A Rare Association Between Herpes Simplex Virus Type 1 and Miller-Fisher Syndrome.

The etiopathogenesis for Guillain-Barré syndrome (GBS) and Miller-Fisher syndrome (MFS), a variant of GBS, is well-documented in the literature. However, the association between MFS and an underlying herpes simplex virus type 1 (HSV-1) infection is very limited. We present a unique case of a 48-year-old man who developed diplopia, bilateral ptosis, and gait instability following an acute diarrheal illness and recurring cold sores. The patient was diagnosed with MFS precipitated by recurrent HSV-1 infection following a Campylobacter jejuni acute infection. The diagnosis of MFS was supported by a positive anti-GQ1b ganglioside immunoglobulin (Ig)G and abnormal MRI-enhancing lesions of the bilateral cranial nerves III and VI. Intravenous immunoglobulin and acyclovir produced a significant clinical response in the patient within the first 72 hours. Our case highlights the rare association between two pathogens and MFS and the importance of recognizing risk factors, symptomatology, and appropriate workup accompanying an atypical MFS case.

Ophthalmoplegia associated with anti-GQ1b antibodies: case report and review.

A 60-year-old man with longstanding bilateral asymmetrical ptosis presented with a partial third nerve palsy. His diplopia improved following an ice pack test. He did not report any symptoms related to the coronavirus disease 2019 (COVID-19), and nasopharyngeal swab was negative. Initial head imaging and blood work-up were normal except for a high titer of anti-GQ1b antibodies. The patient was subsequently diagnosed with acute ophthalmoparesis without ataxia which is part of the anti-GQ1b antibody syndrome spectrum. He made a spontaneous recovery over the following months without the need for immunotherapy. Clinical features, pathophysiology and a review of the literature are discussed herein. It is important to consider anti-GQ1b antibody syndrome in patients with symptoms of diplopia, ptosis or suspected ocular myasthenia.

Anti-GQ1b Antibody Syndrome with Visual Impairment: A Retrospective Case Series.

BACKGROUND: Anti-GQ1b antibody syndrome referred to a clinical spectrum characterized by acute onset of ataxia, ophthalmoplegia and areflexia, while visual deterioration was rarely reported in terms of ocular disorders. This study aimed to describe the clinical characteristics of anti-GQ1b antibody syndrome with visual impairment. METHODS: The database at the First Affiliated Hospital of Sun Yat-sen University was searched from 2014 to 2020. Patients with anti-GQ1b IgG were identified and divided into two groups according to the existence of optic neuropathy. Clinical and laboratory data of these subjects between the two groups were collected and analyzed. All patients were followed up by telephone to assess the outcome. RESULTS: A total of 12 patients with seropositive anti-GQ1b antibody were included, 75% of which got antecedent infection. Of these cases, 3 showed visual deterioration accompanied by abnormal orbital magnetic resonance imaging or visual evoked potentials, and the other 9 didn't show any evidence of vision impairment. Patients in the optic neuropathy group presented prominent visual impairments as initial symptoms and were more likely to suffer from facial weakness. There were 4 patients in normal visual acuity group complaining of blurred vision due to intraocular muscle paralysis, which was distinguished by subsequent examination. The combination of glucocorticoids and intravenous immunoglobulin was applied to treat patients with optic neuropathy. CONCLUSIONS: This study provides strong evidence that anti-GQ1b antibody syndrome can exhibit visual impairment, which helps further expand the clinical spectrum of anti-GQ1b antibody syndrome. More attention should be paid to the physical and supplementary ophthalmological examination to explore the pathogenesis and treatment of anti-GQ1b antibody syndrome.

Atypical presentation of an atypical pneumonia: a case report.

BACKGROUND: Neurologic impediments occur in only 0.1% of Mycoplasma pneumoniae infections. Although direct intracerebral infection can occur in these patients, autoimmune-mediated reactions secondary to molecular mimicry are the most common pathophysiology of such neurological complications. These complications include immune-mediated encephalitis, peripheral neuritis such as Guillain-Barré syndrome, and many others. Miller Fisher syndrome is a one of the variants of Guillain-Barré syndrome that has been rarely linked to Mycoplasma pneumoniae infection. It is a condition classically characterized by the triad of ophthalmoplegia, areflexia, and ataxia. Most patients with Miller Fisher syndrome will have positive anti-ganglioside GQ1b antibodies found in their serum, making this autoantibody a very useful serological confirmation parameter. We report a case of a Miller Fisher syndrome in a woman with Mycoplasma pneumoniae infection. To the best of the authors' knowledge, such cases have been only rarely described in literature. CASE PRESENTATION: A 35-year-old Chinese woman presented with sudden onset of double vision and ataxia 5 days after fever and mild flu symptoms. Her Mycoplasma pneumoniae antigen was positive with 1 over 2560 titer of total mycoplasma antibody and presence of immunoglobulin M antibody, suggesting acute infection, and her nerve conduction study revealed mild sensory axonal polyneuropathy with segmental demyelination. the Miller Fischer syndrome variant of Guillain-Barré syndrome secondary to Mycoplasma pneumonia was suspected and later confirmed by presence of serum anti-GQ1b autoantibody. She was treated with intravenous immunoglobulin 0.4 g/kg once daily for 5 days. CONCLUSIONS: The objective of this report is to share a case of an uncommon neurological complication of Mycoplasma pneumoniae infection, to increase the level of suspicion among clinicians that Miller Fischer syndrome can occur as an atypical presentation of an atypical pneumonia.

Case Report: Takotsubo Cardiomyopathy in Bickerstaff Brainstem Encephalitis Triggered by COVID-19.

Takotsubo cardiomyopathy (TCM) is a stress-induced cardiomyopathy triggered by critical illness including severe neurological disorders. However, an association between TCM and Bickerstaff brainstem encephalitis (BBE) has rarely been described. During the current coronavirus disease 2019 (COVID-19) pandemic, growing evidence indicates that COVID-19 often leads to various neurological disorders, but there are few reports of an association between COVID-19 and BBE. Here we report a case of TCM associated with BBE triggered by COVID-19, which subsided with immunotherapy for BBE. Both transthoracic echocardiography and electrocardiography led to early and accurate diagnosis of TCM. Sustained hemodynamic instability due to TCM was immediately lessened with immunotherapy whereas additional plasmapheresis and immunotherapy were required to treat BBE. This case indicates that BBE might follow COVID-19 and TCM should be considered when hemodynamic status remains unstable in a patient with BBE.

Pattern of Extraocular Muscle Involvements in Miller Fisher Syndrome.

BACKGROUND AND PURPOSE: The most-common initial manifestation of Miller Fisher syndrome (MFS) is diplopia due to acute ophthalmoplegia. However, few studies have focused on ocular motility findings in MFS. This study aimed to determine the pattern of extraocular muscle (EOM) paresis in MFS patients. METHODS: We consecutively recruited MFS patients who presented with ophthalmoplegia between 2010 and 2015. The involved EOMs and the strabismus pattern in the primary position were analyzed. Antecedent infections, other involved cranial nerves, and laboratory findings were also reviewed. We compared the characteristics of the patients according to the severity of ophthalmoplegia between complete ophthalmoplegia (CO) and incomplete ophthalmoplegia (IO). RESULTS: Twenty-five patients (15 males and 10 females) with bilateral ophthalmoplegia were included in the study. The most-involved and last-to-recover EOM was the lateral rectus muscle. CO and IO were observed in 11 and 14 patients, respectively. The patients were aged 59.0±18.4 years (mean±SD) in the CO group and 24.9±7.4 years in the IO group (p<0.01), and comprised 63.6% and 21.4% females, respectively (p=0.049). Elevated cerebrospinal fluid protein was identified in 60.0% of patients with CO and 7.7% of patients with IO (p=0.019) for a mean follow-up time from the initial symptom onset of 3.7 days. CONCLUSIONS: The lateral rectus muscle is the most-involved and last-to-recover EOM in ophthalmoplegia. The CO patients were much older and were more likely to be female and have an elevation of cerebrospinal fluid protein than the IO patients.

Pattern of Extraocular Muscle Involvements in Miller Fisher Syndrome

BACKGROUND AND PURPOSE: The most-common initial manifestation of Miller Fisher syndrome (MFS) is diplopia due to acute ophthalmoplegia. However, few studies have focused on ocular motility findings in MFS. This study aimed to determine the pattern of extraocular muscle (EOM) paresis in MFS patients. METHODS: We consecutively recruited MFS patients who presented with ophthalmoplegia between 2010 and 2015. The involved EOMs and the strabismus pattern in the primary position were analyzed. Antecedent infections, other involved cranial nerves, and laboratory findings were also reviewed. We compared the characteristics of the patients according to the severity of ophthalmoplegia between complete ophthalmoplegia (CO) and incomplete ophthalmoplegia (IO). RESULTS: Twenty-five patients (15 males and 10 females) with bilateral ophthalmoplegia were included in the study. The most-involved and last-to-recover EOM was the lateral rectus muscle. CO and IO were observed in 11 and 14 patients, respectively. The patients were aged 59.0±18.4 years (mean±SD) in the CO group and 24.9±7.4 years in the IO group (p<0.01), and comprised 63.6% and 21.4% females, respectively (p=0.049). Elevated cerebrospinal fluid protein was identified in 60.0% of patients with CO and 7.7% of patients with IO (p=0.019) for a mean follow-up time from the initial symptom onset of 3.7 days. CONCLUSIONS: The lateral rectus muscle is the most-involved and last-to-recover EOM in ophthalmoplegia. The CO patients were much older and were more likely to be female and have an elevation of cerebrospinal fluid protein than the IO patients.

Miller-Fisher Syndrome with Blink Reflex Abnormality

No abstract available.

Acute Bilateral Mydriasis and Abducens Nerve Palsy with anti-GQ1b Antibody / 대한소아신경학회지

Ophthalmoplegia without ataxia has various etiologies. An atypical Miller Fisher syndrome implies an ophthalmoplegia without ataxia, areflexia or both. The presence of anti-GQ1b antibody supports the diagnosis of an atypical Miller Fisher syndrome. A 4-year-old Russian girl visited our hospital because of acute bilateral abducens nerve palsy and mydriasis. Although the muscle power of extremities was normal and she didn't show an ataxia, the deep tendon reflex of both knees and ankles was absent. The results of nerve conduction study and cerebrospinal fluid analysis were normal. Magnetic resonance imaging (MRI) showed an enhancement of the bilateral abducens nerve. The anti-Gq1b antibody titer was elevated. The diagnosis of atypical Miller Fisher syndrome was made and a therapy with intravenous immunoglobulins led to the clinical recovery. We report a girl with atypical Miller Fisher syndrome with acute bilateral abducens nerve palsy and mydriasis, diagnosed by of anti-GQ1b antibody positivity.

Acute Ophthalmoplegia Without Ataxia Associated With Anti-GM1 IgG Antibody

No abstract available.

Elevated in Anti-GQ1b and Anti-GT1a IgG Antibody Titers in an Overlap Case of Pharyngeal-Cervical-Brachial Variant of Guillain-Barre Syndrome and Miller-Fisher Syndrome / 대한임상신경생리학회지

No abstract available.

A Patient Presented With Unilateral Abducens Nerve Palsy: A Variant Form of Guillain-Barre Syndrome With Anti-GT1a Antibody

No abstract available.

Miller Fisher syndrome: a rare variant of Guillain-Barré syndrome.

This report describes the case of a 39-year-old male patient who presented to the emergency room with complaints of impaired balance, diplopia, and nasal voice. The patient had a history of upper respiratory tract infection. The initial physical examination revealed ataxia, ophthalmoplegia, and areflexia, which are consistent with the classic triad of Miller Fisher syndrome, considered a benign variant of Guillain-Barré syndrome. The patient developed peripheral facial paralysis during hospitalization. He underwent a treatment with immunoglobulin for five days, resulting in near complete resolution of the ataxia. However, the ophthalmoplegia and areflexia persisted. He was discharged to outpatient follow-up.