COVID-19-associated Miller-Fischer syndrome

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyed Arash Javadmoosavi, MD[2]

Synonyms and keywords: MFS, fisher syndrome

Overview

Miller Fisher Syndrome (MFS) is an acute peripheral neuropathy that can develop after exposure to a viral or bacterial infection. It includes triad of ophthalmoplegia, areflexia and ataxia. In COVID-19 pandemic period, while COVID-19 typically presents with fever, shortness of breath (SOB) and respiratory symptoms, MFS with prior history of COVID-19 has been seen in several cases all around the world. One retrospective study in 214 patients has shown that 8.9 % of COVID-19 patients have reported peripheral neurological symptoms.

Historical Perspective

The first reported case of MFS with history of covid-19 was detected on January 2020 in Shanghai, who was a middle-age woman diagnosed with MFS presented with areflexia, acute weakness in both legs and severe fatigue. Further reports were announced by medical groups in Spain and the USA which presented neuro-ophtalmological symptoms. [1]

Classification

MFS is a rare variant of Guillain-Barre syndrome, characterized by ophtalmoplegia, areflexia and ataxia.

Pathophysiology

MFS is related to dysfunction of third, forth and sixth cranial nerves. A typical serological finding in patients with MFS and prior history of covid-19 is antibodies against GQ1b ganglioside, though negative test for antibodies does not rule out the diagnosis. The presence of ophtalmoparesis in MFS is related to a action of anti-GQ1b antibodies on the neuromuscular junction between the cranial nerves and ocular muscle. ELISA test is positive in 70% to 90% of patients.[2]

Causes

Although MFS has been detected in some patients with covid-19, other viral and bacterial infections can also cause MFS

Differentiating COVID-19-associated Miller-Fischer syndrome from other Diseases

MFS must be differentiated from other diseases that cause ophthalmoplegia, areflexia, and ataxia, such as:[3][4][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]

Diseases History and Physical Diagnostic tests Other Findings
Motor Deficit Sensory deficit Cranial nerve Involvement Autonomic dysfunction Proximal/Distal/Generalized Ascending/Descending/Systemic Unilateral (UL)

or Bilateral (BL)

or

No Lateralization (NL)

Onset Lab or Imaging Findings Specific test
Guillian-Barre syndrome + - - - Generalized Ascending BL Insidious CSF: ↑Protein

↓Cells

Clinical & Lumbar Puncture Progressive ascending paralysis following infection, possible respiratory paralysis
Acute Flaccid Myelitis + + + - Proximal > Distal Ascending UL/BL Sudden MRI (Longitudinal hyperintense lesions) MRI and CSF PCR for viral etiology Drooping eyelids

Difficulty swallowing

Respiratory failure

Adult Botulism + - + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Diplopia, Hyporeflexia, Hypotonia, possible respiratory paralysis
Infant Botulism + - + + Generalized Descending BL Sudden Toxin test Blood, Wound, or Stool culture Flaccid paralysis (Floppy baby syndrome), possible respiratory paralysis
Eaton Lambert syndrome + - + + Generalized Systemic BL Intermittent EMG, repetitive nerve stimulation test (RNS) Voltage gated calcium channel (VGCC) antibody Diplopia, ptosis, improves with movement (as the day progresses)
Myasthenia gravis + - + + Generalized Systemic BL Intermittent EMG, Edrophonium test Ach receptor antibody Diplopia, ptosis, worsening with movement (as the day progresses)
Electrolyte disturbance + + - - Generalized Systemic BL Insidious Electrolyte panel ↓Ca++, ↓Mg++, ↓K+ Possible arrhythmia
Organophosphate toxicity + + - + Generalized Ascending BL Sudden Clinical diagnosis: physical exam & history Clinical suspicion confirmed with RBC AchE activity History of exposure to insecticide or living in farming environment. with : Diarrhea, Urination, Miosis, Bradycardia, Lacrimation, Emesis, Salivation, Sweating
Tick paralysis (Dermacentor tick) + - - - Generalized Ascending BL Insidious Clinical diagnosis: physical exam & history - History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
Tetrodotoxin poisoning + - + + Generalized Systemic BL Sudden Clinical diagnosis: physical exam & dietary history - History of consumption of puffer fish species.
Stroke +/- +/- +/- +/- Generalized Systemic UL Sudden MRI +ve for ischemia or hemorrhage MRI Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation.
Poliomyelitis + + + +/- Proximal > Distal Systemic BL or UL Sudden PCR of CSF Asymmetric paralysis following a flu-like syndrome.
Transverse myelitis + + + + Proximal > Distal Systemic BL or UL Sudden MRI & Lumbar puncture MRI History of chronic viral or autoimmune disease (e.g. HIV)
Neurosyphilis + + - +/- Generalized Systemic BL Insidious MRI & Lumbar puncture CSF VDRL-specifc

CSF FTA-Ab -sensitive

History of unprotected sex or multiple sexual partners.

History of genital ulcer (chancre), diffuse maculopapular rash.

Muscular dystrophy + - - - Proximal > Distal Systemic BL Insidious Genetic testing Muscle biopsy Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. Gower sign positive.
Multiple sclerosis exacerbation + + + + Generalized Systemic NL Sudden ↑CSF IgG levels

(monoclonal)

Clinical assessment and MRI Blurry vision, urinary incontinence, fatigue
Amyotrophic lateral sclerosis + - - - Generalized Systemic BL Insidious Normal LP (to rule out DDx) MRI & LP Patient initially presents with upper motor neuron deficit (spasticity) followed by lower motor neuron deficit (flaccidity).
Inflammatory myopathy + - - - Proximal > Distal Systemic UL or BL Insidious Elevated CK & Aldolase Muscle biopsy Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.

Epidemiology and Demographics

While the incidence of MFS is one or two person per million each year, the prevalence of MFS associated with covid-19 is still unknown.

Risk Factors

There are no established risk factors for MFS associated with covid-19.

Screening

There is insufficient evidence to recommend routine screening for patients with MFS caused by covid-19.

Natural History, Complications, and Prognosis

There is an increased risk of death in patients over the age of 60 year-old. Hence, the mortality rate is estimated to be 3.6%.
Risk factors for severe illness and poor prognosis include:

Diagnosis

Diagnostic Study of Choice

Although the diagnosis of covid-19 is based on respiratory symptoms, it can be associated with neurological symptoms, of which overlap the diagnosis of MFS. Consequently, in patient with prior history of covid-19, other neurologic diseases should be ruled out and anti-GQ1b antibody test should be considered. Also, in new patients with suspicious symptoms for covid-19 and neurological symptoms, nasal swab test and neurological examination should be considered.
MRI may be performed as a part of diagnostic work up. Although in majority of cases no abnormality is detected, enlargement and prominent enhacement in orbits and retro-orbital region has been reported in some cases.[20]. [21]

History and Symptoms

Symptoms of covid-19 associated with MFS include:

[22]

Physical Examination

Patients with covid-19 associated with MFS present various signs and symptoms related to systematic and neurological presentation. Hence physical examination should be performed based on signs and symptoms include:

Vitals

Abnormal signs associated with covid-19:

neurological

Laboratory Findings

Laboratory findings consistent with the diagnosis of covid-19 include positive PCR nasal swab.
Laboratory test for neurological signs are not diagnostic and should be used with other clinical parameters. They are include:

  • Ganglioside (GM1) Antibodies, IgG and IgM
  • GD1b Antibody, IgM
  • GQ1b Antibody, IgG

Electrocardiogram

There are no ECG findings associated with covid-19.

X-ray

CXR is less sensitive in detection of covid-19 in comparison with CT. However, in some cases lung consolidation and patchy peripheral opacities corresponding to ground glass opacities has been reported.[23]

Echocardiography or Ultrasound

There are no echocardiography findings associated with covid-19.
Lung Ultrasound may be helpful in evaluation of patients with covid-19. It indicates :

  • Multiple B-lines
    • Ranging from focal to diffuse with spared areas
  • Irregular and thickened pleural lines
  • Subpleural consolidations
  • Alveolar consolidations
  • Bilateral A-lines

CT scan

The preliminary findings of CT in COVID-19 associated with MFS include:

MRI

Brain MRI may be helpful in the diagnosis of MFS in patients with prior history of covid-19 and neurological manifestations. Although there can be no abnormalities, multiple cranial nerve enhancement has been reported in some patients.

Other Diagnostic Studies

There are no other diagnostic studies associated with covid-19 with MFS manifestations.

Treatment

Medical Therapy

No specific treatment and vaccine exists for covid-19 yet. However, patients with moderate to severe ARDS and respiratory manifestations can benefit from Mechanical ventilation and extracorporeal membrane oxygenation (ECMO). In some patients the combination of antiviral therapies like protease inhibitors, ritonavir, and lopinavir indicated partial success in treatment of covid-19.
Remdesivir, a drug originally developed to treat Ebola virus, showed positive results against SARS-CoV-2.
Dexamethasone has been announced as an effective treatment in patients with systematic manifestations.

Surgery

Surgical intervention is not recommended for the management of covid-19.

Primary Prevention

Effective measures for the primary prevention of covid-19 include handwashing, wearing of face masks, social distancing, avoidance of large gathering and self-isolation for patients who have mild symptoms.

References

  1. ↑ {{https://n.neurology.org/content/early/2020/04/17/WNL.0000000000009619}}
  2. ↑ {{https://pubmed.ncbi.nlm.nih.gov/10695710}}
  3. ↑ {{https://rarediseases.org/rare-diseases/miller-fisher-syndrome/}}
  4. ↑ 4.0 4.1 Kira R (February 2018). "[Acute Flaccid Myelitis]". Brain Nerve (in Japanese). 70 (2): 99–112. doi:10.11477/mf.1416200962. PMID 29433111.
  5. ↑ Hopkins SE (November 2017). "Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations". Curr Treat Options Neurol. 19 (12): 48. doi:10.1007/s11940-017-0480-3. PMID 29181601.
  6. ↑ Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR (September 2016). "Acute flaccid myelitis: A clinical review of US cases 2012-2015". Ann. Neurol. 80 (3): 326–38. doi:10.1002/ana.24730. PMC 5098271. PMID 27422805.
  7. ↑ Chong PF, Kira R, Mori H, Okumura A, Torisu H, Yasumoto S, Shimizu H, Fujimoto T, Hanaoka N, Kusunoki S, Takahashi T, Oishi K, Tanaka-Taya K (February 2018). "Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015". Clin. Infect. Dis. 66 (5): 653–664. doi:10.1093/cid/cix860. PMC 5850449. PMID 29028962.
  8. ↑ Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters H, Tyler KL, Abzug MJ, Dominguez SR (August 2018). "Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality". Lancet Infect Dis. 18 (8): e239–e247. doi:10.1016/S1473-3099(18)30094-X. PMID 29482893. Vancouver style error: initials (help)
  9. ↑ Chen IJ, Hu SC, Hung KL, Lo CW (September 2018). "Acute flaccid myelitis associated with enterovirus D68 infection: A case report". Medicine (Baltimore). 97 (36): e11831. doi:10.1097/MD.0000000000011831. PMC 6133480. PMID 30200066.
  10. ↑ "Botulism | Botulism | CDC".
  11. ↑ McCroskey LM, Hatheway CL (May 1988). "Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract". J. Clin. Microbiol. 26 (5): 1052–4. PMC 266519. PMID 3290234.
  12. ↑ Lindström M, Korkeala H (April 2006). "Laboratory diagnostics of botulism". Clin. Microbiol. Rev. 19 (2): 298–314. doi:10.1128/CMR.19.2.298-314.2006. PMC 1471988. PMID 16614251.
  13. ↑ Brook I (2006). "Botulism: the challenge of diagnosis and treatment". Rev Neurol Dis. 3 (4): 182–9. PMID 17224901.
  14. ↑ Dimachkie MM, Barohn RJ (May 2013). "Guillain-Barré syndrome and variants". Neurol Clin. 31 (2): 491–510. doi:10.1016/j.ncl.2013.01.005. PMC 3939842. PMID 23642721.
  15. ↑ Walling AD, Dickson G (February 2013). "Guillain-Barré syndrome". Am Fam Physician. 87 (3): 191–7. PMID 23418763.
  16. ↑ Gilhus NE (2011). "Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy". Autoimmune Dis. 2011: 973808. doi:10.4061/2011/973808. PMC 3182560. PMID 21969911.
  17. ↑ Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA (May 2004). "Transverse Myelitis: pathogenesis, diagnosis and treatment". Front. Biosci. 9: 1483–99. PMID 14977560.
  18. ↑ Amato AA, Greenberg SA (December 2013). "Inflammatory myopathies". Continuum (Minneap Minn). 19 (6 Muscle Disease): 1615–33. doi:10.1212/01.CON.0000440662.26427.bd. PMID 24305450.
  19. ↑ Berger JR, Dean D (2014). "Neurosyphilis". Handb Clin Neurol. 121: 1461–72. doi:10.1016/B978-0-7020-4088-7.00098-5. PMID 24365430.
  20. ↑ {{http://www.ajnr.org/content/early/2020/05/28/ajnr.A6609}}
  21. ↑ {{https://rarediseases.org/rare-diseases/miller-fisher-syndrome/}}
  22. ↑ {{http://www.ajnr.org/content/early/2020/05/28/ajnr.A6609}}
  23. ↑ {{https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7141645/}}


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