodies and IL-10 may be considered as markers of nervous system impairment in the course of CD.

Serum IgG antibodies to GD1a and GM1 gangliosides in elderly people

Nowadays, the percentage of elderly people in society grows. Good nutrition and medical care help older people to have a normal life over 80 to 90 years. In the last ten years it is of critical importance to establish the clinical significance of serum IgG anti-GD1a and anti-GM1 ganglioside antibodies as potential biomarkers for neuronal damage in neurodegenerative diseases and immune-mediated neuropathies and demyelination. In the current study, the diagnostic values of IgG anti-GD1a and anti-GM1 antibodies were determined by the ELISA method in serum samples of 18 elderly patients (71-91 years). Significantly elevated serum IgG anti-GD1a and anti-GM1 antibodies titers were detected only in patients over 80 years. These data suggest that the immune-mediated neuropathies, neurodegeneration and demyelination in healthy elderly occur after 80 years old. Therefore, IgG anti-GD1a and anti-GM1 antibodies can serve as biomarkers, showing the nervous system dysfunction.

A 3-year-old boy with Guillain–Barré syndrome and encephalitis associated with Mycoplasma pneumoniae infection

Mycoplasma pneumoniae is a common cause of respiratory tract illness in children. Among the most common extrapulmonary manifestations are disorders of the central nervous system, including meningitis, meningoencephalitis, cerebellitis, polyneuropathy, acute disseminated encephalomyelitis, and Guillain-Barré syndrome. Guillain-Barré syndrome, also known as acute inflammatory demyelinating polyradiculoneuropathy, is an acute-onset, immune-mediated disorder of the peripheral nervous system. The central nervous system is usually intact in patients with Guillain-Barré syndrome. However, there have been some reports of an association of Guillain-Barré syndrome with central nervous system involvement in children. We report a 3-year-old boy with M. pneumoniae infection associated with Guillain-Barré syndrome and encephalitis. Both serum anti-GM1 ganglioside (IgG and IgM) and anti-galactocerebroside IgG antibodies were detected in our patient: the former in the earlier stage of the disease, and the latter in the later stage. We speculate that anti-GM1 ganglioside was associated more with encephalitis, and anti-galactocerebroside antibody was associated more with GBS in our case. Our patient is the youngest report of Guillain-Barré syndrome with central nervous system involvement, and the first report of a pediatric patient with associated M. pneumoniae infection. Such cases are rarely reported, but highlight the need for awareness of the association of the infection with Guillain-Barré syndrome with central nervous system involvement.

Lack of association between autism and anti-GM1 ganglioside antibody

Forty of 54 children with autism were reported to have an elevated antibody response to GM1 ganglioside that correlated with disease severity.1 Anti-ganglioside autoantibodies, especially those directed at GM1, are known to be associated with and play a pathogenic role in some immune-mediated peripheral neuropathies.2,3 The presumed link between autism and anti-GM1 antibodies, therefore, implies that testing may identify a sizable subset of patients who would benefit from immunomodulatory therapy. To evaluate the proposed association between autism and anti-GM1 antibodies, we performed serologic testing on children diagnosed with autism by strict clinical criteria and those without autism, using a standard and validated immunoassay protocol.

Immobilization of carbohydrate clusters on a quartz crystal microbalance sensor surface

The immobilization of carbohydrates on gold surfaces is a prerequisite technology for carbohydrate-related studies, including those of carbohydrate–biomolecule interactions. Glycolipid domains in cell membranes, such as lipid rafts, are thought to play an important role in cell biology through their carbohydrate portions. To understand the recognition of glycolipid domains such as receptors for bacterial toxins and viruses, we immobilized clusters of carbohydrates on a gold surface by using polyamidoamine (PAMAM) dendrimers as a scaffold. The PAMAM dendrimers were adsorbed on the gold-coated surface of a quartz crystal microbalance (QCM) sensor and were observed by means of QCM with dissipation (QCM-D). After adsorption of the PAMAM dendrimers, lysoganglioside-GM1 and 12-aminododecyl-N-acetylglucosaminide (GlcNAc–C12–NH2) were immobilized on the amino groups of PAMAM dendrimers by means of an NH2 cross-linker. Immobilization of the carbohydrates was confirmed by observation of their specific interaction with anti-ganglioside GM1 antibody or wheat germ agglutinin (WGA). Surfaces with different GlcNAc–C12–NH2 cluster sizes and densities were prepared by varying the size of the PAMAM dendrimers or the concentration of GlcNAc–C12–NH2 immobilized on the dendrimers, respectively. Analysis of the binding between the GlcNAc–C12–NH2-immobilized surface and WGA revealed that the size of the PAMAM dendrimers influenced the GlcNAc–C12–NH2–WGA interaction, with larger dendrimers resulting in higher WGA binding constants.

Poster 75 The Importance of Electrodiagnostic Medicine in Diagnosing Compression Neuropathy of the Posterior Tibial Nerve Secondary to a Ganglion Cyst: A Case Report

treated with dilation and curettage. She had generalized weakness, which at the time contributed to dehydration and electrolyte imbalance. The patient was later readmitted for progressive generalized weakness and an inability to ambulate. Ultrasound revealed retained fetal products. Results of an initial physical examination revealed proximal lower extremity weakness and areflexia without sensory deficit. Setting: A tertiary hospital. Results: Initial nerve conduction studies revealed decreased motor amplitudes in the legs, with relatively preserved sensory responses. The motor and sensory studies in the arms were normal. Initial electromyography showed acute denervation and loss of motor units in proximal lower extremity muscles. Acute denervation was also seen in distal leg muscles. The upper extremities or lumbar paraspinals were electrically normal. Subsequent nerve conduction studies revealed a loss of motor and sensory responses in both arms and legs. Repeated electromyography reflected a similar denervation pattern in the upper extremities. She was diagnosed with acute motor and sensory axonal neuropathy subtype of Guillain-Barre syndrome (GBS). The patient had antecedent diarrheal illness but Campylobacter jejuni, antiganglioside GM1 antibodies, monoclonopathy, human immunodeficiency virus, West Nile serologies, and CSF studies were negative. Discussion: GBS is the most common cause of acute flaccid paralysis in the world. It is considered to be a postinfectious, immune-mediated disease targeting peripheral nerves though immune mimicry. There are several GBS subtypes: acute inflammatory demyelinating polyradiculoneuropathy, acute motor axonal neuropathy, and acute motor and sensory axonal neuropathy. The acute motor and sensory axonal neuropathy variant often presents with rapid and severe paralysis with delayed and poorer recovery. In several studies, C jejuni was the most commonly isolated pathogen associated with the axonal subtype. Conclusions: In the presence of multiple negative serologies, this would be the first case report that suggests a hyperimmune response to fetal demise and retained products as a potential etiology of GBS.

First case of anti-ganglioside GM1-positive Guillain–Barré syndrome due to hepatitis E virus infection

A 51-year-old previously healthy woman presented with Guillain-Barré syndrome (GBS) and elevated liver enzymes. Further diagnostic investigations showed the presence of an acute hepatitis E infection associated with anti-ganglioside GM1 antibodies. After treatment with intravenous immunoglobulins, the patient made a rapid recovery. Here, we report the first case of GBS due to acute hepatitis E virus (HEV) infection associated with the presence of anti-ganglioside GM1 antibodies. We also review available literature on the association between acute HEV infection and GBS.

Waterskier’s Hirayama syndrome

Hirayama disease is a segmental inferior cervical myelopathy. Presentation is usually in young males with unilateral or asymmetrical upper limb weakness and atrophy. The clinical features can be similar to the initial presentation of amyotrophic lateral sclerosis, but Hirayama syndrome has a benign course and is typically limited to distal muscles of the upper limbs. The typical teenage onset of the syndrome corresponds with juvenile growth spurt. The disproportionate growth of the vertebral column compared to the spinal cord resulting in the relative shortening of the dorsal roots and the loss of attachment between the posterior dural sac and the subjacent lamina are considered to be contributing factors [1]. Several reports document antecedent events including repetitive movements, competitive sport or strenuous physical work. Jeannet et al. [2] documented the case of a 10-year-old girl who had a nocturnal rhythmic movement disorder, leading to prolonged repetitive neck flexion at night time. Huang et al. [3] reported that 37.5% of their patients with Hirayama disease frequently participated in vigorous sports or physical activity for at least 6 months before the onset of symptoms. These activities included basketball, baseball, martial arts, body-building, strenuous farm work or military training. We describe the case of a competitive waterskier who presented with the typical clinical features of Hirayama syndrome. A 55-year-old international waterski champion presented with a 2-year history of progressive left hand weakness. His symptoms developed following an intensive season of waterskiing. His waterskiing activities include travelling up to speeds of 80 kph prior to jumps, with violent passive neck flexion when landing. On examination he had marked wasting of C8 and T1 innervated muscles with striking preservation of the proximal forearm musculature (Fig. 1). Sensory examination was normal as was remainder of his neurological examination. Concentric needle EMG examination revealed fibrillation potentials and positive sharp waves in the left dorsal interosseous and abductor pollicis brevis. Large amplitude long duration polyphasic motor unit activation potentials with reduced recruitment were present in the remaining C7-T1 innervated muscles on the left. Sensory nerve action potentials were normal. No abnormalities were detected in the remaining limbs. A priority of the diagnostic work up was to rule out multifocal motor neuropathy (MMN). There was no evidence of conduction block on repeated conduction studies and anti GM1 ganglioside antibody titers were negative. CSF examination was normal. Standard, axial and sagittal cervical spine MR imaging in a neutral position showed moderate spondylotic changes, in which the vertebral bodies formed an uneven posterior surface. There was no evidence of cord or nerve root compression. Axial imaging in neck flexion demonstrated cord flattening with marked anterior shifting of the posterior wall of the cervical dural canal Fig. 2. P. Bede (&) A. L. W. Bokde S. C. Byrne M. Elamin O. Hardiman Trinity College Dublin, Dublin, Ireland e-mail: bedepeter@hotmail.com

The presence of Mycoplasma pneumoniae infection and GM1 ganglioside antibodies in Guillain-Barré syndrome

Guillain-Barré syndrome (GBS) is an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infection. GBS patients are known to have antecedent bacterial infections associated with auto-antibodies to various gangliosides. This investigation aimed to evaluate GBS patients for serological evidence of Mycoplasma pneumoniae infection and anti GM1 ganglioside antibodies. This cross-sectional study included 57 pediatric GBS patients, 42 neurological controls (i.e., non-GBS Acute Flaccid Paralysis cases) and 35 non-neurological controls. Enzyme linked immune sorbent assay (ELISA) was performed on the sera of the subjects to detect IgM and IgG antibodies against Mycoplasma (M.) pneumoniae and GM1 gangliosides. The results showed that 15.79% and 21.05% GBS patients were positive for IgG and IgM antibodies against M. pneumoniae as compared to 2.38% (P < 0.05) and 14.2% in non-GBS-AFP and 5.7% and 14.2% in non-neurological controls respectively. Additionally, 43.85% and 38.54% GBS patients were positive for IgG and IgM antibodies against GM1 gangliosides as compared to 38.09% and 28.57% in non-GBS-AFP and 14.2% and 2.84% in non-neurological controls respectively (P < 0.05). Significant difference in levels of IgG antibodies against M. pneumoniae was observed between GBS patients and neurological controls, suggesting M. pneumoniae to be an important antecedent to GBS. Significant difference in levels of anti GM1 ganglioside antibodies (IgG & IgM) was seen between GBS patients and non-neurological controls, highlighting its possible role in the pathogenesis of GBS.

Are anti-ganglioside antibodies of clinical value in multifocal motor neuropathy?

Pestronk and colleagues1 first reported antibodies to GMl ganglioside in a treatable form of multifocal motor neuropathy (MMN) in 1988. In subsequent years, anti-GM1 and other ganglioside antibodies were reported in a variety of other disorders, including motor neuron disease (MND), Guillain-Barre syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), monoclonal gammopathy–associated neuropathy, and, occasionally, idiopathic neuropathy, mononeuritis multiplex, radiculopathy, and plexopathy.2,–,4 In MMN, the prevalence of anti-GM1 antibodies ranges widely from 20% to 85%,2,–,6 in part because there is no consensus on the most reproducible assay for this antibody, prompting different investigators to use different ELISA techniques. The prevalence of anti-GM2 antibodies is less well-studied but is generally considerably lower than that of anti-GM1, and many of those patients with MMN having anti-GM2 antibodies also carry anti-GM1.3,7 Anti-GM2 antibodies are found in other neuromuscular disorders as well, including MND, …