Neurological manifestations was reported in 36.4% of COVID-19 patients[1]. GBS is a typical postinfectious disease that generally occurs within four weeks of disease onset[3]. However, parainfectious GBS related to SARS CoV-2 was reported previously[4]. Neuro-invasion or autoimmune response of the virus via ACE2 receptors in neuronal tissues is thought to play a role in the etiology[4].
GBS mainly progresses with limb weakness and areflexia development[3]. This is how it developed in our case, as well. He had rapid progressive neurological findings resulting in quadriplegia, facial paralysis, and dysphagia. Cranial neuropathies including facial paralysis consist of a rare form of GBS[5]. The diagnostic criteria for GBS can be evaluated with the Brighton Criteria[6], and our patients presented all the defined criteria. The neurological findings and CSF examination were consistent with GBS. CSF examination revealed no pleocytosis but increased protein levels, and albumin-cytological dissociation was identified[5]. In addition, the test for SARS CoV-2 PCR in CSF was negative. Published reports of GBS in the literature have indicated negative results in all tested 32 patients with COVID-related GBS[5].
Electromyography (EMG) is the main tool to determine the subtype of GBS. EMG was performed after his admission to ICU and prolonged distal latencies, conductions block, slowing of conduction velocities, and low action potentials were identified. F waves were absent as were all sensory nerves, except the sural nerve, which has been typically reported in patients with GBS. The needle EMG revealed evidence of abnormal insertional activity in the form of positive waves and fibrillation potentials in the muscles of both upper and lower extremities. Overall, electrical abnormalities were consistent with the demyelinating form of GBS with secondary sensory-motor axonal degeneration.
The review of published 37 COVID-19 cases with GBS revealed that the mean-time between COVID-19 symptoms onset and GBS symptoms onset was 11 ± 6.5 days[2]. Another review of 51 COVID-19-related GBS cases reported that 70.5% of the patients were post-infectious whilst 24.5% were para- infectious [5]. Respiratory failure via GBS and the requirement of mechanical ventilation were reported as 17%-30%[7]. Besides, para- infectious COVID-19-related GBS cases were found riskier for ventilator requirement[5]. In the present case, GBS symptoms developed on the third-day of symptom onset of COVID-19.
Although IVIG treatment was given on the second day of admission, limb weakness progressed and bilateral facial paralysis developed. Hence, plasmapheresis was started. Although the recommended treatment regimens were implemented, rapid progression to quadriplegia developed. He needed intubation via respiratory muscle involvement and needed ICU follow-up, similar to %20-%30 of non-COVID GBS patients[6].
The severity of clinical progress is highly variable in patients with GBS, ranging from mild weakness of muscles to serious weakness resulting in quadriplegia and the need for ventilator support[3]. IVIG and plasmapheresis were accepted as efficient treatment modalities[3,8]. Either of them should be implemented as soon as possible after disease onset to prevent the occurrence of permanent nerve damage[3,9,10]. IVIG(0.4 g/kg per day) or plasma exchange for five days constitute effective treatment alternatives. However, a combination of them was not reported as more beneficial compared to the use alone[3]. There is a clear need for more effective treatment agents since many of the patients have developed progressive weakness despite using IVIG or plasmapheresis[3].
GBS is a life-threatening disease with the mortality rate of 3%-7%[3]. The development of respiratory insufficiency via respiratory muscle involvement constitutes one of the most probable causes of death in patients with GBS[3].
Since there is a risk of mortality due to respiratory muscle involvement in GBS, the rapid diagnosis and early treatment is critical in all patients, especially in patients with COVID-19, which may be characterized by extensive lung involvement. Moreover, since para- infectious COVID-19-related GBS has poorer outcomes, the probability of this syndrome should be kept in mind in patients with neurological findings of COVID-19 to manage cases properly without delay.