Volume 32, Issue 6

Multiple sclerosis (MS) is a neurodegenerative disease associated with inflammatory demyelination and astroglial activation, with neuronal and axonal damage as the leading factors of disability. We aimed to perform a meta-analysis to determine changes in CSF levels of neuronal and glial biomarkers, including neurofilament light chain (NFL), total tau (t-tau), chitinase-3-like protein 1 (CHI3L1), glial fibrillary acidic protein (GFAP), and S100B in various groups of MS (MS versus controls, clinically isolated syndrome (CIS) versus controls, CIS versus MS, relapsing-remitting MS (RRMS) versus progressive MS (PMS), and MS in relapse versus remission. According to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses, we included 64 articles in the meta-analysis, including 4071 subjects. For investigation of sources of heterogeneity, subgroup analysis, meta-regression, and sensitivity analysis were conducted. Meta-analyses were performed for comparisons including at least three individual datasets. NFL, GFAP, t-tau, CHI3L1, and S100B were higher in MS and NFL, t-tau, and CHI3L1 were also elevated in CIS patients than controls. CHI3L1 was the only marker with higher levels in MS than CIS. GFAP levels were higher in PMS versus RRMS, and NFL, t-tau, and CHI3L1 did not differ between different subtypes. Only levels of NFL were higher in patients in relapse than remission. Meta-regression showed influence of sex and disease severity on NFL and t-tau levels, respectively and disease duration on both. Added to the role of these biomarkers in determining prognosis and treatment response, to conclude, they may serve in diagnosis of MS and distinguishing different subtypes.

Depression continues to carry a major disease burden worldwide, with limitations on the success of traditional pharmacological or psychological treatments. Recent approaches have therefore focused upon the neurobiological underpinnings of depression, and on the “individualization” of depression symptom profiles. One such model of depression has divided the standard diagnostic criteria into four “depression subtypes”, with neurological and behavioral pathways. At the same time, attention has been focused upon the region of the brain known as the “default mode network” (DMN) and its role in attention and problem-solving. However, to date, no review has been published of the links between the DMN and the four subtypes of depression. By searching the literature studies from the last 20 years, 62 relevant papers were identified, and their findings are described for the association they demonstrate between aspects of the DMN and the four depression subtypes. It is apparent from this review that there are potential positive clinical and therapeutic outcomes from focusing upon DMN activation and connectivity, via psychological therapies, transcranial magnetic stimulation, and some emerging pharmacological models.

Exercise has been shown to have beneficial effects on brain functions in humans and animals. Exercise can improve memory and learning in age-related neurodegenerative diseases. In animal models, physical exercise regulates epigenetics, promotes synaptic plasticity and hippocampal neurogenesis, regulates the expression levels of neurotrophic factors, and improves cognitive function. Therefore, exercise is very important for brain rehabilitation and remodeling. The purpose of this review is to explore the mechanisms by which exercise exerts positive effects on brain function. This knowledge implies that physical exercise can be used as a non-drug therapy for neurological diseases.

Hemorrhagic stroke (HS) is a major cause of death and disability worldwide, despite being less common, it presents more aggressively and leads to more severe sequelae than ischemic stroke. There are two types of HS: Intracerebral Hemorrhage (ICH) and Subarachnoid Hemorrhage (SAH), differing not only in the site of bleeding, but also in the mechanisms responsible for acute and subacute symptoms. This is a systematic review of databases in search of works of the last five years relating to the comprehension of both kinds of HS. Sixty two articles composed the direct findings of the recent literature and were further characterized to construct the pathophysiology in the order of events. The road to the understanding of the spontaneous HS pathophysiology is far from complete. Our findings show specific and individual results relating to the natural history of the disease of ICH and SAH, presenting common and different risk factors, distinct and similar clinical manifestations at onset or later days to weeks, and possible complications for both.

During COVID-19 pandemic, a wide variety of stroke typologies have been described in patients affected by SARS-CoV-2. Investigating the case reports of acute stroke in COVID-19 patients, published since the beginning of the pandemic, we tried to trace the pathogenic mechanisms of stroke during SARS-CoV-2 infection. We conducted a systematic review analyzing demographic data, cerebrovascular risk factors, NIHSS score, vascular territory involvement and laboratory findings of 168 patients described in 89 studies, from a pool of 1243 records. Based on our results, we have identified different stroke profiles: (1) cerebral large vessel disease (CLVD) profile with a low disability, simultaneous onset of COVID-19 and stroke symptoms, good outcome and low serum levels of D-dimer and CRP; (2) intracranial bleeding (IB) profile with high disability, poor outcome and low levels of serum markers of inflammation and coagulopathy; (3) CLVD profile with a short time-lapse between COVID-19 symptoms and stroke onset, high neurological disability and very high systemic inflammatory markers; (4) multiple thrombo-embolic disease (MTED) profile with older patients, many comorbidities, disabling stroke, poor outcome, evident alteration of coagulation tests and high serum levels of both D-dimer and CRP. We therefore summarized these different profiles in a spectrum similar to that of visible light, where the violet–blue band included IB and CSVD with low inflammation and prothrombotic activity, the green–yellow band included CLVD with high inflammation and moderate prothrombotic activity and the orange–red band for MTED with moderate-high levels of inflammation and very high prothrombotic activity.

The sudden and storming onset of coronavirus 2 infection (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) was associated by severe acute respiratory syndrome. Recently, corona virus disease 19 (COVID-19) has appeared as a pandemic throughout the world. The mutational nature of the virus, along with the different means of entering and spreading throughout the body has involved different organs. Thus, patients are faced with a wide range of symptoms and signs. Neurological symptoms, such as anosmia, agnosia, stroke, paralysis, cranial nerve deficits, encephalopathy, meningitis, delirium and seizures, are reported as common complications affecting the course of the disease and its treatment. In this review, special attention was paid to reports that addressed the acute or chronic neurological manifestations in COVID-19 patients who may present acute respiratory syndrome or not. Moreover, we discussed the central (CNS) and peripheral nervous system (PNS) complications in SARS-Cov2-infected patients, and also the pathophysiology of neurological abnormalities in COVID-19.