We described a case of a 59-year-old Caucasian male who acutely developed four limb distal paraesthesia and postural instability ten days after vaccination with ChAdOx1 nCoV-19 (ABW1277). Because of the symptoms’ persistence on the fifteenth day after vaccination, he underwent a neurological examination. Past medical history was positive only for hypertension and hyperuricemia.

The physical examination showed gait ataxia, global areflexia, and distal paraesthesia both at the lower and upper limbs; pallesthesia was normal. Segmental strength was diffusely preserved (MRC: 5/5). No cranial nerve, vegetative, or sphincter involvement was observed. He had no spine sensory level.

He underwent electromyography (EMG), which revealed motor polyradiculoneuropathy with temporal dispersion of the tibial nerve Compound Muscle Action Potential (cMAP) bilaterally, with F reflex absent in all districts. There was no sensory involvement, particularly no temporal dispersion of the sural nerve Sensory Action Potential (SAP) bilaterally. The electrophysiological findings were compatible with demyelinating motor polyneuropathy.

Based on these findings, the patient was hospitalized for further investigations. The molecular oropharyngeal swab was negative for COVID-19 infection.

Routine laboratory results were clinically non-significant (including thyroid function). Serological test for HBV, HCV, Mycoplasma, Zika, Chikungunya, west Nile virus, Borrelia Burgdorferi, and Cytomegalovirus was negative for active infection. The fecal investigation for Campylobacter jejuni was negative. The autoimmune hematological screening was unremarkable.

In the following 24 h, the patient showed clinical worsening, due to cranial nerves involvement with bilateral facial palsy (House-Brackmann grade V), without dysphagia or dysphonia, ocular motility limitations, or respiratory distress.

Lumbar puncture was performed, and CSF analysis showed elevated proteins: 140 mg/dl (normal values: 20.00–40.00 mg/dl), with normal white blood cell count and glycorrhachia. The liquor and serum antibodies antiGM1 IgG-IgM, GQIb IgG-IgM, GM2 IgG-IgM, anti MAG, anti-sulfatide, and anti-GAD were negative. Brain and cervical MRI with gadolinium infusion were unremarkable, without pathological enhancement.

After acquiring informed consent, patients started IV immunoglobulin (IVIg) 0.4 mg/kg for 5 days. He started physiotherapy. On the fifth day, the patient slowly improved first for the gait, and then for the forehead motility with moderate movement; eyes have complete closure with effort; the mouth was slightly weak with maximum effort (House-Brackmann grade IV).

After 10 days, we repeated the EMG. Not surprisingly, the exam showed worsening of the electrophysiological findings, with diffuse and evident signs of motor nerve demyelination (upper and lower limbs, and cranial district) (Table 1; Fig. 1a and b).

Table 1 Electromyography findings after 10 days Full size table