英语科普小知识 失眠似与多动腿综合症有关联

海量资料下载 免费学习英语 www.englishvip.com/xinlw.htm （申请网址） Johns Hopkins researchers believe they may have discovered an explanation for the sleepless nights associated with restless legs syndrome (RLS), a symptom that persists even when the disruptive, overwhelming nocturnal（夜的） urge to move the legs is treated successfully with medication. Neurologists have long believed RLS is related to a dysfunction in the way the brain uses the neurotransmitter dopamine（多巴胺）, a chemical used by brain cells to communicate and produce smooth, purposeful muscle activity and movement. Disruption of these neurochemical signals, characteristic of Parkinson's disease, frequently results in involuntary movements. Drugs that increase dopamine levels are mainstay treatments for RLS, but studies have shown they don't significantly improve sleep. An estimated 5 percent of the U.S. population has RLS.   The small new study, headed by Richard P. Allen, Ph.D., an associate professor of neurology at the Johns Hopkins University School of Medicine, used MRI to image the brain and found glutamate -- a neurotransmitter involved in arousal -- in abnormally high levels in people with RLS. The more glutamate（谷氨酸盐） the researchers found in the brains of those with RLS, the worse their sleep.   The findings are published in the May issue of the journal Neurology. "We may have solved the mystery of why getting rid of patients' urge to move their legs doesn't improve their sleep," Allen says. "We may have been looking at the wrong thing all along, or we may find that both dopamine and glutamate pathways play a role in RLS."   For the study, Allen and his colleagues examined MRI images and recorded glutamate activity in the thalamus, the part of the brain involved with the regulation of consciousness, sleep and alertness. They looked at images of 28 people with RLS and 20 people without. The RLS patients included in the study had symptoms six to seven nights a week persisting for at least six months, with an average of 20 involuntary movements a night or more.   The researchers then conducted two-day sleep studies in the same individuals to measure how much rest each person was getting. In those with RLS, they found that the higher the glutamate level in the thalamus（丘脑）, the less sleep the subject got. They found no such association in the control group without RLS.   Previous studies have shown that even though RLS patients average less than 5.5 hours of sleep per night, they rarely report problems with excessive daytime sleepiness. Allen says the lack of daytime sleepiness is likely related to the role of glutamate, too much of which can put the brain in a state of hyperarousal -- day or night.   If confirmed, the study's results may change the way RLS is treated, Allen says, potentially erasing the sleepless nights that are the worst side effect of the condition. Dopamine-related drugs currently used in RLS do work, but many patients eventually lose the drug benefit and require ever higher doses. When the doses get too high, the medication actually can make the symptoms much worse than before treatment. Scientists don't fully understand why drugs that increase the amount of dopamine in the brain would work to calm the uncontrollable leg movement of RLS.   Allen says there are already drugs on the market, such as the anticonvulsive gabapentin enacarbil, that can reduce glutamate levels in the brain, but they have not been given as a first-line treatment for RLS patients.   RLS wreaks havoc on sleep because lying down and trying to relax activates the symptoms. Most people with RLS have difficulty falling asleep and staying asleep. Only getting up and moving around typically relieves the discomfort. The sensations range in severity from uncomfortable to irritating to painful.   "It's exciting to see something totally new in the field -- something that really makes sense for the biology of arousal and sleep," Allen says. 约翰霍普金斯大学的研究人员认为，他们可能已经发现了一个解释不眠之夜不宁腿综合征（RLS），症状仍然存在，即使在破坏性的，压倒性夜间（夜的）督促动腿成功治疗用药。神经学家一直认为RLS相关的异常，大脑使用神经递质多巴胺（多巴胺），化学所使用的脑细胞进行沟通和产生光滑，有针对性的肌肉活动和运动的方式。这些神经化学信号中断，帕金森氏病的特征，常常导致不自主运动。增加多巴胺水平的药物的治疗RLS的中流砥柱，但有研究明他们没有显着改善睡眠。据估计，5％的美国人口有RLS。   小新研究中，由理查德·P.艾伦博士，约翰斯·霍普金斯大学医学院神经学副教授在使用MRI脑图像，并发现谷氨酸-一种神经递质参与觉醒-在人与RLS异常高的水平。谷氨酸（谷氨酸盐）的研究人员发现，那些与RLS的大脑，他们的睡眠更糟。   该研究结果发表在五月号的“神经学”杂志上。“，为什么摆脱病人的冲动把他们的腿，并不能改善他们的睡眠，我们可能已经解开了这个谜团，”艾伦说。“我们可能一直在寻找一直在错误的东西，或者我们可能会发现，多巴胺和谷氨酸途径发挥作用的RLS。”   在这项研究中，艾伦和他的同事们研究了MRI的图像和录制的谷氨酸在丘脑的活动，意识，睡眠和警觉性与调控有关的大脑部分。看着他们与RLS 28人及20人无图像。RLS患者纳入研究范围有症状六，七晚一个星期，持续至少6个月，平均20不自主运动一晚或以上。   然后，研究人员进行了为期两天的睡眠研究在同一个人来衡量每个人得到多少休息。在那些与RLS，他们发现较高的谷氨酸水平在丘脑（丘脑），少睡的主了。他们并没有发现这种关联对照组不RLS。   以往的研究表明，即使RLS患者平均每晚睡眠少于5.5小时的，他们很少与白天过度嗜睡问题报告。艾伦说，白天嗜睡可能与缺乏太多谷氨酸的作用，可以把大脑过度反应的状态 - 白天或晚上。   如果得到证实，这项研究的结果可能会改变RLS治疗，艾伦说，可能擦除不眠之夜的条件是最坏的副作用。多巴胺相关药物目前用于在RLS做工作，但许多患者最终失去了药物的利益和要求越来越高剂量。当剂量太高，实际上用药可使症状比治疗前更糟糕。科学家并不完全了解为什么无法控制的腿部运动的RLS药物，提高大脑中的多巴胺量将努力平息。   艾伦说，已经有市场上的药物，如的抗惊厥加巴喷丁enacarbil，可以降低大脑中的谷氨酸含量，但他们并没有被给予作为第一线治疗RLS患者。   RLS肆虐对睡眠，因为平躺并试图放松激活症状。与RLS的大多数人有入睡和保持睡眠困难。只有通常起床走动，减轻不适。感觉不舒服的刺激痛苦的严重程度。   “这是令人兴奋地看到全新的东西在现场 - 这是真正有意义的觉醒和睡眠的生物学，”艾伦说。 “成千上万人疯狂下载。。。。。。 更多价值连城的绝密英语学习资料， 洛基内部秘密英语，技巧，策略 请在 网上 申请报名” 洛基国际英语 竭诚为您服务