gq1b-ganglioside and Diplopia

Topics: Autoantibodies; COVID-19; Diplopia; Female; Gangliosides; Humans; Immunoglobulins, Intravenous; Miller Fisher Syndrome; Movement Disorders; SARS-CoV-2; Speech Disorders; Video Recording; Young Adult

Topics: Action Potentials; Aged; Asymptomatic Diseases; Ataxia; Autoantibodies; Blepharoptosis; Calcium Channels, P-Type; Calcium Channels, Q-Type; Diplopia; Electrodiagnosis; Electromyography; Female; Gangliosides; Humans; Hypesthesia; Lambert-Eaton Myasthenic Syndrome; Median Nerve; Miller Fisher Syndrome; Muscle Weakness; Mydriasis; Neural Conduction; Oculomotor Muscles; Tibial Nerve; Ulnar Nerve

Acute ophthalmoparesis without ataxia was designated as 'atypical Miller Fisher syndrome' as it presents with progressive, relatively symmetrical ophthalmoplegia, but without ataxia nor limb weakness, in the presence of anti-GQ1b antibody. Idiopathic intracranial hypertension is characterized by signs of raised intracranial pressure occurring in the absence of cerebral pathology, with normal composition of cerebrospinal fluid and a raised opening pressure of more than 20 cmH. A 28-year-old gentleman with body mass index of 34.3 was referred to us for management of double vision of 2 weeks duration. His symptom started after a brief episode of upper respiratory tract infection. His best corrected visual acuity was 6/6 OU. He had bilateral sixth nerve palsy worse on the left eye and bilateral hypometric saccade. His deep tendon reflexes were found to be hyporeflexic in all four limbs. No sensory or motor power deficit was detected, and his gait was normal. Plantar reflexes were downwards bilaterally and cerebellar examination was normal. Both optic discs developed hyperaemia and swelling. Magnetic resonance imaging of brain was normal and lumbar puncture revealed an opening pressure of 50 cmH. Acute ophthalmoparesis without ataxia can present with co-occurrence of raised intracranial pressure. It is important to have a full fundoscopic assessment to look for papilloedema in patients presenting with Miller Fisher syndrome or acute ophthalmoparesis without ataxia.

Topics: Abducens Nerve Diseases; Acetazolamide; Acute Disease; Administration, Oral; Adult; Ataxia; Autoantibodies; Diplopia; Diuretics; Gangliosides; Humans; Immunoglobulin G; Magnetic Resonance Imaging; Male; Ophthalmoplegia; Ophthalmoscopy; Pseudotumor Cerebri

Topics: Adult; Ataxia; Autoantibodies; Autoantigens; Autoimmune Diseases; Brain Stem; Cognitive Dysfunction; Diplopia; Encephalitis; Female; Gangliosides; Humans

Miller Fisher syndrome is defined by a triad of symptoms, namely areflexia, ataxia, and ophthalmoparesis. The ophthalmoparesis is mostly severe, undulating weakness of eye movements with ptosis and increased fatigability resembling a neuromuscular transmission disorder. We present a 52-year-old man with severe Miller Fisher syndrome with a high level of anti-GQ1b antibodies and a presynaptic type of neuromuscular transmission disorder. The diagnosis was confirmed by stimulated single-fiber electromyography with the use of a concentric needle electrode and various stimulation rates.

Topics: Ataxia; Autoantibodies; Diplopia; Electromyography; Evoked Potentials, Somatosensory; Gangliosides; Humans; Male; Middle Aged; Miller Fisher Syndrome; Neuromuscular Junction Diseases; Ophthalmoplegia; Reflex, Abnormal

Reported herein is an adult case of Fisher syndrome (FS) that occurred as a complication during the course of community-acquired pneumonia caused by Mycoplasma pneumoniae. A 38-yr-old man who had been treated with antibiotics for serologically proven M. pneumoniae pneumonia presented with a sudden onset of diplopia, ataxic gait, and areflexia. A thorough evaluation including brain imaging, cerebrospinal fluid examination, a nerve conduction study, and detection of serum anti-ganglioside GQ1b antibody titers led to the diagnosis of FS. Antibiotic treatment of the underlying M. pneumoniae pneumonia was maintained without additional immunomodulatory agents. A complete and spontaneous resolution of neurologic abnormalities was observed within 1 month, accompanied by resolution of lung lesions.

Topics: Adult; Anti-Bacterial Agents; Antibodies; Diplopia; Erythrocyte Count; Gangliosides; Humans; Lung; Male; Miller Fisher Syndrome; Pneumonia, Mycoplasma; Tomography, X-Ray Computed

Miller Fisher syndrome is a clinical variant of Guillain-Barré syndrome, characterized by acute-onset ophthalmoplegia, ataxia, and areflexia. It results from an immune response to a cross-reactive antigen between GQ1b ganglioside in human neurons and lipo-oligosaccharides of certain bacteria, e.g., Campylobacter jejuni. Anti-GQ1b antibody is a powerful diagnostic marker for Miller Fisher syndrome. However, only a small number of anti-GQ1b-negative Miller Fisher syndrome cases are documented. A 13-year-old boy demonstrated typical clinical features of Miller Fisher syndrome 1 week after C. jejuni enteritis, but was anti-GQ1b and anti-GM1b antibody-negative.

Topics: Ataxia; Blepharoptosis; Campylobacter Infections; Campylobacter jejuni; Child; Diplopia; G(M1) Ganglioside; Gangliosides; Humans; Male; Miller Fisher Syndrome; Neurologic Examination; Reflex

PURPOSE.: Miller Fisher syndrome (MFS) is a rare immune-mediated neuropathy that commonly presents with diplopia after the acute onset of complete bilateral external ophthalmoplegia. Ophthalmoplegia is often accompanied by other neurological deficits such as ataxia and areflexia that characterize MFS. Although MFS is a clinical diagnosis, serological confirmation is possible by identifying the anti-GQ1b antibody found in most of the affected patients. We report a patient with MFS who presented with clinical signs suggestive of ocular myasthenia gravis but in whom the correct diagnosis was made on the basis of serological testing for the anti-GQ1b antibody. CASE REPORT.: An 81-year-old white man presented with an acute onset of diplopia after a mild gastrointestinal illness. Clinical examination revealed complete bilateral external ophthalmoplegia and left-sided ptosis. He developed more marked bilateral ptosis, left greater than right, with prolonged attempted upgaze. He was also noted to have a Cogan lid twitch. Same day evaluation by a neuro-ophthalmologist revealed mild left-sided facial and bilateral orbicularis oculi weakness. He had no limb ataxia but exhibited a slightly wide-based gait with difficulty walking heel-to-toe. A provisional diagnosis of ocular myasthenia gravis was made, and anticholinesterase inhibitor therapy was initiated. However, his symptoms did not improve, and serological testing was positive for the anti-GQ1b immunoglobulin G antibody, supporting a diagnosis of MFS. CONCLUSIONS.: Although the predominant ophthalmic feature of MFS is complete bilateral external ophthalmoplegia, it should be recognized that MFS has variable associations with lid and pupillary dysfunction. Such confounding neuro-ophthalmic features require a thorough history, neurological examination, neuroimaging, and serological testing for the anti-GQ1b antibody to arrive at a diagnosis of MFS.

Topics: Aged, 80 and over; Antibodies; Diagnosis, Differential; Diplopia; Eye Movements; Gangliosides; Humans; Magnetic Resonance Imaging; Male; Miller Fisher Syndrome; Myasthenia Gravis

Ophthalmoplegia without ataxia, areflexia or both has been designated as atypical Miller Fisher syndrome (MFS) or acute ophthalmoplegia (AO). This entity, first reported by Chiba et al. is associated with anti-GQ1b IgG antibodies.We report a patient with isolated acute ophthalmoplegia with high titer of anti-GQ1b IgG antibody activity in the acute phase in whom treatment with intravenous immunoglobulin (IVIg) led to the clinical recovery and the decrease in antibody titer.

Topics: Acute Disease; Adult; Blepharoptosis; Diplopia; Enzyme-Linked Immunosorbent Assay; Female; Gangliosides; Humans; Immunoglobulin G; Immunoglobulins, Intravenous; Miller Fisher Syndrome; Neural Conduction; Neurologic Examination

Topics: Acute Disease; Adult; Autoantibodies; Autonomic Nervous System Diseases; Blepharoptosis; Bradycardia; Cranial Nerve Diseases; Cranial Nerves; Diplopia; Disease Progression; Early Diagnosis; Gangliosides; Humans; Immunoglobulins, Intravenous; Male; Miller Fisher Syndrome; Oculomotor Nerve Diseases; Ophthalmoplegia; Respiratory Tract Infections; Treatment Outcome; Vagus Nerve Diseases; Virus Diseases

Miller Fisher Syndrome (MFS) is the most frequent variant of the Guillain-Barré Syndrome. It is characterised by the classic triad of ophthalmoplegia, ataxia and areflexia. We present a case of a patient who developed these clinical findings 5 days after flu vaccination.. Miller Fisher Syndrome is an unusual condition seen in ophthalmologic clinical practice. Although respiratory and digestive infections have been reported as antecedent infectious agents in MFS, it has not previously been described in relation to the flu vaccine.

Topics: Antibody Specificity; Autoantibodies; Autoantigens; Diplopia; Facial Paralysis; Gait Disorders, Neurologic; Gangliosides; Humans; Immunoglobulins, Intravenous; Influenza Vaccines; Male; Middle Aged; Miller Fisher Syndrome; Nausea; Ophthalmoplegia; Respiration Disorders

Miller Fisher syndrome (MFS) is a rare and usually monophasic polyradiculoneuropathy characterised by ophthalmoplegia, decreased or absent tendon reflexes, and ataxia. The objective of this study was to report a case of recurrent MFS with a clinical presentation virtually indistinguishable from botulism. The patient was a young man with two episodes of increasing external ophthalmoplegia, ptosis, and ataxia with a long asymptomatic interval in between. The second episode occurred after consumption of rotten fish and was accompanied by gastrointestinal symptoms and an anticholinergic syndrome. Very rarely, MFS can present with a recurrent course. The importance of this case of recurrent MFS lies not only in its long asymptomatic period and identical clinical presentation, but also in its instructiveness regarding the differential diagnosis of MFS, particularly life-threatening botulism.

Topics: Acute Disease; Adult; Autoantibodies; Botulism; Diagnosis, Differential; Diplopia; Gangliosides; Humans; Male; Miller Fisher Syndrome; Recurrence

Topics: Adult; Autoantibodies; Campylobacter Infections; Diarrhea; Diplopia; Enteritis; Gangliosides; Humans; Male; Miller Fisher Syndrome; Oculomotor Muscles; Oculomotor Nerve; Oculomotor Nerve Diseases; Ophthalmoplegia

To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin G (IgG) antibody.. Retrospective observational case series.. Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG.. Clinical features of 21 subjects with AO were analyzed.. Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three.. Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of Miller Fisher syndrome or a regional variant of Guillain-Barré syndrome.

Topics: Abducens Nerve Diseases; Acute Disease; Adolescent; Adult; Aged; Autoantibodies; Autoimmune Diseases; Campylobacter Infections; Campylobacter jejuni; Child; Diplopia; Female; Gangliosides; Gastrointestinal Diseases; Humans; Immunoglobulin G; Male; Middle Aged; Miller Fisher Syndrome; Ophthalmoplegia; Paresthesia; Retrospective Studies

To describe two cases with bilateral abducens nerve paresis associated with serum anti-GQ1b IgG antibody.. Case reports.. Two boys, aged 12 and 10 years, experienced acute onset of diplopia after preceding symptoms and signs of infection. In both boys, examination showed only bilateral abducens nerve paresis. Although routine laboratory data and magnetic resonance imaging demonstrated no pathologic findings, titer of anti-GQ1b IgG antibody in the sera of both patients was increased. Diplopia and signs of bilateral abducens nerve paresis disappeared in 6 weeks without any specific treatment.. The anti-GQ1b IgG antibody in the sera of both patients probably contributed to the bilateral abducens nerve paresis.

Topics: Abducens Nerve Diseases; Antibodies; Child; Diplopia; Eye Movements; Gangliosides; Humans; Immunoglobulin G; Infections; Male; Remission, Spontaneous