Coronavirus disease-19 (COVID-19) pandemic continues to grow all over the world. Several studies have been performed, focusing on understanding the acute respiratory syndrome and treatment strategies. However, there is growing evidence indicating neurological manifestations occur in patients with COVID-19. Similarly, the other coronaviruses (CoV) epidemics; severe acute respiratory syndrome (SARS-CoV-1) and Middle East respiratory syndrome (MERS-CoV) have been associated with neurological complications. Methods: This systematic review serves to summarize available information regarding the potential effects of different types of CoV on the nervous system and describes the range of clinical neurological complications that have been reported thus far in COVID-19. Results: Two hundred and twenty-five studies on CoV infections associated neurological manifestations in human were reviewed. Of those, 208 articles were pertinent to COVID-19. The most common neurological complaints in COVID-19 were anosmia, ageusia, and headache, but more serious complications, such as stroke, impairment of consciousness, seizures, and encephalopathy, have also been reported. Conclusion: There are several similarities between neurological complications after SARS-CoV-1, MERS-CoV and COVID-19, however, the scope of the epidemics and number of patients are very different. Reports on the neurological complications after and during COVID-19 are growing on a daily basis. Accordingly, comprehensive knowledge of these complications will help health care providers to be attentive to these complications and diagnose and treat them timely.

Quantitative magnetization transfer imaging provides in vivo estimates of liquid and semisolid constituents of tissue, while estimates of the liquid subpopulations, including myelin water, can be obtained from multicomponent T 2 analysis. Both methods have been suggested to provide improved myelin specificity compared to conventional MRI. The goal of this study was to investigate the sensitivity of each technique to the progression of acute, gadolinium-enhancing regions of multiple sclerosis. Magnetization transfer and T 2 relaxometry data were acquired longitudinally over the course of 1 year in five relapsing-remitting multiple sclerosis patients and in five healthy controls. Parametric maps were analyzed in enhancing lesions and normal-appearing white matter regions. Quantitative magnetization transfer parameters in lesions were most abnormal at the time of enhancement and followed a pattern of recovery over subsequent months. Lesion myelin water fraction was abnormal but did not show a significant trend over time. Quantitative magnetization transfer was able to track the degree and timing of the partial recovery in enhancing multiple sclerosis lesions in a small group of patients, while the recovery was not detected in myelin water estimates, possibly due to their large variability. Our data suggest the recovery is characterized by quick resolution of inflammation and a slower remyelination process. Key words: quantitative; magnetization transfer; multicomponent T 2 ; multiple sclerosis; acute lesions A few MRI methods have been suggested to provide improved pathologic specificity in human white matter (WM) over conventional MRI sequences. Two techniques proposed to be more specific for myelin are quantitative magnetization transfer imaging (QMTI) and multicomponent T 2 analysis of spin echo data (QT2). In this longitudinal study, both techniques were used to follow the progression of the gadolinium (Gd)-enhancing region of acute lesions of multiple sclerosis (MS).The magnetization transfer (MT) effect can be exploited to produce contrast in MRI (for a review see Henkelman et al. (1) and Tofts (2)) and is sensitive to the principal constituents of myelin in human WM (3). MT can be described using a two-component model, grouping spins into the free (or liquid) pool, consisting of water hydrogen nuclei with long T 2 (T 2f > 10 ms), and the restricted (or semisolid) pool, consisting of hydrogen nuclei of large lipids with T 2 too short to be imaged directly using MRI (T 2r < 100 ls). Detailed information about these spin populations can be mapped using offresonance QMTI techniques, with an appropriate twopool model of MT in tissue (4). QMTI yields the relative size of the restricted proton pool (F), the first-order forward magnetization exchange rate (k f ), and most relaxation parameters of the free and restricted pools (R 1f , T 2f , and T 2r ) (5).While QMTI measurements do not provide absolute specificity to the molecular constituents of tissue, there is convergent evidence that MT changes in WM reflect cha...

The therapeutic mode of action of dimethyl fumarate (DMF), approved for treating patients with relapsing-remitting multiple sclerosis, is not fully understood. Recently, we and others demonstrated that Ab-independent functions of distinct B cell subsets are important in mediating multiple sclerosis (MS) relapsing disease activity. Our objective was to test whether and how DMF influences both the phenotype and functional responses of disease-implicated B cell subsets in patients with MS. High-quality PBMC were obtained from relapsing-remitting MS patients prior to and serially after initiation of DMF treatment. Multiparametric flow cytometry was used to monitor the phenotype and functional response-profiles of distinct B cell subsets. Total B cell counts decreased following DMF treatment, largely reflecting losses of circulating mature/differentiated (but not of immature transitional) B cells. Within the mature B cell pool, DMF had a greater impact on memory than naive B cells. In keeping with these in vivo effects, DMF treatment in vitro remarkably diminished mature (but not transitional B cell) survival, mediated by inducing apoptotic cell death. Although DMF treatment (both in vivo and in vitro) minimally impacted B cell IL-10 expression, it strongly reduced B cell expression of GM-CSF, IL-6, and TNF-α, resulting in a significant anti-inflammatory shift of B cell response profiles. The DMF-mediated decrease in B cell proinflammatory cytokine responses was further associated with reduced phosphorylation of STAT5/6 and NF-κB in surviving B cells. Together, these data implicate novel mechanisms by which DMF may modulate MS disease activity through shifting the balance between pro- and anti-inflammatory B cell responses.