excluded electrolytic abnormalities, heavy metal or drugs toxicity, endocrinological disorders, folate and vitamin B12 deficiency.
Blood analysis showed elevated CPK (461 U/L, normal < 145), CRP (5·65 mg/dL, normal < 0·5), lymphocytopenia (0·68 × 10 9 /L, normal 1·10-4), mild increase of LDH (284 U/L, normal < 248), GOT and GPT (549 and 547 U/L, normal < 35), similarly to COVID-19 patients laboratory profile [10] .
Thus, considering the rapid spread of this infection in our region and its pandemic extent, we decided to perform a RT-PCR for SARS-CoV-2 on nasopharyngeal swab, which resulted positive.
We found elevation of Interleukin 6 (11 pg/mL, normal < 5·9), also associated with Covid-19 disease [10] . She was transferred to Covid-19 department and received a five days course of intravenous immune globulin (IvIg), ritonavir 100 mg and darunavir 800 mg per day with hydroxychloroquine 200 mg twice daily, according to our hospital protocol for COVID-19 treatment. She never developed respiratory symptoms or fever; thoracic CT scan was normal.
Immediately after IvIg, she significantly improved with a MRC scale of 4/5 in distal of upper limbs and 3/5 both proximal and distal in lower limbs, while facial diplegia has developed. About 3 weeks after the onset of neurological symptoms two nasopharyngeal swabs, 24 hours apart, resulted negative and she was transferred to rehabilitation care.
To our knowledge, this is the first case of GBS in patient with asymptomatic COVID-19 and laboratory tests consistent with SARS-COV-2 infection. We think the infection wasn't nosocomial, although we cannot absolutely exclude it, because the swab was performed within twelve hours from hospitalization and isolation protocols of suspected patients had been applied. Patient's relatives did not develop symptoms but were observed in isolation for 2 weeks.
The association between COVID-19 and GBS has recently been described both as parainfectious [3, 7, 8] and as post-infective event [4, 5, 9] , similar to other infections and coronavirus [11, 12] , suggesting a mechanism of molecular mimicry or part of systemic inflammatory cascade triggered by the virus. Facial diplegia seems recurrent in GBS related to COVID-19 [7, 8] .
Interesting in our case a patient asymptomatic for COVID-19 develops neurological impairment as a unique clinical event, probably as part of dysimmune process.
Unfortunately, we could not perform a serological test or CSF PCR for COVID-19.
We believe this association may not be a coincidence, more cases could be evaluated, possibly supported by serological and CSF tests, and underlines the importance of looking for neurological impairment in COVID-19 disease and address the correct treatment, such as IvIg, also for respiratory function worsening independently from pneumonitis.
Author contributions BM treated the patient and collected the clinical information. BM, NI and PDM drafted the manuscript. BM and PDMperformed the NCS analysis. PDM provided guidance for the diagnosis and clinical management of the patient. All authors contributed to the editing of the manuscript and approved the final version.
Availability of data and material De-identified data and material inherent to the case report and not included in the manuscript are available on request to the corresponding author by any qualified investigator. 