格林—巴利综合征患者血清中的抗糖脂抗体

采用固相酶联免疫吸附法对３５例急性期格林－巴利综合征（ＧＢＳ）患者、２８例其他神经系统疾病患者和３０例健康体检者的血清中抗硫脂抗体，抗ＧＱ１ｂ及抗ＧＭ１抗体进行检测。结果：ＧＢＳ患者血清中抗硫脂ＩｇＭ抗体、抗ＧＱ１ｂＩｇＧ抗体和抗ＧＭ１ＩｇＧ抗体阳性率分别为３４％、１１％和３１％，均显著高于正常对照组。５６％的抗硫脂抗体阳性患者均有不同程度感觉障碍，而抗硫脂抗体阴性患者仅１６％（Ｐ＜０．０５）。５例有眼肌运动障碍的ＧＢＳ患者中，４例抗ＧＱ１ｂＩｇＧ抗体阳性，无眼肌麻痹的ＧＢＳ患者无１例抗ＧＱ１ｂ抗体阳性。提示不同的抗糖脂抗体可能在ＧＢＳ发病过程中起不同的作用。     

Anti‐ganglioside antibodies in Guillain–Barré syndrome and chronic inflammatory demyelinating polyneuropathy in Chinese patients

Introduction: In this study we investigated the relationships between anti‐ganglioside antibodies and Guillain–Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). Methods: Samples from 48 Chinese patients diagnosed with GBS and 18 patients diagnosed with CIDP were retrospectively reviewed. Results: In the GBS patients, 62.5% were classified as having acute inflammatory demyelinating polyneuropathy (AIDP), 27.1% were found to have acute motor axonal neuropathy (AMAN), and 10.4% were unclassified. Serum IgG anti‐ganglioside antibodies were detected in 46.2% of the AMAN patients and in 6.7% of the AIDP patients (P < 0.05); 5.6% of the 18 CIDP patients were IgG antibody positive, and 27.8% were IgM antibody positive. Facial palsy and sensory impairment were significantly associated with IgM antibodies. Conclusions: These results suggest that IgG anti‐GM1 antibodies are associated with AMAN, but not with AIDP, and that IgM antibodies against GM1, GM2, and GM3 are associated with facial nerve palsy. Muscle Nerve 55 : 470–475, 2017     

Antibodies to acidic glycolipids in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.

Using an enzyme-linked immunosorbent assay and a thin-layer chromatography-immunostaining procedure, we detected serum antibodies against acidic glycolipids in 36 of 53 patients with Guillain-Barré syndrome (GBS) and 8 of 16 patients with chronic inflammatory demyelinating polyneuropathy (CIDP). Although we also found anti-acidic glycolipid antibodies in 4 of 13 patients with other neurological diseases; 2 of 10 patients with multiple sclerosis; 8 of 33 patients with inflammatory, infectious, allergic or autoimmune disorders and 3 of 32 healthy subjects, the levels of antibodies in these controls were much lower than in GBS patients. There were several patterns of reactivity of GBS sera including antibodies to LM1 and HexLM1, GM1 or GD1b or both, various other gangliosides, sulfated glycolipids, and as yet unidentified glycolipids. Sera from 30% of GBS patients had antibodies against two or more antigenically distinct acidic glycolipid antigens. Levels of anti-acidic glycolipid antibodies correlated with clinical symptoms in 9 of 11 GBS patients. While the increased incidence of antibodies to acidic glycolipids in patients with GBS (P less than 0.001) and CIDP (P less than 0.025) compared to controls could be an epiphenomenon, anti-acidic glycolipid antibodies may play a role in nerve injury in some GBS and CIDP patients.     

N-acetylgalactosaminyl GD1a is a target molecule for serum antibody in Guillain-Barré syndrome

Serum antibodies against such major glycolipids as GM1, GD1b, and LM1 have been reported in patients in the acute phase of Guillain-Barré syndrome (GBS). Because minor unidentified glycolipids also may be targets of antibodies in GBS sera, we assayed serum antibody against a crude ganglioside fraction using thin-layer chromatogram immunostaining. Antibody activity was detected against a band that migrated just below GD1a in 6 of the 50 patients with GBS tested. Antibody titer, as determined by enzyme-linked immunosorbent assay, decreased during the course of the disease. All 6 patients had suffered gastrointestinal infection before the neurological onset of GBS and showed low amplitudes for the compound muscle action potentials and normal or only slightly decreased nerve conduction velocities. Thin-layer chromatogram immunostaining did not show this antibody activity in any of the 16 normal and 119 disease controls. The unidentified glycolipid was isolated by DEAE–Sephadex A-25 column chromatography, sialidase treatment, and Iatrobeads column chromatography. Fast atom bombardment-mass spectra showed it to be N-acetyl-galactosaminyl GD1a.     

Serum antibodies to GM1, GD1b,peripheral nerve myelin,and Campylobacter jejuni in patients with Guillain-Barré syndrome and controls: Correlation and prognosis

Serum antibodies to monosialoganglioside (GM1), disialoganglioside (GD1b), and Campylobacter jejuni, measured by enzyme-linked immunosorbent assay and serum antibodies to peripheral nerve myelin, measured by the C1 fixation and transfer assay, were studied in 58 acute-phase patients with Guillain-Barré syndrome (GBS), 42 disease controls, and 29 normal controls. Anti-peripheral nerve myelin antibodies were elevated in 57 of 58 patients with GBS compared with controls, whereas only 8.6% had increased antibody titers to GM1 and 10.3% to GD1b. Only low antibody titers (GM1) or no antibodies (GD1b) were found in controls. More GBS patients (17.2%) than controls (7%) had antibodies to C jejuni. Poor recovery with inability to walk at 1 year after onset of symptoms was seen in 3 (5%) of the patients with GBS. All 3 patients had serological evidence of recent C jejuni infection but no antibodies to GM1 or GD1b. GBS patients with antibodies to GM1 or GD1b had excellent recovery. Our data indicate that antibodies to GM1 or GD1b do not necessarily mediate the extensive axonal damage seen in these severely affected patients.     

Novel anti‐idiotype antibody therapy for lipooligosaccharide‐induced experimental autoimmune neuritis: Use relevant to Guillain‐Barré syndrome

Campylobacteriosis is a frequent antecedent event in Guillain‐Barré syndrome (GBS), inducing high‐titer serum antibodies for ganglioside antigens in the peripheral nervous system (PNS). Molecular mimicry between the lipooligosaccharide (LOS) component of Campylobacter jejuni and human peripheral nerve gangliosides is believed to play an important role in the pathogenesis of GBS. Conventional treatment strategies for patients with GBS include plasmapheresis, intravenous immunoglobulin (IVIG), and immunosuppression, which are invasive or relatively ineffective. In this study, we used our animal model of GBS, in which Lewis rats were immunized with GD3‐like LOS isolated from C.jejuni. The animals developed anti‐GD3 ganglioside antibodies and manifested neuromuscular dysfunction. To develop novel therapeutic strategies, we treated the animals by intraperitoneal administration of an anti‐GD3 antiidiotype monoclonal antibody (BEC2) that specifically interacts with the pathogenic antibody. The treated animals had a remarkable reduction of anti‐GD3 antibody titers and improvement of motor nerve functions. The results suggest that ganglioside mimics, such as antiidiotype antibodies, may be powerful reagents for therapeutic intervention in GBS by neutralizing specific pathogenic antiganglioside antibodies. © 2010 Wiley‐Liss, Inc.     

Clinical and serological prognostic factors in childhood Guillain‐Barré syndrome: A prospective cohort study in Bangladesh

Guillain‐Barré syndrome (GBS) is the most common cause of acute flaccid paralysis in children. The objective of this study was to investigate the preceding infections, clinical, serological and electrophysiological characteristics and outcome of childhood GBS in Bangladesh. We included 174 patients with GBS aged <18 years from a prospective cohort in Bangladesh between 2010 and 2018. We performed multivariate logistic regression to determine the risk factors for poor outcome. Among 174 children with GBS, 74% (n = 129) were male. Around half of the patients (49%, n = 86) had severe muscle weakness, 65% (n = 113) were bedbound (GBS disability score 4) and 17% (n = 29) patients required mechanical ventilation at admission. Campylobacter jejuni serology and anti‐GM1 IgG antibody were positive in 66% and 21% of the patients respectively. One hundred and forty‐three (82%) patients did not receive standard treatment and half of them recovered fully or with minor deficits at 6‐month. Twenty patients (11%) died throughout the study period. At 3‐month of onset of weakness, complete recovery or recovery with minor deficit was significantly higher in demyelinating GBS patients compared to axonal GBS patients (86% vs 51%, P = .001). Cranial nerve palsy (OR = 4.00, 95%CI = 1.55‐10.30, P = .004) and severe muscle weakness (OR = 0.16, 95%CI = 0.06‐0.45, P = .001) were the important risk factors of poor outcome in children with GBS. Further large‐scale studies are required for better understanding of factors associated with mortality and morbidity in childhood GBS.     

Paraparetic Guillain‐Barré syndrome: Nondemyelinating reversible conduction failure restricted to the lower limbs

Introduction: Paraparetic Guillain‐Barré syndrome (GBS) is a rare subtype of GBS characterized by leg weakness and areflexia in the absence of neurological involvement of the arms, cranial nerves, or respiratory muscles. Onset is characterized by lower back, buttock, or leg pain, followed by development of symmetric flaccid limb weakness in the absence of sensory disturbance. Methods: We describe an elderly woman who developed postinfectious symmetric flaccid leg weakness in the absence of sensory disturbance. Serial nerve conduction studies were carried out over 5 months. Results: Antecedent infection, a monophasic disease course, and the presence of cerebrospinal fluid albuminocytological dissociation suggested a diagnosis of paraparetic GBS. Serial nerve conduction studies demonstrated nondemyelinating reversible conduction failure, which was restricted to the legs. Axonal neuropathy was supported by the presence of anti‐GM1 IgG antibodies. Conclusions: These findings suggest that patients with paraparetic GBS have axonal neuropathy, which is restricted to the lower limbs. Muscle Nerve 55 : 281–285, 2017     

Motor nerve excitability after childhood Guillain‐Barré syndrome

Residual motor nerve dysfunction after pediatric Guillain‐Barré syndrome (GBS) was determined in an observational cross‐sectional cohort study in patients who previously developed GBS during childhood (<18 years). Ulnar motor nerve dysfunction was defined by compound motor action potential (CMAP) scan in patients after a follow up of at least 1 year compared with age‐matched healthy controls, in relation to clinical course and outcome. A total of 37 persons previously diagnosed with GBS in childhood were included with a mean age at current examination of 20.6 years (4–39 years). The median time between diagnosis and follow‐up was 11 years (range: 1–22 years). CMAP scanning indicated ulnar motor nerve dysfunction in 25 (68%) participants. The most frequent abnormality was a reduction in nerve excitability observed both in those with residual limb weakness and in the majority of those with complete recovery. CMAP scan characteristics were not related to prognostic factors or outcome. In conclusion, GBS in childhood results in residual motor nerve excitability disturbances, even in those completely recovered, probably reflecting altered physiology of regenerated peripheral nerves.     

When is facial diplegia regarded as a variant of Guillain‐Barré syndrome?

A variant of Guillain‐Barré syndrome (GBS) with predominant manifestation of facial diplegia (FD) has been described recently. This study aimed to characterize and determine the incidence of this FD‐predominant GBS variant. The clinical and serological information of 900 consecutive patients were reviewed. In total, eight patients were identified between January 2007 and December 2010 as having FD accompanied by some features of GBS. These features were subjective sensory symptoms such as distal paresthesia (7/8, 88%), albumin‐cytological (A/C) dissociation (7/8, 88%), antecedent infection (6/8, 75%), and minor nerve conduction study (NCS) abnormalities (5/7, 71%). One patient presented with the typical NCS feature of demyelinating neuropathy. Only two patients exhibited areflexia (2/8, 25%). None of the patients possessed any anti‐ganglioside antibodies; however, the serum of two patients was positive for anti‐mycoplasma antibody (2/6, 33%). FD variant of GBS occurred in less than 1% of our dataset. FD can be a regional variant of GBS when it is accompanied by supporting features, such as subjective tingling, A/C dissociation, and minor NCS abnormalities.     

Association of antibodies to ganglioside complexes and conduction blocks in axonal Guillain‐Barré syndrome presenting as acute motor conduction block neuropathy

A close relationship between acute motor conduction block neuropathy and antibodies against the complex of GM1 and GalNAc‐GD1a has been reported. This study investigates the hypothesis that conduction block at the early phase of axonal Guillain‐Barré syndrome (GBS) is also associated with such ganglioside complexes. Sera were obtained from seven French patients with initial evidence of isolated conduction blocks that resolved or progressed to acute motor axonal neuropathy. Serum IgG to asialo‐GM1 and gangliosides of LM1, GM1, GM1b, GD1a, GalNAc‐GD1a, GD1b, GT1a, GT1b, and GQ1b as well as their complexes were measured. Five of seven patients progressed within the first month of disease to AMAN. One patient had IgG antibodies against the complex of asialo‐GM1 and each of the other ganglioside antigens. Another patient carried IgG antibodies against GM1 complex with GM1b, GD1a, and GT1a as well as asialo‐GM1 complex with GD1a and GT1a. None had IgG antibodies against GM1/GalNAc‐GD1a complex. Six patients had IgG against single antigens GM1, GD1a, GalNAc‐GD1a, GD1b, and asialo‐GM1. In three patients, a reduced reaction against GM1/GalNAc‐GD1a complex was observed. The presence of conduction block in axonal GBS is not always associated with anti‐GM1/GalNAc‐GD1a complex antibodies.     

Dysmyelinogenesis in animal model of GM1 gangliosidosis.

Magnetic resonance imaging (MRI), pathologic examinations, and biochemical analyses were performed on 2 different canine mutants with GM1 gangliosidosis (i.e., English Springer Spaniel and Portuguese Water Dog) and on age- and sex-matched controls. Serial MRI studies were also performed on a child with infantile-onset GM1 gangliosidosis. The affected dogs had abnormalities on MRI, including a relative increase in gray matter and an abnormal signal intensity of cerebral and cerebellar white matter observed on T2-weighted MRI. White matter changes on MRI were similar to white matter abnormalities observed in a 15-month-old boy with GM1 gangliosidosis. The weight ratio of white to gray matter from the frontal lobe was markedly reduced. Microscopic examination revealed characteristic ballooned neurons which stained lightly with Luxol-fast blue. The central cerebral and cerebellar folia white matter exhibited pallor and gliosis, while the corpus callosum and fornix stained normally with Luxol-fast blue. Axons appeared intact on Bodian staining. Ultrastructural studies revealed fewer myelinated axons in affected puppies. Total gangliosides in gray matter were elevated. Thin-layer chromatography demonstrated GM1 ganglioside as the predominant ganglioside. The amount of cerebrosides and sulfatides was reduced in the gray and white matter when compared to controls but the ratio in gray and white matter remained unchanged. Immunostaining of neutral glycolipids disclosed increased amounts of stage-specific embryonic antigen-1 glycolipid in gray matter. These findings suggest that canine models for GM1 gangliosidosis are associated with abnormal myelin development which may be similar to the human disease.     

Correlation of nerve ultrasound,electrophysiological, and clinical findings in post Guillain‐Barré syndrome

We aimed to correlate functional disability, electrophysiology, and nerve ultrasound in patients after Guillain‐Barré syndrome (GBS). Seventy‐five healthy controls and 41 post‐GBS patients (mean 3.4 years, SD ± 2.91 years after onset) underwent clinical, sonographic, and electrophysiological evaluation. Compared to healthy controls, the post‐GBS patients showed: (1) a mean Rasch‐built Overall Disability Scale score of 31.8 (SD ± 11.6), modified Rasch‐built fatigue severity scale score of 15.6 (SD ± 3.2), Medical Research Council sum score of 22 (SD ± 5.6); (2) electrophysiological signs of permanent axonal loss in the majority of the peripheral nerves; (3) sonographical evidence of higher cross‐sectional area values (CSA) of the ulnar (elbow, p < 0.001), radial (spiral groove, p < 0.001), tibial nerve (popliteal fossa, p < 0.001) and brachial plexus (supraclavicular space, p < 0.001). No correlation between sonographic and electrophysiological findings was found. Neither nerve ultrasound nor electrophysiology correlated with muscle strength, overall disability, and fatigue scale. Compared to healthy controls, post‐GBS patients had significant functional disability. Despite significant abnormalities in both electrophysiology and ultrasound compared to healthy controls, neither electrophysiology nor nerve ultrasound correlated with functional disability of these patients.     

Guillain‐Barré syndrome in Bangladesh: validation of Brighton criteria

Guillain‐Barré syndrome has a diverse clinical phenotype related to geographical origin. To date, the majority of large‐scale studies on Guillain‐Barré syndrome (GBS) have been conducted in developed countries. We aimed to evaluate the key diagnostic features and assess the suitability of the Brighton criteria in 344 adult GBS patients from Bangladesh. All patients fulfilled the National Institute of Neurological Diseases and Stroke (NINDS) diagnostic criteria. Standardized data on demographic characteristics and clinical features, cerebrospinal fluid (CSF) analysis, and nerve conduction study (NCS) results were elaborated to measure the sensitivity of Brighton criteria. Most patients (88%) were admitted to hospital after the nadir weakness. Symmetrical weakness and reduced reflexes were found in 98% of patients. CSF albuminocytologic dissociation was detected in 238/269 (89%) cases and abnormal nerve physiology in 258/259 (>99%) cases. Only 27 (8%) patients received either intravenous immunoglobulin (IVIg) or plasmapheresis. In total, 200 (58%) patients met level 1 of the Brighton criteria; 97 (28%) patients met level 2; 42 (12%) patients met level 3; and 5 (2%) patients met level 4. This analysis showed that despite the heterogeneity of GBS in Bangladesh, the Brighton criteria showed a high sensitivity in the diagnosis of GBS.     

What's new in Guillain‐Barré syndrome in 2007–2008?*

The years 2007 and early 2008 have been an exciting time for Guillain‐Barré syndrome (GBS) research. Epidemiological studies have shown that the incidence of GBS remains stable at about 2/100,000 per year but that there have been changes in hospitalization use, likely due to the widespread availability of IVIg. Research into mechanisms has shown the importance of single amino acids in Campylobacter jejuni and the importance of ganglioside conformation. In a murine model of anti‐ganglioside antibody‐mediated neuropathy, Eculizumab was effective in reversing clinical disease and preventing pathology. This suggests trials of Eculizumab in GBS should be considered. Unfortunately, there are no new randomized controlled trials in GBS to report although the unmet need is great.     

Serum anti-GM2 and anti-GalNAc-GD1a ganglioside IgG antibodies are biomarkers for immune-mediated polyneuropathies in cats

Recent work identified anti-GM2 and anti-GalNAc-GD1a IgG ganglioside antibodies as biomarkers in dogs clinically diagnosed with acute canine polyradiculoneuritis, in turn considered a canine equivalent of Guillain-Barré syndrome. This study aims to investigate the serum prevalence of similar antibodies in cats clinically diagnosed with immune-mediated polyneuropathies. The sera from 41 cats clinically diagnosed with immune-mediated polyneuropathies (IPN), 9 cats with other neurological or neuromuscular disorders (ONM) and 46 neurologically normal cats (CTRL) were examined for the presence of IgG antibodies against glycolipids GM1, GM2, GD1a, GD1b, GalNAc-GD1a, GA1, SGPG, LM1, galactocerebroside and sulphatide. A total of 29/41 IPN-cats had either anti-GM2 or anti-GalNAc-GD1a IgG antibodies, with 24/29 cats having both. Direct comparison of anti-GM2 (sensitivity: 70.7%; specificity: 78.2%) and anti-GalNAc-GD1a (sensitivity: 70.7%; specificity: 70.9%) antibodies narrowly showed anti-GM2 IgG antibodies to be the better marker for identifying IPN-cats when compared to the combined ONM and CTRL groups (P = .049). Anti-GA1 and/or anti-sulphatide IgG antibodies were ubiquitously present across all sample groups, whereas antibodies against GM1, GD1a, GD1b, SGPG, LM1 and galactocerebroside were overall only rarely observed. Anti-GM2 and anti-GalNAc-GD1a IgG antibodies may serve as serum biomarkers for immune-mediated polyneuropathies in cats, as previously observed in dogs and humans.     

Ultrasonography of the peripheral nervous system in the early stage of Guillain‐Barré syndrome

Ultrasonography can be used to visualize peripheral nerve abnormalities in immune‐mediated neuropathies. The objective of this study was to prove the role of ultrasonography (US) in acute phase of Guillain‐Barré syndrome (GBS). Systematic ultrasonic measurements of several peripheral nerves including the vagal nerve as well as the sixth cervical nerve root were performed in 18 patients with GBS at days 1–3 after symptom onset and compared to 21 healthy controls. Nerve conduction studies (NCS) of corresponding nerves were undertaken. Consequently, significant differences between the groups were found in compound muscle action potential amplitudes, F‐wave latency, and persistency. Ultrasonic cross‐sectional areas (CSAs) showed significant enlargement in all nerves except of the ulnar nerve (upper arm) and the sural nerve compared to healthy controls, most prominent in proximal and middle median nerve (p < 0.01). The vagal nerve also showed enlargement compared to controls (p < 0.05), which was most pronounced in patients with autonomic dysfunction compared to patients without (p < 0.05). C6 root diameter showed a significant correlation to the amount of cerebrospinal fluid (CSF)‐protein (Pearson correlation, p < 0.05). US shows nerve enlargement in several peripheral nerves including vagal nerve and C6 root in acute phase of GBS and could be an additional diagnostic tool for example, in GBS of atypical onset and autonomic dysfunction.     

Diagnosis of Guillain‐Barré syndrome and validation of the Brighton criteria in Malaysia

We aimed to evaluate the key diagnostic features of Guillain‐Barré syndrome (GBS) in Malaysian patients and validate the Brighton criteria. This was a retrospective study of patients presenting with GBS and Miller Fisher syndrome (MFS) between 2010 and 2019. The sensitivity of the Brighton criteria was evaluated. A total of 128 patients (95 GBS, 33 MFS) were included. In the GBS cohort, 92 (97%) patients presented with symmetrical limb weakness. Reflexes were depressed or absent in 90 (95%) patients. Almost all patients (94, 99%) followed a monophasic disease course, with 5 (5%) patients experiencing treatment‐related fluctuations. Cerebrospinal fluid (CSF) albuminocytological dissociation was seen in 62/84 (73%) patients. Nerve conduction study (NCS) revealed neuropathy in 90/94 (96%) patients. In GBS patients with complete dataset (84), 56 (67%) patients reached level 1 of the Brighton criteria, 21 (25%) reached level 2, 3 (4%) reached level 3, and 4 (5%) reached level 4. In MFS, the clinical triad was present in 25 (76%) patients. All patients had a monophasic course. CSF albuminocytological dissociation was present in 10/25 (40%) patients. NCS was normal or showed sensory neuropathy in 25/33 (76%) patients. In MFS patients with complete dataset (25), 5 (20%) patients reached level 1 of the Brighton criteria, 14 (56%) reached level 2, 2 (8%) reached level 3, and 4 (16%) reached level 4. Inclusion of antiganglioside antibodies improved the sensitivity of the Brighton criteria in both cohorts. In the Malaysian cohort, the Brighton criteria showed a moderate to high sensitivity in reaching the highest diagnostic certainty of GBS, but the sensitivity was lower in MFS.     

Spectrum of neurological diseases associated with antibodies to minor gangliosides GM1b and GalNAc-GD1a

The authors reported the neurological disease spectrum associated with autoantibodies against minor gangliosides GM1b and GalNAc-GD1a. IgG and IgM antibody reactivity against gangliosides GM1, GM2, GM1b, GD1a, GalNAc-GD1a and GQ1b was investigated in sera from 7000 consecutive patients who had various neurological conditions. The clinical diagnoses for 456 anti-GM1b-positive patients were Guillain-Barré syndrome (GBS, 71%), atypical GBS with preserved deep tendon reflexes (12%), Fisher syndrome (10%), Bickerstaff's brainstem encephalitis (2%), ataxic GBS (2%) and acute ophthalmoparesis (1%). For 193 anti-GalNAc-GD1a-positive patients, the diagnoses were GBS (70%), atypical GBS (16%), Fisher syndrome (10%) and Bickerstaff's brainstem encephalitis (3%). Of the patients with GBS or atypical GBS, 28% of 381 anti-GM1b-positive and 31% of 166 anti-GalNAc-GD1a-positive patients had neither anti-GM1 nor anti-GD1a antibodies. Of those patients with Fisher syndrome, Bickerstaff's brainstem encephalitis, ataxic GBS or acute ophthalmoparesis, 33% of 67 anti-GM1b-positive, and 52% of 25 anti-GalNAc-GD1a-positive patients had no anti-GQ1b antibodies. Autoantibodies against GM1b and GalNAc-GD1a are associated with GBS, Fisher syndrome and related conditions. These antibodies should provide useful serological markers for identifying patients who have atypical GBS with preserved deep tendon reflexes, ataxic GBS, Bickerstaff's brainstem encephalitis or acute ophthalmoparesis, especially for those who have no antibodies to GM1, GD1a or GQ1b. A method to prepare GM1b was developed.