Acute ophthalmoplegia in a patient with anti-GQ1b antibody and chronic facial diplegia

2020 ◽  
Vol 13 (7) ◽  
pp. e234319
Author(s):  
Fanny Huynh Du ◽  
Alexan Yerevanian ◽  
Matthew Shtrahman

A 56-year-old man with a remote history of bilateral recurrent facial palsies presented with a week of ophthalmoplegia with intact deep tendon reflexes and lack of ataxia, cerebrospinal fluid with albuminocytologic dissociation and elevated serum anti-ganglioside Q1b (GQ1b) IgG antibody. We diagnosed the patient with acute ophthalmoplegia without ataxia, a condition under the spectrum of anti-GQ1b antibody syndromes which also includes Miller Fisher syndrome. Given the rarity of recurrent facial palsies and anti-GQ1b antibody syndromes as well as reports associating facial palsies and this syndrome, we suggest that our case may be an unusual presentation of an anti-GQ1b antibody syndrome beginning with recurrent facial palsies several years prior to ophthalmoplegia. Prior studies of human nerves provide insight into the pathophysiology, including ganglioside distribution and cross-reactivities underlying the heterogeneity of anti-GQ1b antibody syndromes. This report may expand the differential diagnosis in patients with recurrent facial palsies and broaden the phenotype of anti-GQ1b syndromes.

2016 ◽  
Vol 10 (1) ◽  
pp. 44-45
Author(s):  
Radheshyam Saha ◽  
Suranjit Kumar Saha ◽  
Muhammad Nurul Islam ◽  
Mohammad Rafiqul Kabir ◽  
Aniruddha Mondal ◽  
...  

Miller Fisher Syndrome (MFS) is characterized by acute onset of ophthalmoplegia, ataxia and loss of tendon reflexes with relative sparing of strength in the extremities and trunk. Our patient Mr. Akter Sheikh, 40 years male, non diabetic, non hypertensive, presented with generalized weakness and difficulty in walking for 7 days preceded by a history of respiratory tract infection. After clinical and CSF examination, he was diagnosed as a case of Miller-Fisher syndrome. With treatment he improved significantly.Faridpur Med. Coll. J. Jan 2015;10(1): 44-45


2010 ◽  
Vol 2010 ◽  
pp. 1-4 ◽  
Author(s):  
Theocharis Papanikolaou ◽  
Cath Gray ◽  
Bernard Boothman ◽  
Gerald Naylor ◽  
George Mariatos

Miller-Fisher syndrome (MFS) is a rare condition characterized by the classical triad of ophthalmoplegia, ataxia, and areflexia (Fisher, 1956). It is considered a variant of Guillain-Barré syndrome (GBS) with which it may overlap, or it can occur in more limited forms. We report a case of a thirty-five-year-old male who presented with a six-day history of diplopia, following a recent chest infection. On examination, he was found to have bilateral sixth nerve palsy, bilateral fourth nerve palsy, bilateral areflexical mydriasis, ataxia and total absence of reflexes. After excluding other conditions, a diagnosis of Miller-Fisher syndrome was made. The patient was administered intravenous immunoglobulin and made an uneventful recovery.


2018 ◽  
Vol 57 (14) ◽  
pp. 2057-2060 ◽  
Author(s):  
Tatsuya Ueno ◽  
Ryoya Kimura ◽  
Tomoya Kon ◽  
Rie Haga ◽  
Haruo Nishijima ◽  
...  

2019 ◽  
Vol 48 (3) ◽  
pp. 030006051986749
Author(s):  
Yu-Ming Liu ◽  
Yan-Li Chen ◽  
Yan-Hua Deng ◽  
Yan-Ling Liang ◽  
Wei Li ◽  
...  

Miller Fisher syndrome (MFS), a variant of Guillain–Barré syndrome, is characterized by ataxia, areflexia and ophthalmoplegia. This case report describes a 40-year old male that presented with a 3-day history of unsteady walking and numbness on both hands, and a 2-day history of seeing double images and unclear articulation. Lumbar puncture revealed an opening pressure of 260 mm H2O. Plasma serology was positive for anti-ganglioside M1-immunoglobulin M (anti-GM1-IgM) antibodies and negative for anti-ganglioside Q1b (anti-GQ1b) antibodies. The patient was diagnosed with MFS based on the clinical course and neurophysiological findings. On the 4th day of treatment with intravenous immunoglobulin (IVIG), his ataxia and unsteady walking improved, but his bilateral eyeballs were fixed, and over the next few days he developed bilateral peripheral facial paralysis. After 5 days of IVIG treatment, methylprednisolone treatment was offered and the patient's symptoms gradually improved. Early intracranial hypertension and delayed facial nerve palsy may be atypical presentations of MFS. Anti-GM1-IgM antibodies may be the causative antibodies for MFS. If the IVIG therapy does not stop the progression of the disease, the addition of corticosteroid therapy may be effective. However, the relationship between IgM type, anti-GM1 antibody and MFS remains unclear and requires further research.


2021 ◽  
Vol 14 (11) ◽  
pp. e246701
Author(s):  
Yew Li Dang ◽  
Alexander Bryson

We describe a patient who developed bilateral oculomotor nerve palsy, ataxia, facial diplegia and lower limb weakness 2 weeks post-Oxford-AstraZeneca SARS-CoV2 vaccination, consistent with Miller-Fisher syndrome (MFS) and Guillain-Barre syndrome (GBS) overlap syndrome. Although some features of the patient’s presentation were typical of recently reported cases of a rare GBS variant post-Oxford-AstraZeneca vaccination, including severe facial weakness and a lack of respiratory involvement, to our knowledge this is the first reported case of MFS associated with SARS-CoV2 vaccination. While postvaccination GBS remains rare, it appears to have a favourable prognosis, and recognising this entity is therefore important for patient counselling and monitoring for potential complications.


2019 ◽  
Author(s):  
Neomal Sawanawadu Dilantha De Silva ◽  
Suranga Singhapathirana ◽  
Chintaka Eshan De Silva

Abstract Background : Miller Fisher Syndrome usually presents with complete ophthalmoplegia, areflexia and ataxia. We present an unusual case which presented with unilateral abducens nerve palsy. Case presentation : A 51 year old female patient presented with a history of difficulty in walking and double vision for 1 week which started 2 weeks following an episode of acute gastroenteritis. She didn’t have any bladder bowel incontinence or difficulty in breathing. On examination there was left side abducens nerve palsy and bilateral significant dysmetria. Upper limb and lower limb power was 4/5 with global areflexia. There was no fatigability or sensory deficit. Higher cortical functions were intact with Glasgow Coma Scale of 15/15. Brain stem cerebro vascular accident, alcohol, toxin or drug mediated disease, myasthenia gravis, Bickerstaff encephalitis and Miller-Fisher syndrome were considered as possible differential diagnosis. There was no history of alcohol consumption or any exposure to drugs or toxins. Her Non contrast brain and MRI brain were normal. Nerve conduction study showed asymmetrical sensory motor and F wave abnormalities consistent with a Guillen-Barre Sydrome variant. Cerebro Spinal Fluid analysis showed albumino-cytological dissociation. These findings suggested the diagnosis of Miller-Fisher Syndrome. She was started on plasmaphareis. Her vital parameters, vital capacity and neurological deficit were closely monitored. With 5 cycles of plasmapharesis she made a complete neurological recovery and she was discharged on 16th day of admission. Conclusion: Miller Fisher Syndrome can present as unilateral abducens nerve palsy and early diagnosis and treatment leads to excellent functional outcome.


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