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