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[求助] 请求翻译杨咏威教授的一篇文章

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发表于 2008-12-31 11:33:12 | 显示全部楼层 |阅读模式
有关治疗脊髓损伤的十个问题
Ten Frequently Asked Questions Concerning Cure of Spinal Cord InjuryDecember 21, 2008 by Wise Young
Ten Frequently Asked Questions Concerning Cure of Spinal Cord Injury
By Wise Young, PhD MD
W. M. Keck Center for Collaborative Neuroscience
Revised 20 December 2008 from 21 July 2004
Many questions recur repeatedly on CareCure every few days.  On 21 July 2004, I posted a summary of answers to the ten most frequently asked questions on CareCure (Link) .  That thread received over 450 responses and over 80,000 page-views. Here, I update some of responses to the questions and will expand each of the answers with sequential articles to follow.
1. Will there be a cure for spinal cord injury?
The answer to this question depends on one’s definition of a cure. If a “cure” requires complete eradication of spinal cord injury, I think that it would unlikely in my lifetime.  If a cure means complete restoration of all functions to pre-injury levels for all people with spinal cord injury, I think that this would also be unlikely.  Not only are we unlikely to be able to reverse aging but we may not be able to reverse all changes in the body due to spinal cord injury.  On the other hand, I believe that there will be therapies that will restore sufficient function to a person with severe spinal cord injury so that a casual third-party observer would not be able to tell that the person had spinal cord injury.  This is a reasonably practical definition of a cure for me and I think that will happen.
2. When will a cure be available?
First generation therapies are already restoring function to people with spinal cord injury, including weight-supported treadmill ambulation training, decompression and untethering of a spinal cord, and Fampridine.  Preliminary data suggest that olfactory ensheathing glia transplants may restore some sensory function but only modest motor function, perhaps because the cells are not HLA-matched and are immune-rejected after a few weeks.  Second generation therapies are in or soon-to-be started clinical trial, including umbilical cord blood mononuclear cells, Schwann cells, and embryonic stem cells.  Several therapies such as Nogo receptor blockers and Nogo antibodies, glial-derived neurotrophic factor, cethrin, and other treatments are already in or are close to clinical trial.  Finally, third generation therapies include combination cell transplants, growth factors, and growth inhibitor blockers.  These should be in clinical trial in the next few years. The timing of clinical trials depends on availability of funding for clinical trials. With sufficient funding, I think that one or more of these clinical trials will yield the first therapies that restore function in chronic spinal cord injury.
3. Will a cure work for chronic spinal cord injury?
I believe there will be effective restorative therapies for chronic spinal cord injury for the following reasons. First, much animal and human data indicate that regeneration of relatively few axons can restore function such as walking, bladder function, and sexual function. This is because the spinal cord contains much of the circuitry necessary to execute and control these functions. Only 10% of the axons in the spinal cord are necessary and sufficient to restore locomotor and other functions.  Second, axons continue to try to regrow for many years after injury. Treatments that provide a path for growth, that negate factors that inhibit growth, and that provide long-term stimulation of axonal growth can restore function.  Third, many people recover function years after injury.  These observations give me hope that there will be therapies that facilitate functional recovery in chronic spinal cord injury.
4. What can I do now to be ready for the cure?
People with spinal cord injury should work hard to take care of their body and to prevent muscle and bone atrophy that may prevent recovery of function. This includes disciplined exercise to maintain their muscle and bone.  They must take care of their skin, bladder, and bowels. People should avoid procedures that cause irreversible loss of peripheral nerve and other functions. On the other hand, it is important to weigh the benefits of procedures such as tendon transfers, which can provide greater functionality and independence for people with weak hands. Likewise, certain procedures such as Mitrofanoff and bladder augmentation to reduce bladder spasticity may provide greater independence but may not be easily reversible.  Finally, many studies have shown that people with the highest levels of education after injury are more likely to have better quality of life and health. It is important that people do not neglect their brain, the most important part of their body.
5. What can I do about spasticity, spasms, and neuropathic pain?
Many people suffer from spasticity (increased tone), spasms (spontaneous movements), and neuropathic pain (in areas below the injury site where there sensory loss). Neurons that have lost their inputs tend to become hyperexcitable. Spasticity is the most common manifestation of spinal motoneurons that have been disconnected from the brain. Several treatments reduce spasticity. The most commonly used anti-spasticity drug is baclofen (a drug that stimulates GABA-B receptors in the spinal cord). Oral doses of baclofen of 80-120 mg/day reduce spasticity.  However, for some people such doses are not enough or have too many side effects.  For these people, it may be necessary to combine lower doses of baclofen with clonidine or tizanidine, which activate alpha-adrenergic receptors. While anti-spasticity drugs reduce spasticity, they also weaken muscles and may cause flaccidity and muscle atrophy. So, people should titrate the dose of anti-spasticity drugs so that they retain some muscle tone.  Unless they are taken in doses high enough to cause flaccidity, anti-spasticity drugs usually do not prevent spasms.  However, neurontin (gabapentin) and other anti-epileptic drug may reduce both spasms and neuropathic pain.  Neuropathic pain results from increased excitability of sensory neurons that have been disconnected and may manifest in “burning”, “freezing”, or “pressure” pain.  People accommodate to gabapentin and higher doses of as much as 4000 mg/day may be necessary for pain relief.  In some people, low doses (20 mg/day) of the tricyclic anti-depressant drug amitriptyline (Elavil) may provide relief from neuropathic pain.  Intrathecal delivery of these baclofen or morphine may be necessary.
6. How can I exercise and will it do any good?
Exercise is difficult for paralyzed people and specialized equipment are necessary and useful. First, most people should get standing frames so that they can stand for an hour or two every day. A device called a Glider 6000 allows both standing and some leg movements for people.  Second, functional electrical stimulation (FES) can be used to activate leg muscles and the legs can be stimulated to pedal an exercise bike.  Third, standing and walking in a swimming pool allows people to walk in an environment where the water supports their weight. Fourth, weight-supported treadmill ambulation training has been shown to improve walking recovery. Finally, people should think about setting aside a month or two every year where they would essentially engage in full-time training. During the rest of the year, they need to maintain the gains that they have achieved by spending an hour or so per day on exercising. Although there have been few formal studies of the subject, many people with spinal cord injury have reported significant increases in the girth of their legs when they use FES regularly.
7. What is osteoporosis, its mechanisms and consequences, and ways to reverse it?
Osteoporosis is bone loss and occurs after spinal cord injury, particularly in the pelvis and leg bones below the injury site. The mechanism is not well understood but appears to be related to loss of gravitational and other mechanical stresses on the bone. In acute spinal cord injury, bone begins to decalcify within days after spinal cord injury, with significant increases in urine calcium (hypercalciuria) within 10 days. The pattern of bone loss is 2-4 times greater than those associated with prolonged bed rest without spinal cord injury. Increased dietary calcium intake may slow down but does not prevent the bone loss.  Parathyroid hormone level is usually low in the first year but may increase above normal after the first year. Substantial (25-43%) decreases in bone mineral densities occur in the leg bones within a year and may exceed 50% loss by 10 years.  People with spasticity have less bone loss than those who are flaccid. Osteoporosis is associated with greater fracture rates. The Model Spinal Cord Injury System, for example, reported a 14% incidence of fracture by 5 years after injury, 28% and 39% by 10 and 15 years, usually in the most demineralized bone. People with complete spinal cord injury and paraplegia have ten times greater fracture rates than incomplete injury or tetraplegia. Weight bearing and bicycling with functional electrical stimulation may prevent osteoporosis. Pswith isphosphonates (Pamidronate) and parathyroid hormone (Teriparatide) can osteoporosis and reduce fracture rates in people with chronic spinal cord injury.  Much research is underway to find effective therapies of osteoporosis.
8. What is autonomic dysreflexia, its mechanisms and consequences, and treatments?
Autonomic dysreflexia (AD) refers to increased activity of the sympathetic nervous system, associated with profuse sweating, rash, elevated blood pressure, and vasodilation above the injury level.  AD usually causes a headache due to vasodilation of brain blood vessels. Heart rate falls and vision may be blurred. Nasal congestion may be present. Between 40-90% of people with spinal cord injury suffer from AD.  It is more severe in people with spinal cord injury above T6. AD can be triggered by many potential causes, including bladder distension, urinary tract infection, and manipulation of the bowel and bladder system, pain or irritation, menstruation, labor and delivery, sexual intercourse, temperature changes, constrictive clothing, sunburns, and insect bites. When AD occurs, doctors usually catheterize the bladder to ensure adequate urinary drainage, check for fecal impaction manually using lidocaine jelly as a lubricant, and eliminate all other potential causes of irritation to the body. Treatment includes use of the calcium channel blocker Nifedipine (Procardia 10 mg capsule) to reduce blood pressure or adrenergic alpha-receptor blocking agent phenoxybenzamine (10 mg twice a day), mecamylamine (Inversine 2.5 mg orally), and Diazoxide (Hyperstat 1-3 mg/kg).  Doctors in emergency room may not know how to handle AD crises in people with spinal cord injury and it may be useful for patients to carry a card that give treatment instructions.
9. What is syringomyelia, its mechanisms and consequences, and treatments?
Syringomyelia refers to the development a spinal cord cyst that results from enlargement of the central canal. The central canal is typically tiny and not visible on magnetic resonance images (MRI) of the spinal cord. As many as 15% of people develop a syringomyelic cyst in their spinal cords and 5% may show symptoms of pain and loss of function associated with cyst enlargement, as early as one month and as late as 45 years after injury. Pain is the most commonly reported symptom associated with syringomyelia. Other symptoms include increased weakness, loss of sensation, greater spasticity, and increased sweating. The symptoms may be aggravated by postural changes and Valsalva maneuver (that increase pressure in the chest).  It may also be associated with changes in bladder reflexes, autonomic dysreflexia, painless joint deformity or swelling, increased spasticity, dissociation of sensation and temperature, respiratory impairment. Syringomyelic cysts can be observed with MRI scans. It is usually associated with scarring of meninges or arachnoid membranes of the spinal cord, observable with CT-scan with myelography. Surgical intervention is recommended when there is progressive neurological loss. Traditionally, syringomyelia has been treated with shunting of the cyst by placement of a catheter between the cyst and the subarachnoid space or pleural cavity. But shunting alone is frequently associated with shunt blockade within a year. More recent studies suggest that meticulous removal of adhesions with duroplasty (repairing the dura by grafting membrane) to re-establish subarachnoid cerebrospinal fluid flow is more effective and may eliminate the cyst in 80% of cases.
10.  How does spinal cord injury affect sexual function and what can be done to improve such function?
Most people with spinal cord injury above the T10 will continue to have reflex erections associated with stimulation. Some people may have prolonged erections called priapism. A majority can have ejaculation although increased stimulation including vibration may be required. In many people, ejaculation may be retrograde, i.e. the ejaculate goes into the bladder rather comes out, because the external sphincter may be open. Retrograde ejaculation should not be harmful or cause urinary tract infections. A serious associated complication of sexual intercourse in both men and women is the occurrence of autonomic dysreflexia (AD) with orgasm, with associated headaches and other symptoms of AD. These can be treated with drugs to lower blood pressure (see answer to AD above). In addition, sexual intercourse may be associated with increased spasticity and spasms. People with injuries below T10 may have damage to the spinal cord centers responsible for erection and ejaculation. Many techniques are available to increase erection, including drugs such as Sildenafil (Viagra), vacuum pumps, cock rings, and penile prostheses. Several studies have reported that women with “complete” spinal cord injury can achieve orgasms, possibly through neural pathways outside of the spinal cord.

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发表于 2008-12-31 13:06:09 | 显示全部楼层
用软件做的翻译,请英文好的朋友修正。

十大常见问题关于治疗脊髓损伤

明智的年轻博士,医学博士
苏惠凯克神经科学中心的合作
经修订的2008年12月20号从2004年7月21日
许多问题出现反复CareCure每隔几天。关于2004年7月21日,我发布了简要的回答十个最常见问题CareCure (链接) 。该线程收到超过450名的答复和80000页的意见。在这里,我更新一些的问题作出答复,并扩大每个答案顺序条款遵循。

1、是否有一种治疗脊髓损伤?  

这个问题的答案取决于一个人的定义治愈。如果一个“治疗”要求彻底根除脊髓损伤,我认为这是不可能在我的有生之年。如果一种治疗手段完全恢复所有功能,以受伤前的水平,所有的人脊髓损伤,我认为这也将是不可能的。我们不仅是不可能扭转衰老,但我们可能无法扭转的所有变化的机构,由于脊髓损伤。另一方面,我相信会有疗法将恢复足够的功能,一个人有严重脊髓损伤,使休闲第三方观察员将无法告诉的人脊髓损伤。这是一个合理的切实可行的定义治愈我,我认为这会发生。

2、当将一种治疗可?  

第一代疗法已经恢复功能,以人与脊髓损伤,包括体重减重平板步行训练,减压untethering的脊髓,并Fampridine 。初步数据显示,嗅鞘胶质细胞移植可能恢复一些感觉功能,但只有轻微的运动功能,也许是因为细胞不HLA匹配和免疫拒绝几周后。第二代疗法或即将开始临床试验,包括脐血单个核细胞,雪旺氏细胞和胚胎干细胞。一些疗法,如Nogo受体阻滞剂和勿动蛋白抗体,胶质细胞源性神经营养因子, cethrin ,和其他治疗方法已在或接近临床试验。最后,第三代疗法包括结合细胞移植,生长因子,以及生长抑制剂阻断。这些应该在临床试验在未来几年。时间的临床试验,取决于资金供应情况进行临床试验。有了足够的资金,我认为,一个或多个这样的临床试验将取得的第一个恢复功能的治疗慢性脊髓损伤。  

3、将一种治疗工作慢性脊髓损伤?  

我相信会有有效的恢复性治疗慢性脊髓损伤的原因如下。首先,许多动物和人类的数据表明,再生轴突相对较少,可以恢复功能,如散步,膀胱功能和性功能。这是因为脊髓包含大量的电路必须执行和控制这些功能。只有10 %的轴突脊髓是必要的和足够的恢复运动和其他功能。第二,继续努力轴突再生后多年损伤。治疗提供了一个路径增长,否定因素,抑制经济增长,并提供长期刺激轴突生长可以恢复功能。第三,很多人多年后恢复功能损伤。这些意见给我希望,将有治疗,促进功能恢复的慢性脊髓损伤。  

4、我能做些什么现在就必须准备好治疗?  

人脊髓损伤要努力照顾他们的身体,防止肌肉和骨骼萎缩可能会妨碍恢复功能。这包括纪律部队工作,以维持其肌肉和骨骼。他们必须照顾他们的皮肤,膀胱,肠子。人们应该避免程序,造成不可逆转的损失,周围神经和其他职能。另一方面,重要的是要权衡利益的程序,如肌腱转移,使他们能提供更强大的功能和独立的人,脆弱的手。同样,某些程序,如Mitrofanoff和膀胱扩大,以减少膀胱痉挛可提供更大的独立性,但可能不容易逆转。最后,许多研究表明,人的最高层次的教育,伤后更可能有更好的生活质量和健康。重要的是,人们不要忽略他们的大脑,最重要的部分身体。  
5、我能做些什么约痉挛,痉挛,与神经性疼痛?  

许多人患有痉挛(提高声调) ,痉挛(自发运动) ,以及神经性疼痛(以下领域中受伤的网站那里感觉丧失) 。神经元失去了他们的意见往往成为hyperexcitable 。痉挛是最常见的表现,脊髓运动神经元已断开大脑。一些治疗减少痉挛。最常用的抗痉挛药物的巴氯芬(一种药物,刺激γ -氨基丁酸一B受体在脊髓) 。口服剂量的巴氯芬在80-120毫克/天减少痉挛。然而,对某些人这种剂量是不够的,或有太多的副作用。对于这些人,也许有必要结合低剂量的巴氯芬可乐定或替扎尼定,其中激活α -肾上腺素受体。虽然抗痉挛药物降低痉挛,也削弱,而且可能会导致肌肉痿和肌肉萎缩。因此,人们应该滴定剂量的抗痉挛药物,使他们保持某种程度的肌肉张力。除非他们采取的剂量很高,足以造成痿,抗痉挛药物通常不会防止痉挛。然而,加巴(加巴喷丁)和其他抗癫痫药物可减少痉挛和神经性疼痛。神经性疼痛的结果增加了兴奋的感觉神经元已断开,并可能体现在“燃烧” , “冻结” ,或“压力”的痛苦。人适应加巴喷丁和高剂量高达4000毫克/天可能是必要的缓解疼痛。在一些人中,低剂量( 20毫克/天)的三环抗抑郁药阿米替林( Elavil )可提供救济神经痛。鞘内提供这些巴氯酚或吗啡可能是必要的。

6、我该如何行使,并将它做什么好?  

运动是困难的瘫痪人民和专门设备是必要和有益的。首先,大多数人应该得到常设框架,使他们能够站在一两个小时,每天。装置称为滑翔机6000允许常务委员会和一些腿部运动的人。其次,功能性电刺激(中文)可以用来激活腿部肌肉和腿部可以刺激到踏板行使自行车。第三,站立和行走在一个游泳池允许人们走在这样一种环境,水支持自己的体重。第四,体重减重平板步行训练已经显示出改善步行复苏。最后,人们应该考虑撤销一两个月内,每年在那里他们将主要从事专职培训。在今年余下的,他们需要维持收益,他们所取得的开支一小时左右每天行使。尽管有少数正式研究这个问题,许多人与脊髓损伤的报道显着增加其腿围时经常使用中文。  

7、什么是骨质疏松症,其机制和后果,以及如何扭转?  

骨质疏松症是骨量丢失和发生脊髓损伤后,特别是在骨盆和腿骨低于损伤的网站。该机制没有得到很好的理解,但似乎是有关损失的引力和其他机械应力对骨。在急性脊髓损伤,骨开始decalcify在几天内脊髓损伤后,有显着增加尿中钙(尿症)在10天之内。格局的骨丢失是2-4倍大于那些与长期卧床无脊髓损伤。增加膳食钙的摄入可能会降低,但并不阻止骨丢失。甲状旁腺激素水平低,通常在头一年可能会增加,但高于正常后的第一年。大幅度( 25-43 % )下降骨密度发生在腿骨在一年之内,并有可能超过50 % ,损失了10年。痉挛的人少骨丢失比谁是弛缓。骨质疏松与骨折率更大。示范脊髓损伤系统,例如,报告说, 14 %发生骨折,伤后5年内, 28 %和39 %的10年和15年,通常在最脱钙骨。人们完全脊髓损伤并截瘫的10倍骨折率比不完全损伤或四肢。负重和骑自行车的功能性电刺激可预防骨质疏松症。 Pswith isphosphonates (帕米膦酸)和甲状旁腺素(特立帕肽)可以减少骨质疏松症和骨折率,患慢性脊髓损伤。大量的研究正在寻找有效的治疗骨质疏松症。  

8、什么是自主dysreflexia ,它的机制和后果,和治疗?  

自主dysreflexia ( AD )的指活动的增加交感神经系统,伴随着丰富的出汗,皮疹,血压升高,并高于损伤血管的水平。广告通常会导致头痛,由于脑血管舒张血管。心率下降和远见可能是模糊的。鼻塞可出席。之间40-90 %的人脊髓损伤遭受反倾销。这是更严重的人,脊髓损伤上述扩建。广告可以引发许多潜在的原因,包括膀胱腹胀,尿路感染,并操纵肠和膀胱制度,疼痛或不适,月经,劳动和分娩,性交,温度变化,缩窄服装,灼伤,和昆虫叮咬。当广告出现,医生们通常导尿膀胱,以确保有足够的尿液引流,检查粪便嵌塞手动使用利多卡因果冻作为润滑剂的作用,并消除所有其他潜在原因刺激身体。治疗包括使用钙通道阻滞剂硝苯地平( Procardia 10毫克胶囊) ,以降低血压或肾上腺素能α -受体阻滞剂酚苄明( 10毫克,每日2次) ,美加明( Inversine 2.5毫克口头)和二氮嗪( Hyperstat 1-3毫克/千克) 。急诊室医生可能不知道如何处理危机的公元人民脊髓损伤,它可能是有用的病人携带一张卡片,让治疗的指示。   

9、什么是脊髓空洞症,其机制和后果,和治疗?  

脊髓空洞症是指发展脊髓囊肿的结果扩大的中央管。中央管通常是不可见的微小和磁共振图像( MRI检查)脊髓。多达15 %的人制定一个syringomyelic囊肿在脊髓和5 %的会出现的疼痛和功能丧失与囊肿扩大,早在1个月,直到45年之后损伤。疼痛是最常见的症状与脊髓空洞症。其他症状包括增加弱点,感觉丧失,更多的痉挛,并增加出汗。这些症状可能会加剧姿势变化和Valsalva动作(即增加压力的胸部) 。它也可能与膀胱反射的变化,自主dysreflexia ,无痛的关节畸形或肿胀,增加痉挛,分离的感觉,温度,呼吸障碍。 Syringomyelic囊肿可以看到核磁共振扫描。它通常与疤痕的脑膜或蛛网膜脊髓,观察到的CT扫描与脊髓。外科干预的建议时,逐步神经损失。传统上,一直在治疗脊髓空洞症与分流的囊肿安置导管之间的囊肿和蛛网膜下腔或肋膜腔。但分流单独现象往往伴随着分流封锁在一年之内。更多最近的研究表明,细致消除粘连与duroplasty (修补硬脑膜嫁接膜) ,以重新建立蛛网膜下腔脑脊液流是更有效和更可消除囊肿80 %的情况下。   

10、如何脊髓损伤影响性功能和能够做些什么来改善这种功能?  

大多数人的脊髓损伤以上在T10将继续反射勃起与刺激。有些人可能延长勃起称为@J异常勃起。大多数射精虽然可以增加刺激包括振动可能需要。在许多人来说,可能是逆行性射精,即射精进入膀胱而出来的,因为外括约肌可能打开。逆行性射精不应有害或造成尿路感染。一个严重的相关并发症的发生性关系的男性和女性的发生是自主dysreflexia ( AD )的与性高潮,与相关的头痛和其他症状的AD 。这些可以治疗药物降低血压(见答案公元段) 。此外,性交可能与增加痉挛和抽搐。受伤的人可能有以下的T10损害脊髓中心负责安装和射精。许多技术可提高勃起,包括药物,如西地那非(伟哥) ,真空泵,公鸡戒指,和@J假体。一些研究报告,妇女与“完整的”脊髓损伤可实现性高潮,可能通过神经通路以外的脊髓。

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发表于 2008-12-31 13:38:43 | 显示全部楼层
有关治疗脊髓损伤的十个问题
十大常见问题关于治疗脊髓InjuryDecember 21 , 2008明智的杨
十大常见问题关于治疗脊髓损伤
明智的年轻博士,医学博士
苏惠凯克神经科学中心的合作
经修订的2008年12月20号从2004年7月21日
许多问题出现反复CareCure每隔几天。关于2004年7月21日,我发布了简要的回答十个最常见问题CareCure (链接) 。该线程收到超过450名的答复和80000页的意见。在这里,我更新一些的问题作出答复,并扩大每个答案顺序条款遵循。
1 。是否有一种治疗脊髓损伤?
这个问题的答案取决于一个人的定义治愈。如果一个“治疗”要求彻底根除脊髓损伤,我认为这是不可能在我的有生之年。如果一种治疗手段完全恢复所有功能,以受伤前的水平,所有的人脊髓损伤,我认为这也将是不可能的。我们不仅是不可能扭转衰老,但我们可能无法扭转的所有变化的机构,由于脊髓损伤。另一方面,我相信会有疗法将恢复足够的功能,一个人有严重脊髓损伤,使休闲第三方观察员将无法告诉的人脊髓损伤。这是一个合理的切实可行的定义治愈我,我认为这会发生。
2 。当将一种治疗可?
第一代疗法已经恢复功能,以人与脊髓损伤,包括体重减重平板步行训练,减压untethering的脊髓,并Fampridine 。初步数据显示,嗅鞘胶质细胞移植可能恢复一些感觉功能,但只有轻微的运动功能,也许是因为细胞不HLA匹配和免疫拒绝几周后。第二代疗法或即将开始临床试验,包括脐血单个核细胞,雪旺氏细胞和胚胎干细胞。一些疗法,如Nogo受体阻滞剂和勿动蛋白抗体,胶质细胞源性神经营养因子, cethrin ,和其他治疗方法已在或接近临床试验。最后,第三代疗法包括结合细胞移植,生长因子,以及生长抑制剂阻断。这些应该在临床试验在未来几年。时间的临床试验,取决于资金供应情况进行临床试验。有了足够的资金,我认为,一个或多个这样的临床试验将取得的第一个恢复功能的治疗慢性脊髓损伤。
3 。将一种治疗工作慢性脊髓损伤?
我相信会有有效的恢复性治疗慢性脊髓损伤的原因如下。首先,许多动物和人类的数据表明,再生轴突相对较少,可以恢复功能,如散步,膀胱功能和性功能。这是因为脊髓包含大量的电路必须执行和控制这些功能。只有10 %的轴突脊髓是必要的和足够的恢复运动和其他功能。第二,继续努力轴突再生后多年损伤。治疗提供了一个路径增长,否定因素,抑制经济增长,并提供长期刺激轴突生长可以恢复功能。第三,很多人多年后恢复功能损伤。这些意见给我希望,将有治疗,促进功能恢复的慢性脊髓损伤。
4 。我能做些什么现在就必须准备好治疗?
人脊髓损伤要努力照顾他们的身体,防止肌肉和骨骼萎缩可能会妨碍恢复功能。这包括纪律部队工作,以维持其肌肉和骨骼。他们必须照顾他们的皮肤,膀胱,肠子。人们应该避免程序,造成不可逆转的损失,周围神经和其他职能。另一方面,重要的是要权衡利益的程序,如肌腱转移,使他们能提供更强大的功能和独立的人,脆弱的手。同样,某些程序,如Mitrofanoff和膀胱扩大,以减少膀胱痉挛可提供更大的独立性,但可能不容易逆转。最后,许多研究表明,人的最高层次的教育,伤后更可能有更好的生活质量和健康。重要的是,人们不要忽略他们的大脑,最重要的部分身体。
5 。我能做些什么约痉挛,痉挛,与神经性疼痛?
许多人患有痉挛(提高声调) ,痉挛(自发运动) ,以及神经性疼痛(以下领域中受伤的网站那里感觉丧失) 。神经元失去了他们的意见往往成为hyperexcitable 。痉挛是最常见的表现,脊髓运动神经元已断开大脑。一些治疗减少痉挛。最常用的抗痉挛药物的巴氯芬(一种药物,刺激γ -氨基丁酸一B受体在脊髓) 。口服剂量的巴氯芬在80-120毫克/天减少痉挛。然而,对某些人这种剂量是不够的,或有太多的副作用。对于这些人,也许有必要结合低剂量的巴氯芬可乐定或替扎尼定,其中激活α -肾上腺素受体。虽然抗痉挛药物降低痉挛,也削弱,而且可能会导致肌肉痿和肌肉萎缩。因此,人们应该滴定剂量的抗痉挛药物,使他们保持某种程度的肌肉张力。除非他们采取的剂量很高,足以造成痿,抗痉挛药物通常不会防止痉挛。然而,加巴(加巴喷丁)和其他抗癫痫药物可减少痉挛和神经性疼痛。神经性疼痛的结果增加了兴奋的感觉神经元已断开,并可能体现在“燃烧” , “冻结” ,或“压力”的痛苦。人适应加巴喷丁和高剂量高达4000毫克/天可能是必要的缓解疼痛。在一些人中,低剂量( 20毫克/天)的三环抗抑郁药阿米替林( Elavil )可提供救济神经痛。鞘内提供这些巴氯酚或吗啡可能是必要的。
6 。我该如何行使,并将它做什么好?
运动是困难的瘫痪人民和专门设备是必要和有益的。首先,大多数人应该得到常设框架,使他们能够站在一两个小时,每天。装置称为滑翔机6000允许常务委员会和一些腿部运动的人。其次,功能性电刺激(中文)可以用来激活腿部肌肉和腿部可以刺激到踏板行使自行车。第三,站立和行走在一个游泳池允许人们走在这样一种环境,水支持自己的体重。第四,体重减重平板步行训练已经显示出改善步行复苏。最后,人们应该考虑撤销一两个月内,每年在那里他们将主要从事专职培训。在今年余下的,他们需要维持收益,他们所取得的开支一小时左右每天行使。尽管有少数正式研究这个问题,许多人与脊髓损伤的报道显着增加其腿围时经常使用中文。
7 。什么是骨质疏松症,其机制和后果,以及如何扭转?
骨质疏松症是骨量丢失和发生脊髓损伤后,特别是在骨盆和腿骨低于损伤的网站。该机制没有得到很好的理解,但似乎是有关损失的引力和其他机械应力对骨。在急性脊髓损伤,骨开始decalcify在几天内脊髓损伤后,有显着增加尿中钙(尿症)在10天之内。格局的骨丢失是2-4倍大于那些与长期卧床无脊髓损伤。增加膳食钙的摄入可能会降低,但并不阻止骨丢失。甲状旁腺激素水平低,通常在头一年可能会增加,但高于正常后的第一年。大幅度( 25-43 % )下降骨密度发生在腿骨在一年之内,并有可能超过50 % ,损失了10年。痉挛的人少骨丢失比谁是弛缓。骨质疏松与骨折率更大。示范脊髓损伤系统,例如,报告说, 14 %的骨折发生率,伤后5年内, 28 %和39 %的10年和15年,通常在最脱钙骨。人们完全脊髓损伤并截瘫的10倍骨折率比不完全损伤或四肢。负重和骑自行车的功能性电刺激可预防骨质疏松症。 Pswith isphosphonates (帕米膦酸)和甲状旁腺素(特立帕肽)可以减少骨质疏松症和骨折率,患慢性脊髓损伤。大量的研究正在寻找有效的治疗骨质疏松症。
8 。什么是自主dysreflexia ,它的机制和后果,和治疗?
自主dysreflexia ( AD )的指活动的增加交感神经系统,伴随着丰富的出汗,皮疹,血压升高,并高于损伤血管的水平。广告通常会导致头痛,由于脑血管舒张血管。心率下降和远见可能是模糊的。鼻塞可出席。之间40-90 %的人脊髓损伤遭受反倾销。这是更严重的人,脊髓损伤上述扩建。广告可以引发许多潜在的原因,包括膀胱腹胀,尿路感染,并操纵肠和膀胱制度,疼痛或不适,月经,劳动和分娩,性交,温度变化,缩窄服装,灼伤,和昆虫叮咬。当广告出现,医生们通常导尿膀胱,以确保有足够的尿液引流,检查粪便嵌塞手动使用利多卡因果冻作为润滑剂的作用,并消除所有其他潜在原因刺激身体。治疗包括使用钙通道阻滞剂硝苯地平( Procardia 10毫克胶囊) ,以降低血压或肾上腺素能α -受体阻滞剂酚苄明( 10毫克,每日2次) ,美加明( Inversine 2.5毫克口头)和二氮嗪( Hyperstat 1-3毫克/千克) 。急诊室医生可能不知道如何处理危机的公元人民脊髓损伤,它可能是有用的病人携带一张卡片,让治疗的指示。
9 。什么是脊髓空洞症,其机制和后果,和治疗?
脊髓空洞症是指发展脊髓囊肿的结果扩大的中央管。中央管通常是不可见的微小和磁共振图像( MRI检查)脊髓。多达15 %的人制定一个syringomyelic囊肿在脊髓和5 %的会出现的疼痛和功能丧失与囊肿扩大,早在1个月,直到45年之后损伤。疼痛是最常见的症状与脊髓空洞症。其他症状包括增加弱点,感觉丧失,更多的痉挛,并增加出汗。这些症状可能会加剧姿势变化和Valsalva动作(即增加压力的胸部) 。它也可能与膀胱反射的变化,自主dysreflexia ,无痛的关节畸形或肿胀,增加痉挛,分离的感觉,温度,呼吸障碍。 Syringomyelic囊肿可以看到核磁共振扫描。它通常与疤痕的脑膜或蛛网膜脊髓,观察到的CT扫描与脊髓。外科干预的建议时,逐步神经损失。传统上,一直在治疗脊髓空洞症与分流的囊肿安置导管之间的囊肿和蛛网膜下腔或肋膜腔。但分流单独现象往往伴随着分流封锁在一年之内。更多最近的研究表明,细致消除粘连与duroplasty (修补硬脑膜嫁接膜) ,以重新建立蛛网膜下腔脑脊液流是更有效和更可消除囊肿80 %的情况下。
10 。如何脊髓损伤影响性功能和能够做些什么来改善这种功能?
大多数人的脊髓损伤以上在T10将继续反射勃起与刺激。有些人可能延长勃起称为@J异常勃起。大多数射精虽然可以增加刺激包括振动可能需要。在许多人来说,可能是逆行性射精,即射精进入膀胱而出来的,因为外括约肌可能打开。逆行性射精不应有害或造成尿路感染。一个严重的相关并发症的发生性关系的男性和女性的发生是自主dysreflexia ( AD )的与性高潮,与相关的头痛和其他症状的AD 。这些可以治疗药物降低血压(见答案公元段) 。此外,性交可能与增加痉挛和抽搐。受伤的人可能有以下的T10损害脊髓中心负责安装和射精。许多技术可提高勃起,包括药物,如西地那非(伟哥) ,真空泵,公鸡戒指,和@J假体。一些研究报告说,妇女与“完整的”脊髓损伤可实现性高潮,可能通过神经通路以外的脊髓。

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发表于 2008-12-31 14:54:02 | 显示全部楼层
谢谢楼上三位朋友,你们辛苦了!

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发表于 2009-1-8 09:38:27 | 显示全部楼层
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谢谢楼上的朋友!

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