Miller Fisher Syndrome Presenting Research Articles

Comments on the case report of “fleeting diplopia and wobbly feet: Miller-Fisher syndrome presenting as bilateral abducent nerve palsy”

Comments on the case report of “fleeting diplopia and wobbly feet: Miller-Fisher syndrome presenting as bilateral abducent nerve palsy”

Fleeting diplopia and wobbly feet: Miller-Fisher syndrome-presenting as bilateral abducent nerve palsy

A case report of a healthy young male, presented with binocular diplopia of sudden onset with mild bilateral abduction limitation, progressed rapidly to near total ophthalmoplegia. Rest of the ophthalmic examination, blood pressure, and magnetic resonance imaging of brain were normal. Basic blood work-up was normal except mildly raised serum triglycerides. He gave a history of mild giddiness and ataxia. Neurological evaluation done showed absent deep tendon reflexes and serum anti-GQ1b antibody was raised. A diagnosis of Miller-Fisher syndrome was made and he was given intravenous immunoglobulin. Post-treatment his ocular motility recovered well, with minimal residual diplopia noted for distance. In individuals with abducent nerve palsy, normal imaging, and no systemic risk factors, a careful history asking for subtle neurological symptoms and a complete central nervous system examination is warranted to rule out conditions like Miller-Fisher syndrome which may not be a familiar entity to many ophthalmologists.

Anti-GD1b-Positive Miller Fisher Syndrome Presenting as Total Ophthalmoplegia

Anti-GD1b-Positive Miller Fisher Syndrome Presenting as Total Ophthalmoplegia

Miller Fisher syndrome presenting with bilaterally impaired adduction in horizontal gaze and dissociated nystagmus of the abducting eyes

AbstractThe patient is a 58‐year‐old woman presenting a 5‐day history of diplopia that started 2 weeks after an upper respiratory tract infection. Neurological examination revealed bilaterally impaired adduction in horizontal gaze with dissociated nystagmus of the abducting eyes, which resembled dissociated nystagmus observed in internuclear ophthalmoplegia (INO). She also exhibited slightly impaired abduction and impaired supraduction in both eyes, right‐sided ptosis, and slight truncal ataxia. There were no abnormal findings on contrast‐enhanced MRI of the brain. The diagnosis of Miller Fisher syndrome was confirmed by positive serum anti‐GQ1b and GT1a antibodies. The patient fully recovered without specific treatment. Impaired adduction in horizontal gaze with dissociated nystagmus of the abducting eye is generally presumed to be indicative of INO, a lesion in the medial longitudinal fasciculus. We presumed that an imbalance between severely restricted adduction and preserved abduction of the opposite eye led to the unique ocular motility disturbances observed in our patient.

Miller-Fisher Syndrome Presenting in an Air Force Recruit with Extensive Maxillary Sinus Disease as Unilateral Ophthalmoplegia (P2.2-109)

Miller-Fisher Syndrome Presenting in an Air Force Recruit with Extensive Maxillary Sinus Disease as Unilateral Ophthalmoplegia (P2.2-109)

Miller fisher syndrome presenting with prodromal thunderclap headache

Objectives We report a case of Miller-Fisher syndrome presenting initially with thunderclap headache. Case A 77 year old male with a history of type 2 diabetes mellitus, hypertension, depression and previous right pontine stroke, presented to our hospital with thunderclap headache and syncope. He reported a brief, non-bloody, diarrhoeal illness five weeks prior but he had otherwise been well. There was recurrent thunderclap headache over the following 24 hours with subsequent vomiting and syncope. He was diagnosed with vagal-induced sinus pause causing syncope. Plain CT brain and CT angiogram were unremarkable. Over the following 48 hours, the patient developed ocular signs, which progressed to complete ophthalmoplegia and complete ptosis. CSF examination was unremarkable (protein 0.30 g/L, acellular). MRI brain, including post-gadolinium enhanced imaging of orbits and cavernous sinus, was unremarkable. Three days after presentation, his reflexes began to diminish in the lower limbs and he developed heel-shin ataxia. The presumptive diagnosis was Miller Fisher syndrome and he was commenced on intravenous immunoglobulin (2 g/kg over three days). Supportive tests returning after initiation of treatment were positive serum anti-GQ1B IgG antibodies and positive stool culture for Campylobacter jejuni . Despite this, the patient’s severe headaches persisted, non-responsive to opiod analgesia and non-steroidal anti-inflammatory agents. Repeat CSF examination was unremarkable, with an opening pressure of 13 cm H2O. Twelve days after initial onset of headache, the patient was trialled on oral nimodipine 60 TDS, with resolution of headache over the following 12 hours. Conclusions Although not radiographically confirmed, we postulate the headache may have been due to reversible cerebral vasoconstriction syndrome (RCVS), given the characteristics of the headache and dramatic response to nimodipine. Although headache is infrequently observed in Miller Fisher syndrome, the exact aetiology is unclear and there has been no previously reported association with RCVS.

Miller Fisher syndrome presenting as palate paralysis

We report a 63-year old patient who presented to our care initially with a hypernasal voice followed by ataxia, ptosis, dysphonia, and paresthesias. The patient's history, physical examination, and additional tests led to a Miller Fisher syndrome (MFS) diagnosis. Palatal paralysis as an inaugurating manifestation of MFS is quite rare and requires special attention from neurologists and otolaryngologists. Although it may present as benign as an acute change in voice, early diagnosis and prompt management may prevent further complications.

G.P.412 - Atypical Miller Fisher syndrome presenting as acute isolated bilateral ophthalmoplegia in young children

G.P.412 - Atypical Miller Fisher syndrome presenting as acute isolated bilateral ophthalmoplegia in young children

PP08.12 – 2493: Atypical Miller Fisher syndrome presenting as acute isolated bilateral ophthalmoplegia: Report of two nex patients with serological specificity

Objective Miller Fisher syndrome (MFS) is an acute polyradiculoneuritis regarded as an uncommon clinical variant of Guillain-Barre syndrome (GBS) asociated with antiGQ 1b positvie serology. MFS is characterized by the acute onset of a clinical triad of ophthalmoplegia, cereballar ataxia and areflexia. Atypical forms of MFS presenting as ophthalmoplegia without ataxia, have been scarcely described. Methods A detailed clinical and serological description of 2 young childhood cases of acute isolated bilateral ophthalmoplegia. Results Case 1 6-year-old boy presented with acute onset of diplopia, ten days after he experienced diarrhea and fever. Neurologic examination showed bilateral isolated sixth nerve palsy, more prominent on the left. Investigations including brain imaging, lumbar puncture and fundoscopic exam were normal. C. jejuni serology showed elevated IgG and IgA. Analysis of anti-ganglioside antibodies by ELISA in serum obtained immediately after admission revealed high levels of anti-GQ1b, anti-GT1a and anti-GD3 IgG and IgM. Case 2 4-year-old boy admitted with limited abduction of both eyes, as well as adduction paresis of the right eye. Two weeks before, the boy suffered from a febrile episode with diarrhea. All investigations carried out on admission were normal. ELISA for anti-ganglioside antibodies was performed on the serum obtained 2 weeks after onset and revealed elevated titers of anti-GQ1b and anti-GT1a IgG and IgM. Serology was positive to C. jejuni. We observed a complete spontaneous resolution 8 weeks after onset in both children. Conclusion The two patients we decribed confirm the rare but possible occurrence of atypical MFS in young children a few weeks following gastrointestinal infection. Identification of high titers of anti-GQ1b IgG associated with positive serology for C. jejuni enabled the diagnosis of atypical MFS. This paper highlights the relevance of measuring serum anti-GQ1b IgG level in the diagnostic work-up of acute isolated ophthalmoplegia of unknown aetiology in a child.

An unusual case of Miller Fisher syndrome presenting with proptosis and chemosis

Miller Fisher syndrome (MFS), a rare variant of Guillan-Barre syndrome, is characterized by ophthalmoplegia, ataxia, and areflexia. In addition to this classic triad, symptoms may include bulbar palsy, weakness, and sensory loss. The anti-GQ1b IgG antibody is a sensitive and specific marker for MFS; it is found in more than 90% of affected patients. We describe an unusual case of MFS that presented with dramatic bilateral proptosis and chemosis.

Familial Miller Fisher Syndrome

Miller Fisher syndrome is an acute inflammatory polyradiculoneuropathy that is generally considered a variant of Guillain-Barré syndrome and is characterized by the clinical triad of ataxia, areflexia, and ophthalmoplegia. Several reports of familial Guillain-Barré syndrome have been reported, indicating a possible underlying genetic and/or environmental predisposition to the development of Guillain-Barré syndrome. A familial association in Miller Fisher syndrome has not previously been described in the literature. We report 2 cases of Miller Fisher syndrome presenting simultaneously in siblings, with a review of recent relevant literature.

Miller Fisher Syndrome Presenting with Pain on Eye Movement

A 19-year-old man noticed a severe tingling pain associated with eye movement six days after the onset of a mild gait disturbance. The pain disappeared when his eyes were still. Physical examination revealed a full range of eye movements (although there was diplopia), mild muscle weakness in the extremities, ataxia, decreased vibration sense and areflexia. Serum anti-GA1 IgG was strongly positive, and anti-GM1 and GQ1b IgG were weakly positive. He was diagnosed with Miller Fisher syndrome and treated with intravenous immunoglobulin, whereupon his symptoms, including the tingling pain, improved within a week.

Headache Associated With Miller Fisher Syndrome

Miller Fisher syndrome, a variant of Guillain-Barre syndrome, is composed of the clinical triad of ophthalmoplegia, ataxia, and areflexia. A variety of other symptoms and signs have been reported in this syndrome, but headache is not a commonly reported symptom. We report a 35-year-old man with anti-GQ(1b) antibody-confirmed Miller Fisher syndrome presenting with severe and persistent headache, and we propose that the headache is caused by antibody-mediated effects on the trigeminovascular pain pathway.

Miller Fisher syndrome: a diagnosis not to be missed

We report a case of Miller Fisher syndrome presenting in an ENT setting. The referral was made on the basis of worsening nasal regurgitation following Campylobacter jejuni enteritis. The aim of this report is not to add to the recorded instances of Miller Fisher syndrome, but to help raise the level of its awareness amongst otolaryngologists. Emphasis is placed on the mode of presentation and management issues, as early diagnosis is crucial and confers a favourable prognosis. In that respect, we consider this case noteworthy and instructive.

Miller Fisher Syndrome Presenting as Pseudotumor

Two female children, ages 9 and 2 years, who presented with pseudotumor cerebri and within 2 to 3 days, were diagnosed with Miller Fisher syndrome are reported from the Hopital Universitaire des Enfants Reine Fabiola, Brussels, Belgium.

Benign intracranial hypertension: atypical presentation of Miller Fisher syndrome?

Acute ocular paresis, nausea, vomiting, and headaches associated with high intracranial pressure without obvious intracranial pathology are typical features of benign intracranial hypertension. We describe two young children whose presentation, initially suggestive of idiopathic or benign intracranial hypertension, evolved to comprise ophthalmoplegia, ataxia, and areflexia. This triad characterizes Miller Fisher syndrome, a clinical variant of Guillain-Barré syndrome that occurs rarely among children. In both patients, this diagnosis was supported by the clinical course and neurophysiologic findings. Plasma serology was positive for Campylobacter jejuni and anti-GQ1b antibodies in one patient and for antimyelin antibodies in the other. This report of two children with Miller Fisher syndrome presenting with intracranial hypertension adds to the findings for a similar patient treated previously, which raises the question concerning the possible role or contribution of benign intracranial hypertension in Miller Fisher syndrome.