Psychology
Plasticity and Functional Recovery of the Brain After Trauma
"Plasticity and Functional Recovery of the Brain After Trauma" refers to the brain's ability to reorganize and adapt following injury or damage. This process involves the formation of new neural connections and the recruitment of alternative brain regions to compensate for lost functions. Understanding plasticity and functional recovery is crucial for developing effective rehabilitation strategies for individuals who have experienced brain trauma.
Written by Perlego with AI-assistance
Related key terms
1 of 5
9 Key excerpts on "Plasticity and Functional Recovery of the Brain After Trauma"
eBook - PDFSynaptic Plasticity
Basic Mechanisms to Clinical Applications
- Michel Baudry, Xiaoning Bi, Steven S. Schreiber(Authors)
- 2005(Publication Date)
- CRC Press(Publisher)
By plasticity in this context, we refer to adap-tive events affecting the morphology, anatomical connections, and the func-tions subserved by neurones. Particular attention is paid to the relationship between host and transplanted cells, the anatomical integration of the grafted cells, and how circuit reconstruction within the host brain might promote functional recovery. Furthermore, we examine the role of the environment and the experience of the individual suffering from brain damage or disease. Together, these data indicate that rehabilitative train-ing has the potential to modify the functional plasticity both of the affected brain and of the transplants. The different mechanisms by which cells from different sources, and following different types of brain damage, can affect host function will also determine their dependence on training and experience for maximizing therapeutic outcome. During the period immediately following injury and during the early stages of disease, the brain is at its most plastic and privileged state, offering a window of opportunity for therapeutic intervention. In contrast to a pes-simistic interpretation of Cajal’s dictum, cited above, spontaneous recovery following injury shows that the adult brain does retain the capacity at some level to reorganize itself functionally. In order to improve the outcome fol-lowing brain damage, cell replacement therapy must both make use of the endogenous potential for recovery of the host and optimize the external circumstances associated with any intervention, such as the source and treatment of the cells, the timing of the intervention, and the experience and the environment of the recipient. The role of these factors in neural plas-ticity and transplant-induced brain repair is examined in more detail in the following sections.
eBook - PDFTraumatic Brain and Spinal Cord Injury
Challenges and Developments
- Cristina Morganti-Kossmann, Ramesh Raghupathi, Andrew Maas(Authors)
- 2012(Publication Date)
- Cambridge University Press(Publisher)
Section 1 Traumatic Brain Injury Chapter 15 Plasticity and recovery of the injured brain Dorothy A. Kozlowski and Theresa A. Jones Introduction Neuroplasticity is the ability of the nervous system to change itself, as it does in response to experiences and to injury. Neuroplasticity is not a novel idea. In 1890, the psychologist, William James, proposed it to be the mechanism underlying the formation of motor, intellectual and professional skills, and other “habits” [1]. Neuroanatomical plasticity was also described in exquisite detail by Ram´ on y Cajal in the late nine- teenth and early twentieth centuries in his studies of the diseased brain [2]. The idea that learning occurs as a result of activity-dependent modifications in neural circuitry gained prominence in 1949, with Donald Hebb’s profoundly influential postulate that (as com- monly simplified) neurons that fire together, wire together [3]. Nevertheless, neural plasticity continued to be viewed as largely a developmental phenomenon. In the 1960s, Hubel and Wiesel strengthened this belief and instituted the idea that there was a “critical period” for neuroplasticity. They found that depriving one eye of visual stimulation during a specific develop- mental time window in young kittens, but not in adult cats, produced blindness and significantly affected the development of the visual cortex by eliminating ocular dominance columns [4]. This idea of neuroplasticity as a developmental phenomenon persisted into the 1970s. It was around this time that Greenough and others found that mature cortical neurons in rats can grow new dendrites and synapses in response to behav- ioral manipulations, such as housing in an enriched environment or maze training. This was found first in rats that were juvenile, but past early critical periods of development [5], and soon after it was found in fully adult rats [6, 7].
- Steven Laureys(Author)
- 2006(Publication Date)
- Elsevier Science(Publisher)
The study of whether, and particularly how, treatments can reduce impairments is thus crucial, and it is in this field that the clinical neurosciences can make a unique contribution. Plasticity in the damaged brain Despite the limited capacity of the central nervous system (CNS) to regenerate there is evidence that improvements in specific impairments do occur. Experiments in both animals and humans show that some regions in the normal adult brain, particularly the cortex, have the capacity to change structure and consequently function in response to environmental change (Schallert et al., 2000). This reorganization at the systems level is often referred to as plasticity. In addition, work in animal models has clearly demonstrated that focal damage in the adult brain can lead to a number of molecular and cellular changes in both perilesional and distant brain regions, normally seen only in the developing brain (Cramer and Chopp, 2000). This suggests that the damaged brain is more able to change structure and function in response to afferent signals. In other words it is more “plastic”. It is hypothesized that similar injury-induced changes occur in the human brain, and that targeted therapy interacts with these changes and thereby provides a means of reducing impairment in patients with focal brain damage via activity-dependent plastic change. These advances are clearly of great interest to clinicians and scientists alike. This review will concentrate on the current level of understanding of the mechanisms of recovery from motor impairment in human patients. Brain research in humans is largely performed at the systems level
eBook - PDFBrain Neurotrauma
Molecular, Neuropsychological, and Rehabilitation Aspects
- Firas H. Kobeissy(Author)
- 2015(Publication Date)
- CRC Press(Publisher)
In fact, the brain some-times actually becomes more sensitive to activity-dependent neural plasticity after stroke-like damage (Jones, 2009; Jones et al., 2008; Kleim and Jones, 2008; Nudo, 2003). Long-term motor dysfunction is common after TBI, yet there are few treatments available. It is assumed that motor rehabilita-tive therapy after TBI will also improve motor function through similar neural plastic mechanisms seen after stroke damage. Yet, recent findings suggest that injury-induced adaptive plas-ticity after TBI is restricted, at least in some aspects, compared with injury-induced plasticity found in stroke models (Jones et al., 2012; Kozlowski et al., 2013). Because adaptive plasticity is reduced, it likely will require a great deal of effort to promote recovery after TBI. Additionally, even in these stroke models, behavioral manipulations often have varying degrees of suc-cess (Jones, 2009; Jones et al., 2008; Wolf et al., 2008), and significant improvements can take weeks or months of effortful training. Therefore, motor recovery after TBI may be greatly improved by combining appropriate experience-dependent practice with treatments that have been shown to alter brain activity, such as CS of the motor cortex. Combining CS and motor practice after TBI injury may facilitate greater neural plasticity because CS has been found to do in stroke survivors and thus may enhance greater motor recovery. 43.3 IMPLANTABLE CS DEVICES ENHANCE MOTOR FUNCTION RECOVERY AND DRIVE NEURAL PLASTICITY Extradural electrical stimulation over the motor cortex was initially used as an experimental treatment for intractable cen-tral pain in humans after stroke.
- Carlo Caltagirone, Fabrizio Piras, Paola Imbriani(Authors)
- 2021(Publication Date)
- Giunti Psychometrics(Publisher)
This type of neural plasticity has implications for the type of rehabilitative train-ing administered post-stroke. Cauraugh and Summers (2005) proposed that mo-tor recovery of the upper limbs may stem from activity-dependent intervention involving interlimb coordination. According to these authors, bilateral movement training facilitates cortical plasticity through motor cortex disinhibition, en-hanced recruitment of ipsilateral pathways, and upregulation of descending com-mands to propriospinal neurons. There are different approaches to improving function after brain damage (Kleim and Jones, 2008). On the one hand, the severity of the initial injury can be limited to minimize loss of function. On the other hand, one can attempt to fa-cilitate brain reorganization by restoring or compensating for compromised func-tions. A critical element of rehabilitative training consists in helping individuals to develop compensatory behavioural strategies. To this end, it is important to un-derstand how training interacts with neural reactions to the brain damage, and to identify the time windows in which training can be optimally applied (Kleim and Jones, 2008). These authors further indicate some principles of experience-de-pendent plasticity that need to be taken into account for rehabilitation. First, they propose the principle Use It or Lose It, related to the notion that failure to drive specific brain functions can lead to functional degradation. The principle of Use It and Improve It instead refers to the idea that training driving a specific brain function can lead to function enhancement. The principle of Specificity states that the nature of the training experience affects the nature of the plasticity. The prin-ciple of Repetition implies that induction of plasticity requires sufficient repeti-tion. The principle of Intensity Matters Induction of plasticity requires sufficient training intensity.
eBook - PDF- Daniel J. DiLorenzo, Joseph D. Bronzino, Daniel J. DiLorenzo, Joseph D. Bronzino(Authors)
- 2007(Publication Date)
- CRC Press(Publisher)
This implied that any injury the brain sustains during the course of a lifetime would translate to a given functional deficit that is irreversible. Damage to the visual area, for example, would mean permanent visual loss. In relatively more recent years, however, this view has been challenged by the demonstration of plasticity in the adult cortex (Chino, 1997; Gilbert, 1998; Kaas, 1994). Approximately a few weeks to three months after visual cortical damage, spontaneous functional recovery may occur, although to a limited degree (Zihl and von Cramon, 1985; Gray et al., 1989; Tiel-Wilck and Koelmel, 1991; Zhang et al., 2006). Poppelreuter (1917) had reported spontaneous recovery of visual functions found in soldiers with gunshot lesion. Subsequent studies have found similar spontaneous visual improvement (Trobe and Miekle, 1973; Bogousslavsky et al., 1983; Hier et al., 1983; Koelmel, 1984, 1988; Zihl and von Cramon, 1985, 1986; Messing and Gaenshirt, 1987; Tiel-Wilck, 1991). This improve-ment has been explained as a result of recovery from the swelling around the area of injury, or of functional revival of partially disrupted neural circuitry. The amount of improvement can range from 7% to as much as 85%. Such inconsistency may be reflected in differences in testing method and criteria of what consti-tuted visual recovery. Interestingly, a common finding was that patients with relatively large transition zones would reliably show a more significant amount of spontaneous recovery. The question arises as to the neurobiological mechanisms of recovery of vision following lesions. In this context, the reorganization of receptive fields is relevant. 23.2.4 Plasticity of Receptive Field Reorganization Hartline (1938) defined the receptive field as the retinal region that must be illuminated to obtain a response in any given fiber.
eBook - PDFBrain Injury
Functional Aspects, Rehabilitation and Prevention
- Amit Agrawal(Author)
- 2012(Publication Date)
- IntechOpen(Publisher)
6. Conclusion The neuroplasticity mediated cognitive rehabilitative processes upon brain injury are frequently divided into two phases: initially a relearling of compromized and/or lost “functions” followed by later compensational processes which support the behavioural abilities without re-establishing what has been lost to injury (e.g. Stein & Hoffman, 2003). According to the REF-model, such a distinction is likely to be somewhat artificial and potentially misleading regarding the possibility of major re-establishment of lost functions – at least if “function” is considered at the level of the EFs. As mentioned above and discussed extensively elsewhere (Mogensen, 2011a), re-establishment of the lost neural substrate of EFs is unlikely to occur. However, as noted by Mogensen & Malá (2009), subtotal lesions of various structures (or more likely substructures) of the brain may allow a degree of “re-establishment” of the original substrate of task mediation via mechanisms such as those suggested by I.H. Robertson & Murre (1999). If such a process leads to re-establishment of the substrate of EFs originally lost to trauma, an actual “relearning” may indeed take place. But in general, a distinction between “relearning” and “compensation” will (according to the REF-model) in most if not all cases reflect the degree to which the surface level phenomena can easily be distinguished from those seen pretraumatically – while both “relearning” and “compensation” in reality reflect the REF-processes. At the theoretical level, the REF-model has provided a framework within which the concepts of localization of function and functional recovery can co-exist. But it has also provided a structure within which connectionist networks (e.g. McClelland et al., 1986; McLeod et al., 1998; Rumelhart & McClelland, 1986) can co-exist with “modularity” (e.g. Fodor, 2000; Pinker, 1999).
eBook - PDF- Jennifer K. E. Steeves, Laurence R. Harris(Authors)
- 2012(Publication Date)
- Cambridge University Press(Publisher)
A minimal number of residual cells was found to be critical for vision restoration to occur, but because of network plasticity, which acts on the rest of the brain, the precise number of surviving cells in the lesion site is a rather poor predictor of restoration (Sautter and Sabel, 1993). Also, local cellular changes such as (re-)activation of surviving cells (Prilloff et al., 2007) or enhancement of their synaptic transmission (synaptic plasticity), are involved. Furthermore, recovery prospects depend not only on how much primary tissue is left but also on the presence of rerouting pathways for visual information, which is only one aspect of network plasticity. Network plasticity refers to all changes in areas that are not primarily dam- aged but are influenced by deafferentiation, including nondeafferented regions involved in the postlesion response. Combined, simultaneous lesions of all alter- native pathways result in more severe deficits, and the probability and/or extent of recovery is markedly reduced. For example, there is less recovery in cats with combined visual cortex and suprasylvian gyrus lesions (Wood et al., 1974) so that when creating combined lesions of different visual areas simultane- ously, there may still be visual sparing (in luminous flux). However, when the suprachiasmatic nucleus was also damaged, removing the last visual structure still available, restoration was practically impossible (Pasik and Pasik, 1973). Receptive Field Plasticity in Deafferented Brain Structures The classic example of network plasticity in the visual system is “receptive field” (RF) reorganization, a field pioneered by Eysel (e.g., Eysel and Gr¨ usser, 1978). RF reorganization was observed after retinal lesions with RF shifts up to 5 to 9 degrees of visual angle and up to tenfold initial increase of RF size followed by shrinkage to nearly normal levels (Darian-Smith and Gilbert, 1995; Waleszczyk et al., 2003; Giannikopoulos and Eysel, 2006).
eBook - PDF- Jon C. Horvitz, Barry L. Jacobs(Authors)
- 2022(Publication Date)
- Cambridge University Press(Publisher)
The irony of this situation should not be lost on us because these same events involving glutamate, its receptors, and Ca2 + are critical processes in virtually all positive forms of plasticity, including learning and memory. So, here we have the classi- cal case of too much of a good thing! KEY CONCEPTS • Neurotrophic factors are released by target neurons to promote the growth and survival of incoming axons. • Long-term potentiation is the strengthening of synaptic connections between neurons. Changes in synaptic strength play an important role in learning and memory. • In addition to trauma to the brain, the environment contains agents that are potentially harmful to the cells of the nervous system. • Excessive neuronal excitation is the primary mechanism underlying cell death. 8.2 PLASTICITY 337 8.2.5 Biological Processes and Technologies Offer Hope for CNS Recovery There is an intense interest in developing treatments that will promote re- covery after injury to the nervous system from disease or accidents. When we ask about nervous system recovery, there are several questions of in- terest. Can the damaged neurons reestablish their connections with their targets? If not, can other neurons that are not damaged take over some of their functions? Even if the damaged neurons fail to reestablish normal connections and healthy neurons do not substitute for them, the person may learn strategies to compensate for the movement difficulties or other disrupt- ed functions. For instance, if brain damage causes paralysis of one arm, the person may gain skill in using the unaffected arm to carry out more tasks. If elbow movements are no longer possible, the person may learn to carry out tasks by moving other joints in ways that compensate for the lost abilities. We begin with a brief discussion of the peripheral nervous system, where damaged neurons can often spontaneously reestablish their con- nections.
Index pages curate the most relevant extracts from our library of academic textbooks. They’ve been created using an in-house natural language model (NLM), each adding context and meaning to key research topics.
