Guillain–Barré syndrome with bilateral facial diplegia secondary to severe acute respiratory syndrome coronavirus-2 infection: a case report

On 1 May 2020, a previously healthy 50-year-old Hispanic male presented with a 2-day history of slurred speech, with particular difficulty in the pronunciation of some consonants and closed vowels, trouble closing eyes, and bilateral facial droop. He reported no numbness, extremity weakness, inability to swallow, or blurry vision, among other neurological manifestations. He had had contact with his father, who died of SARS-CoV-2 infection 1 month prior to the admission. Around the time of this contact, he presented asthenia, ageusia, and hyporexia with two positive reverse-transcription polymerase chain reaction (RT-PCR) results for SARS-CoV-2 infection, the first one 19 days prior to the onset of neurological symptoms and the second one 6 days before arriving at the emergency department. He received management with hydration and paracetamol for symptoms such as asthenia, adynamia, and nasal congestion. He was not taking any medication prior to diagnosis, and he did not smoke or consume alcohol. He denied exposure to environmental toxins or chemicals and was unemployed.

On admission, his vital signs were normal (pulse 78 beats per minute, blood pressure 130/80 mmHg, temperature 36 °C), as was the general physical examination. Because the patient had not signs of respiratory distress (saturation ≥ 90%), thoracic X-rays were not taken. Neurological examination revealed mild dysarthria and bilateral facial palsy (House–Brackmann grade III). No other cranial nerve abnormalities were found. There were no meningeal signs. He had normal gait without limb weakness or areflexia. Blood cell count showed lymphopenia (199 cells/µL) without any other relevant findings. Non-contrasted and contrasted brain MRIs were performed without pathological findings. A lumbar puncture was done at day 6, with the presence of albuminocytologic dissociation (0 cells, proteins 210 mg/dL). Cerebrospinal fluid (CSF) Gram stains and culture were negative. No antiganglioside antibodies were available at our institution. The same day, neurophysiological studies (electromyography and nerve conduction) reported severe acute axonal neuropathy of both right and left facial nerves, with prolongation of latency and severe amplitude reduction in all the motor potentials recorded bilaterally. Also, a drastic reduction was recorded in recruitment patterns in facial muscles, with interference patterns less than 30%. All those changes suggest denervation (see Tables 1, 2, Figure 1 for details). Motor and sensory conduction studies in the upper and lower extremities were normal (see Additional file 1 for details-supplementary material).

In accordance with several guidelines for management of GBS [12, 13], plasmapheresis was offered to the patient by our neurology service. However, the patient declined the procedure for personal reasons. The patient was monitored in hospital for 8 days without developing motor symptoms or additional neurological deterioration and without receiving immunomodulatory treatment. He was discharged with a physical rehabilitation program. At a follow-up performed 30 days after discharge, the patient presented complete recovery.