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Objectives. To compare the viability of the numerical rating scale (NRS) and the visual analogue scale (VAS) as a pain assessment tools among a large cohort of patients who underwent microdiscectomy. Summary of Background Data. The pain intensity (PI) reduction is a parameter of surgical treatment efficacy. The two most commonly used scales of PI are NRS and VAS. Many studies have shown strong similarities between those two scales, but the direct interchange is difficult. Methods. Patients, who underwent microdiscectomy, were prospectively enrolled into the study and assessed using VAS and NRS for the back (NRS-B) and the leg (NRS-L), Short Form of McGill Pain Questionnaire (SF-MPQ) included Pain Rating Index (PRI) and Oswestry Disability Index (ODI) 1 day before and 1 month and 3 months after the procedure. Results. 131 patients were included in the study. NRS-L, NRS-B, VAS, and ODI were significantly lower (p<0.001) 1 month after microdiscectomy. NRS-L and NRS-B ratings remained at a similar level while VAS and ODI decreased after 3 months. The rate of decline of PI measured by NRS-L correlated statistically significant (rs = 0.366; p<0.001) with ODI 1 month after surgery. Before surgery, the most significant correlation was found between ODI and NRS-L (rs = 0.494; p<0.001), the lowest with NRS-B (rs = 0.319; p<0.001). 3 months after surgery, there was higher correlations between ODI and VAS (rs = 0.634) than NRS-L (rs = 0.265). PRI correlated significantly (p<0.001) and more stronger with VAS than with NRS-L and NRS-B in every points of assessment. Conclusion. The results showed that PI measurements by NRS-L/NRS-B and VAS mutually correlate and impair functionality evaluated by ODI (convergent validity) but in different modes (differential validity). NRS and VAS are not parallel scales and assess different aspects of pain. The measurement of NRS-L 1 month after microdiscectomy seems to give quick insight into the effectiveness of the procedure.

Cerebral small vessel disease (CSVD) represents a cluster of various vascular disorders with different pathological backgrounds. The advanced vasculature net of cerebral vessels, including small arteries, capillaries, arterioles and venules, is usually affected. Processes of oxidation underlie the pathology of CSVD, promoting the degenerative status of the epithelial layer. There are several classifications of cerebral small vessel diseases; some of them include diseases such as Binswanger’s disease, leukoaraiosis, cerebral microbleeds (CMBs) and lacunar strokes. This paper presents the characteristics of CSVD and the impact of the current knowledge of this topic on the diagnosis and treatment of patients.

Failed Back Surgery Syndrome (FBSS) occurs in 10-40% of patients treated surgically due to disk herniation (DH). There are several factors which can predispose to FBSS, but the exact patomechanism is not elucidated. The aim of this study was to investigate Metalloproteinase-2 (MMP-2) and Tissue Inhibitor of Metalloproteinase-2 (TIMP-2) activities in the homogeneous group of FBSS patients with epidural fibrosis in comparison to its activity in patients with surgically treated DH. Methods: DH, FBSS and control (CG) groups consisted of 30 subjects. The patients were assessed clinically by the Numerical Rating Scale (NRS), McGill Pain Questionnaire (SF -MPQ), Oswestry Disability Index (ODI) and Beck Depression Inventory (BDI). Serum concentrations of MMP-2 and TIMP-2 were measured, by the immunoenzymatic method.Results:There was a significantly higher MMP-2 expression (medians: 4797.49 vs 2656.65; p<0.0001) and TIMP-2 concentration (medians: 166.40 vs 109.60; p<0.0001) in the DH compared to the CG. Also significantly higher MMP-2 expression (4219.95 vs 2656.65; p<0.0001) and TIMP-2 concentration (medians: 150.17 vs 109.60; p=0.0003) were found in the FBSS compared to the CG. Activity of MMP-2 , measured as MMP-2/TIMP-2 was did not significantly change between the DH, FBSS and CG. MMP2 expression (p<0.0001) and TIMP-2 concentration (p<0.0001) were significantly higher in the DH than FBSS.Results indicate the contribution of MMP-2 and TIMP-2 in DH and FBSS. Unchanged activity of MMP-2 can indicate an insufficiency of MMP-2 repair system, in both diseases.Lower MMP-2 expression and TIMP-2concentration in the FBSS group can reflect the chronicity of process.

An increasing number of studies have indicated the important role of cytokines in the development of depressive disturbances (DD). In medically ill patients, cytokines can provoked sickness behavior, the signs of which resemble DD. This results in alterations in behavior to limit energy expenditure and redirect it to cope with particular diseases. The aim of our study was to investigate the role of pro-inflammatory IL-6, TNF-α, and IL-1β and anti-inflammatory IL-10 and TGF-β in DD observed in patients suffering from pain caused by disk herniation (DH) qualified for surgery. The intensity of DD assessed by using Beck Depression Inventory, pain intensity, and functional impairment were evaluated in 70 patients with DH who were qualified for surgery. Pro-inflammatory serum levels of TNF-α, IL-1, IL-6, anti-inflammatory TGF-β, and IL-10 were measured. Elevated serum levels of TGF-β, IL-10, and IL-6 were found in the group with moderate and severe depressive symptoms (SD) compared with the groups with mild (MD) or no depressive symptoms (ND). TGF-β levels were negatively correlated with pain intensity, as assessed using the Present Pain Intensity scale in SD. Functional impairment measured using the Oswestry Disability Index was the most advanced in SD group. Results of our study can suggest association between depressive disturbances and anti-inflammatory cytokines TGF-β and IL-10. Functional impairment of SD group is more severe but serum levels of TGF-β and IL-10, which are involved in the healing processes, are increased.

Metformin (MET), 1,1-dimethylbiguanide hydrochloride, is a biguanide drug used as the first-line medication in the treatment of type 2 diabetes. The recent years have brought many observations showing metformin in its new role. The drug, commonly used in the therapy of diabetes, may also find application in the therapy of a vast variety of tumors. Its effectiveness has been demonstrated in colon, breast, prostate, pancreatic cancer, leukemia, melanoma, lung and endometrial carcinoma, as well as in gliomas. This is especially important in light of the poor options offered to patients in the case of high-grade gliomas, which include glioblastoma (GBM). A thorough understanding of the mechanism of action of metformin can make it possible to discover new drugs that could be used in neoplasm therapy.

Spinal Cord Injury (SCI) is a common neurological disorder with devastating psychical and psychosocial sequelae. The majority of patients after SCI suffer from permanent disability caused by motor dysfunction, impaired sensation, neuropathic pain, spasticity as well as urinary complications, and a small number of patients experience a complete recovery. Current standard treatment modalities of the SCI aim to prevent secondary injury and provide limited recovery of lost neurological functions. Stem Cell Therapy (SCT) represents an emerging treatment approach using the differentiation, paracrine, and self-renewal capabilities of stem cells to regenerate the injured spinal cord. To date, multipotent stem cells including mesenchymal stem cells (MSCs), neural stem cells (NSCs), and hematopoietic stem cells (HSCs) represent the most investigated types of stem cells for the treatment of SCI in preclinical and clinical studies. The microenvironment of SCI has a significant impact on the survival, proliferation, and differentiation of transplanted stem cells. Therefore, a deep understanding of the pathophysiology of SCI and molecular mechanisms through which stem cells act may help improve the treatment efficacy of SCT and find new therapeutic approaches such as stem-cell-derived exosomes, gene-modified stem cells, scaffolds, and nanomaterials. In this literature review, the pathogenesis of SCI and molecular mechanisms of action of multipotent stem cells including MSCs, NSCs, and HSCs are comprehensively described. Moreover, the clinical efficacy of multipotent stem cells in SCI treatment, an optimal protocol of stem cell administration, and recent therapeutic approaches based on or combined with SCT are also discussed.

Objective: The aim of this study is to evaluate neurological scales, as well as biochemical and radiological parameters measured on day 10 after ischemic stroke (IS), according to their value as predictors of the long-term outcome. Material and methods: 45 patients were assessed according to the Barthel Index (BI) and National Institute of Health Stroke Scale (NIHSS) on day 10, and according to Modified Rankin Scale (mRS) 3 months after the onset of IS. On day 10 of IS, the serum level of C-reactive protein (CRP), albumin, D-dimers (DD), S100BB and Tau proteins was measured and the volume of ischemic focus assessed with the use of Computed Tomography (CT). The patients were divided into groups with good outcome (GO) and mRS 0–2, and with bad outcome (BO) and mRS 3–6. Results: NIHSS and BI scores (p<0.001), the volume of ischemic focus (p<0.01), CRP (p<0.01) and albumin level (p<0.05), but not DD, S100BB and Tau protein levels evaluated on day 10, correlated with mRS after 3 months since IS onset. Patients from the BO group were observed to have lower BI (p=0.001), higher NIHSS (p<0.01) and CRP levels (p<0.05), and bigger volume of ischemic focus (p<0.05) measured on day 10 of IS. In the GO group, there were more patients with atherosclerotic etiology (p=0.02 x2=7.856). Regression analysis showed that only the BI score assessed on day 10 of IS can predict the outcome after 3 months assessed by mRS (OR=1.102, 95%, CI:1.01–1.203; p=0.001). Conclusions: BI assessed on day 10 has a predictive value for the outcome evaluated by mRS 3 months after the onset of IS.

Glioblastoma (GBM) is the most popular primary central nervous system cancer and has an extremely expansive course. Aggressive tumor growth correlates with short median overall survival (OS) oscillating between 14 and 17 months. The survival rate of patients in a three-year follow up oscillates around 10%. The interaction of the proteins programmed death-1 (PD-1) and programmed cell death ligand (PD-L1) creates an immunoregulatory axis promoting invasion of glioblastoma multiforme cells in the brain tissue. The PD-1 pathway maintains immunological homeostasis and protects against autoimmunity. PD-L1 expression on glioblastoma surface promotes PD-1 receptor activation in microglia, resulting in the negative regulation of T cell responses. Glioblastoma multiforme cells induce PD-L1 secretion by activation of various receptors such as toll like receptor (TLR), epidermal growth factor receptor (EGFR), interferon alpha receptor (IFNAR), interferon-gamma receptor (IFNGR). Binding of the PD-1 ligand to the PD-1 receptor activates the protein tyrosine phosphatase SHP-2, which dephosphorylates Zap 70, and this inhibits T cell proliferation and downregulates lymphocyte cytotoxic activity. Relevant studies demonstrated that the expression of PD-L1 in glioma correlates with WHO grading and could be considered as a tumor biomarker. Studies in preclinical GBM mouse models confirmed the safety and efficiency of monoclonal antibodies targeting the PD-1/PD-L1 axis. Satisfactory results such as significant regression of tumor mass and longer animal survival time were observed. Monoclonal antibodies inhibiting PD-1 and PD-L1 are being tested in clinical trials concerning patients with recurrent glioblastoma multiforme.