key: cord-1045988-4may4joi
authors: Faulkner, Dr L.; Scott, Dr S.; Flint, Dr NJ.
title: Miller-Fisher syndrome associated with SARS-CoV-2: a case report
date: 2022-02-28
journal: Microbes Infect
DOI: 10.1016/j.micinf.2022.104954
sha: 31d5fb1d1fdb60ce8f81d04e6c868e6401ff7037
doc_id: 1045988
cord_uid: 4may4joi

SARS-CoV-2 infections are increasingly associated with neurological complications, including immune-mediated neuropathies. Miller-Fisher syndrome is a rare variant of Guillain-Barré syndrome characterised by the triad of ataxia, ophthalmoplegia and areflexia. Here we present a case of Miller-Fisher syndrome following COVID-19 infection. The clinical presentation was a short history of a rapidly-progressive peripheral sensorimotor neuropathy with bulbar dysfunction and facial weakness following mild COVID infection. Examination revealed global areflexia and a broad-based ataxic gait. CSF analysis revealed albuminocytological dissociation and neurophysiological testing later supported the diagnosis. The patient required high flow nasal oxygen therapy for respiratory dysfunction in a level 2 care setting and received immunological treatment with intravenous immunoglobulins. We conclude that Miller-Fisher syndrome needs to be considered in patients presenting with new sensorimotor dysfunction following SARS-COV-2 infection. Early recognition is key given the propensity to cause life-threatening respiratory failure, and early administration of immunological treatment is associated with improved prognosis.

with bulbar dysfunction and facial weakness following mild COVID infection. Examination 23 revealed global areflexia and a broad-based ataxic gait. CSF analysis revealed 24 albuminocytological dissociation and neurophysiological testing later supported the diagnosis. 25 The patient required high flow nasal oxygen therapy for respiratory dysfunction in a level 2 26 care setting and received immunological treatment with intravenous immunoglobulins. 27 We conclude that Miller-Fisher syndrome needs to be considered in patients presenting with 28 new sensorimotor dysfunction following SARS-COV-2 infection. Early recognition is key given 29 the propensity to cause life-threatening respiratory failure, and early administration of 30 immunological treatment is associated with improved prognosis.

Two weeks prior to admission, the patient experienced a persistent, productive cough without 61 anosmia or dysgeusia. Community testing with nasopharyngeal PCR confirmed SARS-CoV-2 62 infection.

Neurological symptoms began with symmetrical paraesthesia of the hands, feet and mouth, 65 followed by ascending lower limb weakness. On attending hospital, he was noted to have a 66 broad-based ataxic gait and required assistance to walk. Symptoms continued to progress 67 following admission, with sensory loss spreading to mid-shins in the lower limbs, and to mid- Baseline laboratory blood tests included full blood count, liver function, renal function and 84 bone profile. Thyroid function, haematinics, blood borne virus screening, lipid profile, γGT, 85 ammonia and magnesium levels were also tested during admission, all of which were within 86 reference ranges. The only laboratory investigation of note was hypokalaemia (2.7 mmol l -1 ) 87 at presentation, probably due to long-term diuretic therapy. Intravenous fluid with potassium 88 was administered in the Emergency Department with no resolution of symptoms. A number of differential diagnoses for the initial sensorimotor disturbance were considered.

The patient did not have diabetes mellitus, a significant alcohol history or any neurological family history, and the rapid onset of symptoms suggested these to be unlikely causes. Early 

The authors have no conflicts of interest to declare 259 J o u r n a l P r e -p r o o f

No acute infarction, intracranial haemorrhage or mass lesion.

Normal ventricles and basal cisterns.

The proximal flow voids are present.

There are spondylitic changes from C3/4 to C6/7. At C3/4 the anterior thecal sac is indented and the cord contacted but no intrinsic cord signal change at this level or elsewhere.

Moderate narrowing of the left C3/4 foramen and bilaterally at C4/5 and C5/6. T4 haemangioma, otherwise unremarkable bone marrow signal.

Heart and mediastinal contours are preserved.

Other than faint atelectasis at the left lung base the lungs appear clear.

Pleural spaces unremarkable. J o u r n a l P r e -p r o o f Sensory Sensory responses from the right median and radial nerves were of low amplitude, the median responses showing moderate slowing across the wrist. Sensory responses from the right ulnar, sural and superficial peroneal nerves were absent.

Motor responses from the right median nerve show a very severe prolongation of distal latency and mild slowing in the forearm. The right ulnar nerve showed patchy slowing, particularly across the elbow in the upper arm. The right tibial nerve gave low amplitude in the foot wither severe prolongation to the distal latency and moderate slowing in the calf. The right peroneal response was normal in tibialis anterior and showed low amplitude in the foot.

The results are typical of Guillain Barre syndrome. 

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