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Introduction: Guillain-Barré syndrome (GBS) is a rare disease that affects almost 0.8-1.9 cases per 100,000 people worldwide every year. This is the most prevalent cause of subacute flaccid paralyzing illness today. It is a subacute inflammatory demyelinating polyradiculoneuropathy; the typical scenario involves ascending symmetrical flaccid paralysis, but in some circumstances, sensory, autonomic, and cranial neuropathy may also be involved. Several vaccines have been found to have complications since the previous century. Numerous case reports of GBS in the literature have been reported following COVID-19 vaccines in recent times. Objective: This study aimed to conduct a comprehensive examination of GBS cases that have been reported after COVID-19 vaccines; to analyze the descriptive statistical analysis of data gathered regarding clinical, laboratory, electrophysiological, and radiological characteristics; to discuss, based on the available evidence, whether the disease has a preference for a particular vaccine type; and to speculate on the potential pathogenesis. Methodology: This review has been carried out by recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Result: Reviewing 60 case reports illustrated that most of them are from the USA (18.1%) and the majority of affected individuals were males (60%). The results favored the association between vector-based SARS-CoV-2 vaccine, particularly AstraZeneca vaccine, and the GBS. The mean of symptoms onset is 11.4 days. The results of diagnostic tests such as LP are consistent mostly with albumin-cytological dissociation (81.81%), where brain and spine MRI was unremarkable in 59.52%. Regarding electrodiagnostic tests, AIDP is the most common variant (61.81%). The management was not consistent among the case reports. However, IVIG is the most frequent way of treating these patients (68.33%). The functional outcome was documented in 47 patients; 65% improved with medical management. Conclusion: This study aimed to conduct a systematic review of reported cases of GBS following COVID-19 vaccines and descriptive statistical analysis of collected data on clinical, laboratory, electrophysiological, and radiological features, to discuss, based on available results, whether the disease has a predilection to a specific vaccine type and to speculate the potential pathogenesis. [ABSTRACT FROM AUTHOR]

IntroductionGuillain–Barré syndrome (GBS) is a rare disease that affects almost 0.8–1.9 cases per 100,000 people worldwide every year. This is the most prevalent cause of subacute flaccid paralyzing illness today. It is a subacute inflammatory demyelinating polyradiculoneuropathy; the typical scenario involves ascending symmetrical flaccid paralysis, but in some circumstances, sensory, autonomic, and cranial neuropathy may also be involved. Several vaccines have been found to have complications since the previous century. Numerous case reports of GBS in the literature have been reported following COVID-19 vaccines in recent times.ObjectiveThis study aimed to conduct a comprehensive examination of GBS cases that have been reported after COVID-19 vaccines; to analyze the descriptive statistical analysis of data gathered regarding clinical, laboratory, electrophysiological, and radiological characteristics; to discuss, based on the available evidence, whether the disease has a preference for a particular vaccine type; and to speculate on the potential pathogenesis.MethodologyThis review has been carried out by recommendations of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.ResultReviewing 60 case reports illustrated that most of them are from the USA (18.1%) and the majority of affected individuals were males (60%). The results favored the association between vector-based SARS-CoV-2 vaccine, particularly AstraZeneca vaccine, and the GBS. The mean of symptoms onset is 11.4 days. The results of diagnostic tests such as LP are consistent mostly with albumin-cytological dissociation (81.81%), where brain and spine MRI was unremarkable in 59.52%. Regarding electrodiagnostic tests, AIDP is the most common variant (61.81%). The management was not consistent among the case reports. However, IVIG is the most frequent way of treating these patients (68.33%). The functional outcome was documented in 47 patients; 65% improved with medical management.ConclusionThis study aimed to conduct a systematic review of reported cases of GBS following COVID-19 vaccines and descriptive statistical analysis of collected data on clinical, laboratory, electrophysiological, and radiological features, to discuss, based on available results, whether the disease has a predilection to a specific vaccine type and to speculate the potential pathogenesis.

While monocyte to high-density lipoprotein cholesterol ratio (MHR) has been reported to be associated with nervous system lesions, the role of MHR has not been determined in patients with Guillain-Barré Syndrome (GBS). The purpose of our study was to explore the role of MHR in patients with GBS. A total of 52 GBS patients were involved in the study retrospectively, including patients with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), and acute motor sensory axonal neuropathy (AMSAN). We used Hughes Functional Grading Scale (HFGS) score to evaluate functional status in GBS patients. Among patients with different subtypes of GBS, MHR was significantly elevated in those with demyelination compared to patients without demyelination (p < 0.001); AIDP patients had an increased MHR compared with AMAN or AMSAN patients (p = 0.001; p = 0.013). There was a positive correlation between MHR and HFGS score (r = 0.463, p = 0.006) in AIDP patients, but not in AMAN or AMSAN. Multiple linear regression analysis revealed that MHR was independently associated with HFGS score (beta = 0.405, p = 0.013) in AIDP patients. Our study suggests that MHR as an inflammatory marker is elevated in patients with AIDP compared to AMAN or AMSAN patients, while MHR has a positive correlation with clinical severity in AIDP patients, suggesting that MHR may provide an additional information to reflect the pathophysiology of AIDP. [ABSTRACT FROM AUTHOR]

We initially described two children who developed Guillain-Barré syndrome (GBS) complicated by rhabdomyolysis (RML), and reviewed five adult patients from the literature. Through analysis of the clinical features, laboratory examination, treatment and prognostic data from these seven patients, we found that when GBS “meets” RML, the most prominent characteristics were the following: male dominance; limb weakness, pain and respiratory failure could be caused by multiple factors; limb weakness and respiratory muscle paralysis were more serious than with GBS alone; and the probability of mechanical ventilation was increased. Neuroelectrophysiological studies revealed axonal lesions. Close monitoring and timely identification and intervention to remedy potentially fatal complications such as electrolyte disorder multisystem complications and kidney injury are crucial. With plasma exchange, peritoneal dialysis and supportive treatment, the long-term outcome of most patients was satisfactory.

Introduction: Guillain-Barré syndrome (GBS) has been classified into demyelinating and axonal subtypes or forms, such as acute motor axonal neuropathy (AMAN) and regional pharyngeal-cervical-brachial variant (PCBv). Objective: To study the relationship between motor nerve conduction blocks (CBs) and prognosis in AMAN and PCBv. Patients and Methods: We retrospectively analyzed six cases of AMAN and PCBv with serial nerve conduction studies (NCS) and electromyography (EMG). Results: The serial NCS (1st−2nd and 3rd week) showed, as the most constant data, a decreased amplitude of the compound muscle action potential (CMAP) in 100% of cases. CBs were present in 66.6% of cases. EMG (3rd week) showed signs of severe denervation in 33.3%. All patients were treated from the 1st−2nd week of evolution with intravenous immunoglobulins (IVIGs). Patients with CBs (1st−2nd and 3rd week), showed reversible CBs or reversible conduction failure (RCF) and complete recovery at 1 month. Patients without CBs, with persistent reduced distal CMAP amplitude (dCMAP), showed severe acute denervation due to axonal degeneration (3rd week and 1st−3rd month) and a slow recovery of several months. Conclusions: Not all axonal forms of GBS have a poor prognosis. This study of AMAN and PCBv shows that patients with CBs can have reversible CBs or RCF, and good prognosis. Patients without CBs, with persistent reduction of dCMAP amplitude decrement, have severe acute denervation, and a worse prognosis. AMAN and PCBv have a continuous spectrum ranging from CBs due to dysfunction/disruption of Nodes of Ranvier, called nodopathies, with reversible CBs or RCF and good prognosis, to axonal degeneration with worse prognosis. [ABSTRACT FROM AUTHOR]

Introduction:Guillain-Barré syndrome (GBS) has been classified into demyelinating and axonal subtypes or forms, such as acute motor axonal neuropathy (AMAN) and regional pharyngeal-cervical-brachial variant (PCBv).ObjectiveTo study the relationship between motor nerve conduction blocks (CBs) and prognosis in AMAN and PCBv.Patients and MethodsWe retrospectively analyzed six cases of AMAN and PCBv with serial nerve conduction studies (NCS) and electromyography (EMG).ResultsThe serial NCS (1st−2nd and 3rd week) showed, as the most constant data, a decreased amplitude of the compound muscle action potential (CMAP) in 100% of cases. CBs were present in 66.6% of cases. EMG (3rd week) showed signs of severe denervation in 33.3%. All patients were treated from the 1st−2nd week of evolution with intravenous immunoglobulins (IVIGs). Patients with CBs (1st−2nd and 3rd week), showed reversible CBs or reversible conduction failure (RCF) and complete recovery at 1 month. Patients without CBs, with persistent reduced distal CMAP amplitude (dCMAP), showed severe acute denervation due to axonal degeneration (3rd week and 1st−3rd month) and a slow recovery of several months.ConclusionsNot all axonal forms of GBS have a poor prognosis. This study of AMAN and PCBv shows that patients with CBs can have reversible CBs or RCF, and good prognosis. Patients without CBs, with persistent reduction of dCMAP amplitude decrement, have severe acute denervation, and a worse prognosis. AMAN and PCBv have a continuous spectrum ranging from CBs due to dysfunction/disruption of Nodes of Ranvier, called nodopathies, with reversible CBs or RCF and good prognosis, to axonal degeneration with worse prognosis.

Introduction: Motor nerve conduction blocks (CBs) could be detected in both acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). We aimed to identify the correlation between CBs and functional outcome in the two subtypes of GBS.Methods: Motor nerve conduction studies were performed in 17 patients with AIDP and 23 with AMAN. All patients were treated with intravenous immunoglobulin, and their disabilities were evaluated with Hughes functional grading scale before treatment, 1 month and 6 months after onset.Results: AMAN with CBs had higher reduction of Hughes grade (indicating more improved outcomes) at 1 month (1.71 ± 0.83 vs. 1 ± 0.67, p = 0.034) than AIDP with CBs. AMAN with CBs had higher reduction of Hughes grade at 1 month (1.71 ± 0.83 vs. 0.56 ± 0.73, p = 0.002) than AMAN without CBs. The reduction of Hughes grade at 1 month showed no significant difference between AIDP with and without CBs.Discussion: Motor nerve CBs in AMAN indicated better prognosis than in AIDP.

Guillain–Barré syndrome (GBS) is an acute peripheral neuropathy that develops as a result of post-infectious immune-mediated nerve injury. It can be classified into classic and variant GBS. Acute motor axonal neuropathy (AMAN) is a subtype of GBS with the key clinical features of pure motor weakness, areflexia, absence of sensory symptoms, and lack of neurophysiologic evidence of demyelination. We reported a case of acute motor axonal neuropathy in association with hepatitis E infection. A young woman was referred to us after a period of nausea, fever, and diarrhea. She had unexplained muscle weakness at admission and has been diagnosed with acute hepatitis E infection. A rigorous clinical neurological assessment revealed bilateral symmetrical weakness, which affects the lower limbs more than the upper limbs, with no evidence of sensory involvement. Neurophysiological measurements indicated acute axonal injury without clues to demyelination. A diagnosis of acute motor axonal neuropathy subtype has been made, to which she only received supportive therapy. The symptoms resolved spontaneously and full recovery of motor function was attained after 35 days of weakness onset with complete normalization of neurophysiologic parameters.

We describe a case report of fulminant Guillain-Barré syndrome mimicking brain death. A previously healthy 60-year-old male was admitted to the neurointensive care unit after developing rapidly progressive weakness and respiratory failure. On presentation, the patient was found to have absent brainstem and spinal cord reflexes resembling that of brain death. Acute motor axonal neuropathy (AMAN), a subtype of Guillain-Barré syndrome, was diagnosed by cerebrospinal fluid and nerve conduction velocity testing. An electroencephalogram showed that the patient had normal, appropriately reactive brain function. Transcranial Doppler ultrasound showed appropriate blood flow to the brain. Guillain-Barré syndrome rarely presents with weakness so severe as to mimic brain death. This article provides a review of similar literature. This case demonstrates the importance of performing a proper brain death examination, which includes evaluation for irreversible cerebral injury, exclusion of any confounding conditions, and performance of tests such as electroencephalography and transcranial dopplers when uncertainty exists about the reliability of the clinical exam.

We describe a case report of fulminant Guillain-Barré syndrome (GBS) mimicking brain death. A previously healthy 60-year-old male was admitted to the neurointensive care unit after developing rapidly progressive weakness and respiratory failure. On presentation, the patient was found to have absent brainstem and spinal cord reflexes resembling that of brain death. Acute motor axonal neuropathy, a subtype of GBS, was diagnosed by cerebrospinal fluid and nerve conduction velocity testing. An electroencephalogram showed that the patient had normal, appropriately reactive brain function. Transcranial Doppler (TCD) ultrasound showed appropriate blood low to the brain. GBS rarely presents with weakness so severe as to mimic brain death. This article provides a review of similar literature. This case demonstrates the importance of performing a proper brain death examination, which includes evaluation for irreversible cerebral injury, exclusion of any confounding conditions, and performance of tests such as electroencephalography and TCDs when uncertainty exists about the reliability of the clinical exam. [ABSTRACT FROM AUTHOR]