Discussion
Only one case series [8] and a few case reports [9, 11] show an association between SARS-CoV-2 infection and GBS. The presented well-documented case report shows all characteristics of a typical, but severe, course of GBS. The association with the SARS-CoV-2 infection in the present case is without a doubt because of the strict time connection. The clinical course regarding the COVID 19 disease and the respiratory symptoms was uncomplicated. The main complaint was the neurological complication with GBS. Severe course of GBS-associated SARS-CoV-2 infections occur also in patients with mild respiratory symptoms, but must be taken into account with seriously ill cases. With COVID-19 disease due to a general impairment, the neurological symptoms can be easily overlooked. Since GBS can cause or exacerbate respiratory symptoms, it should take into account the suspect courses of COVID 19. It would be helpful if clinical, paraclinical, or electrophysiological findings were found that would facilitate the diagnosis of GBS. To date, the previously described courses of the SARS-CoV-2 infection-associated GBS do not describe a special clinical pattern. To date, available references summarizing the following points include a total of nine published cases.
A remarkable clinical pattern in our case was that there was bilateral peripheral facial nerve palsy. This clinical symptom has been reported in one other case report [10] and 3/5 cases in the Italian series reported a facial diplegia in one case and facial weakness in two cases [8]. Therefore, we can describe a bilateral facial involvement in five out of nine patients (55.5%) and a documented bilateral facial diplegia in 3/9 patients (33,3%). Facial nerve involvement in GBS is a common finding in 27–50% [12]. There are no data available for a bilateral seventh nerve involvement in GBS. Estimated data reported up to 12–25% [11].
The CSF parameters show no specific pattern. The SARS-CoV-2 RT-PCR in CSF was performed in our patient and in the Italian series of five patients [8] and was negative in all cases.
Antiganglioside antibodies (GM 1-, GQ1b-antibodies) may indicate special GBS subtypes. They were analyzed in our case and three out of five in the Italian series [8] tested negative.
Nerve conduction studies have been performed in our case and two other case reports [9, 10]. An axonal affection pattern is reported in two out of three cases. Except for the presented case, the clinical course of the other cases is not well documented. So the data do not allow a discussion over a prognostic value of the present electrophysiological data.
So far, attention has mostly focused on complications of the CNS involvement. Taking into account that GBS can cause a considerable impairment of the respiratory system, clinicians dealing with SARS-CoV-2 positive-tested patients should have to pay attention to symptoms of the peripheral nervous system. As far as we know from these few reported cases, there seems to be no association with antiganglioside antibodies or a positive SARS-CoV-2 RT-PCR in CSF. The occurrence of a bilateral facial weakness or bilateral peripheral facial diplegia should be emphasized. This finding and the appearance of specific electrophysiological pattern should be shown in further investigations.