Case Of Miller-Fisher Syndrome Research Articles

The Case Files

The Case Files

An unusual case of Miller Fisher syndrome with unilateral 3<sum>rd</sup> nerve palsy and rapid recovery following intravenous immunoglobulin

The Journal of the Ceylon College of Physicians (JCCP) is a peer-reviewed, open access journal published bi-annually by the Ceylon College of Physicians (CCP) in the last week of June and December.The objective of the Journal is to promote good clinical practice and influence policy making across the medical world through publication of original research and peer reviewed articles on current issues and to foster responsible and balanced debate on issues that affect medicine and health care in Sri Lanka. Contributions to the JCCP reflect its national and multidisciplinary readership and include current thinking across a range of medical specialties.

Additional Steroid Therapy for Delayed Facial Palsy in Miller Fisher Syndrome.

Miller Fisher syndrome (MFS) is a variant of Guillain-Barré syndrome. Delayed facial palsy (DFP) is a symptom that occurs after other neurological symptoms begin to recover within four weeks from the onset of MFS. As there have been few detailed reports about DFP in MFS cases treated with additional immunotherapy, we investigated three cases of DFP in MFS treated with additional steroid therapies. The duration of facial palsy in our cases was 12-24 days. No severe adverse effects were observed. Although adverse side effects should be carefully monitored, additional steroid therapy might be a treatment option for MFS-DFP.

Antibodies to Glycolipids in Guillain-Barré Syndrome, Miller Fisher Syndrome and Related Autoimmune Neurological Diseases.

Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) are acute immune-mediated neuropathies, often preceded by an infection. Anti-glycolipid antibodies are frequently detected in patients' sera in the acute-phase. In particular, IgG anti-GQ1b antibodies are positive in as high as 90% of MFS cases. Anti-glycolipid antibodies are useful for the diagnosis of GBS and MFS. In addition, those antibodies may be directly involved in the pathogenetic mechanisms by binding specifically to the regions where the target glycolipid antigen is densely localized. This was proven by the development of animal models of anti-glycolipid antibody-mediated neuropathies. The presence of antibodies that specifically recognize a new conformational epitope formed by two gangliosides (ganglioside complex) in the acute-phase sera of some GBS patients suggested existence of a carbohydrate-carbohydrate interaction between glycolipids. Further intensive research is needed to clarify this point.

A case of Miller Fisher syndrome with delayed onset peripheral facial nerve palsy after COVID-19 vaccination: a case report

BackgroundTo prevent the spread of the novel coronavirus disease 2019 (COVID-19) infection, various vaccines have been developed and used in a large number of people worldwide. One of the most commonly used vaccines is the mRNA vaccine developed by Moderna. Although several studies have shown this vaccine to be safe, the full extent of its side effects has not yet been known. Miller-Fisher syndrome (MFS) is a rare condition that manifests ophthalmoplegia, ataxia, and loss of tendon reflexes. It is a subtype of Guillain–Barré syndrome and an immune-mediated disease related to serum IgG anti-GQ1b antibodies. Several vaccines including those for COVID-19 have been reported to induce MFS. However, there have been no reports of MFS following Moderna COVID-19 vaccine administration.Case presentationA 70-year-old man was referred to our hospital due to diplopia that manifested 1 week after receiving the second Moderna vaccine dose. The patient presented with restricted abduction of both eyes, mild ataxia, and loss of tendon reflexes. He was diagnosed with MFS based on his neurological findings and detection of serum anti-GQ1b antibodies. The patient was administered intravenous immunoglobulin, and his symptoms gradually improved. Five days after admission, the patient showed peripheral facial paralysis on the right side. This symptom was suggested to be a delayed onset of peripheral facial nerve palsy following MFS that gradually improved by administration of steroids and antiviral drugs.ConclusionThere have been no previous reports of MFS after Moderna COVID-19 vaccination. This case may provide new information about the possible neurological side effects of COVID-19 vaccines.

Miller Fisher syndrome following COVID ‐19 vaccines: A scoping review

Background and PurposeMiller Fisher syndrome (MFS), a variant of Guillain–Barré Syndrome (GBS), could be underestimated in evaluations of its adverse events (AEs) following COVID‐19 vaccination. We aimed to identify and characterize MFS following COVID‐19 vaccination.Materials and MethodsRelevant studies reported on during the COVID‐19 pandemic were identified in the MEDLINE, Embase, and other databases.ResultsNine cases of MFS following COVID‐19 vaccination from various regions were included. Unlike MFS following COVID‐19 infection, patients with MFS following COVID‐19 vaccination frequently presented with anti‐GQ1b antibody positivity (44%, 4/9). Unlike GBS following COVID‐19 vaccination, only two of nine (22%) cases of MFS following COVID‐19 vaccination had developed after viral‐vector‐related vaccine administration.ConclusionsMiller Fisher syndrome following COVID‐19 vaccination seems to have a different pathophysiology from MFS following COVID‐19 infection and GBS following COVID‐19 vaccination. This neurological syndrome with a rare incidence and difficulty in diagnosis should be considered an AE of COVID‐19 vaccination.

Guillain-Barré Syndrome and Miller Fisher Syndrome in Association With an Arboviral Outbreak: A Brazilian Case Series.

IntroductionGuillain-Barré syndrome (GBS) in association with arboviruses, such as Zika, chikungunya, and dengue, has been previously documented; however, Miller-Fisher Syndrome (MFS) and other GBS subtypes are rarely reported.MethodsWe identified a series of GBS and MFS cases that were followed during the Zika virus outbreak in Salvador, Brazil (2015–2016). Blood and CSF samples were collected for virus diagnosis. In addition, serological studies to verify previous arboviral infection and electromyography (EMG) were performed.ResultsOf the 14 patients enrolled, 10 were diagnosed with GBS, including three GBS subtypes (two cases of bifacial weakness with paresthesia and one case of paraparetic GBS), and four as MFS. IgM antibodies against one or more of three arboviruses were present in 11 (78.6%) patients: anti-zika IgM positivity in eight (57%), anti-Chikungunya IgM in three (21%), and anti-Dengue in one (7%) individual. A single case was positive for both anti-Dengue IgM and anti-Chikungunya IgM, suggesting co-infection. EMG revealed an AIDP pattern in all nine patients analyzed.ConclusionThe current case series contributes to our knowledge on the clinical presentation of arbovirus-associated GBS and its subtypes, including MFS, and serves as an alert to clinicians and other healthcare professionals in regions affected by arbovirus outbreaks. We highlight the importance of recognizing arboviruses in diagnosing GBS and its subtypes.

A Rare case of Miller Fisher Syndrome with Ophthalmoplegia with Bulbar Palsy with Bifacial Weakness with Progressive Quadriparesi

A 20 years old female came to ED with c/o giddiness since 4 days, headache since 3 days with diplopia with slurring of speech, lower limb weakness, difficulty in swallowing, and dropping of left eyelid since 1 day. Patient had no any pre-existing comorbidity and not on any regular medication. Last menstrual period was on 5 days back. On examination Patient was vitally and haemodynamically stable. Diplopia on right sided distant vision present. Venous blood gas samples showed Hyponatremia. On CNS examination the Glasgow coma scale was 15/15 with power in upper and lower limb 5/5 bilaterally. There was no neck stiffness. Gag reflex present. Patient was taken immediately on symptomatic supportive treatment and admitted in Intensive care unit. Patient was planned for contrast enhanced MRI brain, lumbar puncture for CSF study, chest x-ray, ultrasound whole abdomen. Blood samples for complete haemogram and other relevant blood investigations with serum electrolytes sent for further study.

Miller Fisher syndrome developed after a previous COVID-19 infection (case report)

Miller Fisher syndrome is one of the forms of Guillain–Barrе́ syndrome, characterized by a clinical triad that includes ophthalmoplegia, ataxia and areflexia, with the possible addition of moderate peripheral tetraparesis. During the year that has passed since the start of the pandemic of the new coronavirus infection COVID‑19, international publications have presented a few cases of Miller Fisher syndrome, which developed in patients at different times after the COVID‑19 infection – from 3–5 days to 3 weeks. The article presents a description of a clinical case of Miller Fisher syndrome, which occurred with 34‑year‑old man 21 days after the COVID‑19 infection. The clinical manifestations of Miller Fisher syndrome were typical and included diplopia, areflexia, and ataxia. At the beginning of the disease, there was a transient episode of speech impairment in the form of mild dysarthria. Oculomotor disorders predominated in the clinical picture over other components of the classical triad. On the background of treatment with human immunoglobulin G, there was a complete regression of symptoms.This description of Miller Fisher syndrome, which developed after the postponed infection with COVID‑19, is the first in Russia. The presented case demonstrates the ability of the SARS‑CoV‑2 virus to induce the development of an autoimmune disease. Practitioners should take into account the possibility of Miller Fisher syndrome developing in the event of an acute onset of diplopia, ataxia and areflexia in patients after a previous COVID‑19 infection.

Anti-Ganglioside Antibody Negative Miller Fisher Syndrome with Atypical Features: A Case Report

Miller Fisher Syndrome (MFS), a variant of Guillain Barre Syndrome (GBS), is an immune-mediated neuropathy presenting with the classical clinical triad of ophthalmoplegia, ataxia, and areflexia. Although the clinical triad is the cardinal diagnostic clue, it can also present with a variety of other atypical neurological symptoms and signs beyond the classical triad. IgG anti-GQ1b antibodies are a powerful serological marker for the diagnosis of MFS, however, they can be absent in 10-15% cases of MFS. Here, we are describing a case of a 55-year old lady with an anti-ganglioside negative case of MFS with ptosis and bulbar palsy, who improved with IVIg.

Miller Fisher syndrome associated with COVID-19: an up-to-date systematic review.

Recently, during the pandemic infection of the novel SARS-CoV-2, some cases of Miller Fisher syndrome (MFS) have been reported. We want to summarize the main features of patients with MFS and COVID-19. A PubMed search was performed on 8 October to identify references reporting cases with MFS associated with COVID-19 from the first report of COVID-19 to 8 October 2020 using the following keywords: “Miller Fisher syndrome” AND “COVID-19” OR “SARS-CoV-2”. A systematic review from the first report of coronavirus disease 2019 (COVID-19) to 8 October 2020 revealed 7 cases with Miller Fisher syndrome (MFS) associated with COVID-19. The 7 cases came from 5 countries but most of these patients were from Europe (85.7%), especially Spain. There are 5 cases of MFS diagnosed after the laboratory confirmation of SARS-CoV-2 infection. The mean onset time of MFS-associated neurological symptoms was 14.75 days after the diagnosis of COVID-19. However, the two remaining cases presented initially with MFS-associated neurological symptoms followed by the diagnosis of COVID-19. The most common symptoms of COVID-19-associated MFS were perioral paresthesias (57.1%), ataxia (57.1%), blurred vision (42.9), ophthalmoplegia (42.9), and generalized areflexia (42.9). However, more cohort and case-control studies are required to establish the epidemiological linkage.

Classic and overlapping Miller-Fisher syndrome: clinical and electrophysiological features in Mexican adults.

Classic and overlapping Miller-Fisher syndrome (MFS) have divergent clinical courses. Few studies have addressed the electrophysiological evaluation of MFS patients, most of them carried out in Asia. This work describes and compares their clinical and neurophysiological characteristics. From a Guillain-Barré syndrome (GBS) patient cohort, we made a selection of twenty MFS cases. We defined classic and overlapping MFS, as stated by Wakerley et al. (Nat Rev Neurol 10(9):537-544, 2014). We describe and compare clinical, biochemical, and electrodiagnostic parameters between groups. Seventy-five percent were men, mean age was 42.2 ± 13.6years, and 45% had a Hughes score ≥ 3. MFS/GBS was the most frequent clinical subtype with 50%. Almost one-third had unaltered electrophysiological studies. Comparative analysis between groups showed statistically significant differences in length of stay, dysautonomia presence, and treatment type. Kaplan-Meier survival analysis showed that 100% of the patients had an independent walk at 3months. This study reports Mexican MFS patient's characteristics and represents the most extensive case series in Latin America. We observed a high proportion of overlapping syndromes, a good recovery profile, and no significant severe complications.

Miller Fisher Syndrome Triggered by Infections: A Review of the Literature and a Case Report.

We reported a case of Miller Fisher syndrome following a breakthrough varicella zoster virus infection in an otherwise healthy 6-year-old male. The objective of this review was to summarize the infectious etiologic agents known to trigger Miller Fisher syndrome. Review of the literature on infections associated with Miller Fisher syndrome. We identified 762 studies after duplicates were removed. Titles, abstracts, and full texts were screened. Finally, 37 studies were included in qualitative synthesis after citations and reference list were checked. The age range of cases reported was 0-78 years, and male sex was predominant in studies where these parameters were reported. The most common causative agent was Campylobacter jejuni followed by Haemophilus influenzae. Our review highlights the importance of recognizing the infections triggering Miller Fisher syndrome. We also present a unique case of Miller Fisher syndrome associated with breakthrough varicella zoster virus infection. Preventive policies may consider population immunization for certain causative agents.

Miller Fisher Syndrome in Patients With Severe Acute Respiratory Syndrome Coronavirus 2 Infection: A Systematic Review.

Background and PurposeMiller Fisher syndrome (MFS) is a subtype of Guillain-Barré syndrome characterized by the triad of ophthalmoparesis, areflexia, and ataxia. Although cases of MFS have been associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, no studies have synthesized the clinical characteristics of patients with this condition.MethodsIn this rapid systematic review, we searched the PubMed database to identify studies on MFS associated with SARS-CoV-2 infection.ResultsThis review identified 11 cases, of whom 3 were hospitalized with motor and/or sensory polyneuropathy as the first sign of SARS-CoV-2 infection. SARS-CoV-2 RNA was not detected in analyses of cerebrospinal fluid, suggesting a mechanism of immune-mediated injury rather than direct viral neurotropism. However, antiganglioside antibodies were found in only two of the nine patients tested. It is possible that target antigens other than gangliosides are involved in MFS associated with SARS-CoV-2 infection.ConclusionsThe present patients exhibited clinical improvement after being treated with intravenous immunoglobulin. Although rare, patients with SARS-CoV-2 infection may present neurological symptoms suggestive of MFS. Early recognition of the MFS clinical triad is essential for the timely initiation of treatment.

Ocular Manifestations of Miller Fisher Syndrome: a Case Report

Background:Miller Fisher syndrome (MFS) is a variant of Guillain-Barré syndrome and is characterised by a clinical triad of ophthalmoplegia, ataxia and areflexia.Objectives:This report presents an atypical case of MFS characterized by ocular and gastrointestinal involvement, and anti-ganglioside antibody-positivity.Methods:A 17-year old boy was referred to our ophthalmology emergency room with signs and symptoms of diplopia and upper lid ptosis of the right eye. He underwent a complete ophthalmologic examination with special reference to strabologic status, as well as a neuropediatric examination with serum antiganglioside antibody panel.Results:Strabologic examination showed horisontal diplopia (near and far), ptosis of the upper eyelid on the right and bilateral ophthalmoplegia (limited elevation). Orthoptic examination revealed esotropia of 8 prism dioptres (PD) at near and 18 PD at far distance. A pediatric neurologist found normal limb power, deep tendon reflexes and flexor plantar responses, but attenuated right patellar reflex. Serum anti-GQ1b IgG (+++), anti-GQ1b IgM (++) and anti-GD1a IgM(++) were positive. Positivity of anti-GQ1b IgG antibody confirmed the existence of incomplete MFS. We treated the patient with systemic intravenous immunoglobulins for five days, and after five months of follow-up, all symptoms resolved.Conclusion:MFS can present itself as a wide range of clinical features and its timely recognition is important. Despite the alarming nature of the disease, patients with MFS tend to have a good recovery of presented symptoms, and without any significant residual deficit.

Miller Fisher syndrome in a patient with pulmonary tuberculosis

Miller Fisher syndrome (MFS) is characterized by the acute ophthalmoparesis, ataxia and areflexia. We describe the case of 70-year-old man with cardinal symptom of MFS and active pulmonary tuberculosis (Tb). A thorough evaluation led to the diagnosis of MFS and treatment with intravenous immunoglobulin (IVIg) was started. The complete resolution of ophthalmoparesis and ataxia was observed from the fourth day of IVIg treatment. This is the first report to describe a case of MFS that developed in patient pulmonary tuberculosis. Key Words: Miller Fisher syndrome · Tuberculosis · Guillain-Barré syndrome.

Reader response: Miller Fisher syndrome and polyneuritis cranialis in COVID-19.

We read with interest the report by Gutiérrez-Ortiz et al.1 Starting from the analysis of 2 cases of Miller Fisher syndrome and cranial polyneuritis, the authors propose some hypotheses regarding the pathogenesis of neurologic manifestations during COVID-19. They affirm that there may be a common pathogenesis among all neurologic clinical features of COVID-19, including chemosensitive disorders, which appear frequently in these patients in Europe.

Ataxia and ophthalmoplegia: an atypical case of Miller Fisher Syndrome (MFS) with anti-GAD antibody (4756)

Ataxia and ophthalmoplegia: an atypical case of Miller Fisher Syndrome (MFS) with anti-GAD antibody (4756)

An Overlapping Case of Miller Fisher Syndrome and the Pharyngeal-Cervical-Brachial Variant of Guillain-Barré Syndrome.

A 55-year-old Caucasian male presented initially to the emergency room (ER) reporting myalgia, chills and fever. Physical examination and laboratory tests were unremarkable and he was discharged with symptomatic care. He returned to our ER 2 weeks later reporting dizziness, loss of balance, blurred vision, mild dysarthria and bilateral hand paraesthesia. On examination, he presented complete bilateral ophthalmoplegia, mild dysarthria, left finger-to-nose dysmetria, ataxia, areflexia and bilateral hand hypoaesthesia without fever. Blood tests and head computed tomography were normal. The patient was admitted to the Internal Medicine department. On the second day on the ward, the patient presented dysphagia. A head magnetic resonance angiogram showed no signs of ischaemia or vascular disease and a lumbar puncture was performed but no pleocytosis, albumin-cytological dissociation or hypoglycorrhachia was present. Despite the normal results we suspected a Guillain-Barré syndrome variant, and started treatment with intravenous immunoglobulin (IVIG) at a dose of 400 mg per kilogram which continued for 5 days with immediate neurological improvement. We present a rare overlapping case of Miller Fisher syndrome and the pharyngeal-cervical-brachial variant of Guillain-Barré syndrome.LEARNING POINTSThe overlap of Miller Fisher syndrome and pharyngeal-cervical-brachial variants of Guillain-Barré syndrome are rarely described in the literature but should be considered when multiple cranial nerves are involved with normal neuroimaging results, even with normal cerebrospinal fluid analysis.Due to similar clinical presentation, a misdiagnosis of cerebral ischaemia, botulism or ocular myasthenia gravis can delay treatment and put patients at risk.In its natural history, this syndrome evolves to respiratory arrest and death, but with accurate diagnosis and prompt treatment, the prognosis improves considerably.

Recurrent Miller Fisher syndrome

Miller Fisher syndrome is an acute, self-limiting neurological disorder presenting with thetriad of opthalmoplegia, ataxia and areflexia. It has a worldwide incidence of 0.09% per 100,000 population. The incidence of recurrent Miller Fisher Syndrome is unknown. A 69 year old female presents with 3 episodes of ataxia, opthalmoplegia and hypo to areflexia in 2005, 2015 and 2018. This was associated with dizziness, diplopia, blurring of vision, ptosis, mild motor weakness, sensory loss, dysphonia and urinary retention. Electrodiagnostics were consistent with Miller Fisher syndrome. Patient was given plasmapheresis and had complete remission after 3 to 4 months. Recurrent cases of Miller Fisher syndrome in 2 retrospective studies document 4 out of 28 recurrent cases over a period of 15 years and 4 out of 34 over a period of 12 years. All of these cases had only 1 recurrent episode with a mean age of onset at 22 years old. Antecedent cause is most commonly an upper respiratory tract infection and autonomic and bulbar symptoms are seen in recurrent attacks. Anti-GQ1B antibodies are present in 85–90% of cases of Miller Fisher syndrome. Immuno modulatory treatments like plasmapheresis and Intravenous Immunoglobulin G have shortens the course of the disease. Our case of recurrent Miller Fisher syndrome has typical and atypical features. Studies on prevalence and incidence as well as studies on risk factors that predispose to recurrence are lacking and there are no randomized placebo-controlled trials on its treatment.