Objective
To report a patient with history of recurrent Bell’s Palsy who developed Bell’s Palsy 36 hours after the administration of the second dose of the Pfizer-BioNTech COVID-19 vaccine.
Case
The patient is a 57-year-old female with past medical history of 3 episodes of Bell’s Palsy. She responded to prednisone treatment and returned to her baseline after each occurrence. Less than 36 hours following the second dose of the vaccine, the patient developed a left Bell’s Palsy. The facial droop progressed in severity over the next 72 hours.
Conclusion
Given the expedited production of the vaccine and the novelty associated with its production, there may be information pertaining to side effects and individual response that remain to be discovered. Since both the Moderna and Pfizer Vaccine trials reported Bell’s Palsy as medically attended adverse events, the association between vaccine administration and onset of symptomatic Bell’s Palsy may warrant further investigation.
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This is a case report in which a patient with SLE had a brainstem variant of PRES, and MRI demonstrated atypical distribution of FLAIR hyperintensity in the thalami and the midbrain sparing the red nuclei bilaterally (Figure 1). This impressive lesion pattern may reveal the disease mechanisms of PRES in patients with SLE.
The COVID-19 pandemic is different from previous pandemic diseases in many ways. One of them relates to the literature. There is an exponential increase in the number of articles since April 2020. Also, and equally drastic, is how readily available they are to the general reader. It will be interesting to analyze (in the future) if advances in information age have played any significant role in the battle against our current pandemic.
Miller Fisher syndrome is a variant of Guillain-Barre syndrome characterized by the classic triad of ophthalmoplegia, ataxia, and areflexia. Pupillary involvement is common in MFS and has been reported in 35–42% of MFS patients. Although case reports have discussed isolated ophthalmoplegia as a presentation of MFS, anisocoria and rapid fluctuation of pupillary diameter have not been reported in anti-GQ1b antibody positive individuals. Here we describe an individual who presented with diplopia and was found to have progressive internal and external ophthalmoplegia with frequent fluctuations in pupillary diameter and anisocoria. These exam findings are not commonly described even in atypical presentations of MFS. The onset of symptoms was preceded by an upper respiratory infection but no gastrointestinal symptoms. Imaging and CSF studies were unremarkable; however serum levels of immunoglobulin G anti-GQ1b antibody and anti-GAD antibody were elevated confirming the diagnosis of MFS. The patient was treated with IVIG and intravenous steroids with mild resolution of external ophthalmoplegia. He did not go on to develop more typical features of MFS such as ataxia or areflexia. This demonstrates that isolated external and internal ophthalmoparesis with rapidly fluctuating pupillary diameter and associated anisocoria can be the sole manifestation of atypical MFS.
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