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生物医学专业交流-Biomedicine Discussion
【求助】脑栓死-用何药物治疗？？ |
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【求助】脑栓死-用何药物治疗？？ 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) allenec21 2010-02-08 05:01 同学父亲在国内得了脑栓死，危险期15天，需要紧急治疗，但是国内现在的技术和药物都还不够完善，希望在此能得到大家的帮助~~ 希望对此有相关了解的给予帮助，用何药物可以帮助病人度过危险期或者治愈这种病~~ 谢谢大家的帮助~ 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) allenec21 2010-02-08 05:01  希望与各位结交朋友…… |
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2010-02-08 05:01
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楼主你好。我是... 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) jianglidanfine 2010-02-08 20:58 楼主你好。我是北京宣武医院神经外科医生，现在UCSF学习的，对这个病很熟悉。可能能给你帮助。 我想知道病人的详细情况。这个病不叫“脑栓死”，而是“脑栓塞”或“脑梗死”，都属于缺血性脑血管病，两种名称对应两种不同的病，临床表现可能一样，但发病机制和治疗方法不一样。你说的“危险期”也不确切。所以我需要病人的详细情况，包括发病情况、既往病史和检查结果。 还有，对于这种缺血性脑血管病，国内现在的技术和药物水平已经很高了，尤其是大城市的大医院，这种病很常见，国内的治疗也很规范。如果你同学方便的话，可以咨询北京宣武医院或者上海华山医院，这两家医院的脑血管病诊治水平是国内最高的。 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) jianglidanfine 2010-02-08 20:58 |
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2010-02-08 20:58
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a answer from Diana 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) doctliu 2010-02-09 00:08 Dear Bo and all: Sorry to hear the bad news about your friend's father. Please take a look at this article that I just read and decide if it's something that might be helpful. http://synapse.ucsf.edu/articles/2010/January/28/stroke.html Regards, Diana Scientists Discover New Strategy to Help Stroke Survivors By Helen Shen Staff Writer Stroke is a leading cause of death and disability in industrialized nations, affecting around 15 million people each year, according to the World Health Organization. Most commonly during a stroke, a blocked blood vessel deprives cells in part of the brain of vital blood flow and oxygen. The damage caused to the brain leaves many stroke survivors with permanent cognitive and physical disabilities. Scientists and physicians agree that one of the biggest challenges in treating strokes is delivering clot-busting medications in time to save neurons in the brain. The critical window may be as short as two hours, after which neurons without blood flow become irreversibly damaged. It is estimated that only 1-3% of stroke victims arrive at the hospital in time to be effectively treated. Now, a study published in the December 2009 issue of Nature Medicine points to a new therapeutic strategy that might save dying neurons and extend the treatment window for stroke patients. These new results could lead to drug developments that would improve the lives of many stroke survivors and their caregivers. Historically, neuron loss was thought to be an inevitable and immediate consequence of stroke. However, research from the past twenty years suggests that neuron death in stroke is a multi-step process that could potentially be interrupted if scientists were to identify the right drug targets. While the exact mechanisms of neuron death in stroke are still unclear, many researchers suspect excessive activation of the NMDA receptor (NMDAR) to be a primary cause. Found on the surface of many neuron types, NMDAR plays an important role in helping neurons communicate with one another. In stroke, however, excessive stimulation of NMDAR overloads neurons, triggering a sequence of toxic events that can kill neurons. Researchers at the University of British Columbia, led by Yu Tian Wang, have discovered that a molecule called SREBP-1 appears to be a key player in NMDAR-related neuron death. SREBP-1 belongs to a class of molecules known as transcription factors, which turn genes on and can control a cell’s response to changing environmental conditions like stroke. Some transcription factors promote cell survival while others, like SREBP-1, can facilitate cell death. “The involvement of SREBP-1 in brain injury following stroke is a novel finding, and we do not know many of the details yet,” says Wang, but his team has developed and tested an experimental drug that blocks SREBP-1 and holds early promise for fighting stroke-related brain damage. The drug, called Indip, works by restricting SREBP-1’s access to the genes it normally turns on when NMDAR is overstimulated. The drug does not end stroke, and does not prevent excessive activation of NMDAR, but by suppressing SREBP-1’s function, it appears to block a crucial step along the pathway from NMDAR overstimulation to cell death. In Wang’s study, rats treated with Indip lost only about half as many neurons following stroke, compared to untreated rats. More importantly, the Indip-treated rats showed fewer behavioral deficits the day after stroke, scoring significantly better in tests measuring posture, vision, touch and other brain functions. Further tests showed that the effective treatment window for Indip may extend up to two hours after stroke, with sustained benefits observable one week later. These results, while preliminary, are of potential interest to many like Andy Josephson, who studies and treats stroke as Medical Director of Inpatient Neurology at UCSF. “We see a lot of patients at UCSF who are outside of the critical treatment window for existing acute stroke therapies. Once neurons are dead, opening up blood vessels doesn’t matter much. Blocking SREBP-1 could be a new strategy for keeping neurons alive longer, extending the window for traditional stroke therapies to work.” The road from rodent study to human clinical trials is a long one, and even Wang admits, it will not be easy. Because SREBP-1 is present in many different tissues and cell types, further studies are needed to fully characterize its normal function, as well as possible side effects from blocking its activity. Wang is also running tests to determine the optimum dosages and therapeutic windows of Indip and other similar compounds. Identifying SREBP-1 as a key player in NMDAR-mediated neuron death has wide-ranging implications beyond the treatment of stroke. NMDAR overstimulation is also suspected to cause neuron death in a variety of other neurological conditions including Huntington’s and Parkinson’s Diseases. Future research may show whether blocking SREBP-1 could be a therapeutic strategy for improving brain function in many different patient groups. This article appeared in the January 28, 2010 issue of Synapse. 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) doctliu 2010-02-09 00:08 |
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2010-02-09 00:08
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谢谢大家的帮助~~ 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) allenec21 2010-02-10 11:54 点击下载附件 Click to Download（JPG 格式， 2493 K）  附件里是病人的病情报告，希望2楼的能够再次帮助分析一下，或者给予帮助~~谢谢~ 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) allenec21 2010-02-10 11:54 希望与各位结交朋友…… |
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2010-02-10 11:54
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脑干梗死 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) jianglidanfine 2010-03-28 13:33 楼主你好，很抱歉前一阵一直没上BBS，现在才看到你的回复。不好意思。 病情报告很详细。从病情报告来看，病人的治疗很及时，诊断无误，措施也很得到，需要考虑的方面都考虑到了。基底动脉供血脑干，是多个生命中枢所在的脑区，包括呼吸、血压、内分泌调节中枢，一旦基底动脉血栓形成，引起脑干梗死，如果累及生命中枢，就很容易有生命危险，甚至来不及抢救。 你所提到的病人发病时即出现闭锁综合症，1天后即出现呼吸衰竭，病情进展很快。但治疗措施很及时。脑梗死病人卧床后最常见的并发症就是发热、感染（包括肺部感染、血液系统感染），由于要积极脱水降颅压，极易引起肾功能不全。肾功不全，引起全身毒素在体内积累，高热不退，病情恶化会很快。所以这个病是很凶险的。但从病情报告来看，初始治疗得当及时，肾功不全后的用药调整也可行，没有什么可质疑的。但如果高热不退，可以试用亚低温治疗。但是我看到回复已经一个多月过去了，所以可能有点晚了。但看这治疗过程，知道病人所在的神经内科也是很有经验的，所以楼主不必特别操心病人该如何治。医生自会全力以赴。但这个病本就凶险，很多病人即使是在积极治疗的情况下仍熬不过并发症而去世，或者成为植物人。即使医术再发达，也有束手无策的时候。 但不管怎样，希望听到楼主的好消息，病人能够慢慢康复。 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) jianglidanfine 2010-03-28 13:33 |
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2010-03-28 13:33
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[url=http://ww... 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) makeud 2010-11-19 00:10 [url=http://www.makeyoudifferent.com/][b]wholesale designer sunglasses[/b][/url] [CCB]2[/CCB] 摘自 加州大学论坛旧版 (Universities in California Bulletin Board System) makeud 2010-11-19 00:10 wholesale brand clothing shoes jeans sunglass bikini etc. www.makeyoudifferent.com |
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2010-11-19 00:10
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