What are the known effects of yoga on the brain in relation to motor performances,body awareness and pain? A narrative review

ObjectiveThe current body of literature was reviewed to evaluate the effects of yoga on the brain in relation to motor performance, body awareness and pain.BackgroundYoga has been increasingly popular in the Western countries especially for its unique integration of the mind and body. Yoga has been studied more intensely in the last decade. Although it has been shown to improve cognitive functions, few studies have looked into the effects of yoga on improving motor performance, body awareness or pain and the possible underlying brain mechanisms associated with them.MethodsA search of the current literature was made using keywords such as: “yoga brain motor”, “yoga brain pain”, “effects yoga brain” and “effects yoga brain motor performance”. The findings were then discussed in relation to motor performance, body awareness and pain and their reported mechanisms of action on the brain.ResultsA total of 61 articles were selected, out of which 29 were excluded because they did not meet our criteria. A total of thirty-two articles were included in this review, which we further subdivided by focus: motor performance (n = 10), body awareness (n = 14) and pain (n = 8).DiscussionOur review shows that yoga has a positive effect on learning rate, speed and accuracy of a motor task by increasing attention and decreasing stress through a better control of sensorimotor rhythms. Yoga also seems to improve sensory awareness and interoception, regulate autonomic input, increase parasympathetic activity and promote self-regulation. Yoga was also shown to reduce the threat signal, increase pain tolerance, decrease pain unpleasantness and decrease the anxiety and distress associated with pain. Those changes are associated with the recruitment of specific brain areas such as the insula, the amygdala and the hippocampus.ConclusionBased on the studies reviewed in this report, we found that the practice of yoga seems to facilitate motor learning, to increase body awareness and to decrease pain. These are associated with a wide variety of changes in terms of brain activity and structure. Further studies are necessary to reveal its precise mechanism of action on the brain and to validate its wider application in clinical settings.     

Association of Bezafibrate Treatment With Reduced Risk of Cancer in Patients With Coronary Artery Disease

ObjectiveTo evaluate the association between bezafibrate, a drug used to treat hypertriglyceridemia, and long-term cancer incidence in patients with coronary artery disease (CAD).Patients and MethodsThe study comprised 2980 patients with CAD (mean age, 60 years; 2729 [91.6%] men) who were free of cancer and were enrolled in the Bezafibrate Infarction Prevention study, a double-blind trial conducted between May 1, 1990, and January 31, 1993, in 18 cardiology departments in Israel. Patients randomized to receive 400 mg of bezafibrate (n=1486) or placebo (n=1494) daily for a median of 6.2 years (range, 4.7-7.6 years) were followed up for incidence of cancer through the Israeli National Cancer Registry and all-cause death through the Population Registry of the State of Israel until December 31, 2013. Cox proportional hazards and Fine and Gray survival models were used to assess the bezafibrate-cancer association.ResultsClinical characteristics and laboratory values were well balanced between the 2 groups at the study entry. Over a median follow-up of 22.5 years (range, 21.2-23.9 years), cancer developed in 753 patients. With death considered a competing event, the cumulative incidence of cancer at the end of the follow-up was lower in the bezafibrate vs the placebo group (23.9%; 95 CI, 21.9%-26.1% vs 27.2%; 95 CI, 25.1%-29.4%; P=.04). The hazard ratio for cancer in the bezafibrate vs placebo groups was 0.86 (95% CI, 0.74-0.99). In mediation analysis, the association between bezafibrate treatment and cancer incidence was not sensitive to adjustment for on-trial lipid levels but was attenuated on adjustment for on-trial fibrinogen levels.ConclusionBezafibrate treatment is associated with reduced risk of cancer among patients with CAD. Fibrinogen, but not lipid lowering, is linked to this association.     

早期高压氧干预对创伤性脑损伤后认知功能障碍影响的DTI研究

目的 观察早期高压氧治疗对创伤性脑损伤后认知功能障碍的临床治疗效果,并通过扩散张量成像（DTI）技术探讨其神经作用机制。 方法 采用随机数字表法将64例创伤性脑损伤后认知障碍患者分为对照组和高压氧组,每组32例。2组患者均给予常规基础治疗及认知康复训练,高压氧组在此基础上辅以高压氧治疗。于治疗前、治疗2个疗程后分别采用简易智能精神状态量表（MMSE）和蒙特利尔认知功能评估量表（MoCA）对2组患者认知功能进行评估。从2组患者中各随机抽取15例于治疗前、后进行常规T1WI平扫及DTI扫描,将影像学数据与量表评估结果进行相关性分析。 结果 治疗后2组患者MMSE评分及MoCA评分均较治疗前有不同程度提高,并且以高压氧组MMSE评分［（22.75±3.50）分］、MoCA评分［（21.47±3.39）分］的改善幅度较显著,与对照组间差异有统计学意义（P<0.05);经Pearson相关性分析发现,对照组脑白质差异区各向异性分数值(FA)与MMSE评分、MoCA评分无显著相关性（P>0.05）,高压氧组胼胝体、双侧内囊前肢、左侧上纵束FA值与MMSE评分及MoCA评分具有正相关性(P<0.05)。 结论 早期高压氧治疗联合常规认知训练能进一步改善创伤性脑损伤患者认知功能;其作用机制可能与调节胼胝体、双侧内囊前肢、左侧上纵束等脑白质区结构与功能有关。     

Effects of Moderate Alcohol Consumption on the Central Nervous System*

The concept of moderate consumption of ethanol (beverage alcohol) has evolved over time from considering this level of intake to be nonintoxicating and noninjurious, to encompassing levels defined as “statistically” normal in particular populations, and the public health-driven concepts that define moderate drinking as the level corresponding to the lowest overall rate of morbidity or mortality in a population. The various approaches to defining moderate consumption of ethanol provide for a range of intakes that can result in blood ethanol concentrations ranging from 5 to 6 mg/dl, to levels of over 90 mg/dl (i.e., 20 mM). This review summarizes available information regarding the effects of moderate consumption of ethanol on the adult and the developing nervous systems. The metabolism of ethanol in the human is reviewed to allow for proper appreciation of the important variables that interact to influence the level of exposure of the brain to ethanol once ethanol is orally consumed. At the neurochemical level, the moderate consumption of ethanol selectively affects the function of GABA, glutamatergic, serotonergic, dopaminergic, cholinergic, and opioid neuronal systems. Ethanol can affect these systems directly, and/or the interactions between and among these systems become important in the expression of ethanol's actions. The behavioral consequences of ethanol's actions on brain neurochemistry, and the neurochemical effects themselves, are very much dose- and time-related, and the collage of ethanol's actions can change significantly even on the rising and falling phases of the blood ethanol curve. The behavioral effects of moderate ethanol intake can encompass events that the human or other animal can perceive as reinforcing through either positive (e.g., pleasurable, activating) or negative (e.g., anxiolysis, stress reduction) reinforcement mechanisms. Genetic factors and gender play an important role in the metabolism and behavioral actions of ethanol, and doses of ethanol producing pleasurable feelings, activation, and reduction of anxiety in some humans/animals can have aversive, sedative, or no effect in others. Research on the cognitive effects of acute and chronic moderate intake of ethanol is reviewed, and although a number of studies have noted a measurable diminution in neuropsychologic parameters in habitual consumers of moderate amounts of ethanol, others have not found such changes. Recent studies have also noted some positive effects of moderate ethanol consumption on cognitive performance in the aging human. The moderate consumption of ethanol by pregnant women can have significant consequences on the developing nervous system of the fetus. Consumption of ethanol during pregnancy at levels considered to be in the moderate range can generate fetal alcohol effects (behavioral, cognitive anomalies) in the offspring. A number of factors–including gestational period, the periodicity of the mother's drinking, genetic factors, etc.–play important roles in determining the effect of ethanol on the developing central nervous system. A series of recommendations for future research endeavors, at all levels, is included with this review as part of the assessment of the effects of moderate ethanol consumption on the central nervous system     

急性脑缺血模型大鼠胃肠黏膜血流变化及组织形态学的改变

目的探讨急性脑缺血模型大鼠早期胃肠黏膜血流变化及组织形态学的改变。方法雄性Wistar大鼠64只,随机分为两组:脑缺血模型组(32只)和假手术对照组(32只),两组大鼠分别按术后6、12、24、48 h时相点分为4个亚组(每组均为8只)。测定胃肠黏膜血流量,光镜和透射电镜下观察肠黏膜组织形态学变化。结果脑缺血组各时相点的胃、肠黏膜血流量(mV)分别为术后6 h(148±13、34．5±3．2),12 h(102±11、22．7±1．9),24 h(125±10、26．2±4．3),48 h(137±15、30．5±4．1),均低于对照组同时相点的术后6 h(285±17、46．8±5．4),12 h(301±21、50．1±3．6),24 h (294±24、45．4±4．1),48 h(318±11、48．7±7．3),两组比较,差异有统计学意义(P相似文献   

Pancreatic carcinoma with brain metastases: case report and literature review

The case of a patient developing multiple brain metastases from carcinoma of the exocrine pancreas has been described. A 56-year-old man with stage IV pancreatic cancer attained a clinical and radiographic response while receiving the G-FLIP chemotherapy regimen (biweekly gemcitabine, irinotecan, 5-fluorouracil, leucovorin and cisplatin). After 4 months of therapy, he developed gait imbalance and weakness in the right hand. An MRI of the brain showed multiple 1-2 mm enhancing nodules in the cerebral hemispheres and pons. A subsequent biopsy confirmed that these were pancreatic carcinoma metastases. The patient experienced a rapid deterioration in his neurological status and died 3 days after brain biopsy. Previously reported cases of brain metastases from pancreatic cancer are reviewed.     

高尿酸血症与冠心病的相关性

为探讨高尿酸血症与冠心病之间的关系 ,对 2 0 0 9例拟诊冠心病行冠状动脉造影的患者测定禁食 12h后静脉血清尿酸值及其它生物化学指标。结果发现 ,冠心病组血清尿酸显著高于正常冠状动脉组 (36 9± 97mmol/L比 35 6± 94mmol/L ,P <0 .0 1)。单因素分析显示 ,高尿酸血症与冠心病显著相关 (χ2 MH=4 .36 4 ,P =0 .0 37,OR值为1.2 4 )。急性心肌梗死患者尿酸增高病例数较正常冠状动脉组明显增多。多因素回归分析显示血清尿酸与冠心病(χ2 wald=4 .76 ,P =0 .0 2 92 ,OR值为 0 .999)和急性心肌梗死 (χ2wald=2 3.4 8,P =0 .0 0 0 1,OR值为 1.0 0 4 )呈显著正相关。糖尿病或吸烟合并高尿酸血症时 ,OR值均明显升高。因此 ,高尿酸血症与冠心病发病显著相关 ,尤其当合并糖尿病或吸烟时该关系更为明显。     

血管紧张素原基因T174M和血管紧张素转换酶基因I/D多态性与急性心肌梗死的相关性

目的探讨中国汉族人群血管紧张素转换酶和血管紧张素原基因型的分布及其与急性心肌梗死的关系。方法应用聚合酶链反应技术,对112例急性心肌梗死患者、128例非冠心病患者血管紧张素转换酶I/D多态性及血管紧张素原T174M多态性进行检测。结果血管紧张素转换酶基因型分布及等位基因频率在病例组及对照组间差异有显著性(P<0.01)。病例组和对照组血管紧张素原基因型及等位基因频率总体分布差异亦有显著性(P<0.05)。联合基因分析显示,急性心肌梗死组血管紧张素转换酶DD基因型 血管紧张素原174MM基因型频率显著高于对照组(P<0.01),具有该联合基因型者发生冠心病的风险比数比(OR=8.467)明显高于单独具有血管紧张素转换酶DD基因型(OR=2.558)或血管紧张素原174MM基因型(OR=6.176)者。结论血管紧张素原T174M基因多态性中M等位基因和血管紧张素转换酶I/D基因多态性基因中的D等位基因是中国汉族人群冠心病发病的危险因素之一。同时具有血管紧张素转换酶DD型及血管紧张素原174MM型发生冠心病的相对风险显著高于单基因血管紧张素转换酶DD型及单基因血管紧张素原174MM型。     

Effects of chronic alcohol consumption on the broad phospholipid signal in human brain: an in vivo 31P MRS study

BACKGROUND: Phosphorus magnetic resonance spectroscopy (31P MRS) allows for the measurement of phospholipids and their breakdown products in the human brain. Fairly mobile membrane phospholipids give rise to a broad signal that co-resonates with metabolic phosphodiesters. Chronic alcohol exposure increases the rigidity of isolated brain membranes and, thus, may affect the amount and transverse relaxation times (T2) of MRS-detectable phospholipids. We tested the hypothesis that subjects who were heavy drinkers have stiffer membranes than controls who were light drinkers, as reflected in a smaller broad signal component and a shorter T2 of the broad signal in 31P MR spectra of the brain. METHODS: Thirteen alcohol-dependent heavy drinkers (mean age 44 years) were studied by localized 31P MRS in the centrum semiovale and compared with 17 nondependent light drinkers of similar age. The broad component signal was separated from the metabolite signal by convolution difference, which is based on the large difference in line widths of these two signals. Longitudinal and T2 relaxation times were measured using standard methods. RESULTS: The broad component integral was 13% lower in the brain of heavy drinkers compared with light drinkers (p < 0.001) and remained significantly smaller after corrections for both longitudinal and transverse relaxations (p < 0.01). The T2 distribution of the broad component consistently showed two resolvable components in both groups. The fast relaxing component had the same T2 in both groups (T2 = 1.9 msec). The slower relaxing component T2 was 0.6 msec shorter in heavy drinkers compared with light drinkers (p = 0.08). CONCLUSIONS: These results, observed in the absence of white matter volume loss, are consistent with biochemical alterations and higher rigidity of white matter phospholipids associated with long-term chronic alcohol abuse. The observed smaller broad signal component in these relatively young heavy drinkers is a sensitive measure of white matter phospholipid damage.