体育运动引起的神经损伤的流行病学调查

在各种竞技运动训练和比赛中,中枢神经系统的损伤比周围神经损伤发生率高。本文就体育运动中神经系统损伤的流行病学、以及在一些运动项目中与体育运动相关的损害性疾病和发生率予以综述。     

Neural crest derived stem cells from dental pulp and tooth-associated stem cells for peripheral nerve regeneration

The peripheral nerve injuries, representing some of the most common types of traumatic lesions affecting the nervous system, are highly invalidating for the patients besides being a huge social burden. Although peripheral nervous system owns a higher regenerative capacity than does central nervous system, mostly depending on Schwann cells intervention in injury repair, several factors determine the extent of functional outcome after healing. Based on the injury type, different therapeutic approaches have been investigated so far. Nerve grafting and Schwann cell transplantation have represented the gold standard treatment for peripheral nerve injuries, however these approaches own limitations, such as scarce donor nerve availability and donor site morbidity. Cell based therapies might provide a suitable tool for peripheral nerve regeneration, in fact, the ability of different stem cell types to differentiate towards Schwann cells in combination with the use of different scaffolds have been widely investigated in animal models of peripheral nerve injuries in the last decade. Dental pulp is a promising cell source for regenerative medicine, because of the ease of isolation procedures, stem cell proliferation and multipotency abilities, which are due to the embryological origin from neural crest. In this article we review the literature concerning the application of tooth derived stem cell populations combined with different conduits to peripheral nerve injuries animal models, highlighting their regenerative contribution exerted through either glial differentiation and neuroprotective/neurotrophic effects on the host tissue.     

等速肌力康复系统对膝关节损伤后力量训练的作用：2例分析

背景：目前越来越多的人把等速训练作为运动员肌力测试和训练的一个重要手段,但应用等速肌力康复系统进行关节损伤后肌力训练的研究并不多见。 目的：探索等速肌力训练系统在关节损伤后肌力训练中的优势,为今后运动员膝关节损伤后的功能康复训练提供科学的依据。 设计、时间及地点：自身前后对照观察,试验于2008-03/05在河北师范大学体育学院实验室进行。 参试者：两名石家庄学院一侧膝关节损伤的女大学生篮球运动员。 方法：对两名女大学生篮球运动员患膝训练前后的屈伸肌群用澳大利亚的Kinitech等速康复系统进行了等速测试和评价。将患膝训练前后的屈伸肌指标、患膝与健膝的屈伸肌指标等一系列数据进行了对比,观察等速力量训练对膝关节屈伸肌恢复的效果。 主要观察指标：膝关节屈伸肌群的峰值力矩。 结果：两名受试者经过8周的等速力量训练,在60(°)/s和240(°)/s测试时的各项力量指标都有不同程度的增长。从PT值来看,受试者1的屈肌比伸肌增长幅度要大,而受试者2的伸肌则比屈肌增长幅度大,受试者1和受试者2在慢速测试时的BP和快速测试时的STW 、AP这几项力量指标上,进步都非常明显,两人在快速测试时的耐力指数也有一定程度的增长。 结论：使用等速康复系统进行等速力量训练,对两人膝关节屈伸肌的力量指标均有明显提高。等速康复力量训练对人体膝关节手术后肌肉功能的恢复有积极的促进作用。     

Repair of chronic spinal cord injury

Advances in medical and rehabilitative care now allow the 10-12,000 individuals who suffer spinal cord injuries each year in the United States to lead productive lives of nearly normal life expectancy, so that the numbers of those with chronic injuries will approximate 300,000 at the end of the next decade. This signals an urgent need for new treatments that will improve repair and recovery after longstanding injuries. In the present report we consider the characteristics of the chronically injured spinal cord that make it an even more challenging setting in which to elicit regeneration than the acutely injured spinal cord and review the treatments that have been designed to enhance axon growth. When applied in the first 2 weeks after experimental spinal cord injury, transplants, usually in combination with supplementary neurotrophic factors, and possibly modifications of the inhibitory central nervous system environment, have produced limited long-distance axon regeneration and behavioral recovery. When applied to injuries older than 4 weeks, the same treatments have almost invariably failed to overcome the obstacles posed by the neurons' diminished capacity for regeneration and by the increasing hostility to growth of the terrain at and beyond the injury site. Novel treatments that have stimulated regeneration after acute injuries have not yet been applied to chronic injuries. A therapeutic strategy that combines rehabilitation training and pharmacological modulation of neurotransmitters appears to be a particularly promising approach to increasing recovery after longstanding injury. Identifying patients with no hope of useful recovery in the early days after injury will allow these treatments to be administered as early as possible.     

Bidirectional Brain‐gut‐microbiota Axis in increased intestinal permeability induced by central nervous system injury

Central nervous system injuries may lead to the disorders of the hypothalamic‐pituitary‐adrenal axis, autonomic nervous system, and enteric nervous system. These effects then cause the changes in the intestinal microenvironment, such as a disordered intestinal immune system as well as alterations of intestinal bacteria. Ultimately, this leads to an increase in intestinal permeability. Inflammatory factors produced by the interactions between intestinal neurons and immune cells as well as the secretions and metabolites of intestinal flora can then migrate through the intestinal barrier, which will aggravate any peripheral inflammation and the central nervous system injury. The brain‐gut‐microbiota axis is a complex system that plays a crucial role in the occurrence and development of central nervous system diseases. It may also increase the consequences of preventative treatment. In this context, here we have summarized the factors that can lead to the increased intestinal permeability and some of the possible outcomes.     

The epidemiology of injuries to the nervous system resulting from sport and recreation

Sports and recreational activities are associated with a variety of injuries. Although many of these injuries are musculoskeletal in nature, both the peripheral nervous system and the central nervous system are at risk for injury as well. This article examines the incidence of nervous system injuries in particular sports. The association between particular forms of injuries and the sports in which they are likely to be incurred are also investigated. Further assessment of preventative measures is provided when possible.     

Coordination of fingertip forces during precision grasping in multiple system atrophy

While the pathology and autonomic nervous system components of multiple system atrophy (MSA) have been well described, little is known about the associated motor dysfunction. One prominent feature of MSA is parkinsonism, although ataxias and pyramidal tract signs are frequently present. To investigate the nature of motor deficits in MSA, a natural grip-lift movement requiring a precision grasp was used to examine force coordination. Subjects were asked to grasp an instrumented object using the fingertips of the thumb and index finger and lift it 10 cm above the table surface. Subjects with MSA demonstrated a prolonged duration between object contact and initiation of the lifting drive that increased with the weight of the object. During this period these subjects produced large grasping forces generating a significant portion of the eventual grip force employed to hold the object. In contrast, control subjects generated grip and load forces in parallel after establishing contact with the object. Therefore, subjects with MSA showed a disrupted performance on both the sequential (grasp, then lift) and simultaneous (grip and load force development) portions of this task. Only after initiation of the vertical lifting drive did subjects with MSA generate forces in a similar manner to control subjects. These findings demonstrate that subjects with MSA exhibit a disrupted coordination of grasp and could suggest a general deficit in motor control resulting from multi-focal neural degeneration.     

The role of neurologists in pediatric neuro-oncology

Because of advances in the diagnosis and management of brain tumors, the opportunity for neurologists to participate in the care of children with central nervous system neoplasms has greatly increased. Data developed by various study groups has allowed a more systematic approach to childhood brain tumors. Much more information will become available. New data must be reviewed and recommendations for therapy made by individuals with clinical neuroscience experience and training. The training needs of such individuals must be met in neurology training programs.     

Oxidant mechanisms in neonatal hypoxia-ischemia

The neonatal brain appears to be selectively vulnerable to oxidative stress. Several potential mechanisms associated with altered reactive oxygen species metabolism would explain the increased susceptibility. They include increased accumulation of hydrogen peroxide with subsequent neurotoxicity. This enhanced neurotoxicity from H2O2 accumulation may be related to inadequate scavenging abilities of the immature nervous system, such as lower glutathione peroxidase activity. Contributing to the immaturity of the scavenging enzymes is the inability of the developing nervous system to maintain glutathione stores. The immature nervous system is rich in iron, and has more free iron than the mature nervous system. As H2O2 accumulates because of these improper defense mechanisms, it is exposed to this free iron. This exposure results in the generation of OH radical (Fenton reaction), a more potent free radical that can cause severe damage. The rapid conversion of H2O2 to OH in the setting of free iron sets up the immature nervous system for increased cytotoxicity. Understanding the molecular mechanisms of oxidative stress will lead to better therapies for neonatal hypoxia-ischemia.     

Neurologic aspects of boxing

The assessment and prevention of potentially adverse neurologic consequences of boxing requires two important considerations. Acute neurologic injuries should be distinguished from chronic brain injuries and the level of competitive boxing (ie, amateur vs professional) must also be taken into account. Acute neurologic injuries such as concussion, post-concussion syndrome, intracranial hemorrhage, and brain contusion are more readily identified than chronic neurologic injuries because of their immediate devastation of the nervous system. In contrast, chronic neurologic injuries differ in their pathophysiologic mechanisms that are exemplified by an insidious onset and progression after the cessation of boxing. Accordingly, the chronic traumatic encephalopathy of boxing poses the most serious neurologic threat of boxing. Amateur boxing differs from professional boxing in the duration of fights, rules and regulatory policies, medical evaluation, and protective devices. These factors could produce a differential effect on the risk of injury to the brain. The prevention of neurologic injuries in boxing requires the integration of proper neurologic evaluation by qualified ring-side physicians, the design and utilization of effective protective devices, and the establishment of national regulatory agencies.     

Bi-directional interaction of NF-κB in nervous system damage,learning and memory

The mechanism of action of nuclear factor-kappa B (NF-κB)’s has been widely studied in nervous system damage and disease since 2000. NF-κB is widely present in eukaryotic cells, and inactive NF-κB is present in the cytoplasm. Activated NF-κB transfers into the nucleus and induces expression of several target genes. Through the action of different downstream effectors, NF-κB plays a bi-directional interactive role in central nervous system damage, as well as learning and memory. While NF-κB can induce pro-inflammation factor release and exacerbate brain injury, it can also exert protective effects on neurons in central nervous system diseases and injuries by upregulating endothelial nitric oxide synthase (eNOS), Mn-superoxide dismutase (Mn-SOD), B-cell lymphoma/leukaemia-2 (Bcl-2), and inhibitors of apoptosis protein (IAPs). Moreover, NF-κB is required for spatial learning and memory and passive avoidance training. However, a decrease in NF-κB activity in the hippocampal dentate gyrus is necessary for active avoidance training. This paper reviews NF-κB’s bi-directional interactive role in these processes.     

Hypoxia: the third wheel between nerve and muscle

Skeletal muscles not only obey carefully all motor commands received via motor nerves from nervous system, but also are ready to modify their structure and function to be more suited to the tasks assigned by nervous system. Thus, nervous system appears as the major modulator of the muscle structure and function. Other factors, however, may interfere with the nerve-muscle partnership and among them, hypoxia plays a pivotal role because skeletal muscles exhibit a great variability of the oxygen fluxes and because hypoxia per se has a powerful influence on muscle fibers. The adaptation of skeletal muscles to nerve-induced activity is particularly evident with low frequency tonic patterns and examples are given by chronic low frequency stimulation and by endurance training. Adaptation includes fiber type transitions towards a slow-oxidative phenotype, increased mitochondrial density and increased capillary/fiber ratio. Hypoxia can trigger some of such changes and this has suggested that low oxygen tension at fiber level might be a mediator, possibly based on HIF and VEGF, of the muscle adaptation to increased contractile activity. Chronic hypoxia can, however, induce opposite modifications, such as a fiber type transition from slow-oxidative to fast-glycolytic and mitochondrial loss. In such conditions, the increased contractile activity can antagonize hypoxia effects. Thus, hypoxia can play a double role in the nerve-muscle relationship, either reinforcing the nerve influence or antagonizing it. This short review aims to re-examine the ambiguous relationships between nerve-induced contractile activity and hypoxic conditions and to suggest possible interpretations of the double role played by hypoxia.     

Mild hypothermia as a treatment for central nervous system injuries Positive or negative effects？

Besides local neuronal damage caused by the primary insult,central nervous system injuries may secondarily cause a progressive cascade of related events including brain edema,ischemia,oxidative stress,excitotoxicity,and dysregulation of calcium homeostasis.Hypothermia is a beneficial strategy in a variety of acute central nervous system injuries.Mild hypothermia can treat high intracranial pressure following traumatic brain injuries in adults.It is a new treatment that increases survival and quality of life for patients suffering from ischemic insults such as cardiac arrest,stroke,and neurogenic fever following brain trauma.Therapeutic hypothermia decreases free radical production,inflammation,excitotoxicity and intracranial pressure,and improves cerebral metabolism after traumatic brain injury and cerebral ischemia,thus protecting against central nervous system damage.Although a series of pathological and physiological changes as well as potential side effects are observed during hypothermia treatment,it remains a potential therapeutic strategy for central nervous system injuries and deserves further study.     

Immunophilins: neuroprotective agents and promoters of neural regeneration

Immunophilins are a family of proteins mainly known because they act as receptors of the immunosuppressant drugs cyclosporin A (CsA) and FK506. Immunophilins serve several general functions, including regulation of mitochondrial permeability, modulation of ion channels stability and acting as chaperones for a variety of proteins. However, immunophilins are also present at high density in the nervous system. CsA, FK506 and other derivatives inhibit the function of immunophilins and, through bloking or activating several intracellular pathways, it has been shown that they exert neuroprotective effects in different experimental models of ischemia, Parkinson's disease and excitotoxic insults. Moreover, FK506 also has neuroregenerative effects, by enhancing the axonal regeneration rate after lesions of the peripheral nervous system. The development of new agents that selectively bind to immunophilins opens new interesting perspectives for the therapy of degenerative diseases and injuries of the nervous system.     

Nerve regeneration and thyroid hormone treatment.

On the basis of 3 reports that thyroid hormone treatment stimulates axon outgrowth in rats with nervous system injuries, a 43-year-old patient with an ulnar nerve laceration was given desiccated thyroid (up to 360 mg/day) following nerve suture. The Hoffmann-Tinel sign of sensory axon outgrowth advanced at a rate of 5.0 mm/day in the forearm, approximately 200% faster than the anticipated rate. A good functional result was obtained in 7 months. On the maximum dosage of desiccated thyroid, the patient developed mild weight loss associated with an increased appetite; there was no other sign or symptom of hyperthyroidism. Further investigation of the role of thyroid hormone during nerve regeneration seems warranted.     

Roles of Eph/ephrin bidirectional signaling during injury and recovery of the central nervous system

Multiple cellular components, including neuronal, glial and endothelial cells, are involved in the sophisticated pathological processes following central nervous system injury. The pathological process cannot reduce damage or improve functional recovery by merely targeting the molecular mechanisms of neuronal cell death after central nerve system injuries. Eph receptors and ephrin ligands have drawn wide attention since the discovery of their extensive distribution and unique bidirectional signaling between astrocytes and neurons. The roles of Eph/ephrin bidirectional signaling in the developmental processes have been reported in previous research. Recent observations suggest that Eph/ephrin bidirectional signaling continues to be expressed in most regions and cell types in the adult central nervous system, playing diverse roles. The Eph/ephrin complex mediates neurogenesis and angiogenesis, promotes glial scar formation, regulates endocrine levels, inhibits myelin formation and aggravates inflammation and nerve pain caused by injury. The interaction between Eph and ephrin is also considered to be the key to angiogenesis. This review focuses on the roles of Eph/ephrin bidirectional signaling in the repair of central nervous system injuries.     

A clinical trial with desglycinamide arginine vasopressin for the treatment of memory disorders in man

In a double-blind cross-over trial the memory effect of the neuropeptide desglycinamide arginine vasopressin (DGAVP) was selected because of its well-documented facilitatory effects on memory components in rodents. Patients with stabilized or progressive amnesic disorders (Korsakoff disease, early stages of Alzheimer dementia, head injuries and other central nervous system diseases) did not respond to the drug. Factors possibly explaining the discrepancy with animal research are discussed.     

Early life predictors of the physiological stress response later in life

People born at a low birth weight are at increased risk of chronic adult disease including coronary heart disease, type 2 diabetes, cognitive decline and depression. Recent human and animal research has suggested programming of physiological stress response as an important linking mechanism. We review evidence from human studies, focusing on biological markers as early life indicators and laboratory-induced stress response as an outcome.Several studies show that indicators such as birth weight or length of gestation are associated with alterations in blood pressure, autonomic nervous system and hypothalamic–pituitary–adrenal axis (HPAA) response. In most studies these associations vary according to sex: low birth weight seems to be associated with higher autonomic nervous system response more clearly in females and with higher peripheral vascular resistance and HPAA response in males.The published studies have established the validity of the concept of early life programming of stress response. We believe that important future directions include focusing on specific early life exposures as predictors and on stress response in everyday life as an outcome.     

Early life predictors of the physiological stress response later in life

People born at a low birth weight are at increased risk of chronic adult disease including coronary heart disease, type 2 diabetes, cognitive decline and depression. Recent human and animal research has suggested programming of physiological stress response as an important linking mechanism. We review evidence from human studies, focusing on biological markers as early life indicators and laboratory-induced stress response as an outcome.Several studies show that indicators such as birth weight or length of gestation are associated with alterations in blood pressure, autonomic nervous system and hypothalamic-pituitary-adrenal axis (HPAA) response. In most studies these associations vary according to sex: low birth weight seems to be associated with higher autonomic nervous system response more clearly in females and with higher peripheral vascular resistance and HPAA response in males.The published studies have established the validity of the concept of early life programming of stress response. We believe that important future directions include focusing on specific early life exposures as predictors and on stress response in everyday life as an outcome.