Hassan Farid is a research assistant at the College of Medicine—University of Basrah and a neurology resident at Al-Basrah Teaching Hospital-Basrah Health Directorate—Iraq. Currently, he is a clinical neurology master student at the Sheffield Institute of Translational Neuroscience (SITraN) at the University of Sheffield and Royal Hallamshire Hospital – NHS foundation trust – United Kingdom. Hassan did much research in the fields of neurology, neurophysiology, and COVID-19 infection, with a special interest regarding the neurological manifestation and complications of COVID-19 infection.

In December 2019, a new disease called novel coronavirus disease, or COVID-19, was spreading around Wuhan, China, and had become a worldwide pandemic. Although pneumonia-like symptoms predominate, many patients are still at risk of having neurological complications such as strokes or Guillain-Barre syndrome. Moreover, intensive care unit (ICU) treatment and long-term ventilatory support increase the risk of critical illness myopathy (CIM) and polyneuropathy (CIN). CIN and CIM traditionally occur as a result of multiple organ failure, muscle immobility, corticosteroids, and neuromuscular blocking medications. The pathogenic mechanisms of COVID-19 are still not well understood. It is possible that it occurred due to direct viral toxic effects or because of the vigorous mechanical ventilation due to severe respiratory damage in the COVID-19 lungs. Furthermore, other possible suggestions include the inflammatory cytokine storm or the neurotoxic side effects of the medication used to treat COVID-19, such as vigorous steroid therapy. In terms of diagnosis, clinically, the patient is critically ill and has limb weakness or difficulty weaning from the ventilator after non-neuromuscular causes such as cardiac and respiratory diseases have been excluded. Electro-physiologically, for CIN, evidence of axonal motor and sensory polyneuropathy in nerve conduction studies and for CIM, needle electromyography of short-duration, low-amplitude motor unit potentials. Biochemically, high neurofilament light chain and glial fibrillary acidic protein levels were detected in COVID-19 patients who later developed CIM or CIN. Additionally, elevated interleukin-6 at admission is a risk-predictor biomarker for CIN developing in COVID-19. The prevalence is widely variable in the literature, but most of them argue that CIN is more prevalent than CIM during the COVID-19 pandemic. Generally, there is a clear distinction between the outcomes of CIN versus CIM, as patients with CIN have a slower or incomplete recovery and a higher mortality rate, whereas patients with CIM often show complete recovery within 6 months. Therefore, CIN and CIM are important to identify during the COVID-19 era since survivors often present with severe residual disability and persistent exercise limitations several years afterwards

Nareen H. Hasrat is a neurophysiology resident at the Basrah Health Directorate and a medical physiology master student in the College of Medicine—University of Basrah. She is working in the EMG and nerve conduction studies clinic in Basrah, southern Iraq. This research is a retrospective cohort study that aims to evaluate the prevalence and characteristics of inflammatory polyneuropathy during the COVID-19 era. It is actually part of her master's dissertation that she is currently working on and aims to evaluate the neurophysiological changes by EMG and NCS among patients with COVID-19 infection. Nareen is a medical doctor licenced to work in Iraq since 2017, and her main research interests are in the fields of neurology and neurophysiology. Her work is done under the supervision of Assistant professor Dr. Haithem J. Kadhum, "Medical physiology specialist," and professor Dr. Ali R. Hashim, "Consultant physician and neurologist," as well as Dr. Zaineb A. Yaqoob, "Neurophysiology specialist."

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. We recommend active surveying and maybe screening programs for those who recovered from COVID-19 and developed neurological symptoms, as well as increasing doctors' and patients’ awareness about these disorders and not referring to the fatigue and walking difficulties as trivial post-COVID-19 manifestations.