Inflammatory Polyneuropathy Research Articles

HERV-W envelope protein is present in microglial cells of the human glioma tumor microenvironment and differentially modulates neoplastic cell behavior

Gliomas are the most common parenchymal tumors of the central nervous system (CNS). With regard to their still unclear etiology, several recent studies have provided evidence of a new category of pathogenic elements called human endogenous retroviruses (HERVs) which seem to contribute to the evolution and progression of many neurological diseases such as amyotrophic lateral sclerosis (ALS), schizophrenia, chronic inflammatory polyneuropathy (CIDP) and, particularly, multiple sclerosis (MS). In these diseases, HERVs exert effects on cellular processes such as inflammation, proliferation, and migration. In previous studies, we demonstrated that in MS, the human endogenous retrovirus type-W envelope protein (HERV-W ENV) interferes with lesion repair through the activation of microglia (MG), the innate myeloid immune cells of the CNS. Here, we now show that HERV-W ENV is also present in the microglial cells (MG) of the tumor microenvironment (TME) in gliomas. It modulates the behavior of glioblastoma (GBM) cell lines in GBM/MG cocultures by altering their gene expression, secreted cytokines, morphology, proliferation, and migration properties and could thereby contribute to key tumor properties.

Top 10 Clinical Pearls in Vasculitic Neuropathies.

Vasculitic neuropathies are a diverse group of inflammatory polyneuropathies that result from systemic vasculitis (e.g., polyarteritis nodosa, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis), vasculitis resulting from rheumatological disorders (e.g., rheumatoid arthritis and Sjögren's syndrome), paraneoplastic conditions, viruses, and medications. Occasionally, vasculitis is restricted to the peripheral nerves and termed nonsystemic vasculitic neuropathy. Presenting with an acute or subacute onset of painful sensory and motor deficits, ischemia to individual peripheral nerves results in the classic "mononeuritis multiplex" pattern. Over time, overlapping mononeuropathies will result in a symmetrical or asymmetrical sensorimotor axonal polyneuropathy. The diagnosis of vasculitic neuropathies relies on extensive laboratory testing, electrodiagnostic testing, and nerve and/or other tissue biopsy. Treatment consists primarily of immunosuppressant medications such as corticosteroids, cyclophosphamide, rituximab, methotrexate, or azathioprine, in addition to neuropathic pain treatments. Frequently, other specialists such as rheumatologists, pulmonologists, and nephrologists will comanage these complex patients with systemic vasculitis. Prompt recognition of these conditions is imperative, as delays in treatment may result in permanent deficits and even death.

Increased CXCL12, a potential CSF biomarker for differential diagnosis of amyotrophic lateral sclerosis

Abstract Amyotrophic lateral sclerosis (ALS) is a debilitating and lethal neurodegenerative disorder marked by the gradual deterioration of motor neurons. Diagnosing ALS is challenging due to the lack of reliable diagnostic tools, with clinical assessment being the primary criterion. Recently, increased levels of neurofilament light chain (NF-L) in CSF have been considered a useful biomarker in disease, correlating with disease progression but not specific for diagnosis. This study utilized ELISA to measure CSF CXCL12 levels in healthy controls (HC), ALS patients, and patients with ALS-mimic disorders, assessing its potential as a diagnostic biomarker and comparing it with NF-L levels. Our results confirmed previous findings, showing increased CXCL12 levels in ALS patients compared to HC (797.07 ± 31.84 pg/mL vs. 316.15 ± 16.6 pg/mL; p=0.000) and increased CSF NF-L levels in ALS (4,565.63 ± 263.77 pg/mL) compared to HC (847.86 ± 214.37 pg/mL; p=0.000). Increased CXCL12 levels were specific to ALS, not seen in ALS-mimic conditions like myelopathies (252.20 ± 23.16 pg/mL; p=0.000), inflammatory polyneuropathies (IP) (270.24 ± 32.23 pg/mL; p=0.000), and other mimic diseases (OMD) (228.91 ± 29.20 pg/mL; p=0.000). In contrast, CSF NF-L levels in ALS overlapped with those in myelopathies (2,900.11 ± 872.20 pg/mL; p=0.821) and OMD (3,169.75 ± 1,096.65 pg/mL; p=0.63), but not with IP (1,156.4 ± 356.6 pg/mL; p=0.000). ROC curve analysis indicated significant differences between the AUC values of CXCL12 and NF-L in their diagnostic capacities. CXCL12 could differentiate between ALS and myelopathies (AUC: 0.99 ± 0.005), IP (AUC: 0.962 ± 0.027), and OMD (AUC: 1.00 ± 0.00), whereas NF-L was only effective in IP cases (AUC: 0.92 ± 0.048), not in myelopathies (AUC: 0.71 ± 0.09) or OMD (AUC: 0.69 ± 0.14). We also evaluated CXCL12 levels in plasma (ALS (2,022 ± 81.8 pg/mL) vs HC (1,739.43 ± 77.3 pg/mL; p=0.015)) but found CSF determination (AUC: 0.97 ± 0.012) to be more accurate than plasma determination (AUC: 0.65 ± 0.063). In plasma, SIMOA NF-L determination (ALS (86.00 ± 12.23 pg/mL) vs HC (12.69 ± 1.15 pg/mL); p=0.000) was more accurate than plasma CXCL12 (AUC: 0.98 ± 0.01405). These findings suggest that CSF CXCL12 levels can enhance diagnostic specificity in distinguishing ALS from ALS-mimic disorders, compared to NF-L. Larger studies are needed to validate these results, but CXCL12 determination shows promising diagnostic potential.

Recent Trends in Diabetic and Nondiabetic Neuropathies: A Retrospective Hospital-based Nationwide Cohort Study

ObjectiveThe aim of this study was to evaluate the trends in the incidence of diabetic neuropathy (DN) and nondiabetic neuropathy (non-DN) in a hospital-based cohort between 2010 and 2019 in Romania. MethodsWe retrospectively analyzed cases with a primary or secondary discharge International Classification of Diseases, Tenth Revision, diagnosis code of neuropathy reported throughout Romania. ResultsA total of 1 725 729 hospitalizations with a diagnosis of neuropathy (DN, 769 324 - 44.6%, and non-DN, 956 405- 55.4%) were identified. Women accounted for more DN cases (40 0 936- 52.1%), and men accounted for more non-DN cases (63 7 968- 61.0%). The incidence rate showed an increasing trend during the index period, by a mean rate of 4.3%/year for non-DN and 1.4%/year for DN. Type 2 diabetes was responsible for the overall increase in the incidence rate of DN, whereas in type 1 diabetes, the incidence rate decreased; in both types of diabetes, diabetic polyneuropathy was predominant, whereas autonomic neuropathy had an incidence rate of 10 to 20 times lower than polyneuropathy. The incidence rates of non-DNs increased mainly due to inflammatory polyneuropathies (+3.8%) and uremic neuropathy (+10.3%). ConclusionUsing a nationally representative database of hospital-admitted cases, we found that the incidence rates of DN and non-DN increased from 2010 to 2019. The main contributors were type 2 diabetes, inflammatory polyneuropathy, and uremic neuropathy.

Genetic analyses of inflammatory polyneuropathy and chronic inflammatory demyelinating polyradiculoneuropathy identified candidate genes

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a rare, immune-mediated disorder in which an aberrant immune response causes demyelination and axonal damage of the peripheral nerves. Genetic contribution to CIDP is unclear and no genome-wide association study (GWAS) has been reported so far. In this study, we aimed to identify CIDP-related risk loci, genes and pathways. We first focused on CIDP, and 516 CIDP cases and 403,545 controls were included in the GWAS analysis. We also investigated genetic risk for inflammatory polyneuropathy (IP), in which we performed a GWAS study using FinnGen data and combined the results with GWAS from UK biobank (UKBB) using a fixed-effect meta-analysis. A total of 1,261 IP cases and 823,730 controls were included in the analysis. Stratified analyses by gender were performed. Mendelian randomization (MR), colocalization, and transcriptome-wide association study (TWAS) analyses were performed to identify associated genes. Gene-set analyses were conducted to identify associated pathways. We identified one genome-wide significant locus at 20q13.33 for CIDP risk among women; the top variant located at the intron region of gene CDH4. Sex-combined MR, colocalization and TWAS analyses identified three candidate pathogenic genes for CIDP, five genes for IP. MAGMA gene-set analyses identified a total of 18 pathways related to IP or CIDP. Sex-stratified analyses identified three genes for IP among males; and two genes for IP among females. Our study identified suggestive risk genes and pathways for CIDP and IP. Functional analysis should be conducted to further confirm these associations.

Pathobiochemical mechanisms of development of idiopathic inflammatory polyneuropathy

The article discusses the pathobiochemical mechanisms of the development of idiopathic inflammatory polyneuropathy. The authors’ analysis of the literature data showed. that the infection is not the direct cause of the disease, but plays the role of a provoking agent that triggers autoim mune mechanisms. Triggering factors may also include blood transfusions, surgery, bone marrow transplantation, and traumatic injuries to peripheral nerves. understanding the etiology, clinical manifestations and diagnosis of peripheral nerve damage is an important problem in the modern world of medicine.

Differentiating recurrent Guillain-Barre syndrome and acute-onset chronic inflammatory polyneuropathy: literature review.

Guillain-Barre syndrome (GBS) is an acute-onset immune-mediated polyneuropathy characterized by ascending symmetrical muscle weakness, diminished reflexes, and sensory symptoms. While GBS typically follows a monophasic course, some patients experience treatment-related fluctuations or recurrences, posing diagnostic challenges in distinguishing GBS from acute-onset chronic inflammatory polyneuropathy (A-CIDP). A-CIDP, may present acutely, simulating GBS, with a nadir in less than 8weeks, subsequently evolving into a chronic or relapsing course. The distinction between recurrent GBS and A-CIDP is crucial, as A-CIDP necessitates long-term immunosuppression. A PubMed search was conducted using the search terms 'recurrent Guillain Barre syndrome' and 'acute onset CIDP' focusing on studies in theEnglish language, published between January 1, 2004 and April 30, 2023. Overlapping clinical features, particularly in the early stages, complicate differentiation between recurrent GBS and CIDP. Electrophysiological studies, ultrasonography, and immunological markers have been explored for discrimination; however, definitive criteria for differentiation remain elusive. Recent follow-up studies have further blurred the boundaries between recurrent GBS and A-CIDP, suggesting the persistence of underlying immune processes even in GBS patients without clinical deterioration. This emphasizes the necessity of reevaluating diagnostic criteria and treatment strategies. In conclusion, distinguishing recurrent GBS from A-CIDP remains an ongoing challenge. Existing evidence questions the categorization of recurrent GBS as a distinct entity, challenging its very existence. Continued research is necessary to refine diagnostic criteria and deepen our understanding of these conditions, ultimately advancing patient care. This review delves into the intricacies of recurrent GBS and A-CIDP differentiation and highlights the need for a reevaluation of therecurrent GBS concept.

The psychometric properties of the Six-Spot Step Test – a systematic review using the COSMIN guidelines

Objective Accurate and reliable balance measures are important for prescribing fall prevention treatments and monitoring their effectiveness. Thus, we aimed to systematically review the psychometric properties of the Six-Spot Step Test, an increasingly used measure of dynamic balance. Data sources A literature search using the free-text term “Six-Spot Step Test” was performed on 12 February 2024, in Medline, Embase, Rehabilitation & Sports Medicine and SPORTDiscus. Eligibility criteria were adults aged 18 or more, trials evaluating the psychometric properties of the Six-Spot Step Test, and English-language articles. Conference abstracts were excluded. Review methods Two investigators screened and selected data independently and assessed the methodological quality and evidence using the COSMIN Risk of Bias checklist and modified GRADE approach. One investigator extracted study characteristics such as design, population and psychometric properties. Results Of the 159 articles identified, 16, evaluating multiple measurement properties, were included in the final analysis. A total of 1319 people participated, including people affected by Stroke, multiple sclerosis, Parkison's disease, chronic inflammatory polyneuropathy and older adults with balance problems. Eight articles assessing reliability (n = 618, intraclass correlations coefficient ≥0.7, minimal detectable change = 22%) and 12 construct validity (n = 1082, 83% true hypothesis, area under the curve >0.7) exhibited sufficient methodological quality with high-level evidence, while two studies (n = 167) examining responsiveness showed very low evidence. Conclusion Apart from responsiveness, robust evidence supports the reliability and validity of the Six-Spot Step Test for assessing dynamic balance in a specific group of individuals with neurological diseases and older adults. Further, it is considered feasible for clinical use.

Risk factors for respiratory failure among hospitalized patients with Guillain–Barré syndrome

BackgroundGuillain–Barré syndrome (GBS) is an acute inflammatory polyneuropathy that can lead to respiratory failure. In this study, we evaluate early clinical risk factors for respiratory failure at the time of hospital admission. MethodsWe studied a retrospective cohort of patients with GBS admitted to a tertiary care center. The potential risk factors studied were sociodemographic characteristics, GBS symptoms, overall and cervical muscle weakness (Medical Research Council [MRC] scores), electromyography findings, and cerebrospinal fluid analysis findings. Unadjusted odds ratios (OR) were calculated and exact logistic regression analysis (adjusted OR) performed to assess the association between baseline risk factors and respiratory failure. ResultsOverall, 13 of 113 (12%) patients included in the study developed respiratory failure. Unadjusted analyses showed that involvement of any cranial nerve (OR: 14.7; 95% CI, 1.8–117.1), facial palsy (OR: 17.3; 95% CI, 2.2–138.0), and bulbar weakness (OR: 10.7; 95% CI, 2.3–50.0) were associated with increased risk of respiratory failure. Lower MRC sum scores (for scores <30, OR: 14.0; 95% CI, 1.54–127.2) and neck MRC scores (for scores ≤3, OR: 21.0; 95% CI, 3.5–125.2) were associated with higher likelihood of respiratory failure. Adjusted analyses showed that presence of bulbar weakness (OR: 7.6; 95% CI, 1.3–43.0) and low neck MRC scores (scores ≤3, OR: 9.2; 95% CI, 3.5–125.2, vs scores >3) were independently associated with respiratory failure. ConclusionsBulbar and neck muscle weakness at admission are clinical predictors of increased risk of respiratory failure in patients with GBS. These findings could guide the adequate management of high-risk patients.

Neuropathic arthropathy of the shoulder associated with chronic inflammatory demyelinating polyneuropathy: A case report

Neuropathic arthropathy is a chronic degenerative arthropathy that results from a neurosensory deficit of the affected joint. According to neurovascular theory, the loss of sensation of the joint is responsible for its formation. Chronic inflammatory demyelination polyneuropathy (CIDP) is a rare disease with sensorimotor involvement in which demyelination and axonal damage occur in the peripheral nerves as a result of an abnormal immune response. A case is presented of a 64-year-old male patient with a diagnosis of CIDP who had Charcot arthropathy of the right shoulder.

Electronic health record-wide association study for atrial fibrillation in a British cohort.

Atrial fibrillation (AF) confers a major healthcare burden from hospitalisations and AF-related complications, such as stroke and heart failure. We performed an electronic health records-wide association study to identify the most frequent reasons for healthcare utilization, pre and post new-onset AF. Prospective cohort study with the linked electronic health records of 5.6 million patients in the United Kingdom Clinical Practice Research Datalink (1998-2016). A cohort study with AF patients and their age-and sex matched controls was implemented to compare the top 100 reasons of frequent hospitalisation and primary consultation. Of the 199,433 patients who developed AF, we found the most frequent healthcare interactions to be cardiac, cerebrovascular and peripheral-vascular conditions, both prior to AF diagnosis (41/100 conditions in secondary care, such as cerebral infarction and valve diseases; and 33/100 conditions in primary care), and subsequently (47/100 conditions hospital care and 48 conditions in primary care). There was a high representation of repeated visits for cancer and infection affecting multiple organ systems. We identified 10 novel conditions which have not yet been associated with AF: folic acid deficiency, pancytopenia, idiopathic thrombocytopenic purpura, seborrheic dermatitis, lymphoedema, angioedema, laryngopharyngeal reflux, rib fracture, haemorrhagic gastritis, inflammatory polyneuropathies. Our nationwide data provide knowledge and better understanding of the clinical needs of AF patients suggesting: (i) groups at higher risk of AF, where screening may be more cost-effective, and (ii) potential complications developing following new-onset AF that can be prevented through implementation of comprehensive integrated care management and more personalised, tailored treatment. NCT04786366.

Peripheral Nerve Ultrasound for the Differentiation between ALS, Inflammatory, and Hereditary Polyneuropathies.

Background and Objectives: Ultrasound (US) is a non-invasive tool for the in vivo detection of peripheral nerve alterations. Materials and Methods: In this study, we applied nerve US to assist the discrimination between the spectrum of amyotrophic lateral sclerosis (ALS, n = 11), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP, n = 5), and genetically confirmed Charcot-Marie-Tooth disease (CMT, n = 5). All participants and n = 15 controls without neurological diseases underwent high-resolution US of the bilateral tibial nerve. The nerve cross-sectional area (CSA) and nerve microvascular blood flow were compared between the groups and related to cerebrospinal fluid (CSF) measures, clinical symptoms, and nerve conduction studies. The analyses are part of a larger multimodal study on the comparison between US and 7 Tesla (7T) magnetic resonance neurography (MRN). Results: The patients and controls were matched with respect to their demographical data. CMT had the longest disease duration, followed by CIDP and ALS. CSA was related to age, weight, and disease duration. CSA was larger in CMT and CIDP compared to ALS and controls. The blood flow was greatest in CIDP, and higher than in CMT, ALS, and controls. In ALS, greater CSA was correlated with greater CSF total protein and higher albumin quotient. The US measures did not correlate with clinical scores or nerve conduction studies in any of the subgroups. Conclusion: Our results point towards the feasibility of CSA and blood flow to discriminate between ALS, CIDP, and CMT, even in groups of small sample size. In ALS, larger CSA could indicate an inflammatory disease subtype characterized by reduced blood-nerve barrier integrity. Our upcoming analysis will focus on the additive value of 7T MRN in combination with US to disentangle the spectrum between more inflammatory or more degenerative disease variants among the disease groups.

Local Inflammatory Mediators Involved in Neuropathic Pain.

Polyneuropathy (PNP) is a term to describe diseases of the peripheral nervous system, 50% of which present with neuropathic pain. In some types of PNP, pain is restricted to the skin distally in the leg, suggesting a local regulatory process leading to pain. In this study, we proposed a pro-inflammatory pathway mediated by NF-κB that might be involved in the development of pain in patients with painful PNP. To test this hypothesis, we have collected nerve and skin samples from patients with different etiologies and levels of pain. We performed RT-qPCR to analyze the gene expression of the proposed inflammatory pathway components in sural nerve and in distal and proximal skin samples. In sural nerve, we showed a correlation of TLR4 and TNFα to neuropathic pain, and an upregulation of TNFα in patients with severe pain. Patients with an inflammatory PNP also presented a lower expression of TRPV1 and SIRT1. In distal skin, we found a reduced expression of TLR4 and miR-146-5p, in comparison to proximal skin. Our findings thus support our hypothesis of local inflammatory processes involved in pain in PNP, and further show disturbed anti-inflammatory pathways involving TRPV1 and SIRT1 in inflammatory PNP.

A Precipitant Less Appreciated: A Glance at Cases of Tuberculosis Manifesting with Guillain Barre Syndrome

Guillain-Barre syndrome (GBS) is an immune triggered inflammatory polyneuropathy precipitated by various triggers by means of cross reactivity and molecular mimicry. Tuberculosis (TB) of any organ, although may produce features of peripheral neuropathy, has rarely been associated with GBS. We describe a middle-aged female patient in whom pulmonary TB manifested with GBS primarily without any prominent constitutional symptoms and review the literature to strengthen our viewpoint in this regard. The treatment with immunomodulators is beneficial with good outcome and thus early diagnosis and intervention is suggested.

Exposure to specific tumour necrosis factor inhibitors and risk of demyelinating and inflammatory neuropathy in cohorts of patients with inflammatory arthritis: a collaborative observational study across five Nordic rheumatology registers

ObjectiveTo compare incidences of neuroinflammatory events, including demyelinating disease (DML), inflammatory polyneuropathies (IPN) and multiple sclerosis (MS), in patients with rheumatoid arthritis (RA) or spondyloarthritis (SpA; including psoriatic arthritis) starting...

Miller Fisher syndrome: a success story

Acute inflammatory demyelination polyneuropathy (AIDP) or acute idiopathic polyneuritis are the other key synonyms for Guillain-Barre syndrome (GBS) with ascending characteristics of weakness, mild sensorium loss, areflexia or hyporeflexia. GBS has been seen most commonly among the younger age group, and a male predominance has been reported. The case reports demonstrate a case of a 66-year-old female admitted to the causality department with abrupt onset of giddiness, diplopia, and headache the patient was diagnosed with myasthenia gravis and atypical GBS and shifted to the ward for further treatment. The patient was in the intensive-care unit due to mild ischemic changes in the MRI brain and bilateral facial neuropathy. The patient was treated with intravenous immunoglobulins and I.V. glucocorticoids. The patient was discharged on the 25th day of admission without support walk and full extraocular movements. The case report demonstrates the essential use of high clinical knowledge and investigation for a prompt treatment for a such rare disorder.

Neurological complications of SARS-CoV-2 infection

SARS-CoV-2 virus was first identified in 2019 in Wuhan (China) and is responsible for the ongoing COVID-19 pandemic. Although the virus causes mild, transient symptoms of an upper respiratory tract infection in most cases, it can also lead to severe pneumonia, respiratory failure and/or death. Approximately 85% of patients experience central and peripheral neurological symptoms. In the acute phase of the disease, ischaemic strokes, intracranial haemorrhages, meningitis and encephalitis, acute demyelinating diseases and acute inflammatory polyneuropathies may occur. However, mild neurological symptoms that can persist for months and significantly affect daily functioning are much more common. These include headache and dizziness, olfactory and gustatory dysfunction, mild cognitive disturbances, as well as depressive, anxiety, and sleep disorders. Some of them are encompassed by popular terms “post-covid syndrome” and “brain fog.” The pathogenesis of neurological complications of SARS-CoV-2 infection is still not fully understood; overproduction of cytokines induced by viral infection may be of great importance. There is no causal treatment, while symptomatic treatment is of limited effectiveness. Primary prevention in the form of SARS-CoV-2 vaccinations is of great importance. In the following review, we would like to present the current knowledge on epidemiology, pathology, pathogenesis and treatment of neurological complications after SARS-CoV-2 infection. Further multi-centre, large-scale clinical studies are necessary to identify the exact pathogenetic mechanisms.

Two possible etiologies of Guillain-Barré syndrome: mRNA-1273 (Moderna) vaccination and scrub typhus: A case report

Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy related to infection with bacteria or virus and vaccination. Cases of GBS after coronavirus infection-19 (COVID-19) vaccination have been reported. However, cases of GBS after inoculation with mRNA-based COVID-19 vaccines, especially mRNA-1273, have rarely been reported compared to after inoculation with adenovirus vector-based COVID-19 vaccines. On 1 hand, GBS occurring after scrub typhus is often reported, but the exact pathological mechanism has not been elucidated. We report the case of a patient with GBS after inoculation with mRNA-1273 COVID-19 vaccine and scrub typhus. A 47-year-old man received COVID-19 vaccination 4 weeks before admission. He had a fever, rash and general weakness 1 day after vaccination. After 3 weeks, the muscle strength of the extremities deteriorated to the extent that walking was impossible. The patient developed quadriplegia with areflexia, axonal-type sensorimotor polyneuropathy was confirmed by nerve conduction study. The patient was diagnosed as GBS. Scrub typhus was also diagnosed as eschar was observed in the chest area and the serologic test of anti-R-tsutsugamushi antibody showed a strongly positive result. The patient received treatment with intravenous immunoglobulin at 0.4 g/kg daily for 5 days. Mechanical ventilation was applied during the intensive care unit. He was treated for scrub typhus simultaneously. Six months after the onset of the disease, the patient showed improvement to the point where he could work and exercise alone. When GBS is suspected, early evaluation and treatment can lead to favorable outcomes. Considering that cases of GBS after COVID-19 vaccination have been reported, it is important to conduct early evaluation and management of patients with muscle weakness after COVID-19 vaccination to ensure early detection of GBS. And even if fever and rash are side effects that can occur frequently after vaccination, it is necessary to consider other diseases in addition to the side effects of the vaccine. This is to prevent delay in diagnosis and treatment of other diseases.

Guillain-Barré Syndrome and It’s Effect on Child Population

Background: Guillian Barre Syndrome (GBS) is the most common cause of minor flaccid paralysis in the world and post-polio eradication is the most common cause on the Indian subcontinent as well. It affects 0.6-4 people per 1 lakh people per year. Guillian-Barre syndrome should be distinguished by a variation associated with inflammation of the cortical area of brain of chronic inflammatory polyneuropathy predicting prognosis and clinical course. Children have a better prognosis than adults and usually recover after a different period. However, in the Pressing event of the disease, the damage can be severe and can lead to mechanical failure and even death. There are a few studies in the indian subcontinent that show the effects of GBS in children and the effect of regional variability of the outcome. This study is therefore designed to study prospective clinicians, as well as the overall effect on children with GBS in India.&#x0D; Objective: Studying the short-term and long-term effect of Guillian Barre Syndrome in children.&#x0D; Methods: This is a health care infrastructurel-based study to be conducted at Acharya Vinoba Bhave Rural hospital (ABVRH) for a period of one year. All children under the age of 18 between August 2019 to July 2020 are admitted to the PICU and completing the comprehending criteria will be comprised in the study. Patient details regarding the progression of the disease, the results of the investigation, the PICU stay, clinical studies in the hospital, the treatment received and the state of discharge will be recorded in the pre-prescribed proforma. The data obtained will be analyzed simultaneously.&#x0D; Conclusion: Information on factors associated with positive and negative outcomes in children with GBS will serve as a guide for your treating pediatrician to plan a treatment plan and will also help them explain their predictions to parents.

Decreased Incidence of Guillain-Barré Syndrome during the COVID-19 Pandemic: A Retrospective Population-Based Study

Background: Guillain-Barré syndrome is an immune-mediated acute inflammatory polyneuropathy that is associated with various triggers, including certain infections and vaccines. It has been suggested that both SARS-CoV-2 infection and vaccination may be triggering factors for Guillain-Barré syndrome, but evidence remains equivocal. Here, we conducted a population-based incidence study of Guillain-Barré syndrome spanning the 3 years immediately prior to and the 2 years during the pandemic. Methods: Cases were identified by searching a regional diagnostic database for the ICD-10 code for Guillain-Barré syndrome. Individuals who fulfilled the Brighton criteria for Guillain-Barré syndrome were included. Information on clinical presentation, laboratory values, and vaccination status were retrieved from medical records. We calculated the incidence immediately prior to and during the pandemic. Results: The Guillain-Barré syndrome incidence rate was 1.35/100,000 person-years for the pre-pandemic period and 0.66/100,000 person-years for the pandemic period (incidence rate ratio: 0.49; p = 0.003). Three cases were temporally associated with SARS-CoV-2 infection and 1 case each to the AstraZeneca and Pfizer-BioNTech COVID-19 vaccines. Conclusions: Our results show that the incidence of Guillain-Barré syndrome decreased during the pandemic. This is most likely due to decreased prevalence of triggering infections due to social restrictions. Our findings do not support a causal relationship between Guillain-Barré syndrome and COVID-19.