Recovery after brain injury: mechanisms and principles
نویسنده
چکیده
The past 20 years have represented an important period in the development of principles underlying neuroplasticity, especially as they apply to recovery from neurological injury. It is now generally accepted that acquired brain injuries, such as occur in stroke or trauma, initiate a cascade of regenerative events that last for at least several weeks, if not months. Many investigators have pointed out striking parallels between post-injury plasticity and the molecular and cellular events that take place during normal brain development. As evidence for the principles and mechanisms underlying post-injury neuroplasticity has been gleaned from both animal models and human populations, novel approaches to therapeutic intervention have been proposed. One important theme has persisted as the sophistication of clinicians and scientists in their knowledge of neuroplasticity mechanisms has grown: behavioral experience is the most potent modulator of brain plasticity. While there is substantial evidence for this principle in normal, healthy brains, the injured brain is particularly malleable. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. This paper reviews selected studies that have demonstrated the neurophysiological and neuroanatomical changes that are triggered by motor experience, by injury, and the interaction of these processes. In addition, recent studies using new and elegant techniques are providing novel perspectives on the events that take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies.
منابع مشابه
Mobilization of stem cell with granulocyte-colony stimulating factor promotes recovery after traumatic brain injury in rat
Introduction: This study was designed to investigate the effects of granulocyte colony-stimulating factor (G-CSF) administration in rats for 6 weeks after traumatic brain injury (TBI). Methods: Adult male Wistar rats (n = 30) were injured with controlled cortical impact device and divided into four groups. The treatment groups (n = 10 each) were injected subcutaneously with recombinant human...
متن کاملP 116: The Effect of Galectin-3 and Lanthionine Ketimine Ester in Neural Recovery after Spinal Cord Injury
Spinal cord injury (SCI) is a trauma that disturbs motor, sensitive and autonomic function and directly impacts the quality of life. After physical damage, releasing of pro-inflammatory proteins and cytokines occurs and with collaboration of immune system cells, an immune response begins in the brain tissue. The result of neuroinflammation is edema, apoptosis and release of axonal growth inhibi...
متن کاملP153: Evaluating the Effect of Lactobacillus Acidophilus Probiotic Supplementation on Sensory-Motor Recovery After a Traumatic Brain Injury
Traumatic brain injury (TBI) is a common cause of death which affects millions of people around the world. TBI is also associated with various neurological impairments. After the primary mechanical injury at the moment of a TBI event, several cellular and molecular processes are activated within the brain tissue as the secondary injury. An important mechanism involved in the secondary injury of...
متن کاملO 27: Traumatic Brain Injury and Inflammation
Traumatic brain injury (TBI) is a significant public health concern in our country, because of placing in top three most common causes of death and substantial direct and indirect costs to society. The incidence of TBI in our country is 1.7 times of international incidence. Traumatic brain injury induced by primary and secondary mechanisms that give rise to death and neurologic morbidity in pat...
متن کاملP 104: Effects of Human Neural Stem Cells in Cure Neuroinflammation of Traumatic Brain Injury
Traumatic brain injury (TBI) is defined as an external mechanical injury to the brain. Neuroinflammation plays a vital role in the pathophysiology of TBI. Microglia and astrocytes play a central role in the initiation and regulation of inflammation. Numerous pro-inflammatory mediators including cytokines, chemokines, reactive oxygen species (ROS) and nitric oxide (NO) released by microglia. In ...
متن کامل