We review the literature on REM parasomnias, and their the underlying mechanisms. Several REM parasomnias are consistent with sleep dissociations, where certain elements of the REM sleep pattern emerge in an inadequate time (sleep paralysis, hypnagogic hallucinations and cataplexy) or are absent/partial in their normal REM sleep time (REM sleep without atonia, underlying REM sleep behavior disorder). The rest of REM parasomnias (sleep related painful erection, catathrenia) may have other still unclear mechanisms. REM parasomnias deserve attention, because in addition to disturbing sleep and causing injuries, they may shed light on REM sleep functions as well as the heterogeneous etiologies of parasomnias. One of them, REM sleep behavior disorder has special importance as a warning sign of evolving neurodegenerative conditions mainly synucleinopathies (some cases synucleinopathies themselves) and it is a model parasomnia revealing that parasomnias may have by autoimmune, iatrogenic and even psychosomatic etiologies.

Prevalence of acute ische­mic stroke (AIS) is increased in patients with coronavirus disease 2019 (COVID-19). A proposed hypothesis is increased virus-induced propensity to hypercoagulation resulting in arterial thrombosis. Our aim was to provide evidence regarding the involvement of neutrophil extracellular trap (NET) formation (NETosis) in COVID-19 related AIS. Twenty-six consecutively enrolled COVID-19+ pneumonia patients with AIS, 32 COVID-19+ pneumonia patients without AIS and 24 AIS patients without COVID-19 infection were included to the study. Clinical characteristics of recruited patients were collected. Serum levels of citrullinated histone H3 (H3Cit; a factor of NETosis), IL-8 and C5a (mediators associated with NETosis) were measured by ELISA (enzyme-linked immunosorbent assay). H3Cit levels were significantly higher in COVID-19+ AIS patients, whereas all study groups showed comparable IL-8 and C5a levels. There were no significant differences among etiological subgroups of AIS patients with or without COVID-19. AIS patients with COVID-19 showed relatively increased white blood cell, lymphocyte, neutrophil, D-dimer, C-reactive protein and procalcitonin levels than control groups. H3Cit levels did not correlate with clinical/prognostic features and inflammation parameters. H3Cit and IL-8 levels were correlated in COVID-19 patients without stroke but not in COVID-19 positive or negative AIS patients. Increased levels of inflammation parameters and H3Cit in COVID-19 related AIS suggest that NETosis may cause susceptibility to arterial thrombosis. However, H3Cit levels do not correlate with clinical severity measures and inflammation parameters diminishing the prognostic biomarker value of NETosis factors. Moreover, the link between IL-8 and NETosis appears to be abolished in AIS.

Neurological symptoms and complications associated with coronavirus 2019 (COVID-19) are well known. It was aimed to evaluate the brainstem and trigeminal/facial nerves and the pathways between these structures in COVID-19 using the blink reflex test. Thirty patients with post COVID-19 (16 males, 14 females) and 30 healthy individuals (17 males, 13 females) were included in this prospective study. Individuals who previously had a positive nose swap polymerase chain reaction test for severe acute respiratory syndrome coronavirus 2 and whose previously clinical features were compatible with COVID-19 were included in the post COVID-19 patient group. Neurological examination of the participants should be normal. Blink reflex test was performed on all participants. R1, ipsilateral R2 (IR2), and contralateral R2 (CR2) waves obtained from the test were analyzed. The mean ages of healthy individuals and post COVID-19 patients were 34.0±6.4 and 38.4±10.6 years, respectively. Both age and gender were matched between the groups. R1, IR2, and CR2 latencies/amplitudes were not different between the two groups. The side-to-side R1 latency difference was 0.5±0.3 and 1.0±0.8 ms in healthy individuals and post COVID-19 patients, respectively (p=0.011). One healthy individual and 12 patients with post COVID-19 had at least one abnormal blink reflex parameter (p=0.001). This study showed that COVID-19 may cause subclinical abnormalities in the blink reflex, which includes the trigeminal nerve, the seventh nerve, the brainstem, and pathways between these structures.

Although severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a novel virus, many central and peripheral nervous system manifestations associated with coronavirus disease-19 (COVID-19) infection have been reported. Beyond the neurologic manifestations, we may still have much to learn about the neuropathologic mechanism of SARS-CoV-2 infection. Here we report a case of post-poliomyelitis syndrome (PPS) related to COVID-19 and attempt to predict the possible pathophysiologic mechanism behind this association.

[Research results in recent years have demonstrated that B-lymphocytes play a crucial role in the pathogenesis of multiple sclerosis (MS). The increased understanding of the disease process has resulted in the development of B cell-targeting antibodies as potential drugs for both relapsing and progressive forms of MS. Therefore, B-cell depletion therapies are becoming more prominent and determining in reducing disease progression. The first B-cell depleting anti-CD20 monoclonal antibody was rituximab, which has also been studied in MS and, following favourable results, new drugs have been developed with a similar point of attack. In 2017, the FDA and in 2018, the EMA approved ocrelizumab, another anti-CD20 monoclonal antibody, for the treatment of relapsing-remitting (RRMS) and primary progressive multiple sclerosis (PPMS). This was a particularly significant advance in the treatment of PPMS, as it was the first medication with a proven effect of reducing progression in PPMS. Ofatumumab, a fully human anti-CD20 monoclonal antibody, has emerged recently as a new player in B-cell depletion therapy. The drug has also recently been approved by the EMA in March 2021 for use in relapsing forms of MS. In this review, we detail the mechanism of action and efficacy of anti-CD20 therapies currently used in MS. ]