Temporal Pattern of Individual Neurological Function Recovery in Guillain-Barré Syndrome.

Background: There is paucity of studies on the temporal pattern of recovery of facial, bulbar, sensory, motor, and autonomic dysfunction in Guillain-Barré syndrome (GBS), although many studies have reported short- and long-term functional outcomes. We report the temporal pattern of recovery of various neurological functions in GBS, and compare the pattern of recovery between acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Methods: Forty-two patients with GBS were prospectively included, and their clinical details, including peak disability on a 0-6 scale, were noted. The day of complete recovery in motor, sensory, facial, bulbar, and autonomic functions during 3 months of follow-up was recorded. Results: Complete recovery of autonomic function occurred in all (median, 12 days), bulbar weakness in 91.3% (median, 15 days), facial weakness in 86.2% (median, 19 days), and sensory functions in 82.1% (median, 20 days). Only 9.5% of patients achieved normal motor function within 3 months. The days of complete recovery of bulbar, facial, autonomic, and motor deficits were comparable between AIDP and AMAN. Demyelinating GBS had an earlier recovery of bulbar and sensory functions. Conclusions: The neurological recovery in GBS occurs first in the autonomic, followed by the bulbar, facial, sensory, and motor functions. The demyelinating type had an earlier recovery of bulbar and sensory functions.

Expanding our understanding of Guillain-Barré syndrome: Recent advances and clinical implications.

Guillain-Barré syndrome (GBS) is a rare yet potentially life-threatening disorder of the peripheral nervous system (PNS), characterized by substantial clinical heterogeneity. Although classified as an autoimmune disease, the immune mechanisms underpinning distinct GBS subtypes remain largely elusive. Traditionally considered primarily antibody-mediated, the pathophysiology of GBS lacks clarity, posing challenges in the development of targeted and effective treatments. Nevertheless, recent investigations have substantially expanded our understanding of the disease, revealing an involvement of autoreactive T cell immunity in a major subtype of GBS patients and opening new biomedical perspectives. This review highlights these discoveries and offers a comprehensive overview of current knowledge about GBS, including ongoing challenges in disease management.

Journey of Guillain Barre syndrome from the pre-pandemic era to the pandemic era: A 4-year retrospective study.

Aims: To study demographic and clinical profiles of Guillain Barre syndrome (GBS) in the pre-pandemic and coronavirus disease 2019 (COVID-19) pandemic era and to compare the GBS incidence, severity, and its outcome in the pre-pandemic and pandemic eras. Methodology: This is a 4-year retrospective study done in a tertiary care hospital in Delhi, India, between March 2018 and March 2022. Patients were divided into the pre-pandemic era and pandemic era (2 years before and 2 years after March 2020). Results: The number of patients (N) was 25 in the pandemic/vaccine era, while N = 49 in the pre-pandemic era. The mean duration of hospitalization was significantly higher (P = 0.03) during the pandemic era (10.68 ± 6.67 days) compared to the pre-pandemic era (7.59 ± 3.55 days). There was no statistical difference in age (P = 0.56), gender (P = 0.70), GBS variants (P = 0.40), clinical spectrum, antecedent infection (P = 0.91), Hughes Disability Score on admission and discharge (P = 0.93 and P = 0.52, respectively), respiratory involvement requiring a ventilator (P = 0.19), and mortality (P = 0.26) in both the eras. Conclusion: Our study showed no association of the incidence of GBS with the ongoing COVID-19 pandemic. The mean hospitalization days were significantly increased during COVID-19 in view of associated respiratory involvement. The commonly held hypothesis of the increase in GBS cases during the pandemic/vaccine era has not been observed in our study.

Effectiveness of Symptomatic Physiotherapy in Enhancing the Psychological Parameters of a Patient With Guillain-Barré Syndrome: A Case Report.

Guillain-Barré syndrome is a polyneuropathy that can be caused by an autoimmune condition or a bacterial infection. In typical GBS cases, there is hypo- or areflexia, symmetrical limb weakness that worsens within four weeks of the symptoms. The facial nerve is involved in this situation, which results in weak facial muscles, which, in turn, affect facial emotions and movements. In this case study, a 21-year-old athlete who suffered from unexpected weakness that resulted in quadriplegia had goal-oriented physical therapy treatment designed for the patient, who recovered quickly. This case study aims to emphasize how goal-oriented physical therapy treatment can help patients recover quickly.

Deciphering the Neuropsychiatric Lupus Enigma: Navigating the Intersection of Acute Inflammatory Demyelinating Polyneuropathy (AIDP), Infection, and Flare.

A 17-year-old male diagnosed with systemic lupus erythematosus (SLE), showing poor compliance with medication, presented to our facility with a 20-day history of fever, polyarthritis, and cough. Additionally, he had experienced a seizure episode, followed by a one-day history of altered mentation. Subsequently, he developed pneumonia, respiratory distress, and shock, necessitating ventilator and inotropic support. Neuropsychiatric lupus (NP-lupus) was suspected, and hence high-dose steroids, hydroxychloroquine, and broad-spectrum antibiotics were initiated. Following successful extubation, he manifested ascending flaccid paralysis. The presence of albumin-cytological dissociation and axonal neuropathy confirmed the diagnosis of acute inflammatory demyelinating polyneuropathy (AIDP). He underwent further management with pulse steroids and plasmapheresis. Upon recovery, he was discharged on a regimen of steroids, cyclophosphamide, and hydroxychloroquine. During follow-up, he maintained ambulatory status with no residual neurological sequelae.

Clinical Worsening of Charcot-Marie-Tooth Disease Due to Overlapping Acute Inflammatory Polyneuropathy.

We report a case of a six-year-old male with Charcot-Marie-Tooth disease (CMT) type 1B due to MPZ gene mutation who experienced an acute worsening of his symptoms a few years after the diagnosis. He was not able to walk without assistance and had transitory paresthesia in his hands, 10 days after suffering from an upper respiratory and diarrheal illness. The investigation revealed elevated cerebrospinal fluid (CSF) protein levels with no pleocytosis, and sensory and motor chronic demyelinating neuropathy without active denervation findings on electrophysiological studies. The patient completely recovered following treatment with intravenous immunoglobulin. We describe the patient's history and engage in a review of the literature to find similar clinical cases. It has been proposed that MPZ gene mutations can change the myelin structure and result in abnormal exposure of the nervous cell components to immune cells. Hence, patients with this type of CMT would be predisposed to concurrent inflammatory forms of neuropathy.

Usefulness and Clinical Impact of Whole-Body MRI in Detecting Autoimmune Neuromuscular Disorders.

Autoimmune neuromuscular diseases are a group of heterogenous pathologies secondary to the activation of the immune system that damage the structures of the peripheric nerve, the neuromuscular junction, or the skeleton muscle. The diagnosis of autoimmune neuromuscular disorders comprises a combination of data from clinical, laboratory, electromyography, imaging exam, and biopsy. Particularly, the whole-body MRI examination in the last two decades has been of great use in the assessment of neuromuscular disorders. MRI provides information about the structures involved and the status of activity of the disease. It can also be used as a biomarker, detect the pattern of specific muscle involvement, and is a useful tool for targeting the optimal muscle site for biopsy. In this work, we summarized the most used technical protocol of whole-body MRI and the role of this imaging technique in autoimmune neuromuscular disorders.

Guillain-Barré Syndrome Following Hand, Foot, and Mouth Disease in an Adult Patient.

Guillain-Barré syndrome (GBS) stands as one of the primary causes of acute flaccid paralysis. It includes acute-onset peripheral nerve lesions and typically follows a monophasic course. Its etiopathogenesis is linked to an immune-mediated response to a prior infection, often respiratory or intestinal. The main variants of GBS are acute inflammatory demyelinating polyneuropathy, which accounts for approximately 90% of cases in the USA and Europe, and acute motor axonal neuropathy, responsible for about 10% of cases in the USA and Europe. From the literature review, only one case of GBS preceded by hand, foot, and mouth disease (HFMD) has been described. The authors report a rare clinical case of typical GBS after HFMD. Recognizing this adult-onset disease as a potential preceding infection of GBS is crucial for early diagnosis and treatment. Additionally, the integration into a rehabilitation program adjusted to the deficits plays an important role in motor and functional recovery.

Nodal-paranodal antibodies in HIV-immune mediated radiculo-neuropathies: Clinical phenotypes and relevance.

BACKGROUND: The frequency of nodal-paranodal antibodies in HIV-infected patients with chronic immune-mediated radiculo-neuropathies (IMRN) has not been previously described. METHODS: HIV-infected patients who met the inclusion criteria for chronic IMRN were screened for immunoglobulin G (IgG) antibodies directed against nodal (neurofascin (NF)186) and paranodal (NF155, contactin-1 (CNTN1) and contactin-associated protein(Caspr1)) cell adhesion molecules, using a live, cell-based assay. To explore potential pathogenicity, binding of human IgG to myelinated co-cultures was assessed by incubation with patients' sera positive for nodal or paranodal antibodies. Normal human serum was added as a source of complement to assess for complement activation as a mechanism for myelin injury. RESULTS: Twenty-four HIV-infected patients with IMRN were included in the study, 15 with chronic inflammatory demyelinating polyneuropathy (CIDP), 4 with ventral root radiculopathies (VRR), and 5 with dorsal root ganglionopathies (DRG). Five patients with CIDP had combined central and peripheral demyelination (CCPD). Three patients (12.7%) tested positive for neurofascin IgG1 antibodies in the following categories: 1 patient with VRR was NF186 positive, and 2 patients were NF155 positive with DRG and mixed sensory-motor demyelinating neuropathy with optic neuritis, respectively. CONCLUSION: The frequency of nodal-paranodal antibodies is similar among IMRN regardless of HIV status. Interpretation of the results in the context of HIV is challenging as there is uncertainty regarding pathogenicity of the antibodies, especially at low titres. Larger prospective immune studies are required to delineate pathogenicity in the context of HIV, and to establish a panel of antibodies to predict for a particular clinical phenotype.

Acute/chronic inflammatory polyradiculoneuropathy.

Autoimmune neuropathy may present acutely or with a more progressive and/or relapsing and remitting course. Acute inflammatory neuropathy or Guillain-Barré syndrome (GBS) has variable presentations but by far the most common is acute inflammatory demyelinating polyradiculoneuropathy which is characterized by rapidly progressive proximal and distal symmetric weakness, sensory loss, and depressed reflexes. The most common chronic autoimmune neuropathy is chronic inflammatory demyelinating polyradiculoneuropathy, which in its most typical form is clinically similar to acute inflammatory demyelinating polyradiculoneuropathy (proximal and distal symmetric weakness, sensory loss, and depressed reflexes) but differs in that onset is much more gradual, i.e., over at least 8 weeks. While the majority of GBS cases result from a postinfectious activation of the immune system, presumably in a genetically susceptible host, less is understood regarding the etiopathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy. Both acute and chronic forms of these inflammatory neuropathies are driven by some combination of innate and adaptive immune pathways, with differing contributions depending on the neuropathy subtype. Both disorders are largely clinical diagnoses, but diagnostic tools are available to confirm the diagnosis, prognosticate, detect variant forms, and rule out mimics. Given the autoimmune underpinnings of both disorders, immunosuppressive and immunomodulating treatments are typically given in both diseases; however, they differ in their response to treatment.

Guillain-Barre Syndrome in Children and Adolescents.

Guillain-Barre syndrome (GBS) is an immune-mediated disease of the peripheral nerves and cause of acute flaccid paralysis in children around the world. The most common type of GBS in North America targets myelin and leads to demyelinating neuropathy. Often there is a history of infection in the weeks preceding motor symptoms. GBS has been associated with different infections, including COVID. Children usually recover motor function, but autonomic instability and respiratory compromise can occur necessitating close observation and potentially intensive care unit admission.

Guillain-Barre Syndrome, a Leptomeningeal Metastasis Mimic, in a Patient With Metastatic Breast Carcinoma.

Leptomeningeal metastasis (LM) is an outcome associated with a terminal prognosis for a patient with metastatic cancer. Symptoms associated with this type of cancer progression can be subtle and nonspecific. Evaluation of LM occurs with a lumbar puncture (LP) and magnetic resonance imaging (MRI). Guillain-Barre Syndrome (GBS) can present with a similar presentation of neurological symptoms to LM. Additionally, both disease states may present with similar MRI findings. The LP can be an important diagnostic evaluation to differentiate LM and GBS. However, an LP may be unremarkable in both disease states. Therefore, a comprehensive assessment of the patient based on clinical history, physical examination, laboratory, and radiologic evaluation is essential for prompt diagnosis and treatment. We present a patient with metastatic breast cancer that presented with generalized weakness. Thorough evaluation allowed the diagnosis and treatment of GBS.

Increased risk of depression after Guillain-Barré syndrome.

INTRODUCTION/AIMS: Guillain-Barré syndrome (GBS) is a potentially life-threatening disorder, and some patients may develop subsequent depression related to traumatic stress or permanent loss of motor function. We determined the short-term (0 to 2 years) and long-term (>2 years) risk of depression after GBS. METHODS: Individual-level data from nationwide registries were linked in this population-based cohort study of all first-time hospital-diagnosed GBS patients in Denmark between 2005 and 2016 and individuals from the general population. After exclusion of individuals with previous depression, we computed cumulative rates of depression, defined as either antidepressant drug prescription or depression hospital diagnosis. We used Cox regression analyses to calculate adjusted depression hazard ratios (HRs) after GBS. RESULTS: We identified 853 incident GBS patients and recruited 8639 individuals from the general population. Depression within 2 years was observed in 21.3% (95% confidence interval [CI], 18.2% to 25.0%) of GBS patients and in 3.3% (95% CI, 2.9% to 3.7%) of those in the general population, resulting in a HR of 7.6 (95% CI, 6.2 to 9.3). The highest depression HR was observed within the first 3 months after GBS (HR, 20.5; 95% CI, 13.6 to 30.9). After the first 2 years, GBS patients and the general population members had similar long-term depression risks with an HR of 0.8 (95% CI, 0.6 to 1.2). DISCUSSION: During the first 2 years after GBS hospital admission, patients with GBS had a 7.6-fold increased hazard of depression compared with individuals in the general population. Two years after GBS, the risk of depression was similar to that of the background population.

Prognostic Implications of Early Albuminocytological Dissociation in Guillain-Barré Syndrome.

BACKGROUND: Half of Guillain-Barré syndrome (GBS) present elevated cerebrospinal fluid (CSF) protein levels within 1 week since symptom onset and 80% within 2 weeks. Our objective was to determine the clinical and prognostic implication of albuminocytological dissociation in early GBS. METHODS: An ambispective cohort study was conducted. Good outcome was considered if the patient was able to walk unaided (Guillain-Barré disability score [GDS] ≤ 2 points) at 3-month follow-up. Patients were classified into two groups: with and without albuminocytological dissociation; we compared clinical and paraclinic characteristics between the groups. We analyzed clinical and electrophysiological factors related to presenting early dissociation through a multivariate model. RESULTS: We included 240 patients who fulfilled Asbury criteria for GBS. On further selection, only 94 patients fulfilled inclusion. Mean age was 45.94 ± 17.1 years and 67% were male. Median time from symptom onset to admission was 5 days (IQR 3-6). Regarding albuminocytological dissociation and electrophysiological variants, we found a significant difference: acute inflammatory demyelinating polyneuropathy (AIDP) [60.6% vs 26.2%, p = 0.002], acute motor axonal neuropathy (AMAN) [21.2% vs 49.1%, p = 0.009] and acute motor sensory axonal neuropathy (AMSAN) [12.1% vs 1.6%, p = 0.05]. We did not observe significant differences in recovery of independent walking in short term between both groups. The presence of conduction block in any variant (OR 3.21, 95% CI 1.12-9.16, p = 0.02) and absence of sural registration (OR 5.69, 95% CI 1.48-21.83, p = 0.011) were independent factors related to early dissociation. CONCLUSIONS: Early dissociation (<7 days) is not associated with any particular clinical feature or unfavorable outcome. It is more common to see in AIDP rather than axonal variants.

Recombinant protein subunit COVID-19 vaccine-induced Guillain-Barré Syndrome in an adolescent: A case report.

Guillain-Barré Syndrome (GBS), an autoimmune neurological disease of peripheral nerves, has been causally associated with COVID-19 vaccination in adults. However, no such report has been published so far in children. We describe a 13-year-old female child who presented to the emergency department with complaints of bilateral upper limb, lower limb and truncal weakness over 3 days following first dose of recombinant protein subunit COVID-19 vaccine (Corbevax). Clinical examination and nerve conduction studies showed pure motor axonal polyneuropathy with absent compound muscle action potential (CMAP) in all sampled nerves of upper and lower limbs which was consistent with the diagnosis of GBS after ruling out possible alternative aetiologies. A temporal association between first dose of protein subunit COVID-19 vaccine administered a day prior and symptom onset was noted. The causality assessment using the World Health Organization (WHO) tool for adverse event following immunization (AEFI) assessment indicated vaccine product-related reaction categorized as A1. The patient's clinical condition improved after seven sessions of plasmapheresis. The purpose of this report is to create awareness among health care professionals about COVID-19 vaccine-induced GBS in children as early diagnosis and management can be critical in avoiding complications and improving patient outcomes.

Dose-Effect Relationship of Motor Nerve Inexcitability on Outcome in Guillain-Barré Syndrome: A Prospective Cohort Study.

Objective: One or more inexcitable motor (IM) nerves are common during electrodiagnostic (EDx) study in Guillain-Barré syndrome (GBS). This study assessed the dose-effect relationship of IM nerves on outcome in patients with acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor and/or sensory axonal neuropathy (AMAN and AMSAN). Materials and Methods: Eighty-eight GBS patients admitted during May 2018-June 2023 underwent detailed clinical evaluation and EDx study. Admission and follow-up disability were assessed on a 0-10 Clinical Grading Scale (CGS). Outcome was recovery at 6 months, defined as good (CGS <3) and poor (CGS ≥3). Binary multivariate logistic regression with backward elimination was used to calculate independent predictors of outcome. Results: Proportion of patients with complete recovery decreased significantly with increasing numbers of IM nerves (P < 0.01). Seventy-six patients were followed for 6 months. Among patients with IM nerves (n = 28), complete recovery was similar between AIDP and axonal GBS (70% vs. 50%, respectively; P = 0.40). However, in patients with recordable compound muscle action potentials (CMAPs) in all the motor nerves (n = 26), axonal GBS had significantly poor recovery compared to AIDP (75% vs. 9.1%; P = 0.01). Among patients receiving intravenous immunoglobulin (IVIg; n = 42), poor recovery was seen in 53.6% with IM nerves compared to 35.7% without (P = 0.28), while it was 37.5% versus 5.6% (P = 0.04), respectively, in those who did not receive IVIg (n = 34). However, only admission disability (odds ratio [OR] 0.88, 95% confidence interval [CI] 0.81-0.97; P = 0.007) was found to be an independent predictor of outcome. Conclusion: Although increasing numbers of IM nerves were associated with poor outcome on univariate analysis, they did not predict 6 months' outcome independently. Outcome did not differ between axonal GBS and AIDP among those with IM nerves. IVIg improved outcome in patients with IM nerves.

A young adult with leptospirosis associated acute inflammatory demyelinating polyneuropathy.

Leptospirosis is a zoonotic disease that commonly affects the liver and kidney. It can rarely affect the neurological system with aseptic meningitis being the commonest neurological presentation. We present the case of a patient with leptospirosis complicated by acute inflammatory demyelinating polyneuropathy. Contribution: To our knowledge, this is the first reported case of acute inflammatory demyelinating polyneuropathy as a complication of leptospirosis in South Africa.

Combined central and peripheral demyelination: a case report.

Overlapping central nervous system (CNS) and peripheral nervous system (PNS) demyelination is a rare clinical entity, more frequently seen in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and multiple sclerosis (MS). This case report showcases a patient with atypical CIDP and CNS demyelination lesions. Demographic data, disease course, treatment responsiveness, neurological examination, laboratory tests, nerve conduction studies (NCS), and brain and spinal cord MRI were registered. The case highlights the difficulty of diagnosis establishment and treatment selection, given the atypical course of the disease and limited answers to the indicated therapies. The data from our report suggest that specific and widely available immunological targets are necessary for diagnosing combined central and peripheral demyelination cases appropriately. The association of different immunotherapeutic agents may be necessary to induce and maintain disease remission.

Patrones clínicos y neurofisiológicos de presentación temprana en la polirradiculoneuropatía inflamatoria desmielinizante crónica de inicio agudo / Clinical and neurophysiological patterns of early presenting symptoms in acute onset chronic inflammatory demyelinating polyradiculoneuropathy

Introducción: Dentro de los fenotipos de polineuropatía desmielinizante inflamatoria crónica (CIDP) existe uno cuyo tiempo de evolución es menor de ocho semanas desde el inicio de los síntomas, denominado de inicio agudo (A-CIDP). Esta entidad puede confundirse con el síndrome de Guillain-Barré, variedad desmielinizante inflamatoria aguda (AIDP), lo que retrasa el inicio del tratamiento. Objetivo: Analizar las diferencias clínicas y electrofisiológicas entre A-CIDP, CIDP clásica y AIDP, con el fin de identificar factores que auxilien al diagnóstico diferencial de forma temprana. Pacientes y métodos: Se realizó un estudio transversal con pacientes atendidos en la clínica de enfermedades neuromusculares del Instituto Nacional de Neurología y Neurocirugía con diagnóstico de CIDP según criterios de la European Federation of Neurological Societies and Peripheral Nerve Society. Los pacientes con CIDP <8 semanas se catalogaron como A-CIDP y fueron comparados con pacientes diagnosticados con CIDP clásica y AIDP. Se obtuvieron y analizaron variables clínicas, paraclínicas y electrofisiológicas. Resultados: Se observaron diferencias significativas en antecedente de infección, afección de nervios del cráneo y disautonomías entre la A-CIDP y la AIDP. Los registros electrofisiológicos describieron diferencias significativas en velocidad de conducción de los nervios motores y en los registros del nervio sural, que fueron menores en el grupo de A-CIDP. Conclusión: El antecedente de infección, la afección de nervios del cráneo y las disautonomías son parámetros importantes que se debe tener en cuenta para el diagnóstico diferencial de estas entidades. El análisis electrofisiológico es similar entre la A-CIDP y la CIDP. El diagnóstico diferencial entre estos tipos de polineuropatía desmielinizante debe basarse en el juicio clínico.(AU)

Introduction: The phenotypes of chronic inflammatory demyelinating polyneuropathy (CIDP) include an acute-onset phenotype (A-CIDP) with an evolution time of less than eight weeks from the onset of symptoms. This entity can be confused with Guillain-Barré syndrome of the acute inflammatory demyelinating variety (AIDP), delaying the start of treatment. Objective: To analyze the clinical and electrophysiological differences between A-CIDP, classic CIDP and AIDP, in order to identify factors that may help in the early differential diagnosis. Patients and methods: A cross-sectional study was carried out with patients seen at the neuromuscular disease clinic of the National Institute of Neurology and Neurosurgery with a diagnosis of CIDP according to the criteria of the European Federation of Neurological Societies and Peripheral Nerve Society. Patients with CIDP <8 weeks were categorized as A-CIDP and were compared with patients diagnosed with classic CIDP and AIDP. Clinical, paraclinical and electrophysiological variables were obtained and analyzed. Results: Significant differences in history of infection, cranial nerve involvement and dysautonomia were observed between A-CIDP and AIDP. Electrophysiological recordings reported significant differences in motor nerve conduction velocity and sural nerve recordings, being lower in the A-CIDP group. Conclusion: A history of infection, cranial nerve involvement and dysautonomia are important parameters to take into account for the differential diagnosis of these entities. Electrophysiological analysis is similar between A-CIDP and CIDP. The differential diagnosis between these types of demyelinating polyneuropathy must be based on clinical assessment.(AU)

Prognostic Significance of Serial Nerve Conduction in GB Syndrome.

Background and Aims: We evaluated dynamic changes in neurophysiology of Guillain-Barré syndrome (GBS) at different time points and the role of demyelination and axonal burden in predicting outcome. Methods: Nerve conduction study (NCS) was done in 44 GBS patients at admission and at 1 and 3 months, and were categorized into acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor sensory axonal neuropathy (AMSAN), equivocal and in-excitable motor nerve (IMN). The demyelinating and axonal burden on motor NCS at admission, 1 and 3 months were computed and correlated with disability at 3 and 6 months. Disability was assessed using Clinical Grading Scale. Results: Twenty-four (54.3%) had AIDP, 5 (11.4%) AMAN, 12 (27.3%) equivocal and 3 (6.8%) had IMN at admission. Maximum instability was noted in equivocal group; majority of whom became AIDP at three months. Neurophysiological subtypes at different time points did not correlate with 6 months disability, but demyelination burden at admission (r = -0.42; P = 0.005) and axonal burden at one month (r = 0.43; P = 0.04) correlated with six months disability. Conclusion: Inverse correlation of axonal burden at one and three months with disability suggests role of secondary axonal damage in predicting outcome. Repeat NCS at one month helps in categorizing GBS and also in prognostication.