Aim Though combination of clopidogrel added to aspirin has been compared to aspirin alone in patients with stroke or transient ischemic attack, limited data exists on the relative efficacy and safety between clopidogrel and aspirin monotherapy in patients with a recent ischemic stroke. We aimed to compare clopidogrel versus aspirin monotherapy in this population. Methods PubMed, Embase, and CENTRAL databases were searched from inception to May 2018 to identify clinical trials and observational studies comparing clopidogrel versus aspirin for secondary prevention in patients with recent ischemic stroke within 12 months. Pooled effect estimates were calculated using a random effects model and were reported as risk ratios with 95% confidence intervals. Results Five studies meeting eligibility criteria were included in the analysis. A total of 29,357 adult patients who had recent ischemic stroke received either clopidogrel (n = 14, 293) or aspirin (n = 15, 064) for secondary prevention. Pairwise meta-analysis showed a statistically significant risk reduction in the occurrence of major adverse cardiovascular and cerebrovascular events (risk ratio 0.72 [95% CI, 0.53–0.97]), any ischemic or hemorrhagic stroke (0.76 [0.58, 0.99), and recurrent ischemic stroke (0.72 [0.55, 0.94]) in patients who received clopidogrel versus aspirin. The risk of bleeding was also lower for clopidogrel versus aspirin (0.57 [0.45, 0.74]). There was no difference in the rate of all-cause mortality between the two groups. Conclusions The analysis showed lower risks of major adverse cardiovascular or cerebrovascular events, recurrent stroke, and bleeding events for clopidogrel monotherapy compared to aspirin. These findings support clinical benefit for single antiplatelet therapy with clopidogrel over aspirin for secondary prevention in patients with recent ischemic stroke.

Vascular cognitive impairment (VCI) and vascular dementia are the most common forms of cognitive disorder associated with cerebrovascular disease and related to increased morbidity and mortality among the older population. Growing evidence suggests the contribution of blood-pressure variability, cardiac arrhythmia, hyperactivation of the renin–angiotensin–aldosterone system, endothelial dysfunction, vascular remodeling and stiffness, different angiopathies, neural tissue homeostasis, and systemic metabolic disorders to the pathophysiology of VCI. In this review, we focus on factors contributing to cerebrovascular disease, neurovascular unit alterations, and novel approaches to cognitive improvement in patients with cognitive decline. One of the important factors associated with the neuronal causes of VCI is the S100B protein, which can affect the expression of cytokines in the brain, support homeostasis, and regulate processes of differentiation, repair, and apoptosis of the nervous tissue. Since the pathological basis of VCI is complex and diverse, treatment affecting the mechanisms of cognitive disorders should be developed. The prospective role of a novel complex drug consisting of released–active antibodies to S100 and to endothelial NO synthase in VCI treatment is highlighted.

Examination of a patient with chronic low back pain (LBP) is aimed at eliminating its specific cause and assessing the social and psychological factors of chronic pain. The diagnosis of chronic nonspecific (musculoskeletal) LBP is based on the exclusion of a specific cause of pain, discogenic radiculopathy, and lumbar stenosis. It is advisable to identify possible pain sources: pathology of intervertebral disc pathology, facet joints, and sacroiliac joint and myofascial syndrome.An integrated multidisciplinary approach (a high level of evidence), including therapeutic exercises, physical activity optimization, psychological treatments (cognitive behavioral therapy), an educational program (back pain school for patients), and manual therapy, is effective in treating chronic musculoskeletal LBP. For pain relief, one may use nonsteroidal anti-inflammatory drugs in minimally effective doses and in a short cycle, muscle relaxants, and a capsaicin patch, and, if there is depressive disorder, antidepressants (a medium level of evidence). Radiofrequency denervation or therapeutic blockages with anesthetics and glucocorticoids (damage to the facet joints, sacroiliac joint), back massage, and acupuncture (a low level of evidence) may be used in some patients.Therapeutic exercises and an educational program (the prevention of excessive loads and prolonged static and uncomfortable postures and the use of correct methods for lifting weights, etc.) are recommended for preventive purposes.

ABSTRACT. Over 44 million people suffer from dementia around the world. Researchers estimated that there will be 48.1 million people with dementia by 2020 and 90.3 million by 2040. In addition to dementia, mild cognitive impairment (MCI) and subjective cognitive decline (SCD) relate to cognitive impairment. It has been established that MCI precedes dementia, however the significance of SCD is still unclear. Recent studies suggest that SCD could be a risk factor for objective cognitive impairment. SCD is defined as а self-estimated decline in cognitive capacity in comparison to an individual’s previous level of functioning, which cannot be determined by neuropsychological tests. Objectives: To perform a systematic review of prospective longitudinal cohort studies that assessed the risk of MCI and dementia among people with SCD. Methods: A search was carried out for all available peer-reviewed articles in English related to SCD in PubMed and PsychINFO databases from database initiation through January 2020. The keywords used for the search were ‘subjective cognitive (or memory) impairment (or decline or complaints)’. Three authors separately determined the inclusion or exclusion of all articles retrieved for full-text evaluation. Results: The chance of progression to dementia in the SCD group was 2.17 (95% confidence interval [95%CI] 1.53‒3.07; p<0.05) compared to normal aging. Furthermore, the SCD group was 2.15 times more likely to progress to MCI than the group without SCD (95%CI 1.39‒3.30; p=0.005). Conclusions: SCD might precede cognitive impairment, however, more detailed longitudinal studies should be conducted.

BackgroundVestibular vertigo is associated with substantially reduced quality of life. Betahistine is effective in improving vertigo-associated symptoms, with longer treatment periods leading to greater improvements; however, it is not known whether these effects persist after treatment cessation.MethodsVIRTUOSO was a prospective, multinational, non-comparative, post-marketing observational programme investigating the effectiveness of betahistine (48 mg/day) and the course of vertigo after the discontinuation of treatment. Patients with vestibular vertigo who were prescribed 48 mg/day betahistine were enrolled in Russia and Ukraine. Treatment duration was up to 2 months, and patients were followed up for 2 months after discontinuation of betahistine. Efficacy endpoints included clinical response (assessed by change in vertigo severity), monthly attack frequency, and physician and patient grading of overall clinical response and improvement of vertigo-associated symptoms.ResultsOverall, 309 patients were enrolled and 305 completed the study. Clinical response was rated as good, very good or excellent in 74.1% of patients at end of treatment, with vertigo severity significantly decreased from baseline (p < 0.001). Monthly vertigo attack frequency decreased significantly during the 2 months of treatment (p < 0.001 from baseline) and further decreased during the 2-month follow-up (p < 0.001 from end of treatment). Overall, clinical response was graded as good or excellent by 94.4% of physicians and 95.4% of patients. Clinical improvement was considered either good or excellent by 82.6–90.5% of physicians and patients for nausea, vomiting and faintness. Only one adverse event was reported, with no serious adverse events.ConclusionOur findings suggest that betahistine (48 mg/day) therapy is effective in treating vertigo in routine clinical settings. The observed effects persisted for 2 months after treatment cessation, suggesting that betahistine may facilitate lasting vestibular compensation.