Effects of Transcranial Direct Current Stimulation on Motor and Cognitive Dysfunction in an Experimental Traumatic Brain Injury Model.

AIM: To investigate the therapeutic and neuroprotective effects of transcranial direct current stimulation (tDCS) application on the traumatic brain injury (TBI)-induced glutamate and calcium excitotoxicity and loss of motor and cognitive functions. MATERIAL AND METHODS: Forty rats were equally divided in the sham, TBI, tDCS + TBI + tDCS, and TBI + tDCS groups. Mild TBI was induced by dropping a 450-g iron weight from a height of 1 m onto the skull of the rats. The tDCS + TBI + tDCS group was prophylactically administered 1 mA stimulation for 30 min for 7 days starting 5 days before inducing TBI. In the TBI + tDCS group, tDCS (1 mA for 30 min) was administered 2 h after TBI, on days 1 and 2. Cognitive and locomotor functions were assessed using the novel object recognition and open field tests. The calcium, glutamate, and N-methyl-D-aspartate receptor 1 (NMDAR1) levels in the hippocampus were measured using enzyme-linked immunosorbent assay. RESULTS: Although the motor and cognitive functions were substantially reduced in the TBI group when compared with the sham, they improved in the treatment groups (p < 0.05). The calcium, glutamate, and NMDAR1 levels were considerably higher in the TBI group than in the sham (p < 0.001). However, they were considerably lower in the tDCS + TBI + tDCS and TBI + tDCS groups than in the TBI groups (p < 0.05). In particular, the change in the tDCS + TBI + tDCS group was higher than that in the TBI + tDCS group. CONCLUSION: Application of tDCS before the development of TBI improved motor and cognitive dysfunction. It demonstrated a neuroprotective and therapeutic effect by reducing the excitotoxicity via the regulation of calcium and glutamate levels.

Cerebellar cavernous angioma associated with developmental venous anomaly presenting as a cerebellopontine angle neoplasm in CT scan.

Association of developmental venous anomaly (DVA) and cavernous malformation (CM) of the posterior fossa is rare. If bleeding occurs, it must be assigned to the CM. Developmental venous anomalies, considered as normal vascular variation, are rarely symptomatic. Indeed, the CMs are true malformations and have a high bleeding potential.

Investigation of serum adropin levels and its relationship with hypothalamic atrophy in patients with multiple sclerosis.

OBJECTIVE: Adropin is expressed in vascular endothelial cells and regulates nitric oxide (NO) bioavailability by upregulating nitric oxide. In recent years, some studies have revealed its relationship with the pathogenesis of multiple sclerosis (MS). Our aim in this study is to determine serum adropin levels in MS patients and to investigate adropin levels's relationship with hypothalamic atrophy. METHODS: A total of 80 people, 40 of whom had MS and 40 of whom were healthy volunteers, were included in the study. Serum samples were taken from all participants. Hypothalamus and pituitary diameters were calculated from magnetic resonance imaging of MS patients. The relationship between serum adropin levels and demographic characteristics, Expanded Disability Status Scale (EDSS), and hypothalamic atrophy were evaluated. RESULTS: The levels of adropin were 848,282±139,229 ng/L in patients with MS and 2957,108±284,034 ng/L in the healthy controls. MS patients had significantly lower levels of adropin than the healthy controls (p = 0.003). Adropin has the highest diagnostic value (AUC=0.874, (95% CI, 0,800-0,947) as cut-off value (838.00), sensitivity (80.43%) and specificity (70.64%) in the MS group. In the study, serum adropin levels were not significantly correlated with 3 ventricle diameter (3VD) and pituitary diameter (PD) size (p = 0,968) and no significant relationships were determined between adropin and other clinical parameters. CONCLUSION: As a potential diagnostic marker, adropin levels were significantly lower in MS patients than in those without. Comprehensive studies are needed to verify this entity.

Investigation of serum adropin levels and its relationship with hypothalamic atrophy in patients with multiple sclerosis.

Objective Adropin is expressed in vascular endothelial cells and regulates nitric oxide (NO) bioavailability by upregulating nitric oxide. In recent years, some studies have revealed its relationship with the pathogenesis of multiple sclerosis (MS). Our aim in this study is to determine serum adropin levels in MS patients and to investigate adropin levels's relationship with hypothalamic atrophy. Methods A total of 80 people, 40 of whom had MS and 40 of whom were healthy volunteers, were included in the study. Serum samples were taken from all participants. Hypothalamus and pituitary diameters were calculated from magnetic resonance imaging of MS patients. The relationship between serum adropin levels and demographic characteristics, Expanded Disability Status Scale (EDSS), and hypothalamic atrophy were evaluated. Results The levels of adropin were 0.85±0.14 ng/mL in patients with MS and 2.96 ng/mL±0.285 ng/mL in the healthy controls. MS patients had significantly lower levels of adropin than the healthy controls (p = 0.003). Adropin has the highest diagnostic value (AUC=0.874, (95% CI, 0,800-0,947) as cut-off value (838.00), sensitivity (80.43%) and specificity (70.64%) in the MS group. In the study, serum adropin levels were not significantly correlated with 3 ventricle diameter (3VD) and pituitary diameter (PD) size (p = 0,968) and no significant relationships were determined between adropin and other clinical parameters. Conclusion As a potential diagnostic marker, adropin levels were significantly lower in MS patients than in those without. Comprehensive studies are needed to verify this entity.

Possible roles of sestrin2 in multiple sclerosis and its relationships with clinical outcomes.

BACKGROUND: Characterized by demyelination, inflammation and axonal damage, multiple sclerosis (MS) is one of the most common disorders of central nervous system led by the immune system. There is an urgent and obvious need for biomarkers for the diagnosis and follow-up of MS. OBJECTIVE: To investigate serum levels of sestrin2 (SESN2), a protein that responds to acute stress, in MS patients. METHODS: A total of 85 participants, 40 patients diagnosed previously with relapsing-remitting MS and 45 healthy controls, were included. Serum SESN2 parameters were investigated in blood samples drawn from each participant in the patient and control groups. RESULTS: SESN2 levels were significantly lower in MS patients than in controls (z: -3.06; p=0.002). In the ROC analysis of SESN2, the predictive level for MS was 2.36 ng/mL [sensitivity, 72.50%; specificity, 55.56%; p=0.002; area under the curve (AUC)=0.693]. For the cut-off value in both groups, SESN2 was an independent predictor for MS [Exp (B)=3.977, 95% confidence interval (95%CI) 1.507-10.494 and p=0.013]. CONCLUSIONS: The decreased expression of SESN2 may play a role in MS pathogenesis, and SESN2 could be used as a biomarker for MS and as immunotherapeutic agent to treat MS.