Case presentation
In May 2021 a 66-year-old woman with a medical history of hypertension and anxious- depressive syndrome in treatment with bupropion, pregabalin and lorazepam was admitted to the emergency department with symptoms of acute progressive weakness of distal lower extremities, especially to the right leg, she had associated symptoms like headache, nausea and vomiting, no urinary and fecal incontinence, no rigor. No previous neurologic history was reported from patient. Neurological manifestations of the patient began with progressive paraesthesia of distal lower extremities, almost four weeks after she received COVID-19 vaccination with a live-attenuated virus.
Brain, cervical and lumbosacral Computed Tomography (CT) was done, it showed a normal finding except for mild herniation of some intervertebral discs and a widespread arthritic degeneration.
On physical examination, the patient was not in hemodynamic instability. She was afebrile and her vitals were: SpO2 98% in ambient air , blood pressure 130/80 mmHg, respiratory rate 18 breaths/minute and heart rate 72 bpm.
The patient was admitted to our Neurology department where the neurological examination revealed a Bell’s palsy with facial asymmetry. Except for the seventh, no other cranial nerve was involved. Upper limbs examination revealed normal trophism and muscle tone in upper limbs. The patient showed progressive failure during Mingazzini I test , without evident lateral deficit. The upper limbs’ examination also revealed a weakness of the interosseous muscles of the hands. Tendon reflexes were absent. Lower limbs examination revealed normal muscle tone but with reduced trophism. The right leg was in an posture of external rotation. The patient could not assume the Mingazzini II position , the iliopsoas muscles were plegic and all limb’ reflexes were absent. Laboratory investigations were blood count, glucose, urea, electrolytes, lactic dehydrogenase, interleukin, PCR, fibrinogen,D-dimer.
Lumbar puncture was performed urgently and the cerebrospinal fluid examination (CSF) revealed clear fluid, normal opening pressure, high protein with normal glucose and cell counts (albumin cytologic dissociation).
Based on physical examination, laboratory investigations, instrumental examinations and CSF findings, a provisional diagnosis of acute, rapidly progressive, inflammatory polyneuropathy like Guillain-Barrè syndrome. Differential diagnosies was made with inflammation or infection of the brainstem or spinal cord for example sarcoidosis, Sjögren syndrome and acute transverse myelitis, brainstem stroke, vitamin deficiency, acute flaccid myelitis were excluded ; also metabolic or electrolyte disorders, some infection for example: Lyme disease, cytomegalovirus, HIV, Epstein–Barr virus or varicella zoster virus, and neuromuscolar junction disease for example: myasthenia gravis and Lambert–Eaton myasthenic syndrome were excluded .
Electrophysiological studies revealed a demyelinating polyneuropathy consistent with Guillain-Barrè syndrome and excluded the subtypes of GBS: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN).
The patient satisfied the level 1 diagnostic certainty of Brighton criteria for GBS. The