Neuroplasticity
Neuroplasticity, also known as neural plasticity or brain plasticity, is the ability of
Neuroplasticity was once thought by
History
Origin
The term plasticity was first applied to behavior in 1890 by William James in The Principles of Psychology where the term was used to describe "a structure weak enough to yield to an influence, but strong enough not to yield all at once".[16][17] The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.[11][18]
One of the first experiments providing evidence for the neuroplasticity phenomenon was conducted in 1793, by Italian anatomist Michele Vicenzo Malacarne, who described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. Malacarne discovered that the cerebellums of the trained animals were substantially larger than the cerebellum of the untrained animals. However, while these findings were significant, they were eventually forgotten.[19] In 1890, the idea that the brain and its function are not fixed throughout adulthood was proposed by William James in The Principles of Psychology, though the idea was largely neglected.[17] Up until the 1970s, neuroscientists believed that the brain's structure and function was essentially fixed throughout adulthood.[20]
While the brain was commonly understood as a nonrenewable organ in the early 1900s, Santiago Ramón y Cajal, father of neuroscience, used the term neuronal plasticity to describe nonpathological changes in the structure of adult brains. Based on his renowned neuron doctrine, Cajal first described the neuron as the fundamental unit of the nervous system that later served as an essential foundation to develop the concept of neural plasticity.[21] He used the term plasticity in reference to his work on findings of degeneration and regeneration in the central nervous system after a person had reached adulthood, specifically. Many neuroscientists used the term plasticity only to explain the regenerative capacity of the peripheral nervous system, which Cajal's conceptual transfer of the term gave rise to a controversial discussion.[22]
The term has since been broadly applied:
Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that it was well defined and that a basic and universal framework served to direct current and future hypotheses and experimentation. Sadly, however, 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 brief, a mutually agreed-upon framework does not appear to exist.[23]
Research and discovery
In 1923,
In 1945, Justo Gonzalo concluded from his research on brain dynamics, that, contrary to the activity of the projection areas, the "central" cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a "maneuvering mass", rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties.[24] He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment,[25] and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder [e.g., see pp 260–62 Vol. I (1945), p 696 Vol. II (1950)].[24] He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.[26]
Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.[27][28]
Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.[20][29]
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, embedded in which were nubs that were made to vibrate in ways that translated images received in a camera, allowing a form of vision via sensory substitution.[30][31]
Studies in people recovering from stroke also provided support for neuroplasticity, as regions of the brain that remained healthy could sometimes take over, at least in part, functions that had been destroyed; Shepherd Ivory Franz did work in this area.[32][33]
Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London's layout in local taxi drivers.[34][35][36] A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media worldwide.
This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, "If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic."[30] Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."[37]
Neurobiology
There are different ideas and theories on what biological process allow for neuroplasticity to occur. The core of this phenomenon is based upon synapses and how connections between them change based on neuron functioning. It is widely agreed upon that neuroplasticity takes on many forms, as it is a result of a variety of pathways. These pathways, mainly signaling cascades, allow for gene expression alterations that lead to neuronal changes, and thus neuroplasticity.
There are a number of other factors that are thought to play a role in the biological processes underlying the changing of neural networks in the brain. Some of these factors include synapse regulation via
JT Wall and J Xu have traced the mechanisms underlying neuroplasticity. Re-organization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.[39]
Types
Christopher Shaw and Jill McEachern (eds) in "Toward a theory of Neuroplasticity", state that there is no all-inclusive theory that overarches different frameworks and systems in the study of neuroplasticity. However, researchers often describe neuroplasticity as "the ability to make adaptive changes related to the structure and function of the nervous system."[40] Correspondingly, two types of neuroplasticity are often discussed: structural neuroplasticity and functional neuroplasticity.
Structural neuroplasticity
Structural plasticity is often understood as the brain's ability to change its neuronal connections. New neurons are constantly produced and integrated into the central nervous system throughout the life span based on this type of neuroplasticity.
Functional neuroplasticity
Functional plasticity refers to the brain's ability to alter and adapt the functional properties of neurons. Functional plasticity can occur in four known ways namely homologous area adaptation, map expansion, cross- model reassignment, and compensatory masquerade.[2] Through homologous area adaptation a cognitive task is shifted from a damaged part of the brain to its homologous area in the brain. Functional changes like this occur usually in children rather than adults. In map expansion, cortical maps related to particular cognitive tasks expand due to frequent exposure to stimuli. Map expansion has been proven through experiments performed in relation to the study: experiment on effect of frequent stimulus on functional connectivity of the brain was observed in individuals learning spatial routes.[43] Cross-model reassignment involves reception of novel input signals to a brain region which has been stripped off its default input. Functional plasticity through compensatory masquerade occurs using different cognitive processes for an already established cognitive task.
The changes can occur in response to previous activity (
Applications and examples
The adult brain is not entirely "hard-wired" with fixed
There is ample evidence[54] for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex.[55] The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The way experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind and neural Darwinism. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies of classical conditioning in invertebrate animal models such as Aplysia.
There is evidence that neurogenesis (birth of brain cells) occurs in the adult, rodent brain—and such changes can persist well into old age.[56] The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but research has revealed that other parts of the brain, including the cerebellum, may be involved as well.[57] However, the degree of rewiring induced by the integration of new neurons in the established circuits is not known, and such rewiring may well be functionally redundant.[58]
Treatment of brain damage
A surprising consequence of neuroplasticity is that the 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 the fundamental issue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to the functional consequences of the injury.
Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in functional outcomes with physical therapy post-stroke. Rehabilitation techniques that are supported by evidence which suggest cortical reorganization as the mechanism of change include
One group has developed a treatment that includes increased levels of progesterone injections in brain-injured patients. "Administration of progesterone after traumatic brain injury[60] (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory-motor recovery."[61] In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections.[62] However, a study published in the New England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.[63]
Binocular vision
For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.[64][65][66]
Phantom limbs
In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60–80% of amputees.[67] An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb.
The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s
In 2009, Lorimer Moseley and Peter Brugger carried out an experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible[clarification needed] configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body.[70] The authors stated that: "In fact, this finding extends our understanding of the brain's 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 truly does change itself."
Chronic pain
Individuals who have chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage,
Meditation
A number of studies have linked meditation practice to differences in cortical thickness or density of
Artistic engagement and art therapy
There is substantial evidence that artistic engagement in a therapeutic environment can create changes in neural network connections as well as increase cognitive flexibility.[84][85] In one 2013 study, researchers found evidence that long-term, habitual artistic training (e.g. musical instrument practice, purposeful painting, etc.) can "macroscopically imprint a neural network system of spontaneous activity in which the related brain regions become functionally and topologically modularized in both domain-general and domain-specific manners".[86] In simple terms, brains repeatedly exposed to artistic training over long periods develop adaptations to make such activity both easier and more likely to spontaneously occur.
Some researchers and academics have suggested that artistic engagement has substantially altered the human brain throughout our evolutionary history. D.W Zaidel, adjunct professor of behavioral neuroscience and contributor at VAGA, has written that "evolutionary theory links the symbolic nature of art to critical pivotal brain changes in Homo sapiens supporting increased development of language and hierarchical social grouping".[87]
Fitness and exercise
Aerobic exercise increases the production of
Deafness and loss of hearing
Due to hearing loss, the auditory cortex and other association areas of the brain in deaf and/or hard of hearing people undergo compensatory plasticity.[97][98][99] The auditory cortex is usually reserved for processing auditory information in hearing people now is redirected to serve other functions, especially for vision and somatosensation.
Deaf individuals have enhanced peripheral visual attention,[100] better motion change but not color change detection ability in visual tasks,[98][99][101] more effective visual search,[102] and faster response time for visual targets[103][104] compared to hearing individuals. Altered visual processing in deaf people is often found to be associated with the repurposing of other brain areas including primary auditory cortex, posterior parietal association cortex (PPAC), and anterior cingulate cortex (ACC).[105] A review by Bavelier et al. (2006) summarizes many aspects on the topic of visual ability comparison between deaf and hearing individuals.[106]
Brain areas that serve a function in auditory processing repurpose to process somatosensory information in congenitally deaf people. They have higher sensitivity in detecting frequency change in vibration above threshold[107] and higher and more widespread activation in auditory cortex under somatosensory stimulation.[108][97] However, speeded response for somatosensory stimuli is not found in deaf adults.[103]
Cochlear implant
Neuroplasticity is involved in the development of sensory function. The brain is born immature and then adapts to sensory inputs after birth. In the auditory system, congenital hearing loss, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system.[109] Due to a sensitive period for plasticity, there is also a sensitive period for such intervention within the first 2–4 years of life. Consequently, in prelingually deaf children, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.[110]
Blindness
Due to vision loss, the
Human echolocation
Attention deficit hyperactivity disorder
Reviews of MRI and electroencephalography (EEG) studies on individuals with ADHD suggest that the long-term treatment of ADHD with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia,[116][117][118] left ventrolateral prefrontal cortex (VLPFC), and superior temporal gyrus.[119]
In early child development
Neuroplasticity is most active in childhood as a part of normal
Neuroplasticity is shown in four different categories in children and covering a wide variety of neuronal functioning. These four types include impaired, excessive, adaptive, and plasticity.[123]
There are many examples of neuroplasticity in human development. For example, Justine Ker and Stephen Nelson looked at the effects of musical training on neuroplasticity, and found that musical training can contribute to experience dependent structural plasticity. This is when changes in the brain occur based on experiences that are unique to an individual. Examples of this are learning multiple languages, playing a sport, doing theatre, etc. A study done by Hyde in 2009, showed that changes in the brain of children could be seen in as little as 15 months of musical training.[124] Ker and Nelson suggest this degree of plasticity in the brains of children can "help provide a form of intervention for children... with developmental disorders and neurological diseases."[125]
In animals
In a single
Some changes occur seasonally in species to enhance or generate response behaviors.Seasonal brain changes
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals.[130] These changes can improve the chances of mating during breeding season.[126][127][128][130][131][132] Examples of seasonal brain morphology change can be found within many classes and species.
Within the class
The
Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common
Traumatic brain injury research
Randy Nudo's group found that if a small stroke (an infarction) is induced by obstruction of blood flow to a portion of a monkey's motor cortex, the part of the body that responds by movement moves when areas adjacent to the damaged brain area are stimulated. In one study, intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys. Some underwent ischemic-infarction procedures and the others, ICMS procedures. The monkeys with ischemic infarctions retained more finger flexion during food retrieval and after several months this deficit returned to preoperative levels.[137] With respect to the distal forelimb representation, "postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex."[137] Understanding of interaction between the damaged and undamaged areas provides a basis for better treatment plans in stroke patients. Current research includes the tracking of changes that occur in the motor areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization process of the brain can be ascertained. Nudo is also involved in studying the treatment plans that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.
Jon Kaas, a professor at Vanderbilt University, has been able to show "how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys."[138] Adult brains have the ability to change as a result of injury but the extent of the reorganization depends on the extent of the injury. His recent research focuses on the somatosensory system, which involves a sense of the body and its movements using many senses. Usually, damage of the somatosensory cortex results in impairment of the body perception. Kaas' research project is focused on how these systems (somatosensory, cognitive, motor systems) respond with plastic changes resulting from injury.[138]
One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Donald Stein[139] and David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer.[62] Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in the estrus cycle, females recovered even better. This difference may be attributed to different levels of progesterone, with higher levels of progesterone leading to the faster recovery from brain injury in mice. However, clinical trials showed progesterone offers no significant benefit for traumatic brain injury in human patients.[140]
Aging
Transcriptional profiling of the frontal cortex of persons ranging from 26 to 106 years of age defined a set of genes with reduced expression after age 40, and especially after age 70.[141] Genes that play central roles in synaptic plasticity were the most significantly affected by age, generally showing reduced expression over time. There was also a marked increase in cortical DNA damage, likely oxidative DNA damage, in gene promoters with aging.[141]
Reactive oxygen species appear to have a significant role in the regulation of synaptic plasticity and cognitive function.[142] However age-related increases in reactive oxygen species may also lead to impairments in these functions.
Multilingualism
The beneficial effect of multilingualism on people's behavior and cognition is well-known nowadays. Numerous studies have shown that people who study more than one language have better cognitive functions and flexibilities than people who only speak one language. Bilinguals are found to have longer attention spans, stronger organization and analyzation skills, and a better theory of mind than monolinguals. Researchers have found that the effect of multilingualism on better cognition is due to neuroplasticity.
In one prominent study, neurolinguists used a voxel-based morphometry (VBM) method to visualize the structural plasticity of brains in healthy monolinguals and bilinguals. They first investigated the differences in density of grey and white matter between two groups and found the relationship between brain structure and age of language acquisition. The results showed that grey-matter density in the inferior parietal cortex for multilinguals were significantly greater than monolinguals. The researchers also found that early bilinguals had a greater density of grey matter relative to late bilinguals in the same region. The inferior parietal cortex is a brain region highly associated with the language learning, which corresponds to the VBM result of the study.[143]
Recent studies have also found that learning multiple languages not only re-structures the brain but also boosts brain's capacity for plasticity. A recent study found that multilingualism not only affects the grey matter but also white matter of the brain.
While it is still debated whether these changes in brain are result of genetic disposition or environmental demands, many evidences suggest that environmental, social experience in early multilinguals affect the structural and functional reorganization in the brain.[145][146]
Novel treatments of depression
Historically, the
See also
- Activity-dependent plasticity
- Brain training
- Environmental enrichment (neural)
- Neural backpropagation
- Neuronal sprouting
- Neuroplastic effects of pollution
- Psychoplastogen
- Psychedelic drug
- Kinesiology
- Spike-timing-dependent plasticity
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- Cohen W, Hodson A, O'Hare A, Boyle J, Durrani T, McCartney E, et al. (June 2005). "Effects of computer-based intervention through acoustically modified speech (Fast ForWord) in severe mixed receptive-expressive language impairment: outcomes from a randomized controlled trial" (PDF). Journal of Speech, Language, and Hearing Research. 48 (3): 715–729. S2CID 15136064. Archived from the original(PDF) on 3 March 2019.
- Giszter SF (January 2008). "Spinal cord injury: present and future therapeutic devices and prostheses". Neurotherapeutics. 5 (1): 147–162. PMID 18164494.
- Mahncke HW, Connor BB, Appelman J, Ahsanuddin ON, Hardy JL, Wood RA, et al. (August 2006). "Memory enhancement in healthy older adults using a brain plasticity-based training program: a randomized, controlled study". Proceedings of the National Academy of Sciences of the United States of America. 103 (33): 12523–12528. PMID 16888038.
- Stein DG, Hoffman SW (July–August 2003). "Concepts of CNS plasticity in the context of brain damage and repair". The Journal of Head Trauma Rehabilitation. 18 (4): 317–341. S2CID 43231369.
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- Videos
- Ramachandran. Phantom Limb Syndrome. about consciousness, mirror neurons, and phantom limb syndrome
- Other readings
- Chorost M (2005). Rebuilt: how becoming part computer made me more human. Boston: Houghton Mifflin. ISBN 978-0-618-37829-6.
External links
- Neuroplasticity at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- Neuro Myths: Separating Fact and Fiction in Brain-Based Learning by Sara Bernard