Guillain-Barré Syndrome Research Articles

A Multidisciplinary Extended Approach to Physiotherapy Rehabilitation in Guillain-Barre Syndrome as Sequelae of COVID-19: A Single Case Study

Introduction: Coronaviruses can cause widespread systemic infections, the most common of which are respiratory complications, which are close to the symptoms of serious acute respiratory syndrome coronavirus (SARS-CoV). Case Description: We report a case of a 16-year-old boy who developed weakness in bilateral lower limbs, difficulty in coughing, and generalized weakness for 2 days. He was diagnosed with post-COVID Guillain-Barre syndrome (GBS). Cerebrospinal fluid (CSF) analysis manifested a CSF protein of 117 mg/dL, a white blood cell count of 6-7/mm3 , and a glucose of too low to comment. Magnetic resonance investigation of the brain revealed mucosal thickening in the bilateral maxillary, ethmoid, and left frontal sinuses. Nerve conduction studies concluded evidence of sensory-motor polyneuropathy. Physiotherapy intervention included patient education, breathing retraining, airway clearance techniques, positioning, a combination of chest proprioceptive neuromuscular facilitation (PNF) techniques, a walking program with supplemented oxygen, and psychological support. Results: Outcome measures have shown enhancement in functional independence and performance of activities of daily living. Conclusion: The evidence from this study suggests that pulmonary rehabilitation plays a pivotal role in managing a patient who is diagnosed with post-COVID GBS, which includes patient education, breathing retraining, airway clearing techniques, a combination of chest PNF techniques, positioning, a walking program with augmented oxygen, and psychological support.

Autoimmune Nodopathy: When to Suspect and How to Treat?

Autoimmune nodopathy (AN) is a rare condition marked by autoantibodies that target specific proteins located within the node of Ranvier or paranodes. This disorder is distinctly different from chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), with AN patients displaying unique clinical symptoms that include acute or subacute onset, primarily distal muscle weakness, sensory ataxia, tremors, and a significant increase in cerebrospinal fluid protein levels. Certain antibodies are linked to specific clinical manifestations; for instance, anti-contactin-1 neuropathy is often accompanied by nephrotic syndrome, whereas anti-pan-neurofascin neuropathy resembles fulminant Guillain-Barre syndrome. In contrast to CIDP patients, who usually experience substantial improvement with intravenous immunoglobulin (IVIG), those with AN may see poor or merely temporary benefits from IVIG therapy. Nonetheless, treatment with the anti-B cell therapy, rituximab, has shown promising results. These findings underscore the critical need for accurate identification of AN's clinical indicators, swift diagnosis of affected individuals, and the application of more effective, targeted treatments for this specific condition.

Autoimmune Nodopathy: When to Suspect and How to Treat?

Autoimmune nodopathy (AN) is a rare condition marked by autoantibodies that target specific proteins located within the node of Ranvier or paranodes. This disorder is distinctly different from chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), with AN patients displaying unique clinical symptoms that include acute or subacute onset, primarily distal muscle weakness, sensory ataxia, tremors, and a significant increase in cerebrospinal fluid protein levels. Certain antibodies are linked to specific clinical manifestations; for instance, anti-contactin-1 neuropathy is often accompanied by nephrotic syndrome, whereas anti-pan-neurofascin neuropathy resembles fulminant Guillain-Barre syndrome. In contrast to CIDP patients, who usually experience substantial improvement with intravenous immunoglobulin (IVIG), those with AN may see poor or merely temporary benefits from IVIG therapy. Nonetheless, treatment with the anti-B cell therapy, rituximab, has shown promising results. These findings underscore the critical need for accurate identification of AN's clinical indicators, swift diagnosis of affected individuals, and the application of more effective, targeted treatments for this specific condition.

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

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. 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). 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. 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.

Buccal Administration of a Zika Virus Vaccine Utilizing 3D-Printed Oral Dissolving Films in a Mouse Model.

Over the years, research regarding the Zika virus has been steadily increasing. Early immunization for ZIKV is a priority for preventing complications such as microencephaly and Guillain-Barré syndrome (GBS). Unlike traditional vaccination approaches, oral dissolving films (ODFs) or mucoadhesive film technology is an emerging, exciting concept that can be used in the field of pharmaceuticals for vaccine design and formulation development. This attractive and novel method can help patients who suffer from dysphagia as a complication of a disease or syndrome. In this study, we investigated a microparticulate Zika vaccine administered via the buccal route with the help of thin films or oral dissolving films (ODFs) with a prime dose and two booster doses two weeks apart. In vitro, the ODFs displayed excellent physiochemical properties, indicating that the films were good carriers for vaccine microparticles and biocompatible with the buccal mucosa. In vivo results revealed robust humoral (IgG, subtypes IgG1 and IgG2a) and T-cell responses (CD4+/CD8+) for ZIKV-specific immunity. Both the Zika MP vaccine and the adjuvanted Zika MP vaccine affected memory (CD45R/CD27) and intracellular cytokine (TNF-α and IL-6) expression. In this study, ZIKV vaccination via the buccal route with the aid of ODFs demonstrated great promise for the development of pain-free vaccines for infectious diseases.

Incidence and Clinical Presentation of Severe Neurotoxicity from Nelarabine in Patients with T-Cell Acute Lymphoblastic Leukemia

BackgroundNelarabine is a purine analog with demonstrated efficacy in the treatment of T-cell Lymphoblastic Leukemia and Lymphoma (T-ALL/LBL). Despite its efficacy and excellent blood-brain barrier penetration, it has a significant side effect profile which is namely concerning for neurotoxicity. Reported neurotoxicity has varied from mild peripheral neuropathy to debilitating grade 4 neurologic complications including Guillain-Barre like syndrome and myelopathy. Patients and MethodsWe conducted a single centered, retrospective case series to study patients who developed severe neurotoxicity after receiving nelarabine as part of T-ALL treatment. One hundred thirty-five patients were identified. Thirteen patients were reviewed for severe neurotoxicity (defined as ≥grade 3), and of those five patients were deemed to have neurotoxicity secondary to nelarabine exposure. ResultsFive patients (4%) developed severe neurotoxicity as manifested by Guillain-Barre like syndrome or myelopathy within a timeframe of eight to fifty-eight days from last nelarabine dose. Upon diagnosis, patients received formal neurologic evaluation by our neuro-oncology specialists including imaging, cerebrospinal fluid testing, and electromyography. Patients were treated with IVIG, and steroids upon diagnosis, but the majority of neuro-deficits were irreversible. ConclusionOur study shows that nelarabine is generally well-tolerated, and the incidence of severe neurotoxicity is rare. Given the potential risk of severe neurotoxicity, we propose capped dose of nelarabine 1000 mg/day, neurological assessment before subsequent dosing, and avoidance of simultaneous IT therapy during nelarabine administration.

Development of a major histocompatibility complex class II conditional knockout mouse to study cell-specific and time-dependent adaptive immune responses in peripheral nerves.

The precise relationship between molecular mimicry and tissue-specific autoimmunity is unknown. Major histocompatibility complex (MHC) class II antigen presenting cell-CD4+ T-cell receptor complex interactions are necessary for adaptive immunity. This study aimed to determine the role of endoneurial endothelial cell MHC class II in autoimmune polyneuropathy. Cryopreserved Guillain-Barré syndrome (GBS) patient sural nerve biopsies and sciatic nerves from the severe murine experimental autoimmune neuritis (sm-EAN) GBS model were studied. Cultured conditional ready MHC Class II antigen A-alpha chain (H2-Aa) embryonic stem cells were used to generate H2-Aaflox/+ C57BL/6 mice. Mice were backcrossed and intercrossed to the SJL background to generate H2-Aaflox/flox SJL mice, bred with hemizygous Tamoxifen-inducible von Willebrand factor Cre recombinase (vWF-iCre/+) SJL mice to generate H2-Aaflox/flox; vWF-iCre/+ mice to study microvascular endothelial cell adaptive immune responses. Sm-EAN was induced in Tamoxifen-treated H2-Aaflox/flox; vWF-iCre/+, H2-Aaflox/flox; +/+, H2-Aa+/+; vWF-iCre/+ and untreated H2-Aaflox/flox; vWF-iCre/+ adult female SJL mice. Neurobehavioral, electrophysiological and histopathological assessments were performed at predefined time points. Endoneurial endothelial cell MHC class II expression was observed in normal and inflamed human and mouse peripheral nerves. Tamoxifen-treated H2-Aaflox/flox; vWF-iCre/+ mice were resistant to sm-EAN despite extensive MHC class II expression in lymphoid and non-lymphoid tissues. A conditional MHC class II knockout mouse to study cell- and time-dependent adaptive immune responses in vivo was developed. Initial studies show microvascular endothelial cell MHC class II expression is necessary for peripheral nerve specific autoimmunity, as advocated by human in vitro adaptive immunity and ex vivo transplant rejection studies.

Tumor necrosis factor α receptor 1A transduces the inhibitory effect on axon regeneration triggered by IgG anti-ganglioside GD1a antibodies

Anti-ganglioside antibodies (anti-Gg Abs) have been linked to delayed/poor clinical recovery in both axonal and demyelinating forms of Guillain-Barrè Syndrome (GBS). In many instances, the incomplete recovery is attributed to the peripheral nervous system's failure to regenerate. The cross-linking of cell surface gangliosides by anti-Gg Abs triggers inhibition of nerve repair in both in vitro and in vivo axon regeneration paradigms. This mechanism involves the activation of the small GTPase RhoA, which negatively modulates the growth cone cytoskeleton. At present, the identity/es of the receptor/s responsible for transducing the signal that ultimately leads to RhoA activation remains poorly understood. The aim of this work was to identify the transducer molecule responsible for the inhibitory effect of anti-Gg Abs on nerve repair. Putative candidate molecules were identified through proteomic mass spectrometry of ganglioside affinity-captured proteins from rat cerebellar granule neurons (Prendergast et al., 2014). These candidates were evaluated using an in vitro model of neurite outgrowth with primary cultured dorsal root ganglion neurons (DRGn) and an in vivo model of axon regeneration. Using an shRNA-strategy to silence putative candidates on DRGn, we identified tumor necrosis factor receptor 1A protein (TNFR1A) as a transducer molecule for the inhibitory effect on neurite outgrowth from rat/mouse DRGn cultures of a well characterized mAb targeting the related gangliosides GD1a and GT1b. Interestingly, lack of TNFr1A expression on DRGn abolished the inhibitory effect on neurite outgrowth caused by anti-GD1a but not anti-GT1b specific mAbs, suggesting specificity of GD1a/transducer signaling. Similar results were obtained using primary DRGn cultures from TNFR1a-null mice, which did not activate RhoA after exposure to anti-GD1a mAbs. Generation of single point mutants at the stalk region of TNFR1A identified a critical amino acid for transducing GD1a signaling, suggesting a direct interaction. Finally, passive immunization with an anti-GD1a/GT1b mAb in an in vivo model of axon regeneration exhibited reduced inhibitory activity in TNFR1a-null mice compared to wild type mice. In conclusion, these findings identify TNFR1A as a novel transducer receptor for the inhibitory effect exerted by anti-GD1a Abs on nerve repair, representing a significant step forward toward understanding the factors contributing to poor clinical recovery in GBS associated with anti-Gg Abs.

When Guillain–Barré Syndrome Defies Expectations: A Case of Atypical Features

Abstract Guillain–Barré syndrome (GBS) is one of the most common causes of acute flaccid paralysis. In typical GBS, there are no central nervous system (CNS) features. GBS with prominent CNS involvement can be seen in uncommon variants of GBS (such as Miller Fisher Syndrome and Bickerstaff brainstem encephalitis [BBE]) or rarely, when it coexists with other conditions such as acute disseminated encephalomyelitis (ADEM). We report a case of a 35-year-old male who presented with fever followed by ascending lower motor neuron type paraparesis suggestive of GBS which progressed rapidly to involve the respiratory muscles necessitating invasive mechanical ventilation. The patient had many atypical features, namely, persistent fever, early bladder and bowel involvement, facial twitching, ophthalmoplegia with ptosis, and a comatose state. Based on these clinical features and the investigations done, a diagnosis of GBS with BBE with a possibility of ADEM was made. The patient was managed intensively, but there was no improvement in the neurological manifestations and the patient succumbed to the illness due to ventilator-associated complications.

New chronic inflammatory demyelinating polyneuropathy/Guillain-Barré syndrome guidelines - impact on clinical practise.

There is no diagnostic biomarker that can reliably detect Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP). Diagnosis relies upon integrating key clinical characteristics and relevant supportive data. Consequently, misdiagnosis and delayed diagnosis are common. Diagnostic criteria have proven valuable resources to improve diagnosis, but are underutilized during routine clinical care. In 2021, the EAN/PNS CIDP criteria was published, and were followed by the EAN/PNS GBS criteria in 2023. Both guidelines utilized GRADE methodology to formulate evidence-based recommendations that are intended to be used by adult and paediatric clinicians across diverse care settings to optimize diagnostic accuracy and improve patient outcomes during routine clinical care. The EAN/PNS GBS and CIDP criteria detail specific clinical, electrophysiological, and laboratory features that raise diagnostic confidence, and call attention to diagnostic mimics. The sensitivity of EAN/PNS and other modern criteria to detect GBS and CIDP is high, but utilization during clinical practice is low. Complexity is one factor limiting widespread application. Strategies are needed to optimize criteria adoption during routine clinical care such that GBS and CIDP diagnosis can be achieved with greater speed and accuracy.

Patterns of Clinical Presentation and In-Hospital Outcome of Adult Patient with Guillain-Barre Syndrome

Patterns of Clinical Presentation and In-Hospital Outcome of Adult Patient with Guillain-Barre Syndrome

A pathologically expanded, clonal lineage of IL-21-producing CD4+ T cells drives inflammatory neuropathy.

Inflammatory neuropathies, which include chronic inflammatory demyelinating polyneuropathy (CIDP) and Guillain Barré syndrome (GBS), result from autoimmune destruction of the PNS and are characterized by progressive weakness and sensory loss. CD4+ T cells play a key role in the autoimmune destruction of the PNS. Yet, key properties of pathogenic CD4+ T cells remain incompletely understood. Here, we used paired single-cell RNA-Seq (scRNA-Seq) and single-cell T cell receptor-sequencing (scTCR-Seq) of peripheral nerves from an inflammatory neuropathy mouse model to identify IL-21-expressing CD4+ T cells that were clonally expanded and multifunctional. These IL-21-expressing CD4+ T cells consisted of 2 transcriptionally distinct expanded cell populations, which expressed genes associated with T follicular helper (Tfh) and T peripheral helper (Tph) cell subsets. Remarkably, TCR clonotypes were shared between these 2 IL-21-expressing cell populations, suggesting a common lineage differentiation pathway. Finally, we demonstrated that IL-21 receptor-KO (IL-21R-KO) mice were protected from neuropathy development and had decreased immune infiltration into peripheral nerves. IL-21 signaling upregulated CXCR6, a chemokine receptor that promotes CD4+ T cell localization in peripheral nerves. Together, these findings point to IL-21 signaling, Tfh/Tph differentiation, and CXCR6-mediated cellular localization as potential therapeutic targets in inflammatory neuropathies.

Guillain-Barre syndrome and link with COVID-19 infection and vaccination: a review of literature.

Guillain-Barré syndrome (GBS) is an autoimmune disease associated with significant morbidity. A wide variety of infectious and non-infectious triggers have been identified to be associated with GBS. COVID-19 has gained attention in recent years for its role in GBS pathogenesis. Our study aims to review the literature on GBS and its epidemiological and pathophysiological association with COVID-19. Recent literature on GBS associated with COVID-19 infections, such as case reports, case series, systematic reviews, and large-scale epidemiological studies, were reviewed. We also reviewed studies that included vaccines against COVID-19 in association with GBS. Studies that focused on understanding the pathobiology of GBS and its association with infectious agents including COVID-19 were reviewed. Despite a lack of consensus, GBS is strongly associated with COVID-19 infection. The exact pathophysiological mechanism regarding COVID-19 as a causative agent of GBS is unknown. Mechanisms, such as the proinflammatory state, triggering of autoimmunity, and direct viral invasion, are postulated and remain to be investigated. Adenovirus vector vaccines are most likely associated with GBS, and the consensual reports clearly suggest mRNA vaccines are associated with low risk and may be protective against GBS by reducing the risk of COVID-19 infection.

A case of variant of GBS with positive serum ganglioside GD3 IgG antibody

BackgroundAcute bulbar palsy-plus (ABPp) syndrome is an unusual variant of Guillain-Barré syndrome (GBS). Anti-GT1a and anti-GQ1b antibodies have been reported in patients with ABPp, but without reports related to GD3 antibodies.MethodsClinical data of a patient diagnosed as ABPp syndrome were reviewed clinically. And we summarized the GBS patients with ABP and facial paralysis reported in the literature.ResultsWe reported a 13-year-old girl presented with asymmetric bifacial weakness, bulbar palsy and transient limb numbness, and had positive serum IgG anti-GD3 antibody. Through reviewing the GBS patients with ABP and facial paralysis reported previously, we found that facial palsy could be unilateral or bilateral. The bilateral facial palsy could present successively or simultaneously, and could be symmetrical or asymmetrical. Other common symptoms included ophthalmoplegia, sensory abnormality and ataxia. IgG anti-GT1a and IgG anti-GQ1b antibodies were the most frequent. Most of the patients had full recovery within two weeks to one year of follow-up.ConclusionsWe reported a patient with asymmetric bifacial palsy and bulbar palsy, which seemed to fit the diagnosis of ABPp syndrome. This was the first report of ABPp variant of GBS with positive serum ganglioside GD3 IgG antibody.

Bioinformatics analysis of the potential biomarkers of Multiple Sclerosis and Guillain-Barré syndrome.

Recent research emphasizes the intricate interplay of genetics and epigenetics in neurological disorders, notably Multiple Sclerosis (MS) and Guillain-Barre Syndrome (GBS), both of which exhibit cardiovascular dysregulation, with GBS often featuring serious bradyarrhythmias requiring prompt recognition and treatment. While cardiovascular autonomic dysfunction in MS is typically less severe, orthostatic intolerance affects around half of MS patients. Their distinction lies in their autoimmune responses, MS is an autoimmune disease affecting the central nervous system, causes demyelination and axon damage, leading to cognitive, ocular, and musculoskeletal dysfunction. In contrast, GBS primarily affects the peripheral nervous system, resulting in paralysis and respiratory complications. Despite their differences, both diseases share environmental risk factors such as viral infections and Vitamin D deficiency. This study aims to explore shared gene expression pathways, functional annotations, and molecular pathways between MS and GBS to enhance diagnostics, pathogenesis understanding, and treatment strategies through molecular analysis techniques. Through the gene expression analysis, five significant genes were found UTS2, TNFSF10, GBP1, VCAN, FOS. Results shows that Common DEGs are linked to apoptosis, bacterial infections, and atherosclerosis. Molecular docking analysis suggests Aflatoxin B1 as a potential therapeutic compound due to its high binding affinity with common differentially expressed proteins.

A Study on the Epidemiology of COVID-19-Related Guillain-Barré Syndrome in the United States.

Several neurological complications have been reported with COVID-19, including Guillain-Barré syndrome (GBS). We looked at incidence, baseline characteristics, and in-hospital outcomes of COVID-19-associated GBS in the United States. We conducted a retrospective analysis using the US National Inpatient Sample database to identify hospitalizations for COVID-19 and GBS, using International Classification of Disease, 10th Revision, codes G610 and G650 for GBS and U071 for COVID-19. The codes used in this study are listed in Supplemental Digital Content 1 (see e Appendix, http://links.lww.com/JCND/A69). In total, 13,705 GBS admissions were recorded nationwide in 2020; of these, 1155 (8.43%) were associated with COVID-19. The frequency of GBS in COVID-19 admissions was 0.07%, compared with 0.08% in non-COVID-19 admissions (P = 0.8166). COVID-19 cohort with GBS had higher utilization of invasive mechanical ventilation (20.8% vs. 11.8%, P < 0.001) in comparison with COVID-19 cohort without GBS. GBS admissions with COVID-19 exhibited significantly higher inpatient mortality (12.2% vs. 3%, P < 0.001) compared with GBS admissions without COVID-19. Our findings underscore GBS as a rare yet severe complication of COVID-19, highlighting a significant difference in mortality when compared with GBS not associated with COVID-19.

Incidence of Guillain-Barré Syndrome (GBS) after COVID-19 Vaccination: a Systematic Review and Meta-Analysis.

Global vaccination against COVID-19 will help nations to overcome the pandemic stage as soon as possible. Guillain-Barré syndrome (GBS) is an acute immune-mediated inflammatory disease of the peripheral nerves (PNS) that is reported as a complication of both COVID-19 and vaccines. Up to now, case reports regarding the incidence of GBS have been reported after different COVID-19 vaccines worldwide. So, the aim of this systematic review and meta-analysis is to estimate the pooled incidence of GBS after COVID-19 vaccination. Two expert researchers conducted a systematic search in PubMed, Scopus, EMBASE, Web of Science, Google Scholar as well as gray literature in order to find relevant articles published before September 2022. After deleting duplicates, we found 1021 articles, of which 458 studies were further evaluated. A final number of 21 studies remained for meta-analysis, with most of those being from the USA, UK and Mexico. Follow-up duration was between 21-42 days. Out of the total number of 2.35x109 patients included in the final meta-analysis, 3654 subjects developed GBS after vaccination, most of whom were males. Incidence of GBS per million ranged between 0.23 and 9.8. The pooled incidence of GBS following vaccination was 0%.

Effectiveness of limited plasma exchange in Guillain-Barré syndrome

Objective: The aim of this study is to compare the efficacy of limited plasma exchange against supportive and standard treatments in treatment of Guillain-Barré syndrome (GBS). Method: A total of 90 GBS patients admitted to Yangon General Hospital, Yangon, Myanmar were recruited over 1.5-year-period from January 2017 to June 2018 and they were divided into 3 groups according to the treatment they received (convenience sampling method): supportive (n=36), limited plasma exchange (LPE) (n=35) and standard (therapeutic plasma exchange - TPE or IVIg) (n=19)). Their clinical features, electrophysiological subtypes and severity were compared at baseline, and outcome (change in GBS disability score (GDS) at 30 days after entry) was assessed and compared. Results: Baseline characteristics such as gender, GBS subtypes and respiratory involvement were comparable, but standard treatment group had older patients, and LPE group had shorter latency to nadir and more cases with antecedent diarrhea, which are poor outcome predictors. At 30 days from entry, mean GDS improvement was 0.9 + 0.6 in supportive, 1.4 + 0.6 in LPE and 1.2 + 0.8 in standard treatment groups respectively. The difference between LPE and supportive treatment was statistically significant (p 0.002) but there was no difference between LPE and standard treatment (p = 0.512). Regarding untoward effects, apart from one transient hypotension and 2 anemic cases, no other serious adverse effects were noted from LPE therapy. Conclusion: LPE may be superior to supportive treatment and may not be inferior to standard treatment. Therefore, LPE may be an alternative effective treatment for GBS patients who are not accessible to standard treatments especially in low income countries with limited resources.

Post-Infectious Guillain Barré Syndrome Related to COVID-19: Unusual Case Report

Guillain-Barré Syndrome (GBS) is a rare immune mediated inflammatory disease of the peripheral nervous system that is presumed to be triggered by preceding infections. In the era of pandemic COVID-19 (coronavirus disease), there is an emerging case of para/post infectious GBS associated to COVID-19 that are described worldwide. Here, we report a 55-years-old man who was admitted for fatigue, fever and cough related to covid-19. Later, after disappearing of covid-19 symptoms he began presenting an ascending areflexic tetraparesis. CSF and NCS were in favour of GBS diagnosis, in particular pure motor AIDP subtype. Antigangliosides antibodies were negative. Lumbosacral MRI showed contrast enhancement of cauda equina roots. The outcome was good after receiving intravenous immunoglobulins treatment.

An open-label, single-center phase II trial of cadonilimab (an anti-PD-1/CTLA-4 bispecific antibody) in combination with platinum-based dual-drug neoadjuvant chemotherapy for locally advanced, resectable head and neck squamous cell carcinoma.

6044 Background: Consensus on neoadjuvant treatment strategies for resectable head and neck squamous cell carcinoma (HNSCC) is not proposed currently. Preclinical and clinical findings suggested that PD-1/CTLA-4 bispecific antibodies may have synergistic anti-tumor activity. This study aimed to explore the safety and activity of cadonilimab in combination with platinum-based dual-drug neoadjuvant chemotherapy in locally advanced, resectable HNSCC. Methods: In this open-label phase II trial, eligible patients with untreated locally advanced, resectable HNSCC (T2N2-3M0、T3-4N0-3M0; stage III-IV, AJCC 8th Edition) were enrolled to receive cadonilimab (10 mg/kg) and platinum-based dual-drug [docetaxel (75 mg/m2) plus cisplatin (60 mg/m2)] on day 1 of each 21-day cycle for three cycles, followed by surgery and postoperative adjuvant therapy. The primary endpoint was objective response rate (ORR) per RECIST1.1. Secondary endpoints included pathologic complete response (pCR), safety, disease-free survival (DFS), and overall survival (OS). Results: Between July 2023 and December 2023, 24 patients were enrolled (median age, 55 years [range 34–69]; 21 men [87.5%]), tumors were located in the oral cavity (10/24, 41.7%), hypopharynx (8/24, 33.3%) and larynx (6/24, 25.0%), 20 (83.3%) patients were clinical T3/4 while 10 patients (41.7%) ≥N2 . After completion of neoadjuvant therapy, the ORR was 87.5% (21/24). Of the 24 patients, 12 (50.0%) patients reached pCR. Treatment-related adverse events (TRAEs) occurred in 14 (58.3%) patients. Grade 3-4 TRAEs were reported in 4 (16.7%) patients, including rash (12.5%), pruritus (12.5%) and Guillain-Barre syndrome (4.2%). DFS and OS data were not yet mature as of the cutoff date (January 1,2024). Conclusions: Cadonilimab plus platinum-based dual-drug neoadjuvant chemotherapy achieved favorable ORR and pCR with manageable toxicities in patients with HNSCC. Follow-up is still underway to obtain long-term survival data. Clinical trial information: NCT06023875 .