经颅磁刺激可改善卒中患者的运动功能

对于健康大脑,两侧半球皮质以一种相似的程度相互抑制,其本质为“相互抵消”。当患者发生卒中时,患侧半球对健侧半球的抑制程度减弱,从而导致健侧大脑半球抑制活性增强。因此,美国哈佛医学院的Mansur等提出一种理论,即如果降低健侧大脑半球活动性,就能消除对患侧半球的抑制作用,进而改善运动功能。最近的研究已表明,无创性皮质脑刺激是一种有效的卒中恢复治疗方法,经颅磁刺激(TMS)能够在意识清醒的受试者中提供无创性和无痛的脑皮质刺激,因此,重复TMS(rTMS)可能有助于调节卒中后大脑的活动性,从而促进卒中后的恢复。为了验证上述理论,M…     

经颅磁刺激用于卒中患者手功能恢复的研究进展

<正>人手所具有的复杂运动功能既依赖于其解剖结构,更需要精确的神经控制。研究手功能的神经调控对进一步认识中枢神经系统对复杂运动的调控过程有重要意义。研究表明,卒中后患侧大脑半球的运动皮质对健侧大脑半球运动皮质的抑制作用减弱,导致卒中后出现健侧大脑半球过度活跃~([1])。在卒中慢性期,处于失衡状态是患侧大脑半球的皮质运动区功能重组的障碍之一。因此,若达到促进卒中患者手功能恢复的目的,一方面需增加受损脑区     

应用脑电非线性动力学分析法研究针刺穴位对不同意识障碍患者的作用

目的应用脑电非线性动力学分析研究针刺穴位对不同意识障碍患者脑电的影响。方法选取卒中后6个月内的意识障碍患者37例,其中最低意识状态（MCS）16例,持续植物状态（PVS）21例。针刺足三里、三阴交、太冲和涌泉穴。比较针刺前（安静闭眼状态）与针刺穴位时,两组患者不同脑区（前额、额、中央、顶、枕、前颞、中颞、后颞区）的脑电非线性指数,包括复杂度（Cx）和近似熵（ApEn）变化。结果①与针刺前比较,针刺患侧时,PVS组患侧所有脑区的Cx、ApEn值变化不明显;MCS组患侧部分脑区的Cx、ApEn值升高（P〈0．05）。②针刺健侧时,与针刺前比较,PVS组健侧少部分脑区的Cx、ApEn值升高（P〈0．05）。MCS组健侧大部分脑区的Cx、ApEn值升高（P〈0．05,P〈0．01）。③针剌前,PVS组和MCS组患侧所测脑区的Cx、ApEn值差异均无统计学意义;针刺患侧穴位时,两组患侧各脑区的Cx差异亦均无统计学意义,而MCS组的前额、前颞、中颞及后颞区的ApEn值高于PVS组（P〈0．05,P〈0．01）。④针刺前,两组健侧大部分脑区的Cx、ApEn值MCS组均高于PVS组（P〈0．05,P〈0．01）;针刺健侧穴位时,健侧所有脑区的Cx、ApEn值MCS组均高于PVS组（P〈0．05,P〈0．01）。结论PVS和MCS患者的皮质活动处于明显抑制状态,MCS较PVS患者皮质受抑制程度相对较轻。针刺能够引起损伤较轻的大脑皮质兴奋性增高,并被脑电非线性分析捕获。     

运用弥散张量成像技术观察头针联合rTMS对卒中病人皮质脊髓束完整性的影响

目的利用弥散张量成像(DTI)观察头针联合低频重复经颅磁刺激(rTMS)改善卒中偏瘫病人皮质脊髓束(CSL)微结构完整性的效果。方法 30例病人随机分为头针组(A组)、低频rTMS组(B组)、头针联合低频rTMS组(C组)。治疗2周后,观察患侧内囊后肢前部CSL的部分各向异性(FA)及临床疗效。结果进行2周治疗后,所有病人病灶侧CSL的FA值及FMA、MBI值均有所提高,但头针联合低频rTMS治疗组的FA值和FMA、MBI值提高更明显。结论头针联合低频rTMS更好地改善卒中偏瘫病人皮质脊髓束微结构的完整性,同时对病人的运动功能及日常生活自理能力改善更明显。     

白芍对大鼠胃电节律失常的影响机制

白芍性微寒、味苦酸,有养血柔肝、缓中止痛、敛阴收汗的功能,临床上常用于治疗胃肠运动性疾病,但其作用机制尚不清楚。目前普遍认为胃电节律失常与胃运动障碍密切相关,临床上十分常见,有研究表明一氧化氮、乙酰胆碱作为胃窦肌间神经丛内一对重要的抑制性和兴奋性神经递质,在调节胃电节律中发挥重要作用。我们研究白芍对胃电节律失常以及胃窦肌间神经丛胆碱能神经、氮能神经的影响,并探讨其作用机制。     

卒中与睡眠-觉醒障碍

睡眠-觉醒障碍既是卒中的危险因素,又是卒中的严重并发症之一.卒中后睡眠-觉醒障碍主要表现为失眠、觉醒障碍、睡眠相关运动障碍和异态睡眠,其发生机制主要与卒中损伤睡眠-觉醒中枢有关.文章综述了卒中后睡眠-觉醒障碍的特点、机制以及早期评估方法和干预策略.     

卒中相关头痛的研究进展

卒中相关头痛即与卒中发生相关联的头痛,可出现于卒中当时、之前或之后,发生率为３％～５７％。年龄、性别、既往偏头痛史,无吸烟史、缺血性心脏病等因素可能与之有关。比较一致的看法是椎基底动脉较颈内动脉供血区、皮质较皮质下以及卒中灶同侧易出现卒中相关的头痛。最近观点认为,三叉神经血管系统与颈神经共同参与头痛的发生机制。     

脑卒中后继发癫痫的临床分析

目的 探讨脑卒中后继发癫痫的临床特点、发病机制及治疗原则。方法 对脑卒中后继发癫痫的病人按卒中发作时间、发作类型、癫痫与卒中部位的关系、治疗方法进行分析比较。结果 脑卒中病灶位于皮质的癫痫发生率较皮质下发生率高，恢复期癫痫临床发作以全身强直阵挛发作多。脑电图表现以慢波为主。结论卒中后癫痫发作与卒中部位有关，早发性癫痫与恢复期癫痫机制有别。     

重复经颅磁刺激治疗卒中后抑郁

卒中后抑郁(post-stroke depression,PSD)是卒中患者的一种常见神经精神并发症,严重影响患者的神经功能恢复和工作生活质量。近年来,作为一种无创性神经调节技术,重复经颅磁刺激(repetitive transcranial magnetic stimulation,rTMS)已应用于卒中的康复治疗,但其在PSD治疗方面也进行了一些研究。文章对rTMS治疗PSD的疗效、可能机制以及局限性进行了综述。     

氟西汀治疗对急性缺血性卒中后运动恢复的影响

偏瘫和轻偏瘫是卒中后最常见的神经功能缺损。一些小样本临床试验提示氟西汀可促进运动功能恢复，但其临床疗效尚不清楚。法国图卢兹大学中心医院神经内科的Chollet等进行了一项随机双盲安慰剂对照试验，旨在评价氟西汀能否促进急性缺血性卒中后运动障碍患者的运动功能恢复。     

Fibrinolysis: an unfinished agenda.

There has been a recent decline in interest in fibrinolysis, suggesting that its physiological basis is sufficiently understood and that therapeutic thrombolysis has reached its limit. The importance of the subject has not diminished since cardiovascular disease is now a leading health problem even in developing countries. Certain highlights and inconsistencies are reviewed. The clinical trials of tissue plasminogen activator (t-PA) revealed a major discrepancy between its fibrinolytic efficacy and its clinical benefit (the 't-PA paradox') that is unexplained. Dose-finding studies also showed that the fibrinolytic efficacy of t-PA required significant nonspecific plasminogen activation. Furthermore, the longstanding belief that t-PA is responsible for physiological fibrinolysis and urokinase-type PA (u-PA) for pericellular plasminogen activation is belied by extensive experimental animal data, but these findings have had little impact on traditional thinking. As a result, the mechanisms responsible for the u-PA paradigm of fibrinolysis have received little attention. Clinical experience with pro-u-PA remains limited and most clinical trials have used infusion rates at which pro-u-PA is largely converted systemically to urokinase. This is due to the unanticipated instability of pro-u-PA in plasma at pharmacological concentrations. Insufficient understanding of basic mechanisms of fibrinolysis has handicapped the design of chimeric or mutant activators. It is submitted that physiological fibrinolysis remains to be better defined, and that it is premature to conclude that therapeutic thrombolysis will be inevitably accompanied by side effects that undermine this method of inducing reperfusion.     

What do we know about how humans cough?

We review the evidence that activation of the cerebral cortex can lead to movements of the vocal folds and possibly to cough. Electrical stimulation of the motor cortex can cause movements of the vocal folds and vocalizatioin, but cough has not been reported. The motor pathways are via the nucleus ambiguous and possibly the nucleus retroambuigualis in the brainstem. In humans, activation of the cerebral cortex by transcranial magnetic stimulation can cause motor potentials in the intrinsic laryngeal muscles and corresponding surface potentials. The relationships between the cortical sensation related to cough, the voluntary control of cough and the involvement of reflex pathways remain to be clarified.     

Mechanisms of use-dependent plasticity in the human motor cortex

Practicing movements results in improvement in performance and in plasticity of the motor cortex. To identify the underlying mechanisms, we studied use-dependent plasticity in human subjects premedicated with drugs that influence synaptic plasticity. Use-dependent plasticity was reduced substantially by dextromethorphan (an N-methyl-d-aspartate receptor blocker) and by lorazepam [a gamma-aminobutyric acid (GABA) type A receptor-positive allosteric modulator]. These results identify N-methyl-d-aspartate receptor activation and GABAergic inhibition as mechanisms operating in use-dependent plasticity in intact human motor cortex and point to similarities in the mechanisms underlying this form of plasticity and long-term potentiation.     

Differences in frontal cortical activation by a working memory task after substitution of risperidone for typical antipsychotic drugs in patients with schizophrenia

Antipsychotic drug treatment of schizophrenia may be complicated by side effects of widespread dopaminergic antagonism, including exacerbation of negative and cognitive symptoms due to frontal cortical hypodopaminergia. Atypical antipsychotics have been shown to enhance frontal dopaminergic activity in animal models. We predicted that substitution of risperidone for typical antipsychotic drugs in the treatment of schizophrenia would be associated with enhanced functional activation of frontal cortex. We measured cerebral blood oxygenation changes during periodic performance of a verbal working memory task, using functional MRI, on two occasions (baseline and 6 weeks later) in two cohorts of schizophrenic patients. One cohort (n = 10) was treated with typical antipsychotic drugs throughout the study. Risperidone was substituted for typical antipsychotics after baseline assessment in the second cohort (n = 10). A matched group of healthy volunteers (n = 10) was also studied on a single occasion. A network comprising bilateral dorsolateral prefrontal and lateral premotor cortex, the supplementary motor area, and posterior parietal cortex was activated by working memory task performance in both the patients and comparison subjects. A two-way analysis of covariance was used to estimate the effect of substituting risperidone for typical antipsychotics on power of functional response in the patient group. Substitution of risperidone increased functional activation in right prefrontal cortex, supplementary motor area, and posterior parietal cortex at both voxel and regional levels of analysis. This study provides direct evidence for significantly enhanced frontal function in schizophrenic patients after substitution of risperidone for typical antipsychotic drugs, and it indicates the potential value of functional MRI as a tool for longitudinal assessment of psychopharmacological effects on cerebral physiology.     

Update on therapy--thalidomide in the treatment of lupus

Thalidomide has been shown to be an effective treatment for cutaneous forms of lupus erythematous refractory to other therapies. Thalidomide has very serious side effects, including teratogenicity and neuropathy, which limit its clinical use in lupus to such severe refractory cases. Efficacy has been confirmed in several studies, although recurrence after discontinuation of treatment is frequent. More recent experience suggests that lower doses than originally used may be effective, which may result in a reduction in side effects. Much effort has been expended in studying the mechanisms of action of thalidomide, although as yet it is unclear which of the mechanisms identified to date contribute to its efficacy in treating cutaneous forms of lupus erythematosus. Identification of patients suitable for thalidomide therapy requires a rigorous selection process. Potential side effects should be clearly explained, particularly teratogenicity as many patients are young women. Written consent and a negative pregnancy test must be obtained prior to commencement of therapy. Reliable contraceptive measures should be strictly observed by patients taking thalidomide. Close clinical and neurophysiological supervision using nerve conduction studies should be undertaken.     

The role of ipsilateral premotor cortex in hand movement after stroke

Movement of an affected hand after stroke is associated with increased activation of ipsilateral motor cortical areas, suggesting that these motor areas in the undamaged hemisphere may adaptively compensate for damaged or disconnected regions. However, this adaptive compensation has not yet been demonstrated directly. Here we used transcranial magnetic stimulation (TMS) to interfere transiently with processing in the ipsilateral primary motor or dorsal premotor cortex (PMd) during finger movements. TMS had a greater effect on patients than controls in a manner that depended on the site, hemisphere, and time of stimulation. In patients with right hemiparesis (but not in healthy controls), TMS applied to PMd early (100 ms) after the cue to move slowed simple reaction-time finger movements by 12% compared with controls. The relative slowing of movements with ipsilateral PMd stimulation in patients correlated with the degree of motor impairment, suggesting that functional recruitment of ipsilateral motor areas was greatest in the more impaired patients. We also used functional magnetic resonance imaging to monitor brain activity in these subjects as they performed the same movements. Slowing of reaction time after premotor cortex TMS in the patients correlated inversely with the relative hemispheric lateralization of functional magnetic resonance imaging activation in PMd. This inverse correlation suggests that the increased activation in ipsilateral cortical motor areas during movements of a paretic hand, shown in this and previous functional imaging studies, represents a functionally relevant, adaptive response to the associated brain injury.     

Motor cortex maps articulatory features of speech sounds

The processing of spoken language has been attributed to areas in the superior temporal lobe, where speech stimuli elicit the greatest activation. However, neurobiological and psycholinguistic models have long postulated that knowledge about the articulatory features of individual phonemes has an important role in their perception and in speech comprehension. To probe the possible involvement of specific motor circuits in the speech-perception process, we used event-related functional MRI and presented experimental subjects with spoken syllables, including [p] and [t] sounds, which are produced by movements of the lips or tongue, respectively. Physically similar nonlinguistic signal-correlated noise patterns were used as control stimuli. In localizer experiments, subjects had to silently articulate the same syllables and, in a second task, move their lips or tongue. Speech perception most strongly activated superior temporal cortex. Crucially, however, distinct motor regions in the precentral gyrus sparked by articulatory movements of the lips and tongue were also differentially activated in a somatotopic manner when subjects listened to the lip- or tongue-related phonemes. This sound-related somatotopic activation in precentral gyrus shows that, during speech perception, specific motor circuits are recruited that reflect phonetic distinctive features of the speech sounds encountered, thus providing direct neuroimaging support for specific links between the phonological mechanisms for speech perception and production.     

Oxidative Stress: a common denominator in the pathogenesis of amyotrophic lateral sclerosis

PURPOSE OF REVIEW: Amyotrophic lateral sclerosis, or Lou Gehrig disease, is a progressive neurodegenerative disease of adult onset characterized by a loss of motor neurons in the spinal cord and motor cortex. In the last several years, substantial progress has been made in defining the pathogenesis of motor neuron injury and relationships between disease mechanisms and the selective vulnerability of the motor neuron in both familial and sporadic forms of amyotrophic lateral sclerosis. RECENT FINDINGS: Current theories have shifted from a neuron-centered pathology to a focus on the interaction between motor neurons and glia, and their respective contributions to pathways implicated in amyotrophic lateral sclerosis. Although multiple mechanisms clearly can contribute to the pathogenesis of motor neuron injury, recent advances suggest that oxidative stress may play a significant role in the amplification, and possibly the initiation, of disease. SUMMARY: This article reviews the clinical aspects of amyotrophic lateral sclerosis and potential mechanisms of disease pathogenesis in the context of recent data supporting a major role for oxidative stress throughout the disease course. Evidence suggesting an important role for intercellular signaling is emphasized.     

Actor's and observer's primary motor cortices stabilize similarly after seen or heard motor actions

We quantified rhythmic brain activity, recorded with whole-scalp magnetoencephalography (MEG), of 13 healthy subjects who were performing, seeing, or hearing the tapping of a drum membrane with the right index finger. In the actor's primary motor (M1) cortex, the level of the approximately 20-Hz brain rhythms started to decrease, as a sign of M1 activation, approximately 2 s before the action and then increased, with a clear rebound approximately 0.6 s after the tapping, as a sign of M1 stabilization. A very similar time course occurred in the M1 cortex of the observer: the activation, although less vigorous than in the actor, started approximately 0.8 s before the action and was followed by a rebound. When the subject just heard the tapping sound, no preaction activation was visible, but a rebound followed the sound. The approximately 10-Hz somatosensory rhythm, which also started to decrease before own and viewed actions, returned to the baseline level approximately 0.6 s later after own actions than observed actions. This delay likely reflects proprioceptive input to the cortex, available only during own actions, and therefore could be related to the brain signature of the sense of agency. The strikingly similar motor cortex reactivity during the first and third person actions expands previous data on brain mechanisms of intersubjective understanding. Besides motor cortex activation before own and observed (predicted) actions, the M1 cortex of both the viewer and the listener stabilized in a very similar manner after brisk motor actions.     

Dorsal anterior cingulate cortex: A role in reward-based decision making

Dorsal anterior cingulate cortex (dACC) is a brain region that subserves cognition and motor control, but the mechanisms of these functions remain unknown. Human neuroimaging and monkey electrophysiology studies have provided valuable insights, but it has been difficult to link the two literatures. Based on monkey single-unit recordings, we hypothesized that human dACC is comprised of a mixture of functionally distinct cells that variously anticipate and detect targets, indicate novelty, influence motor responses, encode reward values, and signal errors. As an initial test of this conceptualization, the current event-related functional MRI study used a reward-based decision-making task to isolate responses from a subpopulation of dACC cells sensitive to reward reduction. As predicted, seven of eight subjects showed significant (P < 10(-4)) dACC activation when contrasting reduced reward (REDrew) trials to fixation (FIX). Confirmatory group analyses then corroborated the predicted ordinal relationships of functional MRI activation expected during each trial type (REDrew > SWITCH > CONrew > or = FIX). The data support a role for dACC in reward-based decision making, and by linking the human and monkey literatures, provide initial support for the existence of heterogeneity within dACC. These findings should be of interest to those studying reward, cognition, emotion, motivation, and motor control.