Neuroplasticity , also known as brain plasticity and neural plasticity , is the brain's ability to change throughout the life of an individual, for example, related brain activity. with the given functionality transferable to a different location, the proportion of gray matter may change, and the synapses may strengthen or weaken over time.
Research in the second half of the 20th century shows that many aspects of the brain can be changed (or "plastic") even into adulthood. This notion contradicts previous scientific consensus that the brain develops during the critical period in early childhood and then remains relatively unchanged (or "static").
Neuroplasticity can be observed at various scales, from microscopic changes in individual neurons to large-scale changes such as cortical remapping in response to injury. Behavior, environmental stimuli, thoughts, and emotions can also cause neuroplastic changes through activity-dependent plasticity, which has significant implications for the development, learning, memory, and healthy recovery of brain damage.
At a single cellular level, synaptic plasticity refers to a change in the relationship between neurons, whereas non-synaptic plasticity refers to changes in intrinsic stimulation.
Video Neuroplasticity
Neurobiology
One of the fundamental principles underlying neuroplasticity is based on the idea that individual synaptic connections are continuously removed or recreated, largely dependent on the activity of the neurons that bear it. Synaptic plasticity-dependence activity is captured in a proverb often used to sum up the Hebbian theory: "a joint fire neuron, a wire together"/"neurons that fire out of sync, fail to connect". If two neurons nearby often produce impulses in close temporal distances, their functional properties can be united. Conversely, neurons that are not regularly activated simultaneously may function less functionally.
Cortical map
The cortical organization, especially in the sensory system, is often described as a map. For example, sensory information from a foot project to a cortical site and a projection of hands targeting another site. Consequently, the cortical representation of sensory input from the body resembles a somatotopic map, often described as a sensory homunculus.
In the late 1970s and early 1980s, several groups began exploring the impact of distorting sensory input on the reorganization of cortical maps. Michael Merzenich, Jon Kaas and Doug Rasmusson are some of these researchers. They found that if the cortical map loses its input, it will activate it at a later time in response to other normally adjacent inputs. Their findings have since supported and expanded by many research groups. Merzenich's (1984) study involved mapping of owl's monkey hands before and after the third digit amputation. Before amputation, there are five different fields, one corresponding to each experimental hand digit. Sixty-two days after the third number cut, the area on the cortical map previously occupied by that digit has been attacked by the previous two and four digits of the previous digit. The areas representing digits one and five are not located right next to the area representing the three digits, so this area remains, for the most part, unchanged cuts. This study shows that only areas that restrict certain areas that invade to change cortical maps. In somatic sensory systems, where this phenomenon has been thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Reorganization does not appear cortically, but occurs at every level in the processing hierarchy; this results in changes in maps observed in the cerebral cortex.
Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological disturbance, to cortical observed plasticity in primate somatosensory systems, with the findings that sensory sites were activated in the improvement of operant behaviors attended in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made a similar effort in the rat rod whisker cortex (also part of the somatosensory system). These two groups differed greatly over the years. The efforts of the rodent mustache barrels to focus on Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Large intrades are made in identifying locus changes as in cortical synapses expressing NMDA receptors, and in the implications of the cholinergic input necessary for normal expression. The work of Ron Frostig and Daniel Polley (1999, 2004) identifies behavioral manipulation that causes a substantial impact on cortical plasticity in the system.
Merzenich and DT Blake (2002, 2005, 2006) continue to use cortical implants to study the evolution of plasticity in both somatosensory and hearing systems. Both systems show similar changes with respect to behavior. When the stimulus is cognitively associated with reinforcement, its cortical representation is amplified and magnified. In some cases, cortical representation may increase two to threefold within 1-2 days when new sensory motor behavior is first obtained, and changes are largely resolved within a few weeks at the most. Control studies show that these changes are not due to sensory experiences alone: ​​they require learning about sensory experiences, they are strongest for reward-related stimuli, and they occur with equal ease in classical operant and conditioning behavior.
An interesting phenomenon involving the plasticity of cortical maps is a phenomenon of ghost sensation. Phantom limb sensations are experienced by people who have undergone amputations in the hands, arms, and legs, but are not limited to the extremities. Although the neurological basis of ghost sensation is not yet fully understood, it is believed that cortical reorganization plays an important role.
Norman Doidge, following in the footsteps of Michael Merzenich, separates the manifestations of neuroplasticity into adaptations that have consequences of positive or negative behavior. For example, if an organism can recover after a stroke to a normal level of performance, that adaptation can be considered as an example of "positive plasticity". Changes such as excessive neuronal growth rates cause tonic spasticity or paralysis, or excessive release of neurotransmitters in response to injuries that can cause neonatal cell death, are considered examples of "negative" plasticity. Additionally, drug addiction and obsessive-compulsive disorder are both considered as examples of "negative plasticity" by Dr. Doidge, because synaptic rewiring that generates this behavior is also very maladaptive.
A 2005 study found that the effects of neuroplasticity occurred faster than previously thought. The brains of medical students are imaged during the study period for their exams. In a matter of months, the gray matter of students increases significantly in the posterior and lateral parietal cortex.
Maps Neuroplasticity
Apps and examples
The adult brain is not completely "programmed" with fixed neural circuits. There are many examples of repetition of cortical and subcortical nerve circuits in response to training and response to injury. There is strong evidence that neurogenesis (the birth of brain cells) occurs in the brains of adults, mammals - and such changes can survive well into old age. The evidence for neurogenesis is primarily limited to hippocampal and olfactory bulbs, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well.
There is now plenty of evidence for active reorganization and depends on the experience of synaptic brain tissue involving various interrelated structures including the cerebral cortex. Specific details about how this process occurs at the molecular and ultrastructural level are active topics of neuroscience research. The way experiences can affect the synaptic organization of the brain is also the basis for a number of theories of brain function including general thought theories and nerve Darwinism. The concept of neuroplasticity is also important for memory theory and learning associated with changes in synaptic structures and functions that are driven by experience in classical conditioning studies on invertebrate animal models such as Aplysia .
Brain damage treatment
A surprising consequence of neuroplasticity is that brain activity associated with a given function can be transferred to a different location; this can result from normal experience and also occurs in the process of recovery from brain injury. Neuroplasticity is a fundamental problem supporting the scientific basis for the treatment of brain injury acquired by a goal-directed therapeutic program in the context of a rehabilitation approach to the functional consequences of injury.
Neuroplasticity gained popularity as a theory that, at least in part, explains the improvement of functional outcomes with post-stroke physical therapy. Rehabilitation techniques supported by evidence showing cortical reorganization as a mechanism of change include constrained-induced gait therapy, functional electrical stimulation, treadmill training with weight support, and virtual reality therapy. Robot-assisted therapy is an emerging technique, which is also hypothesized to work by means of neuroplasticity, although there is currently insufficient evidence to determine the exact mechanism of change when using this method.
One group has developed a treatment that includes increased levels of progesterone injections in patients with brain injury. "Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and improves spatial reference memory and sensory motor recovery." In clinical trials, a group of seriously injured patients had a 60% reduction in death after three days of progesterone injections. However, a study published in the New England Journal of Medicine in 2014 detailing the results of a NIH-funded phase III clinical trial of 882 patients found that acute traumatic brain injury treatment with the hormone progesterone did not give a significant benefit for patients when compared with placebo.
Vision
For decades, researchers assumed that humans should get binocular vision, particularly stereopsis, in early childhood or they would never get it. In recent years, successful improvement in people with amblyopia, convergence mismatch or other stereo vision anomalies has been a prime example of neuroplasticity; improving binocular vision and stereopsis recovery has now become an active field of scientific and clinical research.
Brain training
Some companies have offered so-called cognitive training software programs for various purposes that claim to work through neuroplasticity; one example is Fast ForWord which is marketed to help children with learning disabilities. A systematic meta-analytic review found that "There is no evidence from the analysis that Fast ForWord is effective as a treatment for oral language or reading difficulties of children". The 2016 review found very little evidence supporting one of Fast ForWord's claims and other commercial products, because their task-specific effects failed to generalize other tasks.
Sensory prostheses
Neuroplasticity is involved in the development of sensory function. The birth brain is immature and adapts to the sensory input after birth. In the hearing system, congenital hearing loss, a congenital condition that somewhat often affects 1 in 1000 newborns, has been shown to affect hearing development, and implantation of the sensory prosthesis that activates the hearing system has prevented deficits and led to the functional maturation of the auditory system.. Due to the sensitive period for plasticity, there is also a sensitive period for such interventions within the first 2-4 years of life. As a result, in deaf children, early cochlear implantation, as a rule, allows children to learn the mother tongue and acquire acoustic communication.
Phantom limbs
In the phenomenon of the sensation of a ghost limb, a person continues to feel pain or sensation within the amputated part of his body. This is strangely common, occurring in 60-80% of amputation sufferers. The explanation for this is based on the concept of neuroplasticity, because the cortical maps of the diseased limbs are believed to have been involved with the area around them in the postcentral gyrus. This results in activity around the cortical area which is misinterpreted by the cortical area previously responsible for the limbs that are amputated.
The relationship between the sensation of the phantom limb and neuroplasticity is complex. In the early 1990s, V.S. Ramachandran theorizes that ghost limbs are the result of cortical remapping. However, in 1995 Herta Flor and her colleagues showed that cortical remapping occurs only in patients with phantom pain. His research shows that ghost pain (not the sensation referred to) is the correlation of cortical reorganization perceptions. This phenomenon is sometimes referred to as maladaptive plasticity.
In 2009 Lorimer Moseley and Peter Brugger conducted a remarkable experiment in which they encouraged amputated subjects to use visual imagery to transform their ghostly form into impossible configurations. Four of the seven subjects managed to make the impossible movement of the ghost of the limb. This experiment shows that subjects have modified the neural representation of their ghost limbs and produced the motor commands required to perform impossible motions without any feedback from the body. The authors state that: "In fact, these findings broaden our understanding of brain plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms - the brain completely transforms itself."
Chronic pain
Individuals suffering from chronic pain experience prolonged pain in sites that may have been previously injured, but otherwise are currently healthy. This phenomenon is associated with neuroplasticity due to maladaptive reorganization of the nervous system, both peripherally and centrally. During periods of tissue damage, harmful stimulation and inflammation leads to increased nociceptive input from the periphery to the central nervous system. The prolonged nociceptive of the periphery then elicits a neuroplastic response at the cortical level to alter the somatotopic organization for painful sites, inducing central sensitization. For example, individuals with complex regional pain syndromes exhibit a reduced cortical somatotopic representation of the hands contralaterally and a decrease in the distance between the hands and mouth. In addition, chronic pain has been reported to significantly reduce the gray matter volume in the brain globally, and more particularly in the right prefrontal and thalamus cortex. However, after treatment, these abnormalities in the cortical reorganization and gray matter volume were solved, as well as their symptoms. Similar results have been reported for ghost leg pain, chronic low back pain and carpal tunnel syndrome.
Meditation
Numerous studies have linked meditation practice to differences in gray matter thickness or cortical density. One of the most famous studies to demonstrate was led by Sara Lazar, of Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in collaboration with the Dalai Lama on the effects of meditation on the brain. The results show that long-term or short-term meditative practices produce different levels of activity in areas of the brain associated with qualities such as attention, anxiety, depression, fear, anger, and the body's ability to heal itself. This functional change may be due to changes in the physical structure of the brain.
Fitness and exercise
Aerobic exercise promotes adult neurogenesis by increasing the production of neurotrophic factors (compounds that promote neuronal growth or survival), such as brain-derived neurotrophic factors (BDNF), growth factors such as insulin 1 (IGF-1), and vascular factor endothelial growth (VEGF ). Neurogenesis induced by exercise in the hippocampus is associated with a measurable increase in spatial memory. Consistent aerobic exercise over several months induces significant clinical improvements in executive function (ie, "cognitive control" behavior) and increased gray matter volumes in some brain regions, especially those that enhance cognitive control. The brain structures that show the greatest increase in the volume of gray matter in response to aerobic exercise are the prefrontal and hippocampal cortex; moderate improvement seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens. Higher physical fitness scores (measured by VO 2 max) relate to better executive function, faster processing speed, and hippocampal volume, larger caudate nuclei, and nucleus accumbens.
Human echolocation
Human echolocation is a learned ability for humans to perceive their environment from echoes. This ability is used by some blind people to navigate their environment and feel their environment in detail. Studies in 2010 and 2011 using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adjusted for new skills of ecolocation. Studies with blind patients, for example, show that click echoes heard by these patients are processed by areas of the brain devoted to vision rather than audition.
stimulant ADHD
The review of MRI studies in individuals with ADHD suggests that long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in some parts of the brain, such as the right-tailed nucleus of the basal ganglia.
In children
Neuroplasticity is most active in childhood as part of normal human development, and can also be seen as a very important mechanism for children in terms of risk and endurance. Trauma is considered a major risk because it negatively affects many areas of the brain and puts pressure on the sympathetic nervous system of constant activation. Trauma thus alters the brain connections so that traumatized children may be hyper-alert or overly stimulated. But a child's brain can overcome this adverse effect through the action of neuroplasticity.
In animals
Within a single lifetime, individuals of an animal species may experience various changes in the morphology of the brain. Many of these differences are caused by the release of hormones in the brain; the other is the product of the evolutionary factor or the stage of development. Some changes occur seasonally in species to improve or generate response behavior.
Seasonal brain changes
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals. This change can increase the chances of mating during the breeding season. Examples of seasonal brain morphological changes can be found in many classes and species.
In the Aves class, the black-covered girl experiences an increase in the volume of the hippocampus and the strength of the nerve connection to the hippocampus during the fall. The morphological changes in the hippocampus associated with spatial memory are not limited to birds, as they can also be observed in rodents and amphibians. In singer singing, many songs that control nuclei in the brain get bigger during the mating season. Among birds, changes in brain morphology affect common song patterns, frequency, and volume. Gonadotropin-releasing hormone (GnRH) immunoreactivity, or hormone acceptance, is inherited in European starlings exposed to longer periods of light during the day.
The California marine rabbits, gastropods, have a more successful egg-laying inhibition outside the breeding season due to increased effectiveness of inhibitors in the brain. Changes in the inhibitory properties of the brain region can also be found in humans and other mammals. In Bufo japonicus amphibians, parts of the amygdala are larger before breeding and during hibernation than after breeding.
Seasonal brain variation occurs in many mammals. Part of the female parent hypothalamus is more readily accepted for GnRH during the mating season than at other times of the year. Humans experience a change in "the size of the hypothalamic suprachiasmatic nucleus and the vasopressin-immunoreactive neurons in it" during the fall, when this section is larger. In spring, they reduce size.
Research of traumatic brain injury
Randy Nudo's group found that if small strokes (infarcts) are caused by obstruction of blood flow to the ape's motor cortex, the body parts that respond to movements move when the area adjacent to the damaged area of ​​the brain is stimulated. In one study, intracortical micrometulation mapping techniques (ICMS) were used in nine normal monkeys. Some are undergoing ischemic-infarction procedures and others, ICMS procedures. Monkeys with ischemic infarct retain more finger flexion during feeding and after a few months this deficit returns to preoperative levels. With respect to the distal frontal representation, "the postinfarction mapping procedure reveals that the representation of movement undergoes reorganization across the adjacent and undamaged cortex." Understanding the interaction between damaged and undamaged areas provides the basis for a better treatment plan in stroke patients. Current research includes tracking changes occurring in the cerebral cortex motor area as a result of stroke. Thus, events occurring in the brain reorganization process can be ascertained. Nudo is also involved in studying treatment plans that can improve recovery from stroke, such as physiotherapy, pharmacotherapy, and electrical stimulation therapy.
Jon Kaas, a professor at Vanderbilt University, has been able to show "how somatosensory nucleus 3b and ventroposterior (VP) regions of the thalamus are affected by unilateral dorsal-column long lesions at the cervical level of ape monkeys." The adult brain has the ability to change as a result of injury but the extent to which the reorganization depends on the extent of the injury. His research has recently focused on the somatosensory system, which involves his sense of body and movement using many senses. Usually, somatosensory cortical damage causes a disruption of body perception. Kaas's research project focused on how this system (somatosensory, cognitive, motor system) responded with the plastic changes resulting from injuries.
One recent study of neuroplasticity involves the work done by a team of doctors and researchers at Emory University, in particular Dr. Donald Stein and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injury while also causing no known side effects and being cheap to manage. Dr. Stein noticed that female mice seemed to recover from better brain injury than male rats, and at certain points in the estrous cycle, females recovered better. This difference can be attributed to different levels of progesterone, with higher levels of progesterone leading to faster recovery of brain injury in mice. However, clinical trials suggest progesterone does not provide significant benefits for traumatic human brain injury patients.
History
Origin
The term "plasticity" was first applied to behavior in 1890 by William James in the The Principles of Psychology . The first person to use the term nerve plasticity seems to be the Polish neurologist Jerzy Konorski.
In 1793, the Italian anatomist Michele Vicenzo Malacarne described an experiment in which he paired animals, coached one pair extensively for years, and then dissected both. He found that the trembling of much trained animals is much greater. But these findings are finally forgotten. The notion that his brain and function were not improved throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, although the idea was largely ignored. Until about the 1970s, neuroscientists believed that the structure and function of the brain remained essentially throughout adulthood.
This term has since been widely seen applied:
Given the importance of neuroplasticity, outsiders will be forgiven for assuming that it is well defined and that the basic and universal framework serves to direct current and future hypotheses and experiments. Unfortunately, this is not the case. While many neuroscientists use the word neuroplasticity as an umbrella term it means different things to different researchers in different subfields... In short, a mutually agreed framework does not seem to exist.
Research and discovery
In 1923, Karl Lashley conducted experiments on rhesus monkeys that showed a change of nerve pathway, which he concluded as evidence of plasticity. However, and other studies suggesting plasticity occur, neurologists do not accept much of the idea of ​​neuroplasticity.
In 1945, Justo Gonzalo concluded from his study of the dynamics of the brain, which is contrary to the activity of the projection area, the "central" cortical mass (more or less equidistant from the visual, touch and auditive projection area), would be "mass maneuvering," rather unspecific or multisensor, with the capacity to increase nerve stimulation and rearrange activity through plasticity properties. He gives as an example the first adaptation, to look upright by reversing the glasses in Stratton's experiments, and in particular, some cases of first-hand brain injury in which he observes the dynamic and adaptive nature of their disorders, particularly in reverse perception disorders [eg, see pp 260- 62 Vol. I (1945), p 696 Vol. II (1950)]. He stated that the sensory signal in the projection area would only be a reversed and limited boundary that would be enlarged due to an increase in brain mass being recruited, and reversed due to some cerebral plasticity effect, in a more central region, following spiral growth.
Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, which published his research in 1964.
Other important evidence was produced in the 1960s and beyond, mainly from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.
In the 1960s, Paul Bach-y-Rita invented a device that was tested on a small number of people, and involved a person sitting in a chair, where embedded nubs were made to vibrate in a way that translated images received in camera, through [sensory substitution]].
Studies in people who recover from stroke also provide support for neuroplasticity, because the areas of the brain remain healthy can sometimes take over, at least in part, function that has been destroyed; Shepherd Ivory Franz works in this field.
Eleanor Maguire documented changes to the hippocampal structure associated with acquiring knowledge of the London layout in local taxi drivers. The redistribution of gray matter is indicated in the London Taxi Drivers as compared to the controls. This work on hippocampal plasticity is not only interested scientists, but it also involves the public and the media around the world.
Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for over three decades. He has made some of the "most ambitious claims for this field - that brain exercise may be as useful as medicine for treating schizophrenic diseases - plasticity exists from cradle to grave, and radical increase in cognitive function - how we learn, think, feel, and remember it may happen even to the elderly. "Merzenich's work is influenced by the important discoveries made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing a closed eye and recording cortical brain maps. Hubel and Wiesel noticed that the part of the kitten's brain associated with the closed eye was not idle, as expected. Instead, it processes visual information from the open eye. It is "... as if the brain does not want to waste the 'cortical real estate' and has found a way to change itself."
Source of the article : Wikipedia
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