Neurographic Evidence of Inflammatory Polyneuropathies in Peri-COVID-19 Circumstances and Their Relationship With Acute Disease Severity and Inflammatory Storm

Recently, there has been increasing evidence among people infected with coronavirus disease 2019 (COVID-19) of being diagnosed with the typical acute post-infectious inflammatory polyneuroradiculopathy that was formerly known as Guillain-Barré syndrome (GBS), and it is not uncommon that some of them develop chronic inflammatory demyelinating polyneuroradiculopathy (CIDP). However, there is still a large debate and controversy about the link between COVID-19 and polyneuropathy. As a result, a multicentric retrospective cohort study was conducted in Basrah Governorate in the south of Iraq that included 2240 patients over a period of six months. Of those, 1344 patients had a history of COVID-19 in the previous year, and 1.14% of them developed inflammatory polyneuropathy, while only 0.29% (896 patients) of those with no history of COVID-19 had developed inflammatory polyneuropathy. This difference is highly significant, with a relative risk equal to six. The majority of the inflammatory polyneuropathy (44.4%) was diagnosed four to 12 weeks after the COVID-19 infection, with GBS being the most common type (72.2% of cases). Moreover, the nerve conduction velocity, the distal latency, and the amplitude of the most studied nerves were slower, more prolonged, and lower, respectively, among the COVID-19 groups compared with the non-COVID-19 group. Furthermore, there is an inverse correlation between the nerve conduction velocity in the majority of studied nerves and certain inflammatory biomarkers, such as serum ferritin, interleukin-6, and c-reactive protein. Although the occurrence of inflammatory polyneuropathy is more common among the less severe groups of COVID-19, if it occurs in the severe groups, it shows a more aggressive presentation.