Therapeutic plasma exchange has been a well-known treatment method for many years and is widely available. It leads to the improvement of neurological symptoms in autoimmune neurological diseases by the removal of antibodies. The aim of this study was to present therapeutic plasma exchange responses and procedure-related adverse events in patients with autoimmune neurological diseases based on our 11-year experience.

A retrospective evaluation was conducted on adult patients who underwent a therapeutic plasma exchange procedure due to neurological diseases between January 2013 and January 2024. Data were gathered from electronic and written hospital and apheresis unit records.

A total of 265 patients underwent 1274 procedures with a preliminary diagnosis of autoimmune neurological disease. Five patients were excluded from the analysis due to their final diagnoses. The most common clinical indications were Guillain-Barré syndrome (45.4%), myasthenia gravis (26.1%), and multiple sclerosis (19.2%). The overall response rate was 81.3%, with 21.7% exhibiting a complete response and 59.6% demonstrating a partial response. With the exception of one patient (hypertensive crisis), no complications necessitating the termination of the procedure were observed. The most prevalent complication was an easily manageable allergic reaction.

Therapeutic plasma exchange has been demonstrated to be an efficacious and safe treatment option in autoimmune neurological diseases, with a favorable overall response rate and a manageable mild-to-moderate side effect profile.

Guillain-Barré syndrome (GBS) is associated with significant muscle loss, which can result in prolonged intensive care. The aim of this study was to evaluate muscle atrophy in GBS patients using serial ultrasound measurements of rectus femoris cross-sectional area (RFCSA).

A prospective study was carried out among GBS patients admitted to the intensive care unit (ICU). All clinical and demographic variables were recorded at admission.Ultrasound measurement of RFCSA was done at baseline and 3, 7, and 14 days after ICU admission. Clinical outcomes such as the ICU stay and duration of mechanical ventilation were studied at discharge.

A total of 25 patients were studied. The mean age was 48.96 ± 14.82 years, 44% were female, and 25% experienced significant muscle atrophy in the first 72 hours. The percentage changes in the RFCSA were 5.21 (3.38-8.39), 9.18 (5.52-11.76), and 12.63 (8.65-15.09) on days 3, 7, and 14, respectively. A greater muscle atrophy rate was strongly positively correlated with longer ventilation periods [atrophy day 14 (r = 0.88, p < 0.001)] and atrophy day 7 (r = 0.87, p < 0.001) and total number of ICU days [atrophy day 14 (r = 0.93, p < 0.001)].

Muscle ultrasound (MUSG) shows potential as a tool for monitoring muscle atrophy in GBS patients. However, its ability to reliably identify patients at risk for prolonged ICU stays and mechanical ventilation requires cautious interpretation and further validation due to the absence of a comparator.

The findings of this study highlight the utility of bedside MUSG as a non-invasive tool for monitoring muscle atrophy in neuromuscular diseases and critically ill patients.Early identification of significant muscle loss allows for timely interventions, risk stratification, and resource optimization, ultimately improving ICU outcomes and patient recovery trajectories.

Naik SS, Desai M, Krishnakumar M, Nashi S, Varadarajan B. The Utility of Muscle Ultrasound as a Predictor of Outcome in Guillain-Barré Syndrome Patients in the Intensive Care Unit: A Prospective Cohort Study. Indian J Crit Care Med 2025;29(3):262-267.

Guillain-Barré syndrome (GBS) is an inflammatory disorder of the peripheral nervous system, causing acute flaccid paralysis. There have been occasional reports linking Hepatitis A virus (HAV) to GBS. Here we aimed to evaluate the current literature on the association between GBS and HAV, exploring potential mechanisms and clinical implications.

We conducted a systematic search using PRISMA guidelines in PubMed, Web of Science, Embase, and Scopus. Only published case reports or conference abstracts presenting cases of confirmed HAV infection and GBS were included. Data extraction was performed independently by two reviewers, and quality assessment was conducted using the Joanna Briggs Institute critical appraisal tool.

Out of 581 studies identified, 46 studies encompassing 47 cases met the inclusion criteria. The mean age of patients was 29.47 years, with a male predominance (70.2 %). Geographically, most cases were reported in Asia (74.5 %). Clinical manifestations of HAV included fever, malaise, and jaundice, while GBS presented with muscle weakness and areflexia. Laboratory findings showed albuminocytological dissociation in 76.2 % of cases. Nerve conduction studies predominantly indicated AIDP subtype (32/46, 69.6 %). Treatment involved IVIG, plasmapheresis, and supportive care, with recovery times ranging from one week to 18 months. One fatality was reported.

This review suggests a potential link between HAV infection and GBS, proposing a mechanism: molecular mimicry. It emphasizes the need for increased awareness and preventive measures, especially in areas with lower health standards. However, further research is needed to clarify the possible mechanisms and deepen our understanding.

Acute motor and sensory axonal neuropathy (AMSAN) is a rare and severe form of acute axonal injury caused by immune damage to the axonal membrane. AMSAN is an axonal variant of GBS. GBS occurs from immune injury to the myelin sheath, axonal variants of GBS (AMSAN and AMAN) differ in that insult is to the axonal membrane. AMSAN is seldom seen, especially in pediatric and adolescent patients. Unlike acute motor axonal neuropathy (AMAN), which has been well-described in literature to be secondary to Campylobacter jejuni infection, there is no known etiology of AMSAN. Here, we present a case of an otherwise healthy 15-year-old female who presented with new-onset facial and bulbar weakness that rapidly progressed to functional paralysis requiring intubation. With no clear diagnosis and after failure in improvement with high-dose steroids, Intravenous Immunoglobulin (IVIG), and plasma exchange transfusion, diagnosis was finally made with electromyography (EMG) and nerve conduction study (NCS). In addition, extensive laboratory work was completed and was only notable for primary acute EBV infection. This case represents a new presenting symptom of AMSAN, a unique finding of concomitant primary EBV infection, the possibility of primary Epstein-Barr virus (EBV) infection as the triggering event in AMSAN and stresses the importance of EMG and NCS when evaluating patients with weakness.

Arboviruses pose significant public health challenges globally, particularly in Pakistan, where deforestation, climate change, urbanization, inadequate sanitation, and natural disasters have all contributed to the spread of mosquito-borne flavivirus diseases like dengue fever. The lack of a thorough national surveillance system has made it difficult to determine the extent and distribution of these diseases. Concern has been raised by recent outbreaks of West Nile virus (WNV) and chikungunya (CHIKV) epidemics, which may lead to Zika virus (ZIKV) outbreaks in the future. Additionally, hospital-based surveillance has detected the Japanese encephalitis virus (JEV) in the region. Evidence also points to the presence of additional arboviruses in healthy populations, such as the Karshi virus (KSV), Tamdy virus (TAMV), Crimean-Congo hemorrhagic fever virus (CCHFV), and severe fever with thrombocytopenia syndrome virus (SFTSV). This review aims to address the risk factors linked to these diseases, provide specific policy recommendations for efficient disease prevention and control, and describe the epidemiological trends of these diseases in Pakistan while emphasizing the critical need for improved surveillance and thorough epidemiological investigations.

Immune-mediated neuropathies encompass a range of neurological disorders, including chronic inflammatory demyelinating polyradiculoneuropathy, Guillain-Barré syndrome, multifocal motor neuropathy, autoimmune autonomic neuropathies, and paranodal nodopathies. Recognizing clinical patterns is key to narrowing the broad range of differential diagnoses in immune-mediated neuropathies. Electrodiagnostic testing is a useful tool to support the diagnosis of immune-mediated neuropathies. Our understanding of autoimmune demyelinating neuropathies is rapidly advancing, particularly with the discovery of nodal and paranodal antibodies. Recent advances in neuropathy treatment include the utilization of neonatal Fc receptors to reduce antibody recycling, and the development of complement inhibitors to reduce inflammatory damage, offering promising new therapeutic avenues. Timely identification of immune-mediated neuropathies is imperative as delay in diagnosis and treatment may lead to irreversible disability.

Malaria is an infectious disease caused by Plasmodium parasites, transmitted to humans by infected female Anopheles mosquitoes. Five Plasmodium species infect humans: P. vivax, P. falciparum, P. ovale, P. malariae, and P. knowlesi. Guillain-Barré Syndrome (GBS) is an inflammatory condition that can lead to paralysis, autonomic dysfunction, respiratory failure, and sensory symptoms. GBS typically follows an infection with Campylobacter bacteria, commonly found in undercooked poultry, but is rarely associated with malaria.

A 16-year-old female patient presented to our emergency department with a 1-day history of altered mentation. She had experienced a severe global headache and fever for 3 days prior to presentation. The patient tested positive for falciparum malaria and was admitted to the ward, where she received IV artesunate and other supportive management. After 3 days of admission, she noticed weakness and numbness in her lower extremities. Subsequently, the weakness progressed upward to involve her upper extremities. After extensive workup, the patient was managed with consideration of Guillain-Barré Syndrome (GBS), and she made a complete recovery after 12 weeks.

Guillain-Barré Syndrome (GBS) is an acute paralytic illness often triggered by infections, particularly viral ones. It is the leading cause of sudden muscle weakness, typically following respiratory or gastrointestinal infections, with Campylobacter jejuni being the most common cause. This patient's neurological symptoms pointed to paralysis of the lower motor neurons. Guillain-Barré Syndrome is also suggested by elevated protein levels and a lack of cells in the cerebrospinal fluid. This clinical picture emerged following a Plasmodium falciparum infection. Although the specific subtype (demyelinating or axonal) was not determined in this case due to the absence of a nerve conduction study, demyelinating subtypes have been found in GBS following Plasmodium infection.

In conclusion, while malaria is an exceptionally rare cause of Guillain-Barré Syndrome (GBS), it should be considered in patients with recent malaria infection who present with symptoms of lower motor neuron lesions.

Zika virus (ZIKV) causes a variety of peripheral and central nervous system complications leading to neurological symptoms such as limb weakness. We used a mouse model to identify candidate genes potentially involved in causation or recovery from ZIKV-induced acute flaccid paralysis. Using Zikv and Chat chromogenic and fluorescence in situ RNA hybridization, electron microscopy, immunohistochemistry, and ZIKV RT-qPCR, we determined that some paralyzed mice had infected motor neurons, but motor neurons are not reduced in number and the infection was not present in all paralyzed mice; hence infection of motor neurons were not strongly correlated with paralysis. Consequently, paralysis was probably caused by by-stander effects. To address this, we performed bioinformatics analysis on spinal cord RNA to identify 2058 differentially expressed genes (DEGs) that were altered during paralysis and then normalized after paralysis. Of these "biphasic" DEGs, 951 were up-regulated and 1107 were down-regulated during paralysis, followed by recovery. To refine the search for candidate DEGs we used gene ontology analysis and RT-qPCR to select 3 DEGs that could be involved with the node of Ranvier function and 5 DEGs that could be involved with synaptic function. Among these, SparcL1:Sparc DEG ratios were identified to be inversely correlated with ZIKV-induced paralysis, which is consistent with the known function of SPARC protein to antagonize the synaptogenesis of SPARCL1. Ank3, Sptbn1, and Epb41l3 affecting the structures at and near the nodes of Ranvier were significantly downregulated during ZIKV-induced paralysis. The primary contribution is the identification of 8 candidate genes that may be involved in the causation or recovery of ZIKV-induced paralysis.

Guillain-Barré syndrome (GBS) is an autoimmune disease that affects the peripheral nervous system leading to motor, sensory, and sometimes autonomic manifestations. Therapeutic plasma exchange (TPE), which involves the selective removal of pathological molecules, such as auto-antibodies, from plasma, has proven to be safe and effective in adults with GBS. However, its application in pediatric patients lacks sufficient evidence. This study aims to evaluate the efficacy and safety of TPE in pediatric patients with severe GBS, in a low-resource setting.

This is a single-center retrospective study of 36 GBS patients aged between 2 and 13 years. A total of 122 TPE sessions were administered, with a median of four sessions per patient. A human albumin solution was the exchange fluid in all the sessions. Clinical improvement was evaluated through general examination and muscle power assessment using the Medical Research Council (MRC) scale.

All patients showed clinical improvement upon treatment with TPE. The grade of power in the upper extremities increased from a mean of 1.7 ± 1.1 at the peak of illness to 3.7 ± 0.9 at discharge, indicating an increase of 2.0 ± 1.1 (95% CI, 1.6 to 2.4, p< 0.001). Alternatively, in the lower extremities, it increased from 1.2 ± 1.1 to 2.5 ± 0.8, indicating a significant rise of 1.4 ± 0.8 (95% CI, 1.1 to 1.6, p< 0.001). There was a significant improvement in the cranial, autonomic, and respiratory functions among all patients. Half of the patients were available for follow-up and showed full recovery, with six of them still exhibiting minimal residual deficits. TPE-related complications were mostly mild or moderate, with tachycardia, hypotension, and mild anemia being the most common. However, serious complications occurred in three of the patients, necessitating the discontinuation of the treatment in two of them. There was no mortality related to TPE in this study.

TPE shows promise in treating pediatric GBS. In this study, TPE was associated with the recovery of neurological functions, yielding positive outcomes with only minimal residual deficits. However, balancing its benefits with potential risks requires careful clinical judgment and rigorous monitoring to ensure patient safety and optimize outcomes. TPE was a more cost-effective and accessible option than IVIG in this financially restricted, low-income setting.

Guillain-Barré syndrome (GBS) and its variants represent a spectrum of acute, immune-mediated polyneuropathies with heterogeneous clinical presentations and underlying etiologies. While infectious triggers are common precursors to these disorders, the association between viral infections and autoimmune neurological conditions remains an area of active investigation. Here, we report a case of GBS/Miller-Fisher syndrome overlap syndrome in an 80-year-old male presenting with dysarthria, dysphonia, ophthalmoplegia, areflexia, and postural instability following an upper respiratory tract infection. Cerebrospinal fluid analysis revealed the unexpected detection of herpes simplex virus type 1 DNA. Treatment with intravenous immunoglobulin therapy and acyclovir resulted in a progressive recovery of neurological symptoms. This case emphasizes the role of viral infections in differential diagnosis or as potential triggers for autoimmune neurological disorders highlighting the efficacy to addressed therapy in such complex cases.

Guillain-Barré syndrome (GBS) is a common entity in neurology clinics. A variety of etiologies have been implicated in the presentation of GBS. Although rarely reported, traumatic brain injury (TBI) has also been reported to cause GBS. In this article, we report a similar case of GBS that occurred following TBI and the patient presented with acute flaccid paraparesis with intact strength in upper limbs. Paraparesis progressed to quadriparesis simulating a case of spinal injury, without any correlating imaging findings. Nerve conduction study findings, cerebrospinal fluid studies, and clinical examination led to the diagnosis of post-TBI GBS. A review of similar cases reported in literature is also attached. High index of suspicion should be maintained for GBS in all cases of imaging-negative post-TBI limb weakness which may simulate acute spinal injury.

Background: Guillain-Barré syndrome (GBS) is an immune-mediated polyradiculoneuropathy that represents a leading cause of motor impairment. Robot-assisted therapy (RAT) has been widely applied in various neurological conditions. However, the use of RAT in GBS remains underexplored. This systematic review (SR) aims to evaluate the preliminary evidence regarding the efficacy of RAT in terms of motor recovery in people with GBS (pwGBSs). Secondly, the study protocol for a randomized RCT is reported. Methods: A comprehensive SR was conducted on PubMed, Scopus, EMBASE, Cochrane Library, and Epistemikos. Risk of bias was assessed using the National Institute of Health (NIH) study quality assessment. The SR's protocol was recorded in the PROSPERO database. Results: Out of 116 articles found, four studies published in the past four years met the inclusion criteria. These studies investigated the effects of RAT on lower limbs (three studies) and upper limbs (one study) in four pwGBSs. The results showed improvements in motor function and patient engagement, but it is impossible to generalize the findings. Conclusions: Our SRs supports the rationale for an RCT to assess the efficacy of RAT in pwGBSs. We present the protocol for a double-blind RCT to evaluate the effects of RAT on upper limb motor function in pwGBSs.

Guillain-Barré syndrome represents a heterogeneous group of immune-mediated peripheral neuropathies that are characterized by various clinical manifestations. Reporting this clinical case emphasizes the rarity of Guillain-Barré syndrome, the diagnostic challenges faced by healthcare providers, and the risk of delayed diagnosis for both the mother and fetus. A 34-year-old pregnant woman at 33 weeks of gestation presented to the inpatient ward complaining of paresthesia in the lower and upper limbs, muscle pain, balance disturbances, moderate headache, nausea and vertigo, general weakness, and pronounced fatigue. The patient had experienced an acute viral respiratory infection 4 weeks before presenting to the hospital. The patient was admitted to the intensive care unit with a preliminary diagnosis of acute viral respiratory infection and nasopharyngitis. The patient's condition worsened dynamically, manifesting bulbar syndrome (swallowing problems), paresthesia of the anterior abdominal wall, reduced perception of fetal movements, numbness of the tongue, and low fever (37.2°C). A diagnosis of acute inflammatory demyelinating polyradiculopathy (Guillain-Barré syndrome) was established. Despite treatment, the neurologic symptoms worsened. The paravertebral radicular type pains were difficult to manage with administered analgesic therapy, and there was a progression of the bulbar syndrome. Treatment with intravenous immunoglobulin was initiated. Consequently, it was recommended by the multidisciplinary council to perform an emergency cesarean delivery, in the interest of the mother and fetus. Guillain-Barré syndrome is a rare condition that occurs during pregnancy and requires thorough evaluation, prompt multidisciplinary assessment, and individualized management of delivery to improve maternal and fetal prognosis.

In Guillain-Barré syndrome (GBS), patients with dysautonomia demonstrate sympathetic overactivity (SO). This study assessed the role of prazosin (α1-blocker) in the management of SO.

This cohort study was conducted from January 2022 to September 2023. Thirty-two GBS patients with SO received prazosin (2.5-10 mg three times a day) (prazosin group). For comparison, we included historical controls that included 33 GBS patients having SO with similar baseline characteristics, including median age and disability, who did not receive prazosin, from a GBS registry of patients admitted during February 2018-December 2021. The primary endpoint was days to resolution of SO. Secondary endpoints were daily fluctuations in the systolic (SBP) and diastolic blood pressure (DBP), duration of hospital stay, in-hospital mortality, and disability at 3 months.

The median ages of both the treatment and the control groups were 36 (IQR 25-49) years and 43 (66.2%) were males. The demographic and clinical parameters were comparable. Prazosin resulted in significantly earlier normalization of SO compared to the control group (median 15 vs. 20 days; p = .01). The mean fluctuations in the SBP and DBP at 15 days were significantly lower in the prazosin group. However, the duration of hospital stay and good recovery at 3 months were comparable. Three patients developed hypotension, while two patients died (ventilator-associated pneumonia) in the prazosin group.

This study provides new evidence supporting the role of prazosin in SO, and needs randomized trials to confirm our findings.

The Zika virus (ZIKV) is classified within the Flavivirus genus of the Flaviviridae family and is categorized as an arbovirus. The virus was initially identified in a rhesus monkey in Uganda in 1947 and later in a human in Nigeria in 1952. Since 2007, the prevalence of the virus has been on the rise, culminating in a major outbreak in the United States (US) in 2015. During this outbreak, the adult population was severely impacted, experiencing a range of symptoms, including organ failure, microcephaly, fetal death, and Guillain-Barré syndrome (GBS). Additionally, skin rash, limb swelling, fever, headache, and heightened sensitivity are found in most adults with Zika syndrome. Although the virus can be transmitted through blood, vertical transmission from mother to child, and sexual contact, the primary way of transmission of the virus is through the Aedes mosquito. Cells such as neurons, macrophages, peripheral dendritic cells, and placental cells are among the target cells that the virus can infect. The TAM AXL receptor plays a crucial role in infection. After the virus enters the body through the bloodstream, it spreads in the body with a latent period of 3 to 12 days. Currently, there is no specific treatment or publicly available vaccine for the ZIKV. Limited laboratory testing has been conducted, and existing drugs originally designed for other pathogens have been repurposed for treatment. Given the Aedes mosquito's role as a vector and the wide geographical impact of the virus, this study aims to comprehensively investigate Zika's pathogenesis and clinical symptoms based on existing knowledge and research. By doing so, we seek to enhance our understanding of the virus and inform future prevention and treatment strategies.

Rheumatoid arthritis (RA) is often treated with anti-tumor necrosis factor α (anti-TNF-α) medications. While these drugs can cause common side effects such as injection-site and infusion reactions, rare cases of Guillain-Barré syndrome (GBS) have been reported. It's a potentially life-threatening condition characterized by progressive, ascending weakness of the extremities and areflexia, with an incidence of about 1.5 cases per 100,000 annually and a mortality rate of around 5%. It has been linked to various triggers, including infections, vaccinations, and medications like TNF inhibitors. Anti-TNF-α treatments may induce GBS by activating latent infections, increasing susceptibility, triggering autoimmune responses, or disrupting the balance of TNF-α in the peripheral nervous system. We report a 39-year-old female with a 26-year history of RA, initially treated with methotrexate until it was discontinued due to myelosuppression. She was then prescribed etanercept. A few weeks later, she developed numbness and burning pain in her limbs. GBS was suspected based on her symptoms, and nerve conduction studies confirmed the diagnosis. She was successfully treated with plasmapheresis.

Here we report an enzymatic approach to synthesize N-formylneuraminic acid (Neu5Fo) containing sialosides, through a five-enzyme cascade. This method stands as an alternative to traditional chemical syntheses, aiming for precision and efficiency in generating sialosides with a tailored N-formyl group generated directly from formic acid. The newly synthesized Neu5Fo was characterized using various NMR techniques revealing a conformational equilibrium at the amide bond of the formyl group in slow exchange on the NMR time scale with a trans : cis ratio of ∼2 : 1. This work not only suggests potential for exploring the biological roles of sialosides but also points to the possibility of developing novel therapeutic agents.

This study aims to systematically review the existing literature and perform a meta-analysis to evaluate the prevalence of hyponatremia among Guillain Barre Syndrome (GBS) patients and its relationship with disease prognosis. We comprehensively searched PubMed, Embase, Medline, Web of Science, Science Direct, and the Cochrane Library databases from 1995 to 2024 for observational studies on the prevalence of hyponatremia in GBS. The meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) guidelines. Heterogeneity among the included studies was calculated with the I2 for each analysis. We used the Comprehensive Meta-Analysis software (Version 3.3.070; Biostat, Englewood, USA). Eight observational studies met our inclusion criteria. The meta-analysis showed that the pooled prevalence of hyponatremia among GBS patients was 12% (95% CI: 0.107-0.149). The results exhibited high heterogeneity (I² = 99%), indicating significant variability among the studies. Hyponatremia rates reported in these eight studies ranged from 11.5% to 48% in GBS patients. The prevalence of hyponatremia was found to be 12% in GBS patients, which is relatively lower compared to some reports. Hyponatremia was found to be associated with prolonged hospital stay, mortality, and mechanical ventilation as poor prognostic factors. Further prospective studies are needed to elucidate the mechanisms underlying hyponatremia in GBS and to develop targeted interventions to address this issue.

This article reviews autoimmune neuromuscular disorders and includes an overview of the diagnostic approach, especially the role of antibody testing in a variety of neuropathies and some other neuromuscular disorders.

In the past few decades, multiple antibody biomarkers associated with immune-mediated neuromuscular disorders have been reported. These biomarkers are not only useful for better understanding of disease pathogenesis and allowing more timely diagnosis but may also aid in the selection of an optimal treatment strategy.

Recognition of autoimmune neuromuscular conditions encountered in inpatient or outpatient neurologic practice is very important because many of these disorders are reversible with prompt diagnosis and early treatment. Antibodies are often helpful in making this diagnosis. However, the clinical phenotype and electrodiagnostic testing should be taken into account when ordering antibody tests or panels and interpreting the subsequent results. Similar to other laboratory investigations, understanding the potential utility and limitations of antibody testing in each clinical setting is critical for practicing neurologists.

Patients with Guillain-Barré syndrome (GBS) occasionally have residual gait disturbance one year after disease onset. We hypothesized that providing hip joint movement assistance can improve gait in patients with GBS and residual gait disturbance. A 78-year-old man with GBS showed improvement in gait following conventional rehabilitation and gait training using GAIT TRAINER HWA-01 (HWA-01; Honda Motor Co., Ltd., Tokyo, Japan), which is a hip-wearable exoskeleton robot. Initially, he presented with gastrointestinal symptoms, subsequently flaccid quadriplegia, and respiratory muscle paralysis. He was diagnosed with acute motor axonal neuropathy and was transferred to our hospital on day 185 after the disease onset. Seven months after rehabilitation, his walking ability plateaued. On day 382, a single-case study with ABABA design intervention, with conventional gait training in phase A and gait training using HWA-01 in phase B, was conducted. The primary outcomes included a comfortable walking speed, stride length, and cadence. Comfortable walking speed, stride length, and cadence statistically improved after gait training using HWA-01. Furthermore, improvement in exercise capacity and activities of daily living exceeded the minimal clinically important difference for the intervention. The use of the HWA-01 gait trainer potentially improves gait in patients with GBS who have residual gait disturbance.

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.

The discovery of the anti-GQ1b antibody has expanded the nosology of classic Miller Fisher syndrome to include Bickerstaff brainstem encephalitis, Guillain-Barré syndrome with ophthalmoplegia, and acute ophthalmoplegia without ataxia, which have been brought under the umbrella term anti-GQ1b antibody syndrome. It seems timely to define the phenotypes of anti-GQ1b antibody syndrome for the proper diagnosis of this syndrome with diverse clinical presentations. This review summarizes these syndromes and introduces recently identified subtypes.

Although ophthalmoplegia is a hallmark of anti-GQ1b antibody syndrome, recent studies have identified this antibody in patients with acute vestibular syndrome, optic neuropathy with disc swelling, and acute sensory ataxic neuropathy of atypical presentation. Ophthalmoplegia associated with anti-GQ1b antibody positivity is complete in more than half of the patients but may be monocular or comitant. The prognosis is mostly favorable; however, approximately 14% of patients experience relapse.

Anti-GQ1b antibody syndrome may present diverse neurological manifestations, including ophthalmoplegia, ataxia, areflexia, central or peripheral vestibulopathy, and optic neuropathy. Understanding the wide clinical spectrum may aid in the differentiation and management of immune-mediated neuropathies with multiple presentations.

Solid organ transplant recipients are prone to developing a wide range of complications associated with the procedure itself, as well as with immunosuppressants. Guillain-Barré syndrome, which is part of the spectrum of inflammatory neuropathies, is not expected to occur early after organ transplant when immunosuppression is at its highest point. We describe the clinical case of a patient who underwent an urgent liver transplant due to acute liver failure secondary to drug-induced liver injury and developed Guillain-Barré syndrome early after the transplant.

To establish a method to induce Campylobacter jejuni colonization in the intestines of C57BL/6 mice through antibiotic-induced microbiome depletion.

Fifty-four female C57BL/6 mice were divided into the normal, control, and experimental groups. The experimental group was administered intragastric cefoperazone sodium and sulbactam sodium (50 mg/mL) for 2 days; then, the experimental and control mice were intragastrically administered 200 µL C. jejuni, which was repeated once more after 2 days. Animal feces were collected, and the HipO gene of C. jejuni was detected using TaqMan qPCR from day 1 to day 14 after modeling completion. Immunofluorescence was used to detect intestinal C. jejuni colonization on day 14, and pathological changes were observed using hematoxylin and eosin staining. Additionally, 16S rDNA analyses of the intestinal contents were conducted on day 14. In the experimental group, C. jejuni was detected in the feces from days 1 to 14 on TaqMan qPCR, and immunofluorescence-labeled C. jejuni were visibly discernable in the intestinal lumen. The intestinal mucosa was generally intact and showed no significant inflammatory-cell infiltration. Diversity analysis of the colonic microbiota showed significant inter-group differences. In the experimental group, the composition of the colonic microbiota differed from that in the other 2 groups at the phylum level, and was characterized by a higher proportion of Bacteroidetes and a lower proportion of Firmicutes.

Microbiome depletion induced by cefoperazone sodium and sulbactam sodium could promote long-term colonization of C. jejuni in the intestines of mice.

This study compared the clinical and electrodiagnostic (EDX) features and long-term outcomes of patients with very early Guillain-Barré syndrome (VEGBS, duration of illness ≤4 days) and those with early/late (>4 days)-presenting GBS.

One hundred patients with GBS were clinically evaluated and categorized into VEGBS and early/late GBS groups. Electrodiagnostic studies were performed on the bilateral median, ulnar, and fibular motor nerves and the bilateral median, ulnar, and sural sensory nerves. Admission and peak disability were assessed using the 0 to 6 Guillain-Barré Syndrome Disability Scale (GBSDS). The primary outcome was disability at 6 months, which was categorized as complete (GBSDS ≤1) or poor (GBSDS ≥2). The secondary outcomes were frequencies of abnormal electrodiagnostic findings, in-hospital progression, and mechanical ventilation (MV).

Patients with VEGBS had higher peak disability (median 5 vs. 4; P = 0.02), frequent in-hospital disease progression (42.9% vs. 19.0%, P < 0.01), needed MV (50% vs. 22.4%; P < 0.01), and less frequent albuminocytologic dissociation (52.4% vs. 74.1%; P = 0.02) than those with early/late GBS. Thirteen patients were lost to follow-up at 6 months (nine patients with VEGBS and four patients with early/late GBS). The proportion of patients with complete recovery at 6 months was comparable (60.6% vs. 77.8%; P = ns ). Reduced d-CMAP was the most common abnormality, noted in 64.7% and 71.6% of patients with VEGBS and early/late GBS, respectively ( P = ns). Prolonged distal motor latency (≥130%) was more common in early/late GBS than in VEGBS (36.2% vs. 25.4%; P = 0.02), whereas absent F-waves were more frequent in VEGBS (37.7% vs. 28.7%; P = 0.03).

Patients with VEGBS were more disabled at admission than those with early/late GBS. However, 6 month's outcomes were similar between the groups. F-wave abnormalities were frequent in VEGBS, and distal motor latency prolongation was common in early/late GBS.

Brain- and blood-derived protein analysis in the cerebro-spinal fluid (CSF) in various studies performed abroad found that some proteins and their isoforms were altered significantly in Guillain-Barre´ syndrome (GBS) patients in comparison to controls. However, data are lacking in India with respect to the blood- or brain-derived proteins in patients of GBS.

This study aimed to identify the role of apolipoprotein A IV (Apo A IV) and haptoglobin as potential protein markers in CSF of patients with GBS in our population.

The study comprised 28 participants where 12 confirmed cases of GBS and 16 control subjects admitted for non-infectious neurological disorders were recruited after obtaining approval from the Institutional Ethics Committee. CSF glucose, protein, and adenosine deaminase were analyzed using an autoanalyzer. The concentrations of Apo A IV and haptoglobin were estimated with enzyme-linked immuno-sorbent assay (ELISA) kits.

The CSF protein concentrations of cases were higher as compared to controls. The concentrations of haptoglobin and Apo A IV were higher in the confirmed cases of GBS as compared to the control subjects, and this difference was found to be significant. The receiver operating characteristic curve analysis for haptoglobin revealed that the area under the curve (AUC) was 0.867 (95% CI: 0.732-1.001), with a sensitivity of 83.8% and a specificity of 63.3%. The AUC for Apo A IV was 0.883 (95% CI: 0.758-1.009), with a sensitivity of 91.7% and a specificity of 73.3%.

Haptoglobin along with Apo A IV can emerge as a potential biochemical marker in CSF for the diagnosis of GBS.

Acute canine polyradiculoneuritis (ACP) is a common peripheral neuropathy in dogs, and is generally self-limiting and benign. Electrodiagnostic (EDX) tests are typically performed after 7-10 days. Delaying the definitive diagnosis may hamper the treatment of other causes of acute weakness, which may require specific treatments and may carry different prognoses. This retrospective multicenter study aims to assess whether EDX performed within the first 6 days of clinical signs onset can detect alterations indicative of ACP, and aims to characterize the most prevalent alterations. A total of 71 dogs with suspected ACP were retrospectively analyzed and classified into two groups based on EDX timing: early group (EG, 1-6 days after symptom onset) and late group (LG, 7-15 days after symptom onset). In our study, no significant differences were found between the two groups in motor nerve conduction studies (MNCSs) and F-wave analysis, indicating that EDX is able to demonstrate abnormalities even in the first 6 days from onset. Although the LG showed significantly greater degrees of electromyographic (EMG) alterations compared to the EG, frequent muscle alterations were still observed in the EG group. These findings support the use of EDX in patients with suspected ACP within the first 6 days from the clinical onset. Prompt neurophysiological examinations for suspected ACP patients can be performed effectively and can help allow for early diagnosis and facilitate appropriate treatment.

Anti-sulfatide antibodies are key biomarkers for the diagnosis of Guillain-Barré syndrome (GBS). However, case reports on anti-sulfatide antibody-related GBS are rare, particularly for atypical cases.

A 63 years-old man presented with limb numbness and diplopia persisting for 2 weeks, with marked deterioration over the previous 4 days. His medical history included cerebral infarction, diabetes, and coronary atherosclerotic cardiomyopathy. Physical examination revealed limited movement in his left eye and diminished sensation in his extremities. Initial treatments included antiplatelet agents, cholesterol-lowering drugs, hypoglycemic agents, and medications to improve cerebral circulation. Despite this, his condition worsened, resulting in bilateral facial paralysis, delirium, ataxia, and decreased lower limb muscle strength. Treatment with intravenous high-dose immunoglobulin and dexamethasone resulted in gradual improvement. A 1 month follow-up revealed significant neurological sequelae.

A 53 years-old woman was admitted for adenomyosis and subsequently experienced sudden limb weakness, numbness, and pain that progressively worsened, presenting with diminished sensation and muscle strength in all limbs. High-dose intravenous immunoglobulin, vitamin B1, and mecobalamin were administered. At the 1 month follow-up, the patient still experienced limb numbness and difficulty walking. In both patients, albuminocytologic dissociation was found on cerebrospinal fluid (CSF) analysis, positive anti-sulfatide antibodies were detected in the CSF, and electromyography indicated peripheral nerve damage.

Anti-sulfatide antibody-related GBS can present with Miller-Fisher syndrome, brainstem encephalitis, or a combination of the two, along with severe pyramidal tract damage and residual neurological sequelae, thereby expanding the clinical profile of this GBS subtype. Anti-sulfatide antibodies are a crucial diagnostic biomarker. Further exploration of the pathophysiological mechanisms is necessary for precise treatment and improved prognosis.

Guillain Barre syndrome (GBS) following Varicella zoster is a rare presentation and has only been reported in a few cases around the world. Of the reported cases, the type of GBS is not specified in the majority, and where specified is of the acute inflammatory demyelinating polyradiculoneuropathy (AIDP) type. We report a case of acute motor axonal neuropathy (AMAN) type GBS following herpes zoster in a 27-year-old male who presented with bilateral lower limb weakness and left sided lower motor neuron type facial nerve palsy a week after herpes zoster infection.

Guillain-Barré syndrome (GBS), a post-infectious, immune-mediated, acute demyelinating disease of the peripheral nerves and nerve roots, represents the most prevalent and severe acute paralyzing neuropathy. Purinergic P2X7 receptors (P2X7R) play a crucial role in central nervous system inflammation. However, little is known about their role in the immune-inflammatory response within the peripheral nervous system.

Initially, we assessed the expression of purinergic P2X7R in the peripheral blood of patients with GBS using flow cytometry and qRT-PCR. Next, we explored the expression of P2 X7R in CD4+ T cells, CD8+ T cells, and macrophages within the sciatic nerves and spleens of rats using immunofluorescence labeling and flow cytometry. The P2X7R antagonist brilliant blue G (BBG) was employed to examine its therapeutic impact on rats with experimental autoimmune neuritis (EAN) induced by immunization with the P0180 - 199 peptide. We analyzed CD4+ T cell differentiation in splenic mononuclear cells using flow cytometry, assessed Th17 cell differentiation in the sciatic nerve through immunofluorescence staining, and examined the expression of pro-inflammatory cytokine mRNA using RT-PCR. Additionally, we performed protein blotting to assess the expression of P2X7R and NLRP3-related inflammatory proteins within the sciatic nerve. Lastly, we utilized flow cytometry and immunofluorescence labeling to examine the expression of NLRP3 on CD4+ T cells in rats with EAN.

P2X7R expression was elevated not only in the peripheral blood of patients with GBS but also in rats with EAN. In rats with EAN, inhibiting P2X7R with BBG alleviated neurological symptoms, reduced demyelination, decreased inflammatory cell infiltration of the peripheral nerves, and improved nerve conduction. BBG also limited the production of pro-inflammatory molecules, down-regulated the expression of P2X7R and NLRP3, and suppressed the differentiation of Th1 and Th17 cells, thus protecting against EAN. These effects collectively contribute to modifying the inflammatory environment and enhancing outcomes in EAN rats.

Suppression of P2X7R relieved EAN manifestation by regulating CD4+ T cell differentiation and NLRP3 inflammasome activation. This finding underscores the potential significance of P2X7R as a target for anti-inflammatory treatments, advancing research and management of GBS.

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.

Human autoantibodies (auto-Abs) neutralizing type I IFNs were first discovered in a woman with disseminated shingles and were described by Ion Gresser from 1981 to 1984. They have since been found in patients with diverse conditions and are even used as a diagnostic criterion in patients with autoimmune polyendocrinopathy syndrome type 1 (APS-1). However, their apparent lack of association with viral diseases, including shingles, led to wide acceptance of the conclusion that they had no pathological consequences. This perception began to change in 2020, when they were found to underlie about 15% of cases of critical COVID-19 pneumonia. They have since been shown to underlie other severe viral diseases, including 5%, 20%, and 40% of cases of critical influenza pneumonia, critical MERS pneumonia, and West Nile virus encephalitis, respectively. They also seem to be associated with shingles in various settings. These auto-Abs are present in all age groups of the general population, but their frequency increases with age to reach at least 5% in the elderly. We estimate that at least 100 million people worldwide carry auto-Abs neutralizing type I IFNs. Here, we briefly review the history of the study of these auto-Abs, focusing particularly on their known causes and consequences.

Guillain-Barré syndrome (GBS) is a condition characterized by acute and progressive weakness that impacts the limbs, facial muscles, and bulbar muscles due to acute polyneuro-radiculopathy. Typically, an infection that results in immune-mediated nerve dysfunction is what starts the disease. Patients often encounter paresthesia or discomfort before progressing to muscle weakness, initially in the lower extremities (which may include some proximal components) and subsequently in the upper extremities. The features of polyneuropathy identified during electrophysiology tests, bolstered by evidence of acquired demyelination in the nerve conduction study (NCS), support the clinical diagnosis of GBS. In peripheral neuropathies, NCS often reveals abnormalities in nerve conduction parameters. A specific pattern observed in the sensory nerve conduction study (SNCS), referred to as "sural sparing," signifies that the sural nerve, located near the calf muscles, remains relatively unaffected compared to other sensory nerves. Very few studies have been conducted to investigate improvements in sensory nerve conduction (SNC) parameters before and after intravenous immunoglobulin (IVIG), offering limited clinical correlation for the recovery and prognosis of the disease. The study aimed to observe the NCS parameters of the sensory nerves in both the upper and lower limbs, before and after the infusion of IVIG.

This study was an observational investigation conducted in the neurophysiology laboratory of the Physiology Department at a rural medical college in central India. Fifty clinically diagnosed cases of GBS aged between 18 and 60 years were referred from the Department of Medicine to the Physiology Department for conducting the NCS. Basic sociodemographic information, along with clinical history, was collected. Subsequently, the RMS EMG EP Mark-II machine was employed to examine the sensory nerve action potentials (SNAPs), such as amplitude (in mV) and conduction velocity (in ms), of the sensory nerves in both the upper and lower limbs before and after IVIG infusion. The IVIG infusion occurs within one week of clinically diagnosing GBS. Following an initial NCS, a second NCS follow-up study was conducted one week after the IVIG infusion to analyze the changing trend in sensory nerves.

Upon analysis, no significant correlation was observed between the pre- and post-IVIG SNAPs of the median and ulnar nerves. However, the sural nerve conduction velocity's p-value of 0.033 demonstrated statistical significance, suggesting that the sural nerve is comparatively spared, confirming sural sparing. However, the SNAP of the sensory nerves in GBS patients showed a significant improvement overall, and only NCS quantified the percentage of improvement.

According to the study, the NCS of sensory nerves showed a positive change in the parameters examined before and after the infusion of IVIG. This underscores the timely intervention of GBS with IVIG, and conducting the sensory conduction study diligently will enhance knowledge about the recovery period. Additionally, it supports the treating physician in making informed interventions based on the results post-IVIG infusion. This enhancement in the sensory nerves can only be quantified through NCS.

Acroparesthesia is a symptom characterized by a subjective sensation, such as numbness, tingling, prickling, and reduced sensation, affecting the extremities (fingers and toes). Despite its frequency, data regarding its diagnostic approach and management are scarce. The etiological diagnosis of acroparesthesia is sometimes challenging since it can be due to abnormality anywhere along the sensory pathway from the peripheral nervous system to the cerebral cortex. Acroparesthesia can reveal several diseases. It can be associated with rheumatic complaints such as arthritis or myalgia. Further cautions are required when paresthesia is acute (within days) in onset, rapidly progressive, severe, asymmetric, proximal, multifocal, or associated with predominant motor signs (limb weakness) or severe dysautonomia. Acroparesthesia may reveal Guillain-Barré syndrome or vasculitis, requiring rapid management. Acroparesthesia is a predominant symptom of polyneuropathy, typically distal and symmetric, often due to diabetes. However, it can occur in other diseases such as vitamin B12 deficiency, monoclonal gammopathy of undetermined significance, or Fabry's disease. Mononeuropathy, mainly carpal tunnel syndrome, remains the most common cause of acroparesthesia. Ultrasonography contributes to the diagnosis of nerve entrapment neuropathy by showing nerve enlargement, hypoechogenic nerve, and intraneural vascularity. Besides, it can reveal its cause, such as space-occupying lesions, anatomical nerve variations, or anomalous muscle. Ultrasonography is also helpful for entrapment neuropathy treatment, such as ultrasound-guided steroid injection or carpal tunnel release. The management of acroparesthesia depends on its causes. This article aimed to review and summarize current knowledge on acroparesthesia and its causes. We also propose an algorithm for the management of acroparesthesia.

Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy; a disease involving the peripheral nervous system which is the most common cause of acute flaccid paralysis worldwide. So far, it is still lack of a comprehensive overview and understanding of the national epidemiological, clinical characteristics, and the risk factors of GBS in China, as well as differences between China and other countries and regions in these respects. With the global outbreak of the coronavirus disease 2019 (COVID-19), an epidemiological or phenotypic association between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and GBS has attracted great attention. In this review, we outlined the current clinical data of GBS in China by retrieving literature, extracting and synthesizing the data of GBS in China from 2010 to 2021. Besides, we compared the characteristics of epidemiology, preceding events and clinical profiles of GBS between China and other countries and regions. Furthermore, in addition to conventional intravenous immunoglobulin (IVIG) and plasma exchange (PE) therapy, the potential therapeutic effects with novel medications in GBS, such as complement inhibitors, etc., have become the research focus in treatments. We found that epidemiological and clinical findings of GBS in China are approximately consistent with those in the International GBS Outcome Study (IGOS) cohort. We provided an overall picture of the present clinical status of GBS in China and summarized the global research progress of GBS, aiming to further understand the characteristics of GBS and improve the future work of GBS worldwide, especially in countries with the middle and low incomes.

Guillain-Barre syndrome (GBS) is an immune-mediated inflammatory peripheral neuropathy. This study aimed to conduct a systematic analysis of the serum lipids profile in GBS.

We measured the serum lipids profile in 85 GBS patients and compared it with that of 85 healthy controls matched for age and sex. Additionally, we analyzed the correlation between lipids and the severity, subtypes, precursor infections, clinical outcomes, clinical symptoms, immunotherapy, and other laboratory markers of GBS.

Compared to the healthy controls, GBS exhibited significantly elevated levels of Apolipoprotein B (APOB), Apolipoprotein C2 (APOC2), Apolipoprotein C3 (APOC3), Apolipoprotein E (APOE), triglycerides (TG), and residual cholesterol (RC). Conversely, Apolipoprotein A1 (APOA1), Apolipoprotein A2 (APOA2), and high-density lipoprotein (HDL) were substantially lower in GBS. Severe GBS displayed noticeably higher levels of APOC3 and total cholesterol (TC) compared to those with mild disease. Regarding different clinical outcomes, readmitted GBS demonstrated higher RC expression than those who were not readmitted. Moreover, GBS who tested positive for neuro-virus antibody IGG in cerebrospinal fluid (CSF) exhibited heightened expression of APOC3 in comparison to those who tested negative. GBS with cranial nerve damage showed significantly reduced expression of HDL and APOA1 than those without such damage. Additionally, GBS experiencing limb pain demonstrated markedly decreased HDL expression. Patients showed a significant reduction in TC after intravenous immunoglobulin therapy. We observed a significant positive correlation between lipids and inflammatory markers, including TNF-α, IL-1β, erythrocyte sedimentation rate (ESR), white blood cells, monocytes, and neutrophils in GBS. Notably, APOA1 exhibited a negative correlation with ESR. Furthermore, our findings suggest a potential association between lipids and the immune status of GBS.

The research demonstrated a strong connection between lipids and the severity, subtypes, clinical outcomes, precursor infections, clinical symptoms, immunotherapy, inflammation, and immune status of GBS. This implies that a low-fat diet or the use of lipid-lowering medications may potentially serve as an approach for managing GBS, offering a fresh viewpoint for clinical treatment of this condition.

Guillain-Barré syndrome occurs via molecular mimicry when a trigger sets off an immune response on peripheral nerve epitopes. Patients typically report an antecedent infection, such as an upper respiratory infection or Campylobacter jejuni gastroenteritis. It is typically characterized by progressive, symmetric muscle weakness with absent/decreased deep tendon reflexes. Most cases in the literature report that the paralysis begins in the legs distally and ascends to the extremities. Patients may have sensory symptoms or dysautonomia as well. Notable variant forms include acute motor axonal neuropathy, acute motor/sensory neuropathy, Miller Fisher syndrome, and Bickerstaff brainstem encephalitis. Diagnosis is confirmed if a lumbar puncture shows albuminocytologic dissociation (typically 45 to 200 mg/dL). Nerve conduction studies may also be considered but are not necessary. Management is largely supportive, but intravenous immunoglobulin and/or plasmapheresis for more severe cases may be considered.

Guillain-Barré syndrome (GBS) is an acute inflammatory neuropathy. The Erasmus GBS Respiratory Insufficiency Score (EGRIS) and the modified Erasmus GBS Outcome Score (mEGOS) are prognostic models used in the prediction of mechanical ventilation and outcome. Thus far, there are only few biomarkers for the prognosis prediction of GBS patients, and albumin level is one that is promising.

Patients diagnosed with GBS from 2013 to 2022 at Renmin Hospital, Wuhan University, China, were included. Patients hospitalized between 2016 and 2022 underwent short- and long-term follow-ups. The correlations between EGRIS/mEGOS and mechanical ventilation and outcome were evaluated. Serum albumin level was examined the day after admission. Furthermore, we also investigated whether the level of serum albumin was useful in predicting disease severity or poor outcome.

In all, 145 patients were enrolled. Nineteen patients (13.1%) who required mechanical ventilation had higher Hughes GBS disability score (HGDS) at admission and discharge (P < 0.05 and P < 0.0001, respectively), shorter time from onset to admission and treatment (P < 0.01 and P < 0.001, respectively) and longer hospital stays (P < 0.001) than patients who did not require mechanical ventilation. High EGRIS scores were linked with the need for mechanical ventilation (r = 0.427, P < 0.001, AUC = 0.623). Seventy-one patients were admitted between 2016 and 2022. Of these, 65 patients had a 4-week follow-up and 61 had a 6-month follow-up. Higher mEGOS scores at admission and 7 days after admission significantly correlated with short- (P < 0.0001 and P < 0.0001) and long-term (P < 0.05 and P < 0.05) outcomes, respectively. No significant difference in outcome was found between different subtypes (4 weeks [P = 0.099] and 6 months [P = 0.172]). Patients with lower albumin level tended to have higher HGDS (at admission P < 0.05, at nadir P < 0.001, and at discharge P < 0.001) and higher properties of the need of mechanical ventilation (P < 0.05) and ICU stay (P < 0.05) than those with normal albumin levels. Those with low albumin levels were also unable to walk independently at 6 months (P < 0.01).

mEGOS scores predicted the outcomes of GBS patients in China, and EGRIS score predicted the need for mechanical ventilation in these patients. Albumin level at admission correlated well with disease severity and outcomes.

Dysesthesia is an abnormal sensation in the skin that occurs in the absence of any extraordinary stimulus or other primary cutaneous disorders, excluding any delusions or tactile hallucinations. Clinicians have characterized dysesthesias to include sensations such as burning, tingling, pruritus, allodynia, hyperesthesia, or anesthesia. The etiology and pathogenesis of various generalized dysesthesias is largely unknown, though many dysesthesias have been associated with systemic pathologies including malignancy, infection, autoimmune disorders, and neuropathies. Dermatologists are often the first-line clinicians for patients presenting with such cutaneous findings, thus it is crucial for these physicians to be able to methodically work-up generalized dysesthesias to build a working differential diagnosis, follow up with key labs and/or imaging, and offer patients evidence-based treatment to relieve their symptoms. This broad literature review is an attempt to centralize key studies, cases, and series to help guide dermatologists in their assessment and evaluation of complaints of abnormal cutaneous sensations.

Guillain-Barré syndrome (GBS) is the leading cause of non-polio acute flaccid paralysis worldwide, emphasizing the importance of epidemiological studies on this condition. Therefore, well-designed epidemiological studies in different populations can provide a better understanding of the characteristics of patients with GBS and the nature of the disease. To our knowledge, no previous study has attempted to describe the characteristics of patients with GBS in Kingdom of Saudi Arabia (KSA) based on disease subtypes and clinical features in both adult and pediatric patients. This study aimed to assess the frequencies of GBS subtypes and their relationships with patient characteristics and clinical data in a tertiary hospital in Jeddah, KSA.

This was a retrospective review of patients diagnosed with GBS between January 2000 and January 2018 at King Abdulaziz University Hospital (KAUH), a tertiary center in Jeddah, KSA.

In total, 47 patients with GBS (median age: seven years for pediatric and 36 years for adult patients) were included in the current study. There were six male and three female pediatric patients and 19 male and 19 female adult patients. Among patients with GBS who were classified into a specific electrophysiological subtype (n = 28), 13 (46.2%) had acute inflammatory demyelinating polyneuropathy (AIDP), 11 (39%) had an axonal subtype, and four (14%) had Miller Fisher syndrome (MFS). Patients required prolonged hospitalization of approximately 20 ± 22 days (2.83 ± 3.11 weeks). Patients with MFS were more likely to have higher cytoalbuminologic dissociation than those with other subtypes.

AIDP was the most frequent type of GBS, followed by the axonal type. Patients required prolonged hospitalization of approximately 20 ± 22 days (2.83 ± 3.11 weeks). Patients with MFS were more likely to have higher cytoalbuminologic dissociation than those with other subtypes. GBS type did not show a relationship with ICU admission or mechanical ventilation use. There was no association between specific therapies and different GBS subtypes and no significant difference in outcomes between different patterns of clinical presentation. Intravenous immunoglobulin (IVIg) and plasma exchange (PE) treatments both had the same efficacy in relation to outcomes for patients with GBS.

Guillain-Barré syndrome (GBS), an immune-mediated disease of the peripheral nervous system, is mainly characterized by rapidly progressive ascending weakness of the limbs with reduced or absent deep tendon reflexes. The exact cause of GBS is unknown, but it often occurs after a gastrointestinal or respiratory infection. The present study represents a case of GBS in which multiple antecedent antigenic stimuli may have contributed to the development of GBS. The patient, a 28-year-old immunocompetent man with no significant medical history, presented to the emergency department (ED) with acute ascending flaccid paralysis that persisted for a few days. His initial symptoms included tingling in his legs, which started at his shin and calf and developed into numbness, which extended to his upper limbs and arms. A CT scan of the lumbar and cervical spine indicated minor L4-L5 and L5-S1 disc herniation as well as slight bulging in C5-C6 and C7. The patient was discharged but returned to the ED for urgent treatment the next day after he weakened rapidly, losing the ability to walk or maintain balance. Based on his clinical presentation of ascending weakness and generalized hyporeflexia, he was diagnosed with GBS. Abnormal liver function and positive blood tests for anti-cytomegalovirus (anti-CMV) and anti-Epstein-Barr virus (anti-EBV) IgG and IgM antibodies diagnosed hepatitis, CMV, and EBV, respectively. The patient was treated with intravenous immunoglobulin therapy (IVIG; 27 g/day) and antiviral medicine (ganciclovir; 340 mg IV/day) for five days. His nonexistent deep tendon reflexes began to improve two to three days following treatment. He was able to ambulate longer distances with a walker, and his upper extremities regained full strength. This case highlights the importance of a multiple-treatment approach to the treatment of GBS, wherein multiple antigenic triggering factors may be involved.

Rhinolalia aperta (hypernasal speech) is rarely reported in patients with Miller-Fisher syndrome (MFS). Here, we report a patient with MFS who presented with rhinolalia aperta. A 35-year-old man with a history of alcohol abuse and hepatic cirrhosis presented with a three-day acute hypernasal voice change and numbness of both hands/thighs. After admission, the exam also revealed palatal hypomobility, decreased bilateral hand/thigh sensation, ataxic gait, dysmetria, areflexia, and bilateral abducens palsy. Serum immunoglobulin G (IgG) anti-GQ1b antibody titer was elevated (1:6400). A five-day intravenous IgG was administered with a robust clinical response. Oropharyngeal involvement in MFS can initially manifest with isolated hypernasal speech.

Guillain-Barré syndrome is a rare, rapidly progressive, and potentially fatal immune-mediated neuropathy. A 17-year-old male patient with a fever of 38°C developed masticatory impairment a few days later. Although the fever resolved after one week, the restricted mouth opening and decreased bite force persisted. Thirty-five days after disease onset, the patient was referred to our clinic and reported severe masticatory dysfunction due to a significant reduction in maximum bite force (left: 0 N, right: 12.7 N). His maximal mouth opening was 24 mm without jaw deviation. An electrophysiological study revealed Guillain-Barré syndrome (acute motor axonal neuropathy). The patient was closely monitored as he underwent rehabilitation comprising mouth opening and mastication training. The patient's bite force and masticatory impairment due to the weakness of the muscles of mastication gradually improved. At one year and five months after disease onset, the masticatory impairment had fully resolved. His maximum bite force two years after disease onset was 158.3 N on the left side and 172.2 N on the right side.

Guillain-Barré syndrome is an immune-mediated disease of the peripheral nerves characterized by rapidly progressing symmetric weakness, areflexia, and albuminocytological dissociation. Most patients reach their nadir within 2 weeks. Disease severity can be mild to severe, with 20% of patients requiring mechanical ventilation. Intravenous immunoglobulin and plasma exchange are equally effective treatments. Monitoring strength, respiratory function, blood pressure, and heart rate, as well as pain management and rehabilitative therapy are important aspects of management. About 20% of patients require assistance to walk at 6 months. Older age, preceding diarrhea, and lower Medical Research Council (MRC) sum scores predict poor outcome. Death from cardiovascular and respiratory complications can occur in the acute or recovery phases of the illness in 3 to 7% of the patients. Risk factors for mortality include advanced age and disease severity at onset. Neuropathic pain, weakness, and fatigue can be residual symptoms; risk factors for these include axonal loss, sensory involvement, and severity of illness.

In the context of the global vaccination campaign against COVID-19, several cases of postvaccinal Guillain-Barré syndrome (GBS) were reported. Whether a causal relationship exists between these events has yet to be established. We investigated the clinical and electromyographic characteristics of patients who developed GBS after COVID-19 vaccination and compare these with findings in patients with GBS, without a history of recent vaccination. We included 91 cases between March 2020 and March 2022, treated at 10 referral hospitals of Buenos Aires, Argentina. Of these, 46 had received vaccination against COVID-19 within the previous month. Although Medical Research Council sum-scores were similar in both groups (median 52 vs. 50; P = 0.4), cranial nerve involvement was significantly more frequent in the postvaccination group (59% vs. 38%; P = 0.02), as was bilateral facial paralysis (57% vs. 24%; P = 0.002). No differences were found in clinical or neurophysiological phenotypes, although 17 subjects presented the variant of bilateral facial palsy with paresthesias (11 vs. 6; P = 0.1); nor were significant differences observed in length of hospital stay or mortality rates. Future vaccine safety monitoring and epidemiology studies are essential to demonstrate any potential causal relationship between these events.