Guillain-Barre Syndrome

Miller Fisher syndrome (MFS), considered a clinical variant of Guillain-Barré syndrome (GBS), is characterized by ophthalmoplegia, ataxia and areflexia 1 . Antecedent of respiratory and/or gastrointestinal symptoms is frequent (up to 70%), with an average symptom-free interval of 10 days and the immune-mediated process is often associated with acute phase anti-GQ1b IgG antibodies in up to 95% of all cases 2 . A closely related condition is Bickerstaff's brainstem encephalitis (BBE), which presents additionally alteration of consciousness or long tract signs, but is less frequently associated with anti-GQ1b antibodies 3 . Their relation and nosological position have been subject of extensive discussion in the literature. Idiopathic intracranial hypertension (IIH) comprises signs of increased intracranial pressure occurring in the absence of obvious cerebral pathology 4 . Some studies have reported cases of intracranial hypertension associated with GBS, very few with MFS, but none with BBE.

The impact of plasma exchange (PE) on the treatment of severe Guillain-Barre syndrome (GBS) was studied by comparing all the 16 patients treated with PE in a London teaching hospital between January 1985 and August 1987, with 64 historical controls drawn from a series of patients observed during a prospective study in South East England in 1983 and 1984. There were no GBS-related deaths in the PE treated group but seven in the historical controls (2P=0.39). The median duration of ventilation was only 20 days (range 7-64) in the PE group compared with 36 days (range 14-365) in the surviving patients in the control group (2P=0.06, 95% confidence interval ofdifference in medians -36 to 0 days). The PE group walked earlier without aid (median 55.5 compared with 86 days, 2P=0.04, 95% confidence interval of difference in medians -88 to -2 days). Three months after the onset of neuropathy all PE treated patients were able to walk with support or better, whereas 19 of the surviving historical controls were unable to walk even with support (2P=0.009). The costs of PE were offset by savings in intensive care unit and hospital expenditure.

A 68-year-old woman and a 72-year-old man presented with distal weakness of the limbs and numbness following an influenza vaccination within 2 weeks. Moreover, Guillain-Barré syndrome (GBS) was diagnosed in two patients. Pericarditis was diagnosed in the first patient who also had precordial chest pain with referral to trapezius ridge, and nephrotic syndrome, was observed in the second patient who had leg edema and proteinuria. The relationship among GBS, pericarditis and nephrotic syndrome after an influenza vaccination is discussed.

Acute inflammatory demyelinating polyneuropathy (AIDP) is a type of Guillain-Barré syndrome (GBS) characterized by primary nerve demyelination sometimes with secondary axonal degeneration. Studies on the fine structure of dorsal root ganglia in AIDP are lacking. Our aim was to investigate the cytology and nuclear organization of primary sensory neurons in AIDP with axonal injury using ultrastructural and immunohistochemical analysis. The light cytology of the L5 dorsal ganglion showed the characteristic findings of neuronal axonal reaction. The organization of chromatin, nucleolus, Cajal bodies, and nuclear pores corresponded to transcriptionally active neurons. However, the hallmark of the nuclear response to axonal injury was the formation of numerous nuclear bodies (NBs; 6.37 F 0.6, in the AIDP, vs. 2.53 F 0.2, in the control, mean F SDM), identified as promyelocytic leukemia (PML) bodies by the presence of the protein PML. In addition to PML protein, nuclear bodies contained SUMO-1 and the transcriptional regulators CREB-binding protein (CBP) and glucocorticoid receptor (GR). The presence of proteasome 19S was also detected in some nuclear bodies. We suggest that neuronal PML bodies could regulate the nuclear concentration of active proteins, a process mediated by protein interactions with PML and SUMO-1 proteins. In the AIDP case, the proliferation of PML bodies may result from the overexpression of some nuclear proteins due to changes in gene expression associated with axonal injury.

The objective of this study was to examine factors impacting long-term functional outcomes and psychological sequelae in survivors of breast cancer (BC). A clinical assessment and structured interview assessed the impact of BC on participants' (n ¼ 85) current activity and restriction in participation, using validated questionnaires: Functional Independence Measure (FIM), Perceived Impact Problem Profile (PIPP) and Depression Anxiety Stress Scale (DASS). Participants showed good functional recovery (median motor FIM score ¼ 78). Three-quarters (74%) reported pain, 32% reported upper limb weakness, 31% pain limiting shoulder movement and 29% lymphoedema. One third (32%) reported greatest impact on psychological wellbeing. A substantial number of participants reported high levels of depression (22%), anxiety and stress (19% each). Factors associated with poorer current level of functioning and wellbeing included: younger participants, recent diagnoses, aggressive tumour types, receiving chemotherapy, shoulder limitation due to pain, and lymphoedema. BC survivors require long-term management of psychological sequelae impacting activity and participation.

Patients with a personal or familial history of Charcot-Marie-Tooth disease (CMT) are extremely sensitive to the vinca alkaloids. CMT neuropathy, also called hereditary motor sensory neuropathy, is a heterogeneous group of disorders of peripheral nerves. Methotrexate has also been implicated in neurotoxicity, in as many as 30% of patients receiving intrathecal (IT) methotrexate. Patients with personal or familial history of CMT or other neuropathy may develop profound neuropathy when treated with vincristine, methotrexate or other potentially neurotoxic agents. To our knowledge, only 17 patients have been reported in the literature. Our experience with such a patient documents this hypersensitivity. J.G. was a previously healthy 5-year-old Caucasian male, born by full term normal spontaneous vaginal delivery and with normal developmental milestones (sat at 5 months, crawled at 8 months, walked at 15 months, able to run, jump, hop, skip, and doing well in kindergarten). He was well until 3 days prior to presentation when he developed a nonproductive cough, hoarseness, 1 day of neck swelling, increased work of breathing, voice changes, and snoring. His neurologic status was normal, except for possible ''thin leg muscles'' and occasional clumsiness, according to his mother. Family history was remarkable for a paternal grandmother with breast cancer at 48 years of age and subsequent leukemia and a father with gait disturbance, which was described as ''Charcot-Marie-Tooth like,'' diagnosed when he was 15 years old. The patient's diagnostic chest X-ray film and neck and chest CT scan revealed airway compression from a large anterior-superior mediastinal mass extending into the neck. Staging evaluation confirmed localized involvement. Following histologic confirmation of presumed lymphoma with incisional biopsy of the mass and bone marrow sampling under conscious sedation, he promptly received a dose of 70 mg intrathecal cytarabine (IT Ara-C) and one dose of dexamethasone (dex) on the day of admission. The diagnosis of T cell lymphoblastic lymphoma was finalized the next day, and he began daily dex (6 mg/m 2 /day), weekly vincristine (VCR) (1.5 mg/m 2 / dose), weekly daunomycin (30 mg/m 2 /dose), and thrice weekly asparaginase (6,000 IU/m 2 /dose). The mass rapidly regressed.

Introduction: Dr. C. Miller Fisher described the appearance of unilateral facial palsy after resolution of ataxia in a patient with the eponymic Miller Fisher syndrome (MFS). However, there have been very few reports of delayed appearance of facial weakness in Guillain-Barré syndrome (GBS) and MFS when the other neurological signs reached nadir or started improving. Methods: In this study we reviewed the clinical and laboratory findings of consecutive patients with GBS (n = 195) and MFS (n = 68). Results: Delayed facial weakness occurred in 12 (6%) GBS and 4 (6%) MFS patients and was unilateral in 5 (42%) GBS and 2 (50%) MFS patients. In those patients with delayed facial weakness, neither limb weakness nor ataxia progressed, and facial weakness disappeared without immunotherapy. Conclusions: Because facial weakness can lead to further morbidity, it would be prudent for clinicians to warn patients of this possibility, although additional immunotherapy is usually not required. Muscle...

Previous histochemical studies in the demyelinating form of Guillain-Barré syndrome (GBS), acute inflammatory demyelinating polyneuropathy (AIDP), have shown complement deposition on the surface of Schwann cells, and therefore unknown epitopes would be present on the outer surface of Schwann cells. We used a proteomic-based approach to search for the target molecules of AIDP in the extracted proteins from schwannoma cells. Sera were obtained from 40 patients with GBS, 31 controls with inflammatory disease, and 46 normal controls. We found that patients with AIDP after cytomegalovirus (CMV) infection have serum autoantibodies against membrane-organizing extension spike protein (moesin), which is expressed in the Schwann cell processes at the nodes of Ranvier and is crucial for myelination. Of the 40 patients with GBS, 6 had recent CMV infection and 5 of them (83%) had high levels of serum immunoglobulin G antibodies against moesin. The anti-moesin antibodies were found in none of the...

Guillain-Barre syndrome (GBS) is a rapid-onset muscle weakness caused by the immune system attacking the peripheral nervous system. Although the causes still remain elusive, many studies in the past have linked GBS to vaccinations, such as influenza, but pneumococcal vaccine remains to be studied. This case report highlights a woman who developed severe respiratory failure from Guillain-Barre a month after administration of the PCV vaccine. Possible etiology could be linked to the T-dependent stimulation response of GBS to the G1-specific B cells found in the peripheral blood. Full recovery is often rare in the syndrome, but rapid administration of IVIg and extensive therapy has proved to show a good long-term outcome.

Biomechanical tests of post hoc probability have been proposed by prior authors as reliable tests of causation in forensic settings. Biomechanical assessment of injury kinetics and kinematics is a potentially important tool in forensic medicine, but there is also the potential for misapplication. The most reliable application is when biomechanical analysis is used to explain injury mechanisms, such as how an injury may have occurred. When a biomechanical analysis is used as a means of determining whether, rather than how an injury has resulted from a traumatic exposure, then a lack of reliability of the methodology limits its application in forensic medicine. Herein, we describe a systematic assessment of causation by adapting established general causation principles to specific causation scenarios, and how biomechanical analysis of injury mechanics is properly used to augment such an approach in conjunction with the principles of forensic epidemiology. An example calculation of relative risk associated with cervical spine injury is provided as a representative probabilistic metric for assessing causation. The statistical benefits and limitations of biomechanical analysis are discussed as an adjunct to forensic medicine.

Acute motor axonal neuropathy (AMAN) is a pure motor axonal subtype of Guillain-Barré syndrome (GBS) that was identifi ed in the late 1990s. In Asia and Central and South America, it is the major subtype of GBS, seen in 30-65% of patients. AMAN progresses more rapidly and has an earlier peak than demyelinating GBS; tendon refl exes are relatively preserved or even exaggerated, and autonomic dysfunction is rare. One of the main causes is molecular mimicry of human gangliosides by Campylobacter jejuni lipo-oligosaccharides. In addition to axonal degeneration, electrophysiology shows rapidly reversible nerve conduction blockade or slowing, presumably due to pathological changes at the nodes or paranodes. Autoantibodies that bind to GM1 or GD1a gangliosides at the nodes of Ranvier activate complement and disrupt sodium-channel clusters and axoglial junctions, which leads to nerve conduction failure and muscle weakness. Improved understanding of the disease mechanism and pathophysiology might lead to new treatment options and improve the outlook for patients with AMAN.

Guillain-Barré syndrome (GBS) is a classic failure of the immune system with a life-threatening attack upon a critical self-component. The active phase of the disease is short, concordant with the latency of a primary adaptive immune response. Triggers for GBS include infection and (rarely) vaccination; cross-reactivity between infectious and neural epitopes has been well demonstrated, particularly for Campylobacter jejuni and motor axonal forms of GBS in which non-protein gangliosides are antigenic. Most people are probably exposed to a GBS trigger, but only rarely does the disease develop. We propose that GBS illustrates competing determinants of the immune system's decision about whether to mount a response, and that in unlucky affected individuals, copresentation of cross-reactive antigens with danger signals activating pattern-recognition receptors overcomes normal self-recognition such that a primary response is initiated that attacks the nerve. Then, in most cases of GBS, the response rapidly turns off, and second attacks rarely occur. This suggests active restoration of tolerance, and specific privileged site attributes of nerve and declining danger signals as the trigger wanes may contribute to this restoration. Standard immunosuppression has not been effective in GBS. We suggest this is because immune tolerance is already being restored by the time such therapies are initiated. This in turn suggests that improvements in GBS outcomes are likely to come from better protection of the nerve cells under attack while normal resumption of tolerance is permitted to proceed rather than exploring more aggressive immunosuppressive approaches.

Guillain-Barre syndrome (GBS) is the rubric encompassing highly variable phenotypic subgroups of acute, postinfectious, immune-mediated peripheral neuropathy. The hallmark of GBS phenomenology is a rapidly progressive ascending lower extremity weakness. GBS taxonomy includes a motor and sensory axonal neuropathy (AMSAN). Nitrous oxide (NO) abuse may create a pattern of neurological dysfunction almost identical to subacute combined degeneration. We report an adult with myeloneuropathy due to NO abuse that mimicked the presenting features of the GBS-subtype AMSAN.

Objectives: We performed responsiveness comparison between the patient-reported Inflammatory Rasch-built Overall Disability Scale (I-RODS) and the widely used clinician-reported Inflammatory Neuropathy Cause and Treatment-Overall Neuropathy Limitation Scale (INCAT-ONLS) in patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and immunoglobulin M-monoclonal gammopathy of undetermined significance related polyneuropathy (IgM-MGUSP).

Objective To discover the extent to which persons with Guillain-Barré syndrome receive treatment by a physiotherapist (as inpatients and outpatients), and to assess whether the amount of treatment received is related to outcome. Design Survey method using self-administered questionnaires distributed through a national database. Results In total, 884/1535 (58%) complete responses were received. Nearly 10% of respondents had not received treatment by a physiotherapist in hospital despite their average functional level being the same as respondents who had received treatment in hospital. One-quarter of respondents said that they had not received treatment following hospital discharge despite the identification of relatively high levels of disability. Those who did not receive treatment by a physiotherapist following discharge were less severely disabled. This may indicate that physiotherapists tend to offer treatment to more severely disabled patients. The majority of patients reported disabling fatigue; whilst not statistically related to receipt of treatment by a physiotherapist, this highlights the importance of assessing fatigue in treatment plans to improve physical functioning. Conclusion Improvements to policy and practice can be made by widening inpatient accessibility to treatment by a physiotherapist and increasing outpatient provision of treatment for patients with Guillain-Barré syndrome of all degrees of severity. Crown

PCR-restriction fragment length poymorphism (PCR-RFLP) is a simple, robust technique for the rapid identification of isoniazid-resistant Mycobacterium tuberculosis. One hundred consecutive isolates from a Vietnamese tuberculosis hospital were tested by MspA1I PCR-RFLP for the detection of isoniazid-resistant katG_315 mutants. The test had a sensitivity of 80% and a specificity of 100% against conventional phenotypic drug susceptibility testing. The positive and negative predictive values were 1 and 0.86, respectively. None of the discrepant isolates had mutant katG_315 codons by sequencing. The test is cheap (less than $1.50 per test), specific, and suitable for the rapid identification of isoniazid resistance in regions with a high prevalence of katG_315 mutants among isoniazid-resistant M. tuberculosis isolates.

Purpose: This systematic review examines the literature to identify the context and extent of implementation of the International Classification of Functioning, Disability and Health (ICF) model to understand the experience of health and functioning in persons with chronic conditions from the person perspective. Method: The literature search was conducted through five electronic databases between 2001 and December 2012. Reference lists of included papers were also searched. Articles in which the ICF was used to understand the health and functioning experience of adults with chronic conditions from the person-perspective were included. Data were extracted and analysed to identify the year of publication, geographical location, health condition, context of ICF use, authors' remarks and identified limitations of the ICF. Results: Thirty-seven qualitative and mixed-methods studies were included representing 18 countries and a range of chronic conditions. The ICF was found to be used to elicit and analyse people's narratives, with the majority of studies reporting that the ICF provides a comprehensive analysis of experiences and needs from the person perspective. Some limitations to its use and the need to classify the ''personal factors'' component were reported. Conclusion: The ICF has been used to provide a comprehensive understanding of health and functioning in persons with chronic conditions from the person perspective, although there are currently relatively few studies which have used the ICF in this context. Limitations regarding its use were reported which should be considered by users of the model and during its revision process.

The cases of Guillain Barre Syndrome (GBS) have been reported following the coronavirus disease 2019 (COVID-19). Here, we describe a case that evolved from GBS to chronic inflammatory demyelinating polyneuropathy (CIDP) after COVID-19 in terms of contributing to the literature due to its different aspects. In the cerebrospinal fluid examination of the acute onset mixed type polyneuropathy case, albuminocytological dissociation was not detected. The patient was given a loading dose and monthly maintenance intravenous immunoglobulin (IVIG) for six months. Blood ferritin levels gradually decreased in parallel with clinical improvement. Four months after the IVIG treatment was terminated, the findings recurred and the CIDP was developed and IVIG treatment was continued. Long-term follow-up of post-COVID-19 GBS patients is important in terms of recurrence and chronicity. Ferritin level may be a biochemical marker in the clinical follow-up of these cases.

Neurologists commonly use therapeutic plasma exchange (TPE, also known as plasmapheresis or therapeutic apheresis) to treat a number of conditions. This concise review examines the most common neurologic indications for therapeutic plasma exchange. It focuses on Guillain-Barrè syndrome and myasthenia gravis and also the role of TPE in chronic inflammatory demyelinating polyneuropathy, Lambert-Eaton syndrome, multiple sclerosis, neuromyelitis optica, paraproteinemic polyneuropathy, and Sydenham's chorea. As with any treatment, the proven efficacy, cost, side effects, and availability must be considered before initiation of therapy.

Background: Most studies of Campylobacter infection triggering Guillain-Barré Syndrome (GBS) are conducted in western nations were Campylobacter infection and immunity is relatively rare. In this study, we explored Campylobacter infections, Campylobacter serotypes, autoantibodies to gangliosides, and GBS in Egypt, a country where Campylobacter exposure is common.

Study Design. A case report. Objective. To present improvement of paraplegia due to spinal vascular malformation after delivery with no intervention. Summary of Background Data. Pregnancy has been reported rarely in patients with Klippel-Trenaunay syndrome (KTS). A combined case of spinal arteriovenous malformations (AVMs) within KTS has not been reported before. Methods. A case report of KTS with paraplegia is presented and the pertinent literature is then reviewed. Results. A pregnant woman who was diagnosed with KTS in childhood presented with newly developed paraplegia due to spinal AVMs. Magnetic resonance image showed a vascular malformation at the T9-T12 levels without evidence of spinal cord hemorrhage. Diagnostic angiography that was performed after delivery revealed a high-fl ow arteriovenous fi stula with AVM. Conclusion. Pregnancy complicated by paraplegia is thought to be secondary to venous engorgement and to the resulting spinal cord ischemia in this case. Her neurological symptoms and signs gradually improved over the few days after cesarean delivery.

Background: Guillain-Barré Syndrome (GBS) is an autoimmune disease that may occur after infections. As Coronavirus Disease 2019 (COVID-19) may bring about GBS, it is important to assess the effect of the COVID-19 pandemic on this disease Objectives: This study aimed to compare the distribution and characteristics of GBS during and before the COVID-19 pandemic in an academic referral hospital in the north of Iran. Materials & Methods: This retrospective study assessed GBS distribution and characteristics during the COVID-19 pandemic period (from March 2020 to the end of February 2021) and before the pandemic (from March 2019 to the end of February 2020) on 5340 patients referred to the Neurology Ward of Poursina Hospital of Guilan Province, in Iran. Results: There was no significant difference between GBS distribution during (0.03%) and before (0.04%) the COVID-19 pandemic (P=0.413). There were also no differences between the two periods regarding the gender (P=0.659) and age (P=0.417) of the patients. The most common subtype of GBS during the COVID-19 pandemic was Acute Motor and Sensory Axonal Neuropathy (AMSAN) (71.4%). In both periods, the most common type of treatment was intravenous administration of immune globulin. There was no significant difference between the two periods (P=0.838) regarding the patients' treatment response. Conclusion: The distribution of GBS, its subtypes, type of treatment, and response to treatment were not different between the two study periods.

Objective: To use the International Classification of Functioning, Disability and Health (ICF) to describe and compare patient-reported disability in Guillain-Barré syndrome survivors and persons with multiple sclerosis, and to identify relevant environmental factors. Methods: Cross-sectional survey of 77 survivors of Guillain-Barré syndrome in the community. Their Guillain-Barré syndrome-related problems were linked with ICF categories (second level) using an open-ended questionnaire, consensus between health professionals and the "linking rules", and compared with similar data collected previously for 101 persons with multiple sclerosis. Results: Guillain-Barré syndrome survivors were male (59%) and older than persons with multiple sclerosis (mean age 55 vs 49 years). Of 170 ICF categories, 113 were relevant for Guillain-Barré syndrome survivors (mean number 30 vs 18 for persons with multiple sclerosis). The linked categories for Guillain-Barré syndrome included: body function 27 (56%) compared with 48 (42%) for persons with multiple sclerosis; body structure 11 (68%) vs 16 (34%); activities and participation 48 (70%) and 68 (58%); and for environmental factors 27 (71%) compared with 38 (51%) for persons with multiple sclerosis. The main areas linked in the activities and participation domain were mobility, major life areas and interpersonal relationships; and environmental factors included support and relationships, attitudes and products and technology. Conclusion: This is the first study to use ICF in Guillain-Barré syndrome survivors and towards development of the ICF Core Set for Guillain-Barré syndrome from a broader international perspective.

Guillain-Barre syndrome (GBS) is a postinfectious inflammatory polyradiculo-neuropathy characterized bý flaccid paralysis. Antibodies directed against glycolipid structures (gangliosides), which are highly expressed in the peripheral nervous system, are frequently detected in sera from GBS patients. These antibodies interfere with nerve conduction and have been shown to activate phagocytes via IgG receptors (FcgR). These findings support an important role of glycolipid-specific antibodies in the pathogenesis of GBS. ᮊ

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. D

Acute motor axonal neuropathy (AMAN), an axonal subtype of Guillain-Barré syndrome (GBS), is characterized by pure motor involvement, frequent antecedent infection by Campylobacter jejuni, association with anti-GM1 or anti-GD1a immunoglobulin G (IgG) antibodies, and the electrophysiological features of axonal degeneration and reversible conduction block. Molecular mimicry exists between GM1 and GD1a gangliosides and lipooligosaccharides (LOSs) of C. jejuni isolates from AMAN. Sensitization of rabbits with GM1 or C. jejuni LOS induces anti-GM1 IgG antibodies and subsequent flaccid paralysis. Pathological changes seen in rabbit model peripheral nerves are identical to those in human AMAN. Immunohistochemistry of AMAN rabbits shows disruption of nodal sodium channel clusters and detachment of paranodal myelin terminal loops, similar to paranodal demyelination, which would significantly reduce the safety factor for impulse transmission and might be responsible for the rapidly reversible conduction block frequently present in human AMAN. C. jejuni sialyltransferase (Cst-II), which functions in the biosynthesis of ganglioside-like LOSs, determines the transferase activity. Strains with cst-II (Thr51) express GM1 and GD1a epitopes, whereas GBS patients infected with cst-II (Thr51) strains have anti-GM1 or anti-GD1a IgG antibodies. The cst-II gene is responsible for the development of GBS. Immunological, pathological, electrophysiological, and bacteriological studies have provided strong evidence of carbohydrate mimicry being a cause of AMAN and clarified the mechanisms of nerve conduction failure in AMAN.