“COVID-19: PARALYZED WITH FEAR OR WITH ANTIBODY?”

Case Presentation: A 63 year-old male with a history of mantle cell lymphoma on rituximab, T2DM and hypertension, recently treated for COVID-19, presented again with fever, worsening shortness of breath and new onset bilateral foot weakness/numbness to the ankles. He tested COVID-19 positive 27 days prior to this admission and had a typical COVID-19 presentation including fevers, shortness of breath, non-productive cough, and loss of taste and smell. He received high dose steroids and convalescent plasma for COVID-19 management. He described his lower extremities as feeling “heavy” and “numb”. His weakness was not progressive, and not affecting his bilateral upper extremities. Physical examination revealed 0/5 bilateral foot dorsi or plantar flexion and 0/5 bilateral ankle dorsi or plantar flexion. His knee and hip flexion/extension and upper extremity examination were all normal. Loss of sensation was appreciated bilaterally to the ankle above the lateral malleolus. Plantar and ankle reflexes were mute while knee reflexes were 2+ bilaterally. The remainder of the neurological exam was normal.His inflammatory labs were mildly elevated. CT Head was unremarkable. Doppler ultrasound and CT Angio of lower extremities were negative for clotting. Patient’s lower extremity numbness/weakness did not ascend; however, due to concern for demyelinating autoimmune syndrome a lumbar puncture was performed; CSF protein 65, glucose 136, lymphocytes 59, neutrophils 0, WBC 1, RBC 0. Given the albumino-cytologic dissociation of the CSF, a diagnosis of an atypical (motor predominant) acute demyelinating neuropathy (Guillain-Barre syndrome) was made and considered secondary to recent COVID-19. Patient was started on IVIG.

Discussion: GBS is a rare complication of infection and less commonly, vaccination and surgery. The exact etiology of this demyelinating auto-immune syndrome is not entirely understood but is believed to be an immunologic response to a preceding infection that cross-reacts with peripheral nerve components due to molecular mimicry. Certain vaccines, including the influenza, rabies, and swine flu vaccines, have been linked to increased GBS incidence. GBS symptoms can be variable depending on severity. Most commonly, GBS presents with neurologic symptoms such as numbness, pain, or weakness ascending from the lower extremities. In the most severe cases, paralysis and respiratory dysfunction may develop. This patient’s neurologic symptoms did not present as ascending numbness or weakness and GBS was not initially suspected. DVT was an initial concern due to the patient’s increased risk for hypercoagulation in the setting of malignancy and COVID-19. This case poses significant implications for the future as COVID-19 vaccines become commercially available. Regardless of vaccine type- mRNA vs vector- the immunogenic antigen may introduce the risk of GBS. It will be imperative for physicians to acknowledge GBS, especially in the setting of atypical presentations, as the therapeutic and preventive management of COVID-19 continues to develop.

Conclusions: This case demonstrates the importance of including GBS as a potential complication when evaluating patients diagnosed with COVID-19, particularly in atypical presentations. Due to the devastating effects of this pandemic, physicians will be faced with an unprecedented number of COVID-19 cases and thus vaccinations, leading to the possibility of increased GBS incidence.