Isolated Acute Dysphagia as a Probable Rare Presentation of Guillain-Barré Syndrome with Complete Recovery: A Case Report.

Dysphagia is prevalent among the elderly and can lead to serious complications, often manifesting as a clinical symptom of various neurological or muscular pathologies, including Guillain-Barré Syndrome (GBS). GBS is an acute immune-mediated polyradiculoneuropathy, and dysphagia may arise during its course due to cranial nerve involvement. In rare GBS variants, dysphagia may present as the initial or sole clinical manifestation, posing diagnostic challenges. In this study, we present the case of an elderly female patient with dysphagia, eventually diagnosed with an atypical variant of GBS. Initially, the patient required nasogastric tube feeding; however, complete recovery was achieved through immunotherapy. This case underscores the importance of clinicians conducting thorough evaluations of factors influencing the swallowing mechanism and remaining vigilant about identifying uncommon causative factors. Such approaches enable the implementation of effective disease-modifying therapies, potentially leading to the resolution of dysphagic symptoms.

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

BACKGROUND: Acute 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. METHODS: Clinical 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. RESULTS: We 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. CONCLUSIONS: We 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.

Multiple cerebral infarctions after intravenous immunoglobulin for Guillain-Barré syndrome: two case reports and review of the literature.

Background: Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy mediated by the immune system and is the primary reason for acute flaccid paralysis. Intravenous immunoglobulin (IVIg) is a recognized immunotherapeutic drug that can accelerate recovery from GBS. Limited literature exists concerning cerebral infarction complications with IVIg following its use in the treatment of GBS. Case presentation: A patient was diagnosed with the acute inflammatory demyelinating polyradiculoneuropathy subtype of GBS, while another patient was diagnosed with the acute bulbar palsy variant of GBS 2 years prior and experienced a relapse of GBS. Both patients received immunoglobulin therapy, during which multiple acute cerebral infarctions were detected using magnetic resonance imaging. Both patients had a history of coronary artery atherosclerotic heart disease and vertebral artery stenosis, and D-dimer and fibrinogen degradation products were significantly elevated after immunoglobulin therapy. Conclusions: The risk of cerebral infarction associated with IVIg is generally low in patients with different GBS variants. Nevertheless, the occurrence of cerebral infarction associated with IVIg might not be insignificant in older patients with vascular risk factors and should be carefully monitored.

Anti-GT1a and anti-GQ1b immunoglobulin G antibody positivity with overlapping Miller Fisher/Guillain-Barré syndromes and prominent headache: a case report.

Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) are acute immune-mediated peripheral neuropathies. In addition to their classic presentations, a variety of other signs and symptoms have been reported; however, headache appears to be relatively uncommon. We describe a 53-year-old woman who presented with acute bulbar palsy as the first symptom of overlapping MFS/GBS accompanied by severe headache. The first important clinical impairment of the patient was acute bulbar palsy along with prominent headache, without limb weakness. Although her initial diagnosis was acute bulbar palsy plus, she subsequently developed lower limb diffuse weakness, and her final clinical diagnosis was overlapping MFS/GBS. Anti-ganglioside antibodies were positive for anti-GQ1b and anti-GT1a immunoglobulin G. The patient received intravenous immunoglobulin on day 2 of admission. Early identification of these overlapping syndromes is important for the management of patients, to avoid respiratory failure or severe weakness with axonal degeneration. We therefore remind clinicians of the importance of further examination in patients with headache and acute bulbar palsy of unknown origin.

Guillain-barré syndrome without limb weakness: A rare variant with acute bulbar palsy.

A 76-year-old male was brought to the emergency room with an acute onset of breathlessness and difficulty swallowing. Examination revealed bilateral ptosis, bilateral vocal cord abductor palsy with diaphragmatic paralysis. He did not have any limb weakness. A diagnosis of acute bulbar palsy was made. Cerebrospinal fluid showed albumino-cytological dissociation. Magnetic resonance imaging of the brain (MRI) was normal, and a nerve conduction study (NCS) showed Acute Motor and Sensory Axonal Neuropathy (AMSAN). Guillain-Barré syndrome with acute bulbar palsy was considered. Here, we report a case of suspected Acute Bulbar Palsy plus (ABPp) syndrome. ABPp may be considered as a variant of GBS between the Miller-fisher and Pharyngeal-cervical-brachial variant and does not have any definite limb weakness. This patient also had ABPp with diaphragmatic palsy. However, whether this syndrome is an isolated variant of GBS or a continuum between the Miller-fisher syndrome (MFS) and Pharyngo-cervical brachial (PCB) variants remains to be elucidated. This case is relevant to primary care physicians as the disability with GBS remains high and may render a large burden to carers. The initial symptom of acute dysphagia must lead on the primary care physician to keep this disease in mind to prevent an unwarranted delay in diagnosis.

A Severe Pharyngeal-Sensory-Ataxic Variant of Guillain-Barré Syndrome With Transient Cardiac Dysfunction and a Positive Anti-sulfatide IgM.

Guillain-Barré syndrome (GBS) is a heterogeneous group of acute immune-mediated polyradiculoneuropathy that typically presents with classic axonal or demyelinating sensory-motor type. However, there are variants of GBS with atypical presentation. We report a rare case of severe pharyngeal-sensory-ataxic variant of GBS associated with poor cardiac systolic function, elevated troponin, and positive anti-sulfatide IgM. The sensory symptom atypically started in the hands in an ascending pattern, which progressed to involve the trunk and face and, later, all limbs. It was associated with severe dysphagia, ataxia, and generalized areflexia but with preserved muscle strength in all extremities. Recognizing the atypical pattern of presentation and the ability to perform an accurate clinical localization are the utmost important initial steps in making the diagnosis. The patient showed complete recovery after immunoglobulin therapy.

Case Report: Acute Bulbar Palsy Plus Syndrome: A Guillain-Barré Syndrome Variant More Prone to Be a Subtype Than Overlap of Distinct Subtypes.

Objective: Acute bulbar palsy plus (ABPp) syndrome is a rare regional variant of Guillain-Barré syndrome (GBS) characterized by acute bulbar palsy combined with other cranial symptoms or ataxia without limb and neck weakness. We aim to investigate characteristics of ABPp syndrome and analyze its nosological position within the GBS spectrum. Methods: A patient with ABPp syndrome was reported, and previous case reports of patients who met the criteria for ABPp syndrome from the literature were reviewed. Results: A total of 28 patients were included in our study. Median age was 32 years. Most of the patients (78.6%) were from Asia, and 75.0% had preceding infection. The main accompanying symptoms were ophthalmoplegia (85.7%), facial palsy (60.7%), and ataxia (50.0%). There existed asymmetric weakness in the form of unilateral facial palsy (32.1%) and ptosis (3.6%). Approximately half of the patients had albuminocytological dissociation. All the tested patients were seropositive for antiganglioside antibodies, of which the two most common were immunoglobulin G (IgG) anti-GT1a (77.3%) and anti-GQ1b (59.1%) antibodies. Over one-third of the patients who underwent electrophysiological assessment showed subclinical neuropathy beyond cranial nerves. The outcome was generally favorable as 89.3% of patients made full recovery within 5 months. Conclusion: The hitherto largest case series of ABPp syndrome advances our understanding of this disease. Serologically, the presence of IgG anti-GT1a and anti-GQ1b antibodies predicts and contributes to the disease. Phenotypically, ABPp syndrome is more prone to be a separate subtype of GBS than overlap of distinct subtypes and has the potential to complement current diagnostic framework of GBS.

Acute bulbar palsy plus syndrome: A rare variant of Guillain-Barre syndrome.

Guillain-Barre syndrome (GBS) is the most common cause of acute flaccid paralysis worldwide both in adult and pediatric population. Although flaccid paralysis is the hallmark of this disease, there are some rare variants which may be easily missed unless suspected. Here, we present a very rare variant of GBS - acute bulbar palsy plus syndrome in a pediatric patient. A 13-year-old female child presented with right-sided lower motor neuron type of facial palsy and palsy of bilateral glossopharyngeal and vagus nerve of 2 weeks duration. On detailed neurological examination, motor and sensory system were normal, but the deep tendon reflexes were absent universally. Nerve conduction study showed demyelinating motor neuropathy. Based on typical clinical course and electrophysiological studies, the diagnosis was made. To the best of our knowledge, this is the first pediatric case of unilateral facial palsy with bulbar involvement without any motor abnormality.