Bell’s palsy is a mononeuropathy of the facial nerve that typically causes unilateral facial paralysis. The incidence of unilateral Bell’s palsy is not uncommon, but sequential or simultaneous bilateral Bell’s palsy is exceedingly rare. While unilateral Bell’s palsy is oftentimes idiopathic, bilateral Bell’s palsy is almost exclusively explained by an identifiable trigger. In pre-clinical trials, Bell’s palsy cases were recorded at higher rates in the vaccine cohort than the placebo cohort. Herein, we present a case of isolated sequential bilateral Bell’s palsy that after an extensive workup, proved to be idiopathic. Notably, in the setting of a recent coronavirus disease 2019 (COVID-19) vaccine and absence of identifiable etiology, our case highlights a potential correlation of the COVID-19 vaccine and bilateral Bell’s palsy.

All modern vaccines share the risk of neurological adverse effects. Only a few cases of Parsonage-Turner syndrome (PTS), an uncommon peripheral nerve condition associated with coronavirus disease 2019 (COVID-19) immunization, have been reported to date. We describe a case of COVID-19 vaccineinduced PTS and provide a brief literature review. A 78-year-old male non-smoker with a medical history of coronary artery disease presented with non-exertional, constant chest pain for one hour and new onset of bilateral hand weakness for three days. He had no neurological disease or allergies and denied any recent trauma or infection. Three weeks before the onset of the symptoms, the patient received a second dose of the BNT162b2 COVID-19 vaccine, which was administered 21 days after the first dose. Physical examination was significant for weakness in right-hand grip and wrist flexion. There were no other motor deficits, upper motor neuron signs, bulbar weakness, or sensory deficits. Diagnostic workup for the underlying diabetes mellitus, infections, or other autoimmune diseases was negative. Imaging workup revealed no demyelination, fracture deformity, traumatic subluxation, or compressive myelopathy. Nerve conduction studies, including needle electromyography, showed decreased motor unit recruitment in the bilateral first dorsal interosseous and right deltoid, biceps, and triceps muscles confirming PTS. The patient was treated with 40 mg/day of oral prednisone and occupational therapy to maintain range of motion and activities of daily living. PTS is also known as neuralgic amyotrophy, brachial plexus neuritis, brachial plexopathy, and shoulder-girdle syndrome. It is characterized by asymmetrical, chronic, resistant upper extremity neuropathic pain and neurological defects such as paralysis and paresthesia. There are two different types of PTS: non-hereditary and inherited. The etiology and pathophysiology of PTS are not fully understood. Various aspects such as genetic, environmental, and immunological predisposition may play a role in developing the syndrome. Infections, vaccines, and injuries are typical causes of non-hereditary forms. After the COVID-19 epidemic and the commencement of a global immunization effort, similar instances happened. Presently there is no available test that unequivocally confirms or excludes PTS itself. Electrodiagnostic study and imaging modalities help to rule out other differential diagnoses. Also, there is no specific treatment available; however, it may resolve independently of treatment with supportive care.

A 44-year-old woman with a history of factor V Leiden deficiency and recurrent pulmonary emboli was diagnosed with coronavirus disease 2019 (COVID-19) three weeks prior presented to her local ED with severe chest pain. She was found to have a large hemorrhagic pericardial effusion by cardiac MRI with echocardiographic signs of tamponade. She underwent the creation of a pericardial window and was treated with colchicine with improvement in symptoms.

A 27-year-old female patient initially presented with fever, myalgia, sore throat that progressed to multifocal pneumonia, and cerebral sinus venous thrombosis. A combination of upper respiratory symptoms with tooth infection, positive blood culture for Fusobacterium nucleatum, computed tomography (CT) chest finding of multifocal pneumonia, and magnetic resonance imaging (MRI) finding of internal jugular vein thrombosis (IJVT) and cerebral venous sinus thrombosis (CVST) suggested Lemierre syndrome. The patient was managed with fluids, antibiotics, and anticoagulants. The patient survived and discharged from the hospital. The patient’s symptoms improved at 2 months of follow-up.

Anti-synthetase syndrome usually comprises interstitial lung disease, myositis, arthralgias, and Raynaud phenomenon. The anti-PL-12 antibody is directed against the enzyme alanyl-tRNA synthetase and has been associated with interstitial lung disease in the absence of inflammatory myositis. We report the case of a 33year-old woman with complaints of progressive dyspnea, a persistent dry cough, along with intermittent low-grade fever for a few months. A computed tomography (CT) scan of the chest showed the presence of patchy bilateral airspace opacities and infiltrates. It also showed significant mediastinal and hilar lymphadenopathy. Bronchoscopy with transbronchial biopsy was performed, and histopathology changes were consistent with connective tissue disease related to interstitial lung disease. Further workup revealed the presence of anti-PL-12 antibodies. This case illustrates a rare association of interstitial lung disease with the anti-PL-12 antibody.