椎间盘退变的基因治疗进展

跟腱断裂修复后采用传统的重力垂足位长腿石膏固定,势必使跟腱处于无张力甚至是“失用性”的负性平衡体系下愈合,这种状态可能会抑制跟腱愈合过程中感应“主动”机械信号刺激的关键时机,在此过程中给予的超声波、振动等治疗,也只能使跟腱“被动、间歇”地接受机械刺激。如果在术后采用早期功能锻炼的运动疗法,可以提高跟腱在组织修复过程中功能维持及再塑形的能力,有助于跟腱生物力学特性的恢复。蛋白质组学技术便于从高通量的分子水平揭示运动疗法促进跟腱愈合的机制。     

跟腱损伤修补后的运动疗法：组织学及生物力学评价

背景：开放性跟腱断裂修复后康复时间长、并发症多、功能恢复不尽人意。目前尚缺乏系统、科学、简便、易行的运动疗法促进康复。 目的：观察运用运动疗法对跟腱损伤修补后的组织形态学和力学特性的影响。 方法：日本大耳白兔48只,随机分成制动组和运动组,在距跟腱止点2.0 cm处切断跟腱,建立跟腱损伤模型,缝合线缝合腱周组织后,制动组使用石膏绷带进行传统的重力垂足位长腿石膏固定;运动组不予固定处理。术后7,14,21d分别取跟腱标本,观察肌腱粘连情况及最大断裂应力。 结果与结论：制动组肌腱粘连较运动组明显(P < 0.05)。正常运动组跟腱的最大断裂应力明显高于制动组(P < 0.05)。说明在肌腱愈合的过程中,早期给予动态应力刺激,对促进组织的愈合、减少后遗症等十分有利。     

c/000应用Mitek Anchor系统辅助加固治疗急性闭合性跟腱断裂的临床研究

目的 探讨采用 Mitek Anchor系统辅助加固在修复急性闭合性跟腱断裂中的作用。 方法 12例急性闭合性跟腱断裂患者采用改良Kessler法修补跟腱,后用Mitek Anchor钉各1枚置于跟腱内外侧跟骨内,采用Bunnell方法将尾线由远向近穿经跟腱断端,加固缝合后的跟腱。随访伤口愈合情况,负重行走时间、足跟部疼痛和跟腱再断裂情况,采用Arner-Lindholm方法评价踝关节功能。 结果 术后无切口感染或者皮肤坏死病例。12例患者术后随访14月～25月,平均17月。无足跟部疼痛和再断裂病例发生,根据Arner-Lindholm踝关节功能评定标准,优4例,良8例。结论 采用Mitek Anchor系统辅助加固治疗急性闭合性跟腱断裂疗具有可早期负重,减少跟腱再断裂的发生,是一种理想的治疗方法。     

Bobath联合电刺激疗法对急性脑梗死偏瘫患者运动功能恢复的影响

目的探讨Bobath疗法联合电刺激疗法对急性脑梗死偏瘫患者运动功能恢复的影响。方法选取350例急性脑梗死偏瘫患者为研究对象,根据治疗方式分为对照组和治疗组,每组175例,对照组在常规药物基础上采用Bobath疗法治疗,治疗组在常规药物基础上采用Bobath疗法联合电刺激疗法治疗,治疗28d后观察2组临床疗效,采用四肢简化运动功能评分和改良Barthel指数日常生活活动能力对患者进行评定。结果治疗组总有效率为92.57%,对照组为78.86%,2组比较差异有统计学意义(χ~2=12.343,P=0.000 1)。治疗组运动功能评分和日常生活活动能力评分分别为(70.23±13.52)分和(65.59±14.46)分,改善程度显著高于对照组,差异均有统计学意义(P0.01)。结论 Bobath疗法联合电刺激疗法治疗急性脑梗死偏瘫临床疗效满意,可明显改善患者日常生活活动能力,增强运动功能,值得临床推广应用。     

微创吻合器小切口跟腱吻合修复急性跟腱断裂★

背景：切开手术治疗急性跟腱断裂对跟腱的血运和腱周组织造成较大的破坏，容易发生跟腱粘连，延缓跟腱愈合。 目的：观察跟腱微创吻合器吻合修复急性跟腱断裂的效果。 方法：对2008-02/2009-08采用跟腱微创吻合器治疗的急性跟腱断裂并获得随访的22例患者，进行早期功能操练，并按照美国骨科协会足踝外科分会的标准评价踝关节功能，评价跟腱微创吻合器的治疗效果。 结果与结论：22例均获得随访，随访期为7~14个月(平均11.4个月)，所有患者伤口愈合良好，未发生跟腱再断裂，无腓肠神经支配区的感觉缺失，吻合后3个月AOFAS标准评分为95分，吻合后6个月为98分。说明跟腱微创吻合器能微创治疗急性跟腱断裂并获得良好效果。     

运动想象疗法联合第三代功能性电刺激术对急性缺血性卒中患者上肢运动功能的影响

目的探讨运动想象疗法联合第3代功能性电刺激术对急性缺血性卒中偏瘫患者上肢运动功能的改善作用。方法共40例急性缺血性卒中患者于发病后48 h内随机接受第3代功能性电刺激术(FES组)或联合运动想象疗法(联合治疗组),2周后采用简化Fugl-Meyer运动功能评价量表(FMA)和上肢动作研究测验量表(ARAT)评价上肢运动功能、量角器测量腕关节背伸活动范围。结果与治疗前相比,两组患者治疗2周后FMA、ARAT评分和腕关节背伸活动范围均改善(P=0.000),联合治疗组患者FMA评分(t=-2.528,P=0.016)、ARAT评分(t=-2.562,P=0.014)和腕关节背伸活动范围(t=-2.469,P=0.018)改善程度均优于FES组;且治疗方法与观察时间点之间存在交互作用(均P0.05)。结论运动想象疗法联合第3代功能性电刺激术对改善急性缺血性卒中患者上肢运动功和腕关节背伸活动范围有较好疗效。     

精神疗法联合运动疗法在脑卒中偏瘫患者恢复期的运用

目的研究精神疗法联合运动疗法在脑卒中偏瘫患者恢复期的运用效果。方法选择2015年10月至2016年月2月期间收治入院的脑卒中偏瘫患者患者82例,按照入院ID号随机平均分为对照组与观察组,对照组采用常规康复训练,观察组在对照组基础上采用精神疗法联合运动疗法。比较患者康复训练后步行功能、平衡功能、下肢运动功能改善情况。结果两组患者治疗前的步行功能、平衡功能、下肢运动功能和生活质量的评估组间比较,差异不明显(P0.05)。治疗后两组患者的步行功能、平衡功能、下肢运动功能较级生活质量评估治疗前均有改善(P0.05);而且观察组患者的上述功能指标评分均显著优于对照组患者,存在统计学差异(P0.05。结论在脑卒中偏瘫患者恢复期运用精神疗法联合运动疗法进行康复训练可更显著改善患者预后情况,提高患者生活质量,可在临床治疗中推广应用。     

血管内皮生长因子对兔跟腱内源性愈合作用的量效关系

背景: 多种生长因子在肌腱愈合过程中参与调控细胞的增生和基质合成,血管内皮生长因子在组织愈合和再生中发挥重要作用。目前对于血管内皮生长因子在肌腱内源性愈合方面的研究尚不多。 目的：观察兔跟腱局部硅胶管阻隔后,应用血管内皮生长因子对跟腱内源性愈合作用的量效关系。 设计、时间及地点：随机对照动物实验,于2007-11/2008-04在中南大学湘雅二医院中心实验室完成。 材料：健康家兔48只,体质量2.5~3.0 kg,随机均分成空白组、血管内皮生长因子100,50,10 ng组,每组12只,用于建立跟腱损伤模型。 方法:切开家兔右侧跟腱表面皮肤、皮下组织,钝性分离跟腱的腓肠肌束支和比目鱼肌束支,于跟骨止点上方约2 cm处横行切断跟腱腓肠肌束支,将2 cm长硅胶管套入一侧断端,5-0缝合线改良Kessler法缝合跟腱,缝合后将硅胶管覆盖跟腱缝合处,空白组硅胶管内不加药,其他3组于手术当日及术后第7,14,21天往硅胶管内加入血管内皮生长因子100,50,10 ng。 主要观察指标：术后2,4,6周,每组各取4只家兔行大体标本肉眼观察及组织学观测。 结果：术后6周,各组硅胶管外与周围组织粘连较2,4周时减轻,需钝性或用手术刀分离一面,各组肌腱粘连程度分级差异均无显著性意义(P > 0.05),管内跟腱断端完全被牢固的新生跟腱纤维组织所连接,各组均愈合良好,血管内皮生长因子100,50,10 ng组较空白组愈合质量好(P < 0.05)。术后2,4,6周,血管内皮生长因子100,50 ng组成纤维细胞数较血管内皮生长因10 ng组多(P < 0.05),血管内皮生长因子100,50 ng组成纤维细胞计数差异无显著性意义(P > 0.05),3组胶原水平无差异,血管内皮生长因子100,50,10 ng组成纤维细胞计数及胶原水平均高于空白组(P < 0.05)。 结论：不同剂量外源性血管内皮生长因子均能促进成纤维细胞的增殖和成熟,增加胶原的分泌,促进胶原纤维的成熟,从而促进跟腱的内源性愈合。100,50 ng血管内皮生长因子对促进跟腱愈合效果要优于应用10 ng,100 ng与50 ng之间无明显差异。     

NMES疗法及单纯吞咽训练对脑卒中后吞咽障碍的疗效观察

目的分析脑卒中后吞咽障碍患者采用神经肌肉电刺激疗法(NMES)联合单纯吞咽训练治疗的疗效。方法选取本科2013年1月至2015年1月的脑卒中后吞咽障碍患者90例,随机分为NMES联合治疗组和常规单纯运动训练组,常规单纯运动训练组予以单纯吞咽功能训练,NMES联合治疗组在常规单纯运动训练组基础上加用NMES疗法。对比两组患者治疗前后的各项吞咽功能评分和临床疗效。结果治疗3个疗程后,NMES联合治疗组和常规单纯运动训练组的洼田饮水试验分级、口面运动功能评分显著低于治疗前,吞咽X线电视透视检查(VFSS)评分、藤岛一郎吞咽疗效评分显著高于治疗前(P0.05);治疗3个疗程后,NMES联合治疗组的洼田饮水试验、口面运动功能评分显著低于对照组,VFSS评分、藤岛一郎吞咽疗效评分显著高于常规单纯运动训练组(P0.05)。治疗3个疗程后,NMES联合治疗组的总有效率为95.55%(43/45)显著高于常规单纯运动训练组77.78%(35/45)(P0.05)。结论对于脑卒中后吞咽障碍患者单纯吞咽训练联合采用NMES疗法,疗效更佳。     

运动疗法治疗脑卒中后疲劳35例疗效观察

目的研究运动疗法治疗脑卒中后疲劳(Po SF)的疗效。方法分析35例Po SF患者的临床资料,运动疗法治疗4w后,采用疲劳严重程度量表(FSS)评价疲劳程度,采用Fugl-Meyer量表评价运动功能,采用Barthel指数(BI)评估日常生活活动(ADL)能力,分析运动疗法对Po SF患者的影响。结果经治疗后,患者疲劳程度减轻,上下肢运动功能加强,ADL能力提高,与治疗前相比较,差异有统计学意义(P0.05)。结论通过对Po SF患者进行运动疗法,能有效地改善运动功能,加强ADL能力,恢复快,预后好。     

Mapping increased glycogen phosphorylase activity in dorsal root ganglia and in the spinal cord following peripheral stimuli

A histochemical technique has been used to map the distribution and the relative proportion of the active and inactive form of the enzyme glycogen phosphorylase in the primary afferent cell bodies of lumbar dorsal root ganglia and within the lumbar spinal cord of the rat. The glycogen phosphorylase was found to be present in large and small diameter primary afferent cell bodies and in the grey matter of the spinal cord, except in lamina 2. Most of the glycogen phosphorylase in control rats was in the inactive form. Peripheral innocuous mechanical and thermal stimuli failed to alter the activity of glycogen phosphorylase in the lumbar spinal cord, but noxious mechanical, chemical, and thermal stimuli when applied to the hindlimb of decerebrate rats increased the enzyme activity in the ipsilateral dorsal horn within 10 minutes. The number of primary afferent cell bodies with active glycogen phosphorylase also increased. These changes are likely to be due to the conversion of the inactive "b" form of the enzyme to the active "a" form under the influence of a calcium or cyclic AMP activated phosphorylase b kinase. Pentobarbitone anaesthesia diminished but did not completely suppress the noxious stimulus-evoked glycogen phosphorylase activity changes. Graded electrical stimulation of the sciatic nerve was performed to simulate the effects of the peripheral noxious stimuli in a controlled fashion. Stimulation at a strength that activated only large myelinated afferents produced no greater effect on the distribution of the active form of the enzyme in the dorsal horn than that produced by exposure of the nerve, but stimulation of the thin myelinated A-delta afferents and unmyelinated C-fibres produced a widespread increase in glycogen phosphorylase activity in the spinal cord and in the L4 dorsal root ganglion. The increased activity could be detected after stimulation for as short a period of time as 5 minutes. The mechanisms underlying the stimulus-evoked increase in glycogen phosphorylase activity in the spinal cord and dorsal root ganglia are not yet known, nor have we positively established which elements in the spinal cord, neurones, or glia are responsible for the changes in the glycogen phosphorylase activity. Nevertheless, it is clear that the neural activity generated by certain types of high threshold input is associated with the activation of glycogen phosphorylase, and this may be a useful tool for studying the spatial distribution of some activity-related changes in the nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)     

Biphasic effects of angiotensin II and receptor antagonism on aggregability and protein kinase C phosphorylation in human platelets

In order to define the role of angiotensin II (AngII) receptor subtypes, AT1 and AT2, in platelet activation, we examined the effects of AngII and receptor antagonists on both aggregability and phosphorylation status of protein kinase C (PKC) isoforms in human platelets obtained from 56 healthy volunteers. AngII promoted both spontaneous and agonist (collagen and ADP) stimulated platelet aggregation at concentrations of 10 nM or less, but the promotion effects were lost at 100 nM. Antagonism of AT1 receptor inhibited the promotion effects of AngII at 10 nM or less. On the other hand, antagonism of AT2 receptor enhanced platelet aggregability modestly with AngII at 10 nM or less, and markedly with 100 nM AngII. Furthermore, with 10 nM AngII, phospho-PKCalpha/betaII expression in platelets was increased after collagen stimulation and was inhibited by antagonism of AT1 receptor. With 100 nM AngII, expression levels of phospho-PKCalpha/ betaII remained low even after collagen stimulation but were markedly enhanced by antagonism of AT2 receptor. These findings suggest that at 10 nM or below, AngII promotes aggregability and PKC phosphorylation in human platelets through the AT1 receptor, which can be inhibited by AT1 receptor antagonists, but at higher concentrations, the promotion effects were lost through the opposing action of the AT2 receptor. The present study may provide an additional mechanism for AT1 receptor antagonism, which would provide clinical benefit to patients with stroke or cardiovascular disease accompanied by hypertension.     

Asymmetry in voltage-dependent movements of isolated outer hair cells from the organ of Corti

The electrically induced movements of outer hair cells (OHC) were studied using the whole-cell voltage-clamp technique and video analysis. Cell shortening occurs during depolarization and elongation occurs during hyperpolarization from holding potentials near -70 mV. However, a marked asymmetry in response magnitude exists such that depolarization produces larger cell length changes than do comparable levels of hyperpolarization. The response is such that at normal resting potentials in vivo, displacements are about 2 nm/mV, but increase to about 15 nm/mV as the cell is depolarized. This mechanical rectification in the depolarizing direction manifests itself during symmetrical sinusoidal voltage stimulation as a "DC" reduction in cell length superimposed upon "AC" length changes. The observed OHC mechanical rectification may be involved in the reported production of "DC" basilar membrane displacements during suprathreshold acoustic stimulation (LePage, 1987). Estimates of the magnitude of OHC movements at acoustic threshold levels induced by receptor potentials in the high-frequency region of the cochlea indicate a disparity between basilar membrane and OHC movements on the order of 21 dB. Thus, it appears questionable whether OHC mechanical movements solely underlie the "active process" thought to be responsible for the high degree of neural tuning at sound pressures near 0 dB.     

Brain-computer interfaces in the continuum of consciousness

PURPOSE OF REVIEW: To summarize recent developments and look at important future aspects of brain-computer interfaces. RECENT FINDINGS: Recent brain-computer interface studies are largely targeted at helping severely or even completely paralysed patients. The former are only able to communicate yes or no via a single muscle twitch, and the latter are totally nonresponsive. Such patients can control brain-computer interfaces and use them to select letters, words or items on a computer screen, for neuroprosthesis control or for surfing the Internet. This condition of motor paralysis, in which cognition and consciousness appear to be unaffected, is traditionally opposed to nonresponsiveness due to disorders of consciousness. Although these groups of patients may appear to be very alike, numerous transition states between them are demonstrated by recent studies. SUMMARY: All nonresponsive patients can be regarded on a continuum of consciousness which may vary even within short time periods. As overt behaviour is lacking, cognitive functions in such patients can only be investigated using neurophysiological methods. We suggest that brain-computer interfaces may provide a new tool to investigate cognition in disorders of consciousness, and propose a hierarchical procedure entailing passive stimulation, active instructions, volitional paradigms, and brain-computer interface operation.     

Transcranial electrical stimulation (tES - tDCS; tRNS, tACS) methods

Weak transcranial direct current stimulation (tDCS) with a homogenous DC field at intensities of around 1?mA induces long-lasting changes in the brain. tDCS can be used to manipulate brain excitability via membrane polarisation: cathodal stimulation hyperpolarises, while anodal stimulation depolarises the resting membrane potential, whereby the induced after-effects depend on polarity, duration and intensity of the stimulation. A variety of other parameters influence tDCS effects; co-application of neuropharmacologically active drugs may most impressively prolong or even reverse stimulation effects. Transcranial alternating stimulation (tACS) and random noise stimulation (tRNS) are used to interfere with ongoing neuronal oscillations and also finally produce neuroplastic effects if applied with appropriate parameters.     

Starting and stopping the ventilator for patients with amyotrophic lateral sclerosis

Only a minority of patients who have ALS require, request, and receive assisted or supported ventilation. Usually, when a mechanical ventilator is needed, nonsurgical methods can be used for prolonged periods of time. Appropriately timed discussions can reduce the need for emergency management of breathing failure. The doctrine of informed consent applies to decisions about life support. It involves both the physician (to exercise clinical judgment on behalf of the patient) and the patient (to make personal decisions). They must interact. The patient's firm decision must be clear but need not be in the form of a "living will," and it does not need to be sought repeatedly or reiterated endlessly. Just as a considered decision cannot be arbitrarily overthrown in a time of crisis, neither can a change of mind be willfully ignored. In practice, this may test the capability of even the most experienced and understanding physician, and may result in less-than-ideal outcomes, as our examples show. As in any other area of medical practice, personal experience teaches valuable lessons. Unfortunately, even extended publications discussing clinical management of ALS have failed to address the subject of discontinuing ventilatory support, and ethicists have not always been helpful. Bernat and Beresford have, however, successfully summarized the ethical issues involved. Failure to sustain breathing mechanically or withdrawing artificial support of breathing from a requesting patient who, in the terminal stage of ALS, has become unable to breathe without a mechanical ventilator cannot be called assisted suicide, mercy killing, or either passive or active euthanasia. It is allowing a competent person to die naturally of the incurable illness that afflicts him. The state has no legal interests to be served by intervening in the process just described, which bears no relationship to issues of malpractice, much less to criminal negligence or homicide. Neurologists have not uniformly understood these points, as demonstrated by previous publications addressing the issue and by the findings of our own survey of neurologists who have special experience in the area of neuromuscular diseases. In regard both to starting and to stopping the ventilator, we believe strongly that it is time to lay aside the moral, legal, and ethical conflicts that have needlessly delayed or prevented physicians from complying with the resolute decisions that competent patients have made about their own lives. We urge doctors to act in these cases, as in all others, with their best medical judgment.(ABSTRACT TRUNCATED AT 400 WORDS)     

Corneal reflex in normal and pathological subjects

The orbicularis oculi response can be evoked both by mechanical stimulation of the cornea (corneal reflex) and by electrical stimulation of the skin overlying the supraorbital nerve (blink reflex). Mechanical stimuli to the cornea activate A delta and C free nerve endings of the corneal mucosa. Electrical stimuli to the supraorbital nerve activate A beta, A delta and C fibers of the nerve trunk. Both reflexes present a bilateral late response, but the blink reflex shows in addition an early ipsilateral component (R1), which has never been observed with the corneal stimulation in man. We have developed a simple technique of electrical stimulation of the cornea which provides stable responses and allows precise measurements of threshold and latency of the reflex. In normal subjects, the threshold ranged from 50 to 350 microA, and the maximal stimulus that the subject could bear (tolerance level) ranged from 1000 to 2500 microA. The minimal latency to tolerance level stimuli was 39 +/- 3 msec. The latency difference between the direct responses evoked from the two opposite corneas never exceeded 8 msec and the difference between the direct and consensual responses elicited from the same cornea never exceeded 5 msec. An early ipsilateral component similar to the R1 response of the blink reflex was not observed, even with supramaximal stimulation. The electrically evoked corneal reflex was normal in 10 cases of essential trigeminal neuralgia, while the responses showed significant abnormalities in 18 subjects submitted to thermocoagulation of the Gasserian ganglion as a treatment of neuralgic pain, as well as in 2 cases of symptomatic neuralgia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Excitation of supraoptic vasopressin cells by stimulation of the A1 noradrenaline cell group: failure to demonstrate role for established adrenergic or amino acid receptors

The effects of adrenergic and excitatory amino acid antagonists on supraoptic nucleus (SON) neurosecretory cell responses to stimulation of the A1 noradrenaline (NA) cell group were examined in anaesthetized male rats. As in previous studies, delivery of cathodal pulses (100 microA, 1 ms pulses, 1 Hz) to the A1 region of the caudal ventrolateral medulla excited spontaneously active, antidromically identified neurosecretory cells, the majority of which were identified as arginine vasopressin (AVP) secreting on the basis of basal discharge patterns and responses to abrupt increases in arterial blood pressure. Administration of alpha- and beta-adrenoreceptor antagonists, by systemic or intracerebroventricular delivery of a bolus, or by direct pressure injection into the SON, did not alter neurosecretory cell responses to A1 stimulation, even when doses applied exceeded that required for blockade of excitations elicited by local application of NA. Application of the broad spectrum excitatory amino acid antagonist kynurenic acid (5-40 mM) blocked the excitatory effects of locally applied glutamate (100 microM) and transiently inhibited spontaneous activity, but failed to alter the excitatory effects of A1 region stimulation on SON cells. Identical effects were obtained with a selective kainate/quisqualate receptor antagonist. These data indicate that neurosecretory cell responses to activation of the A1 cell group are unaltered by antagonists of alpha- and beta-adrenoreceptors, or excitatory amino acid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)