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[[Image:Brain 2.jpg|right|thumb|300px|Neuroplasticity challenges the idea that brain functions are fixed in certain locations.]]
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[[File:Brain 2.jpg|right|thumb|320px|Contrary to common ideas as expressed in this diagram, brain functions are not confined to certain fixed locations.]]
'''Neural plasticity''' or '''Neuroplasticity''' (also variously referred to as '''''brain plasticity''','' '''cortical plasticity''' or '''cortical re-mapping''') refers to the changes that occur in the organization of the [[brain]] and [[nervous system|nervous system as]] a result of experience. The coining of the term plasticity in regards to neuronal process is attributed to Polish neuroscientist [[Jerzy Konorski]]. <ref name=LeDoux>"Synaptic Self", Joseph LeDoux 2002, p. 137</ref>
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'''Neuroplasticity''' (from neural - pertaining to the nerves and/or brain and plastic - moldable or changeable in structure), also known as '''brain plasticity''', refers to changes in neural pathways and synapses which are due to changes in behavior, environment and neural processes, as well as changes resulting from bodily injury.<ref name="Pascual-Leone et al. 2011"/> Neuroplasticity has replaced the formerly-held position that the brain is a physiologically static organ, and explores how - and in which ways - the brain changes throughout life.<ref name="Pascual-Leone et al. 2005"/>
   
The concept of neuroplasticity pushes the boundaries of the brain areas that are still re-wiring in response to changes in environment. Several decades ago, the consensus was that lower brain and neocortical areas were immutable after development, whereas areas related to memory formation, such as the [[hippocampus]] and [[dentate gyrus]], where new neurons continue to be produced into adulthood, were highly plastic.<ref>"Neurogenesis in adult primate neocortex: an evaluation of the evidence" Nature Reviews Neuroscience 3, 65-71 January 2002</ref> [[Hubel]] and [[Torsten Wiesel|Wiesel]] had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, were largely immutable after the [[critical period]] in development.<ref>"The period of susceptibility to the physiological effects of unilateral eye closure in kittens"J Physiol Vol 206 1970, Issue 2 pp 419-436</ref> Critical periods also were studied with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and other parts of the brain, including the cerebellum<ref name=Ponti>Ponti et al. Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits. PLoS ONE, 2008; 3 (6): e2366 DOI: 10.1371/journal.pone.0002366</ref>.
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Neuroplasticity occurs on a variety of levels, ranging from cellular changes due to learning, to large-scale changes involved in ''cortical remapping'' in response to injury. The role of neuroplasticity is widely recognized in healthy development, learning, memory, and recovery from brain damage. During most of the 20th century, the general consensus among neuroscientists was that brain structure is relatively immutable after a [[critical period]] during early childhood. This belief has been challenged by findings revealing that many aspects of the brain remain plastic even into adulthood.<ref name="Rakic 2002" />
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[[Hubel]] and [[Torsten Wiesel|Wiesel]] had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, were largely immutable after the [[critical period]] in development.<ref name="Hubel et al 1970" /> Critical periods also were studied with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and other parts of the brain, including the [[cerebellum]].<ref name="Ponti et al 2008" />
   
Decades of research have now shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. According to the theory of neuroplasticity, thinking, learning, and acting actually change both the brain's physical structure, or [[anatomy]], and functional organization, or [[physiology]] from top to bottom. Neuroscientists are presently engaged in a reconciliation of critical period studies demonstrating the immutability of the brain after development with the new findings on neuroplasticity which reveal the mutability of both structural and functional aspects. A substantial paradigm shift is now under way: Canadian psychiatrist [[Norman Doidge]] has in fact stated that neuroplasticity is "one of the most extraordinary discoveries of the twentieth century."<ref name=Doidge>Doidge, Norman. ''The Brain that Changes Itself''. Viking, 2007, p. xv.</ref>
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Decades of research<ref>Chaney, Warren, Dynamic Mind, 2007, Las Vegas, Houghton-Brace Publishing, pp 33-35, ISBN 0-9793392-0-0 [http://openlibrary.org/works/OL15675542W/Dynamic_Mind]</ref> have now shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. Neuroscientific research indicates that experience can actually change both the brain's physical structure ([[anatomy]]) and functional organization ([[physiology]]). Neuroscientists are currently engaged in a reconciliation of critical period studies demonstrating the immutability of the brain after development with the more recent research showing how the brain can, and does, change.<ref>Chaney, Warren, Workbook for a Dynamic Mind, 2006, Las Vegas, Houghton-Brace Publishing, page 44, ISBN 00979339219{{Please check ISBN|reason=Invalid length.}} [http://openlibrary.org/works/OL15675542W/Dynamic_Mind]</ref>
   
== Brain plasticity and cortical maps ==
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== Neurobiology ==
Cortical organization, especially for the [[sensory system]]s, is often described in terms of [[cortical map|maps]].<ref> CORTICAL PLASTICITY: From Synapses to Maps DV Buonomano, MM Merzenich - Annual Review of Neuroscience, 1998 </ref> For example, sensory information from the foot projects to one cortical site and the projections from the hand target in another site. As the result of this somatotopic organization of sensory inputs to the cortex, cortical representation of the body resembles a map (or [[homunculus]]).
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One of the fundamental principles of how neuroplasticity functions is linked to the concept of [[synaptic pruning]], the idea that individual [[synapse|connections]] within the [[brain]] are constantly being removed or recreated, largely dependent upon how they are used. This concept is captured in the aphorism, "neurons that fire together, wire together"/"neurons that fire apart, wire apart." If there are two nearby neurons that often produce an impulse simultaneously, their [[cortical map]]s may become one. This idea also works in the opposite way, i.e. that neurons which do not regularly produce simultaneous impulses will form different maps.
   
In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the [[sensation|sensory inputs]]. [[Michael Merzenich]] and [[Jon Kaas]] used the cortical map as their [[dependent variable]]. They found&mdash;and this has been since corroborated by a wide range of labs&mdash;that if the cortical map is deprived of its input it will become activated at a later time in response to other, usually adjacent inputs. At least in the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Re-organization is not cortically [[emergence|emergent]], but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.<ref>Wall JT, Xu J, Wang X.
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=== Cortical maps ===
"Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body." Brain Res Brain Res Rev. 2002 Sep;39(2-3):181-215. </ref>.
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Cortical organization, especially for the [[sensory system]]s, is often described in terms of [[cortical map|maps]].<ref name="Buonomano et al 1998" /> For example, sensory information from the foot projects to one cortical site and the projections from the hand target in another site. As the result of this somatotopic organization of sensory inputs to the cortex, cortical representation of the body resembles a map (or [[homunculus]]).
   
Merzenich and William Jenkins (1990) initiated studies relating [[sensory experience]], without pathological perturbation, to cortically observed plasticity in the [[primate]] [[somatosensory system]], with the finding that sensory sites activated in an attended [[operant behavior]] increase in their [[cortical representation]]. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the [[rodent]] [[whisker]] [[barrel cortex]] (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, Kevin Fox, and Dan Feldman, and great inroads were made in identifying the locus of change as being at cortical [[synapse]]s [[gene expression|expressing]] [[NMDA receptor]]s, and in implicating [[cholinergic]] inputs as necessary for normal expression. However, the rodent studies were poorly focused on the [[behavioral]] end, and Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.
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In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the [[wikt:sensation|sensory inputs]]. [[Michael Merzenich]], [[Jon Kaas]] and [[Doug Rasmusson]] used the cortical map as their [[dependent variable]]. They found&mdash;and this has been since corroborated by a wide range of labs&mdash;that if the cortical map is deprived of its input it will become activated at a later time in response to other, usually adjacent inputs. Merzenich’s (1984) study involved the mapping of [[owl monkey]] hands before and after [[amputation]] of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third [[Digit (anatomy)|digit]], the area in the [[cortical map]] formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation.<ref name="Merzenich et al 1984" /> This study demonstrates that only those regions bordering a certain area will invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. Re-organization is not cortically [[emergence|emergent]], but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.<ref name="Wall et al 2002" />
   
[[Michael Merzenich|Merzenich]] and DT Blake (2002, 2005, 2006) went on to use [[cortical implant]]s to study the evolution of plasticity in both the [[somatosensory]] and [[auditory]] systems. Both systems show similar changes with respect to [[behavior]]. When a stimulus is cognitively associated with [[reinforcement]], its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1-2 days at the time at which a new sensory motor behavior is first acquired, and changes are largely finished within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, and are strongest for the stimuli that are associated with reward, and occur with equal ease in operant and classical conditioning behaviors.
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Merzenich and William Jenkins (1990) initiated studies relating [[sensory experience]], without pathological perturbation, to cortically observed plasticity in the [[primate]] [[somatosensory system]], with the finding that sensory sites activated in an attended [[operant behavior]] increase in their [[cortical representation]]. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the [[rodent]] [[whisker]] [[barrel cortex]] (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, Kevin Fox and great inroads were made in identifying the locus of change as being at cortical [[synapse]]s [[gene expression|expressing]] [[NMDA receptor]]s, and in implicating [[cholinergic]] inputs as necessary for normal expression. However, the rodent studies were poorly focused on the [[behavioral]] end, and Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.
   
An interesting phenomenon involving cortical maps is the incidence of [[phantom limb]]s. This is most commonly described in people that have undergone [[amputation]]s in hands, arms, and legs, but it is not limited to extremities. The phantom limb feeling, which is thought<ref name=Doidge>Doidge, Norman. The Brain that Changes Itself. Viking, 2007</ref> to result from disorganization in the brain map and the inability to receive input from the targeted area, may be [[annoying]] or [[pain]]ful. Incidentally, it is more common after unexpected losses than planned amputations. There is a high [[correlation]] with the extent of physical remapping and the extent of phantom pain. As it fades, it is a fascinating functional example of new neural connections in the human adult brain.
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[[Michael Merzenich|Merzenich]] and DT Blake (2002, 2005, 2006) went on to use [[cortical implant]]s to study the evolution of plasticity in both the [[somatosensory]] and [[auditory system]]s. Both systems show similar changes with respect to [[behavior]]. When a stimulus is cognitively associated with [[reinforcement]], its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1–2 days at the time at which a new sensory motor behavior is first acquired, and changes are largely finished within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, and are strongest for the stimuli that are associated with reward, and occur with equal ease in operant and classical conditioning behaviors.
   
The concept of plasticity can be applied to molecular as well as to environmental events<ref>Georgetown University Medical Center (2008, July 12). Learning Suffers If Brain Transcript Isn't Transported Far Out To End Of Neurons. ScienceDaily. Retrieved July 13, 2008, from http://www.sciencedaily.com­ /releases/2008/07/080710120503.htm</ref><ref>Harvard University (2004, July 26). Scientists Pinpoint Molecules That Generate Synapses. ScienceDaily. Retrieved July 13, 2008, from http://www.sciencedaily.com­ /releases/2004/07/040726084801.htm</ref> The phenomenon itself is complex and can involve many levels of organization. To some extent the term itself has lost its explanatory value because almost any changes in brain activity can be attributed to some sort of "plasticity". For example, the term is used prevalently in studies of axon guidance during development, short-term visual adaptation to motion or contours, maturation of cortical maps, recovery after amputation or stroke, and changes that occur in normal learning in the adult.
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An interesting phenomenon involving cortical maps is the incidence of [[phantom limb]]s. Phantom limbs are experienced by people that have undergone [[amputation]]s in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limbs is still not entirely understood it is believed that cortical reorganization plays an important role.<ref name="Doidge 2007" />
   
Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". An excessive level of [[neuronal growth]] leading to [[spasticity]] or [[tonic paralysis]], or an excessive release of [[neurotransmitter]]s in response to injury which could kill nerve cells; this would have to be considered a "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive<ref>Doidge, Norman. The Brain that Changes Itself. Viking, 2007</ref><ref>[http://www.childrenofthecode.org/interviews/merzenich.htm] Interview with Merzenich in 2004</ref>.
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Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". Changes such as an excessive level of [[neuronal growth]] leading to [[spasticity]] or [[tonic paralysis]], or an excessive release of [[neurotransmitter]]s in response to injury which could kill nerve cells, would have to be considered "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.<ref name="Doidge 2007"/><ref>[http://www.childrenofthecode.org/interviews/merzenich.htm Interview with Merzenich], 2004</ref>
   
==Treatment of brain damage==
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A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students' brains were imaged during the period when they were studying for their exams. In a matter of months, the students' gray matter increased significantly in the posterior and lateral parietal cortex.<ref>Draganski et al. "[http://www.jneurosci.org/cgi/content/abstract/26/23/6314 Temporal and Spatial Dynamics of Brain Structure Changes during Extensive Learning]" The Journal of Neuroscience, June 7, 2006, 26(23):6314-6317</ref>
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== Applications and examples ==
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=== Treatment of brain damage ===
 
A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move 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 (neuropsychology)|rehabilitation]] approaches to the functional consequences of the injury.
 
A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move 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 (neuropsychology)|rehabilitation]] approaches to the functional consequences of the injury.
   
The adult brain is not "[[hard-wired]]" with fixed and immutable [[neuronal circuit]]s. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that [[neurogenesis]], the formation of new nerve cells, occurs in the adult, mammalian brain--and such changes can persist well into old age.<ref>"Neurogenesis in adult primate neocortex: an evaluation of the evidence" Nature Reviews Neuroscience 3, 65-71 January 2002</ref> The evidence for neurogenesis is mainly restricted to the [[hippocampus]] and [[olfactory bulb]], but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well<ref name=Ponti>Ponti et al. Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits. PLoS ONE, 2008; 3 (6): e2366 DOI: 10.1371/journal.pone.0002366</ref>. In the rest of the brain, neurons can die, but they cannot be created. However, there is now ample evidence for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The manner in which 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 epistemology referred to as [[Neural Darwinism]] and developed by immunologist Nobel laureate [[Gerald Edelman]]. 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]]. This latter program of neuroscience research has emanated from the ground-breaking work of another Nobel laureate, [[Eric Kandel]], and his colleagues at [[Columbia University College of Physicians and Surgeons]].
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The adult brain is not "[[hard-wired]]" with fixed [[neuronal circuit]]s. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that [[neurogenesis]] (birth of brain cells) occurs in the adult, mammalian brain—and such changes can persist well into old age.<ref name="Rakic 2002"/> The evidence for neurogenesis is mainly restricted to the [[hippocampus]] and [[olfactory bulb]], but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well.<ref name="Ponti et al 2008"/>
   
== '''Applications of [[Neuroplasticity]]''' ==
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In the rest of the brain, neurons can die, but they cannot be created. However, there is now ample evidence for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The manner in which 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 epistemology referred to as [[Neural Darwinism]] and developed by immunologist Nobel laureate [[Gerald Edelman]]. 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]]. This latter program of neuroscience research has emanated from the ground-breaking work of another Nobel laureate, [[Eric Kandel]], and his colleagues at [[Columbia University College of Physicians and Surgeons]].
   
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[[Paul Bach-y-Rita]], deceased in 2006, was the "father of sensory substitution and brain plasticity."<ref>"[http://www.salus.edu/nclvi/honoring/bach_y_rita.htm Remembering Leaders in the Field of Blindness and Visual Impairment]." National Center for Leadership in Visual Impairment. Salus University. 20 Nov. 2008</ref> In working with a patient whose vestibular system had been damaged he developed BrainPort,<ref>{{cite web|url=http://mindstates.tribe.net/thread/a8b9f33f-7a6f-4af8-9c0c-588719606271 |title=BrainPort, Dr. Paul Bach-y-Rita, and ... - Mind States - tribe.net |publisher=Mindstates.tribe.net |date=2005-03-30 |accessdate=2010-06-12}}</ref> a machine that "replaces her vestibular apparatus and [will] send balance signals to her brain from her tongue."<ref name="Doidge 2007" /> After she had used this machine for some time it was no longer necessary, as she regained the ability to function normally. Her balancing act days were over.<ref>{{cite web|url=http://www.uwalumni.com/home/onwisconsin/archives/spring2007/balancingact.aspx |title=Wisconsin Alumni Association - Balancing Act |publisher=Uwalumni.com |date= |accessdate=2010-06-12}}</ref>
   
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Plasticity is the major explanation for the phenomenon. Because her vestibular system was "disorganized" and sending random rather than coherent signals, the apparatus found new pathways around the damaged or blocked neural pathways, helping to reinforce the signals that were sent by remaining healthy tissues. Bach-y-Rita explained plasticity by saying, "If you are driving from here to Milwaukee and the main bridge goes out, first you are paralyzed. Then you take old secondary roads through the farmland. Then you use these roads more; you find shorter paths to use to get where you want to go, and you start to get there faster. These "secondary" neural pathways are "unmasked" or exposed and strengthened as they are used. The "unmasking" process is generally thought to be one of the principal ways in which the plastic brain reorganizes itself."<ref name="Doidge 2007" />
   
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[[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 will move 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.<ref name="Frost et al 2003" /> With respect to the distal forelimb representation, "postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex."<ref name="Frost et al 2003">{{cite journal |last1=Frost |first1=S.B. |last2=Barbay |first2=S. |last3=Friel |first3=K.M. |last4=Plautz |first4=E.J. |last5=Nudo |first5=R.J. |year=2003 |title=Reorganization of Remote Cortical Regions After Ischemic Brain Injury: A Potential Substrate for Stroke Recovery |journal=[[Journal of Neurophysiology]] |volume=89 |issue= 6|pages=3205–3214 |url=http://jn.physiology.org/cgi/reprint/89/6/3205.pdf |doi=10.1152/jn.01143.2002 |pmid=12783955}}</ref> 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.
   
[[Neuroplasticity]] is one of the most important and developing topics in Neuroscience today. Dr. Donald Stein, who wrote one of the first books on brain plasticity, ''Brain Injury and Recovery'', defined “Brain plasticity as the ability for the organism to adapt to the changes in its environment in a positive and adaptive way because it’s not just enough to change…”[14] Norman Doidge’s book, ''The Brain that Changes Itself'' has ample examples of plasticity and is a great resource. There have been several great pioneers through this idea of neuroplasticity. Between 30 to 40 years ago there was this notion that each point on your body directly correlates with a specific point on the ‘brain map, essentially, “anatomically hard-wired at birth.”[5] There was no hope for people suffering from a brain injury according to the doctors that believed the hardwired system. A few key scientists did not believe in this “truth” and proceeded to seek another answer.
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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 have evidence to suggest cortical reorganization as the mechanism of change include [[Constraint-induced movement therapy]], [[functional electrical stimulation]], treadmill training with body weight support, and [[virtual reality therapy]]. [[Robot#Healthcare|Robot assisted therapy]] is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.<ref>{{cite journal | author = Young J. A., Tolentino M. | year = 2011 | title = Neuroplasticity and its Applications for Rehabilitation | url = | journal = American Journal of Therapeutics | volume = 18 | issue = | pages = 70–80 }}</ref>
   
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[[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 long standing unilateral dorsal column lesions at cervical levels in macaque monkeys."<ref name="Jain et al 2008" /> 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 when people damage the somatosensory cortex, impairment of the body perceptions are experienced. He is trying to see how these systems (somatosensory, cognitive, motor systems) are plastic as a result of injury.<ref name="Jain et al 2008">{{cite journal |last=Jain |first=Neeraj |date=October 22, 2008 |title=Large-Scale Reorganization in the Somatosensory Cortex and Thalamus after Sensory Loss in Macaque Monkeys |journal=The Journal of Neuroscience |volume=28 |issue=43 |pages=11042–11060 |publisher= |location= |pmid= 18945912|pmc= 2613515|doi=10.1523/JNEUROSCI.2334-08.2008 |url= |last2=Qi |first2=HX |last3=Collins |first3=CE |last4=Kaas |first4=JH }}</ref>
   
===Paul Bach-y-Rita ===
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One of the most recent applications of neuroplasticity involves work done by a team of doctors and researchers at [[Emory University]], specifically Dr. [[Donald Stein]] (who has been in the field for over three decades)<ref>{{cite web|url=http://www.bme.gatech.edu/facultystaff/faculty_record.php?id=31 |title=Coulter Department of Biomedical Engineering: BME Faculty |publisher=Bme.gatech.edu |date= |accessdate=2010-06-12}}</ref> and Dr. 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.<ref name="stein_interview" /> Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice. Also in females, he noticed that at certain points in the estrus cycle females recovered even more. After lots of research, they attributed this difference due to the levels of progesterone. The highest level of progesterone present led to the fastest recovery of brain injury in these mice.
   
[http://www.engr.wisc.edu/bme/newsletter/2007/in_memoriam.html Paul Bach-y-Rita], deceased in 2006, was the “father of sensory substitution and brain plasticity.”[12] In working with a patient whose vestibular system had been damaged he developed [http://mindstates.tribe.net/thread/a8b9f33f-7a6f-4af8-9c0c-588719606271 BrainPort], a machine that “replaces her vestibular apparatus and [will] send balance signals to her brain from her tongue.”[5] After she had used this machine for some time it was no longer necessary, as she regained the ability to function normally. Her [http://www.uwalumni.com/home/onwisconsin/archives/spring2007/balancingact.aspx balancing act] days were over. Plasticity is the major explanation for the phenomena. Because her vestibular system was “disorganized” and sending random rather than coherent signals, the apparatus found new pathways around the damaged or blocked neural pathways, helping to reinforce the signals that were sent by remaining healthy tissues. Bach-y-Rita explained plasticity by saying, “If you are driving from here to Milwaukee and the main bridge goes out, first you are paralyzed. Then you take old secondary roads through the farmland. Then you use these roads more; you find shorter paths to use to get where you want to go, and you start to get there faster. These “secondary” neural pathways are “unmasked” or exposed and strengthened as they are used. The “unmasking” process is generally thought to be one of the principal ways in which the plastic brain reorganizes itself.”[5]
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They developed a treatment that includes increased levels of progesterone injections to give to brain injured patients. "Administration of progesterone after traumatic brain injury<ref>[http://whsc.emory.edu/press_releases_video.cfm?id=brain_trauma Traumatic Brain Injury] (a story of TBI and the results of ProTECT using progesterone treatments) Emory University News Archives</ref> (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhance spatial reference memory and sensory motor recovery."<ref name="Cutler et al 2005">{{cite journal |last1=Cutler |first1=Sarah M. |last2=Hoffman |first2=Stuart W. |last3=Pettus |first3=Edward H. |last4=Stein |first4=Donald G. |year=2005 |month=October |title=Tapered progesterone withdrawal enhances behavioral and molecular recovery after traumatic brain injury |journal=Experimental Neurology |volume=195 |issue=2 |page= |pages=423–429 |publisher=Elsevier |doi=10.1016/j.expneurol.2005.06.003 |url= |language= |pmid=16039652}}</ref> In their clinical trials, they had a group of severely injured patients that after the three days of progesterone injections had a 60% reduction in mortality.<ref name="stein_interview" /> Sam* was in a horrific car accident that left him with marginal brain activity; according to the doctors, he was one point away from being brain dead. His parents decided to have him participate in Dr. Stein’s clinical trial and he was given the three-day progesterone treatment. Three years after the accident, he had achieved an inspiring recovery with no brain complications and the ability to live a healthy, normal life.<ref name="stein_interview">Stein, Donald. "Plasticity." Personal interview. Alyssa Walz. 19 Nov. 2008.</ref>
   
In addition to helping patients with their balance problems, Bach y Rita invented a device that allowed blind people to read, perceive shadows, and distinguish between close and distant objects. This “machine was one of the first and boldest applications of neuroplasticity.”[5] The patient sat in an electrically stimulated chair that had a large camera behind it which scanned the area, sending electrical signals of the image to four hundred vibrating stimulators on the chair against the patient’s skin. The six subjects of the experiment were eventually able to recognize a picture of the supermodel Twiggy.[5] It must be emphasized that these people were congenitally blind and had previously not been able to see. Bach-y-Rita believed in [[sensory substitution]]; if one sense is damaged, your other senses can sometimes take over. He thought skin and its touch receptors could act as a retina ([http://www.pbs.org/kcet/wiredscience/video/286-mixed_feelings.html using one sense for another]). In order for the brain to interpret tactile information and convert it into visual information, it has to learn something new and adapt to the new signals. The brain's capacity to adapt implied that it possessed plasticity. He thought, “We see with our brains, not with our eyes.”[5]
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Stein has done some studies in which beneficial effects have been seen to be similar in aged rats to those seen in youthful rats. As there are physiological differences in the two age groups, the model was tweaked for the elderly animals by reducing their stress levels with increased physical contact. During surgery, anesthesia was kept at a higher oxygen level with lower overall isoflurane percentage and "the aged animals were given subcutaneous [[Lactated Ringer's solution|lactated ringers solution]] post-surgery to replace fluids lost through increased bleeding."<ref name="Cutler et al 2007">{{cite journal |last1=Cutler |first1=Sarah M. |last2=Cekic |first2=Milos |last3=Miller |first3=Darren M. |last4=Wali |first4=Bushra |last5=VanLandingham |first5=Jacob W. |last6=Stein |first6=Donald G. |date=September 24, 2007 |title=Progesterone Improves Acute Recovery after Traumatic Brain Injury in the Aged Rats |journal=Journal of Neurotrauma |volume=24 |issue=9 |pages=1475–1486 |url= |doi=10.1089/neu.2007.0294 |pmid=17892409}}</ref> The promising results of progesterone treatments "could have a significant impact on the clinical management of TBI."<ref name="Cutler et al 2007" /> These treatments have been shown to work on human patients who receive treatment soon after the TBI. However, Dr. Stein now focuses his research on those persons who have longstanding traumatic brain injury in order to determine if progesterone treatments will assist them in the recovery of lost functions as well.
   
A tragic stroke that left his father paralyzed inspired Bach-y-Rita to study brain rehabilitation. His brother, a physician, worked tirelessly to develop therapeutic measures which were so successful that the father recovered complete functionality by age 68 and was able to live a normal, active life which even included mountain climbing. “His father’s story was firsthand evidence that a ‘late recovery’ could occur even with a massive lesion in an elderly person.”[5] He found more evidence of this possible brain reorganization with [http://rkthomas.myweb.uga.edu/Franz.htm Shepherd Ivory Franz]’s work. One study involved stroke patients who were able to recover through the use of brain stimulating exercises after having been paralyzed for years. “Franz understood the importance of interesting, motivating rehabilitation: ‘Under conditions of interest, such as that of competition, the resulting movement may be much more efficiently carried out than in the dull, routine training in the laboratory’(Franz, 1921, pg.93).”[2] This notion has led to motivational rehabilitation programs that are used today.
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=== Treatment of learning difficulties ===
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[[Michael Merzenich]] developed a series of "plasticity-based computer programs known as [[Fast ForWord]]." FastForWord offers seven brain exercises to help with the language and learning deficits of dyslexia. In a recent study, experimental training was done in adults to see if it would help to counteract the negative plasticity that results from age-related cognitive decline (ARCD). The ET design included six exercises designed to reverse the dysfunctions caused by ARCD in cognition, memory, motor control, and so on [9]. After use of the ET program for 8–10 weeks, there was a "significant increase in task-specific performance."[9] The data collected from the study indicated that a neuroplasticity-based program could notably improve cognitive function and memory in adults with ARCD.
   
===Michael Merzenich===
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=== Neuroplasticity during operation of brain-machine interfaces ===
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[[Brain-machine interface]] (BMI) is a rapidly developing field of [[neuroscience]]. According to the results obtained by Mikhail Lebedev, [[Miguel Nicolelis]] and their colleagues,<ref>{{cite journal |first1=Mikhail A. |last1=Lebedev |first2=Jose M. |last2=Carmena |first3=Joseph E. |last3=O'Doherty |first4=Miriam |last4=Zacksenhouse |first5=Craig S. |last5=Henriquez |first6=Jose C. |last6=Principe |first7=Miguel A. L. |last7=Nicolelis |date=May 11, 2005 |title=Cortical Ensemble Adaptation to Represent Velocity of an Artificial Actuator Controlled by a Brain-Machine Interface |journal=The Journal of Neuroscience |volume= 25|series= |issue=19 |pages=4681–4693 |publisher= |location= |doi=10.1523/JNEUROSCI.4088-04.2005 |url=http://www.jneurosci.org/cgi/content/full/25/19/4681 |accessdate=2010-01-31 |pmid=15888644}}</ref> operation of BMIs results in incorporation of artificial actuators into brain representations. The scientists showed that modifications in neuronal representation of the monkey's hand and the actuator that was controlled by the monkey brain occurred in multiple cortical areas while the monkey operated a BMI. In these single day experiments, monkeys initially moved the actuator by pushing a joystick. After mapping out the motor neuron ensembles, control of the actuator was switched to the model of the ensembles so that the brain activity, and not the hand, directly controlled the actuator. The activity of individual neurons and neuronal populations became less representative of the animal's hand movements while representing the movements of the actuator. Presumably as a result of this adaptation, the animals could eventually stop moving their hands yet continue to operate the actuator. Thus, during BMI control, cortical ensembles plastically adapt, within tens of minutes, to represent behaviorally significant motor parameters, even if these are not associated with movements of the animal's own limb.
   
[[Michael Merzenich]] is a neuroscientist who has been one of the pioneers of brain plasticity for over three decades. He has made some of “the most ambitious claims for the field - that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia - that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning - how we learn, think, perceive, and remember are possible even in the elderly.”[5] Merzenich’s work was affected by a crucial discovery made by [[David Hubel]] and [[Torsten Wiesel]] in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was“… as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself.”[5] This implied brain plasticity during the critical period. However, Merzenich argued that brain plasticity 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 tht was 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.”[5]
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Active laboratory groups include those of [[John Donoghue (neuroscientist)|John Donoghue]] at Brown, [[Richard Andersen]] at Caltech, [[Krishna Shenoy]] at Stanford, [[Nicholas Hatsopoulos]] of University of Chicago, [[Andy Schwartz]] at [[University of Pittsburgh]], [[Sandro Mussa-Ivaldi]] at Northwestern and [[Miguel Nicolelis]] at Duke. Donoghue and Nicolelis' groups have independently shown that animals can control external interfaces in tasks requiring feedback, with models based on activity of cortical neurons, and that animals can adaptively change their minds to make the models work better. Donoghue's group took the implants from Richard Normann's lab at Utah (the "Utah" array), and improved it by changing the insulation from polyimide to parylene-c, and commercialized it through the company [[Cyberkinetics]]. These efforts are the leading candidate for the first human trials on a broad scale for motor cortical implants to help [[quadriplegic]] or [[Locked-in syndrome|locked-in]] patients communicate with the outside world.
   
Early in his career Merzenich collaborated with a group of people to develop the cochlear implant, which allows congenitally deaf people to hear. He also developed a series of “plasticity-based computer programs known as [[Fast ForWord]] ®,” [5] which were of tremendous assistance for autistic children and those with severe receptive/expressive language impairments. [3] FastForWord® offers seven brain exercises to help with language and learning deficits. In a recent study, experimental training was done in adults to see if it would help to counteract the negative plasticity that results from age-related cognitive decline (ARCD). The ET design included six exercises designed to reverse the dysfunctions caused by ARCD in cognition, memory, motor control, and so on [9]. After use of the ET program for 8-10 weeks, there was a “significant increase in task-specific performance.”[9] The data collected from the study indicated that a brain plasticity-based program could notably improve cognitive function and memory in adults with ARCD.
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===Sensory prostheses===
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Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, 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 <ref>{{cite journal | author = Kral A, Sharma A | year = 2012 | title = Developmental Neuroplasticity after Cochlear Implantation | url = | journal = Trends Neurosci | volume = 35 | issue = 2| pages = 111–122 }}</ref> 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 to learn mother language and acquire acoustic communication.<ref>Kral A, O'Donoghue GM. Profound Deafness in Childhood. New England J Medicine 2010: 363; 1438-50</ref>
   
===Vilanyanur S. Ramachandran===
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===Phantom limbs===
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[[File:Mirror-box-comic.jpg|thumb|right|200px|A diagrammatic explanation of the mirror box. The patient places the good limb into one side of the box (in this case the right hand) and the amputated limb into the other side. Due to the mirror, the patient sees a reflection of the good hand where the missing limb would be (indicated in lower contrast). The patient thus receives artificial visual feedback that the "resurrected" limb is now moving when they move the good hand.]]
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{{Main|Phantom limb|Mirror box}}
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The experience of [[Phantom limb]]s is a phenomenon in which a person continues to feel pain or sensation within a part of their body which has been amputated. This is strangely common, occurring in 60-80% of amputees.<ref>{{cite journal|last=Beaumont|first=Geneviève|coauthors=Mercier, Pierre-Emmanuel, Malouin, Jackson|title=Decreasing phantom limb pain through observation of action and imagery: A case series|journal=Pain Medicine|year=2011|volume=12|issue=2|pages=289–299|doi=10.1111/j.1526-4637.2010.01048.x|accessdate=2/6/2012}}</ref> An [[Phantom limb#Neurological basis|explanation]] for this refers to 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.
   
Among his many other accomplishments in neuroscience, [[Vilayanur S. Ramachandran]] is famous for his work regarding phantom limbs, or “…the vivid impression that the limb is not only still present but also painful,”[11] which is called [http://neurophilosophy.wordpress.com/2006/10/05/ramachandran-on-concsiousness-mirror-neurons-phantom-limb-sydrome/ phantom limb syndrome ]. This phenomenon arises from tragic limb loss through accident, amputation or other means. Those who suffer from this syndrome experience painful sensations in their stumps described as feeling like spasmodic clenching of the hands caused by “nails digging into my palm. [11] A possible explanation for this is that the brain is sending signals to the missing hand, and in the absence of feedback from the missing arm the signals are continuously sent without the availability of a shutoff mechanism. To counteract this, Ramachandran reasoned, the brain needs to receive visual feedback that the arm is moving in the correct manner. [http://cbc.ucsd.edu/ramabio.html Ramachandran] and William Hirstein “constructed a ‘virtual reality box,’” ([[mirror box]]) to allow “patients to perceive movement in a non-existent arm.”[11] The box has a mirror and a place to put the existing and phantom arms. The patient sees his real arm in the mirror, which creates the illusion of two arms. When the patient sends motor commands to both arms, they receive visual feedback that his phantom hand is moving properly. For many patients, this technique has been effective in relieving phantom limb pain.
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The relationship between phantom limbs and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Herta Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.<ref>{{cite journal | author = Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N ''et al.'' | year = 1995 | title = Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation | url = | journal = Nature | volume = 375 | issue = | pages = 482–484 }}</ref> Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.<ref>Flor H, Cortical Reorganization And Chronic Pain: Implications For Rehabilitation, J Rehabil Med, 2003, Suppl.41:66-72</ref> This phenomenon is sometimes referred to as maladaptive plasticity.
   
===Randy Nudo===
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In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible 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.<ref>Moseley, Brugger, Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb, PNAS, Sept 16, 2009,[http://www.pnas.org/content/early/2009/10/23/0907151106]</ref> 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."
   
[http://www.kumc.edu/physiology/nudo.html Randy Nudo], a professor at [[The University of Kansas]], is another important scientist in the field of brain plasticity research. He found that if a small stroke (an infarction)is induced by impedance of blood flow to a portion of a monkey’s motor cortex, the part of the body that responds by movement will move 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. [6] With respect to the distal forelimb representation, “postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex.” [6] 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.
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===Chronic Pain===
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{{Main|Chronic pain}}
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Individuals who suffer from 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 nervous system, both peripherally and centrally. During the period of tissue damage, [[Noxious stimulus|noxious stimuli]] and [[inflammation]] cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged [[nociception]] from periphery will then elicit a neuroplastic response at the cortical level to change its [[Somatotopic arrangement|somatotopic organization]] for the painful site, inducing [[central sensitization]].<ref>Seifert, F. & Maihöfner, C. Functional and structural imaging of pain-induced neuroplasticity. Current Opinion in Anaesthesiology 2011; 24: 515–523.</ref> For instance, individuals experiencing [[complex regional pain syndrome]] demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.<ref>Maihöfner C., Handwerker H.O., Neundorfer B., Birklein F. Patterns of cortical reorganization in complex regional pain syndrome" ''Neurology'' 2003; 61:1707–1715.</ref> Additionally, chronic pain has been reported to significantly reduce the volume of [[grey matter]] in the brain globally, and more specifically at the [[prefrontal cortex]] and right [[thalamus]].<ref>{{cite journal | author = Apkarian A.V., Sosa Y., Sonty S ''et al.'' | year = 2004 | title = Chronic back pain is associated with decreased prefrontal and thalamic gray matter density | url = | journal = J Neurosci | volume = 24 | issue = | pages = 10410–10415 }}</ref> However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain,<ref>{{cite journal | author = Karl A., Birbaumer N., Lutzenberger W. ''et al.'' | year = 2001 | title = Reorganization of motor and somatosensory cortex in upper extremity amputees with phantom limb pain | url = | journal = J Neurosci | volume = 21 | issue = | pages = 3609–18 }}</ref> [[Low back pain#Chronic pain|chronic low back pain]]<ref>Flor H., Braun C., Elbert T., ''et al.'' Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neurosci Lett 1997;224:5–8.</ref> and [[carpal tunnel syndrome]].<ref>{{cite journal | author = Napadow V., Kettner N., Ryan A. ''et al.'' | year = 2006 | title = Somatosensory cortical plasticity in carpal tunnel syndrome: a cross-sectional fMRI evaluation | url = | journal = Neuroimage | volume = 31 | issue = | pages = 520–530 }}</ref>
   
===Jon Kaas===
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===Meditation===
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{{Main|Research on meditation}}
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A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by [[Sara Lazar]], from Harvard University, in 2000.<ref>{{Cite journal |last1=Lazar |first1= S. |last2=Kerr |first2=C. |last3=Wasserman |first3=R. |last4=Gray |first4 = J.| last5 = Greve| first5 = D. | date = 2005-11-28| title = Meditation experience is associated with increased cortical thickness| journal = NeuroReport| volume = 16 | pages = 1893–97 | issue = 17 | pmc=1361002 | pmid=16272874 | doi=10.1097/01.wnr.0000186598.66243.19 |last6=Treadway |first6=Michael T. |last7=McGarvey |first7=Metta |last8=Quinn |first8=Brian T. |last9=Dusek |first9=Jeffery A.}}</ref> [[Richard Davidson]], a neuroscientist at the [[University of Wisconsin]], has led experiments in cooperation with the [[Dalai Lama]] on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as [[attention]], [[anxiety]], [[Depression (mood)|depression]], [[fear]], [[anger]], the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.<ref>{{Cite journal |last1=Lutz |first1= A. |last2=Greischar |first2=L.L. |last3=Rawlings |first3=N.B. |last4=Ricard |first4 = M.| last5 = Davidson| first5 = R. J.| date = 2004-11-16| title = Long-term meditators self-induce high-amplitude gamma synchrony during mental practice| journal = PNAS| volume = 101| pages = 16369–73 |url=http://www.pnas.org/cgi/content/full/101/46/16369 |accessdate=2007-07-08 |doi=10.1073/pnas.0407401101| issue = 46 |pmid=15534199 |pmc=526201 |postscript=<!--None-->}}</ref><ref>{{cite news|date=20 Jan 2007 |author=Sharon Begley |publisher=Wall Street Journal |url=http://www.dalailama.com/news.112.htm |title=How Thinking Can Change the Brain}}</ref><ref>{{Cite journal |last1=Davidson |first1=Richard |last2=Lutz |first2=Antoine |title=Buddha's Brain: Neuroplasticity and Meditation |journal=IEEE Signal Processing Magazine| month=January |year=2008 |url=http://brainimaging.waisman.wisc.edu/publications/2008/DavidsonBuddhaIEEE.pdf |postscript=<!--None-->}}</ref><ref>{{cite news |title=Stop meditating, start interacting |author=Chris Frith |newspaper=''[[New Scientist]]'' |date=17 February 2007 |url=http://www.newscientist.com/article/mg19325912.400-stop-meditating-start-interacting.html }}</ref>
   
[[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 long standing unilateral dorsal column lesions at cervical levels in macaque monkeys.” [8] 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 when people damage the somatosensory cortex, impairment of the body perceptions are experienced. He is trying to see how these systems (somatosensory, cognitive, motor systems) are plastic as a result of injury. [8]
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===Fitness and exercise===
===Donald Stein===
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In a 2009 study, scientists made two groups of mice swim a water maze, and then in a separate trial subjected them to an unpleasant stimulus to see how quickly they would learn to move away from it. Then, over the next four weeks they allowed one group of mice to run inside their rodent wheels, an activity most mice enjoy, while they forced the other group to work harder on minitreadmills at a speed and duration controlled by the scientists. They then tested both groups again to track their learning skills and memory. Both groups of mice improved their performances in the water maze from the earlier trial. But only the extra-worked treadmill runners were better in the avoidance task, a skill that, according to neuroscientists, demands a more complicated cognitive response.<ref>{{cite journal | author = Liu Yu-Fan, Chen Hsuin-ing, Wul Chao-Liang, Kuol Yu-Min, Yu Lung, Huang A-Min, Wu Fong-Sen, Chuang Jih-Ing, Jen Chauying J. ''et al.'' | year = 2009 | title = Differential effects of treadmill running and wheel running on spatial or aversive learning and memory: Roles of amygdalar brain-derived neurotrophic factor and synaptotagmin I. | url = | journal = Journal of Physiology | volume = 587 | issue = 13| pages = 3221–3231 | doi = 10.1113/jphysiol.2009.173088 }}</ref>
   
One of the most recent applications of neuroplasticity involves work done by a team of doctors and researchers at [[Emory University]], specifically Dr. [http://www.bme.gatech.edu/facultystaff/faculty_record.php?id=31 Donald Stein] (who has been in the field for over three decades) and Dr. 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. [14] Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice. Also in females, he noticed that at certain points in the estrus cycle females recovered even more. After lots of research, they attributed this difference due to the levels of progesterone. The highest level of progesterone present led to the fastest recovery of brain injury in these mice.
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The mice who were forced to run on the treadmills showed evidence of molecular changes in several portions of their brains when viewed under a microscope, while the voluntary wheel-runners had changes in only one area. "Our results support the notion that different forms of exercise induce neuroplasticity changes in different brain regions," Chauying J. Jen, a professor of physiology and an author of the study, said.<ref name="Reynolds 2009"/>
They developed a treatment that includes increased levels of progesterone injections to give to brain injured patients. “Administration of progesterone after [http://whsc.emory.edu/press_releases_video.cfm?id=brain_trauma traumatic brain injury]^^ (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhance spatial reference memory and sensory motor recovery.”[4] In their clinical trials, they had a group of severely injured patients that after the three days of progesterone injections there was a 60% reduction in mortality. [14] Sam* was in a horrific car accident that left him with marginal brain activity; according to the doctors, he was one point away from being brain dead. His parents decided to have him participate in Dr. Stein’s clinical trial and he was given the three-day progesterone treatment. Three years after the accident, he had achieved an inspiring recovery with no brain complications and the ability to live a healthy, normal life. [14]
 
   
Stein has done some studies in which beneficial effects have been seen to be similar in aged rats to those seen in youthful rats. As there are physiological differences in the two age groups, the model was tweaked for the elderly animals by reducing their stress levels with increased physical contact. During surgery, anesthesia was kept at a higher oxygen level with lower overall isoflurane percentage and “the aged animals were give subcutaneous lactated ringers solution post-surgery to replace fluids lost through increased bleeding.”[1] The promising results of progesterone treatments “could have a significant impact on the clinical management of TBI.” [1] These treatments have been shown to work on human patients who receive treatment soon after the TBI. However, Dr. Stein now focuses his research on those persons who have longstanding traumatic brain injury in order to determine if progesterone treatments will assist them in the recovery of lost functions as well.
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===Human echolocation===
   
Major advancements in the field of neuroplasticity have enabled the development of novel techniques that do not require expensive or invasive medicines or surgery. “The only goal of rehabilitation in this context would be to teach the patient new strategies to overcome those lost by the injury, and plasticity would be defined by the extent to which such substitution is possible.”[13] Most of society has finally relinquished the archaic belief that the brain is fixed and immutable; this has facilitated recognition of empirical scientific evidence corroborating the existence of brain plasticity [14&15]. “An increased understanding of plasticity of the brain and spinal cord, and of behavior of innate modular mechanism in intact and [in] injured systems, will likely assist in future developments.”[7]
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[[Human echolocation]] is a learned ability for humans to sense their environment from echoes. This ability is used by some [[blindness|blind]] people to navigate their environment and sense their surroundings in detail. Studies in 2010 <ref>Human Echolocation, Journal of Vision August 13, 2010 vol. 10 no. 7 article 1050 http://www.journalofvision.org/content/10/7/1050.abstract</ref> and 2011 <ref>Neural Correlates of Natural Human Echolocation in Early and Late Blind Echolocation Experts,PLoS One, May 25, 2011, {{doi|10.1371/journal.pone.0020162}}, http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0020162</ref> using [[Functional magnetic resonance imaging]] techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation.
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==Etymology==
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Plasticity was first applied to behavior in 1890 by [[William James]] in ''[[The Principles of Psychology]]'',<ref name="James 1890" /> though the idea was largely neglected for the next fifty years{{Citation needed|date=March 2012}}. The first person to use the term ''neural plasticity'' appears to have been the Polish neuroscientist [[Jerzy Konorski]].<ref name="LeDoux 2002" />
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{{quote|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.<ref name="Shaw 2001" />
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}}
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== History ==
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=== Proposal ===
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Until around the 1970s, an accepted idea across neuroscience was that the nervous system was essentially fixed throughout adulthood, both in terms of brain functions, as well as the idea that it was impossible for new [[neuron]]s to develop after birth.<ref name="Train your brain">Meghan O'Rourke [http://www.slate.com/id/2165040/pagenum/all/#p2 Train Your Brain] April 25, 2007</ref>
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In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But, these findings were eventually forgotten.<ref>{{cite journal |last1=Rosenzweig |first1=Mark R.|year=1996 |title=Aspects of the search for neural mechanisms of memory |journal=Annual Review of Psychology |volume=47 |pages=1–32 |doi=10.1146/annurev.psych.47.1.1 |pmid=8624134 }}</ref> The idea that the brain and its functions are not fixed throughout adulthood was proposed in 1890 by [[William James]] in ''[[The Principles of Psychology]]'', though the idea was largely neglected.<ref name="James 1890" />
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=== Research and discovery ===
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In 1923, [[Karl Lashley]] conducted experiments on [[rhesus monkey]]s which demonstrated changes in neuronal pathways, which he concluded to be evidence of plasticity, although despite this, as well as further examples of research suggesting this, the idea of neuroplasticity was not widely accepted by neuroscientists. However, more significant evidence began to be 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.<ref name="Train your brain"/><ref>''Brain Science Podcast'' Episode #10, "Neuroplasticity"</ref>
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In the 1960s, [[Paul Bach-y-Rita]] invented a device that allowed blind people to read, perceive shadows, and distinguish between close and distant objects. This "machine was one of the first and boldest applications of neuroplasticity."<ref name="Doidge 2007" /> The patient sat in an electrically stimulated chair that had a large camera behind it which scanned the area, sending electrical signals of the image to four hundred vibrating stimulators on the chair against the patient’s skin. The six subjects of the experiment were eventually able to recognize a picture of the supermodel Twiggy.<ref name="Doidge 2007" />
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It must be emphasized that these people were congenitally blind and had previously not been able to see. Bach-y-Rita believed in [[sensory substitution]]; if one sense is damaged, your other senses can sometimes take over. He thought skin and its touch receptors could act as a retina (using one sense for another<ref>{{cite web|url=http://www.pbs.org/kcet/wiredscience/video/286-mixed_feelings.html |title=Wired Science . Video: Mixed Feelings |publisher=PBS |date= |accessdate=2010-06-12}}</ref>). In order for the brain to interpret tactile information and convert it into visual information, it has to learn something new and adapt to the new signals. The brain's capacity to adapt implied that it possessed plasticity. He thought, "We see with our brains, not with our eyes."<ref name="Doidge 2007" />
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A tragic stroke that left his father paralyzed inspired Bach-y-Rita to study brain rehabilitation. His brother, a physician, worked tirelessly to develop therapeutic measures which were so successful that the father recovered complete functionality by age 68 and was able to live a normal, active life which even included mountain climbing. "His father’s story was firsthand evidence that a ‘late recovery’ could occur even with a massive lesion in an elderly person."<ref name="Doidge 2007" /> He found more evidence of this possible brain reorganization with [[Shepherd Ivory Franz]]'s work.<ref>{{cite web|url=http://rkthomas.myweb.uga.edu/Franz.htm |title=Shepherd Ivory Franz |publisher=Rkthomas.myweb.uga.edu |date= |accessdate=2010-06-12}}</ref> One study involved stroke patients who were able to recover through the use of brain stimulating exercises after having been paralyzed for years. "Franz understood the importance of interesting, motivating rehabilitation: ‘Under conditions of interest, such as that of competition, the resulting movement may be much more efficiently carried out than in the dull, routine training in the laboratory’(Franz, 1921, pg.93)."<ref>{{cite journal |last1=Colotla |first1=Victor A. |last2=Bach-y-Rita |first2=Paul |year=2002 |title=Shepherd Ivory Franz: His contributions to neuropsychology and rehabilitation |journal=Cognitive, Affective & Behavioral Neuroscience |volume=2 |issue=2 |pages=141–148 |url=http://htpprints.yorku.ca/archive/00000236/01/Colotla_Bach-y-Rita_2002.pdf |doi=10.3758/CABN.2.2.141 }}</ref> This notion has led to motivational rehabilitation programs that are used today.
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[[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 the field - that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia - that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning - how we learn, think, perceive, and remember are possible even in the elderly."<ref name="Doidge 2007" /> Merzenich’s work was affected by a crucial discovery made by [[David Hubel]] and [[Torsten Wiesel]] in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was"… as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself."<ref name="Doidge 2007" />
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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 was 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."<ref name="Doidge 2007" />
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==Other workers of interest==
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* [[William Newsome]]
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* [[Michael M. Merzenich]]
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* [[Edward Taub]]
   
== Brain plasticity during operation of [[brain-machine interface]]s ==
 
[[Brain-machine interface]] (BMI) is a rapidly developing field of [[neuroscience]]. According to the results obtained by Mikhail Lebedev, [[Miguel Nicolelis]] and their colleagues {{ref_harvard|Lebedev|Lebedev ''et al.'' 2005|none}}, operation of BMIs results in incorporation of artificial actuators into brain representations. The scientists showed that modifications in neuronal representation of the monkey's hand and the actuator that was controlled by the monkey brain occurred in multiple cortical areas while the monkey operated a BMI. In these single day experiments, monkeys initially moved the actuator by pushing a joystick. After mapping out the motor neuron ensembles, control of the actuator was switched to the model of the ensembles so that the brain activity, and not the hand, directly controlled the actuator. The activity of individual neurons and neuronal populations became less representative of the animal's hand movements while representing the movements of the actuator. Presumably as a result of this adaptation, the animals could eventually stop moving their hands yet continue to operate the actuator. Thus, during BMI control, cortical ensembles plastically adapt, within tens of minutes, to represent behaviorally significant motor parameters, even if these are not associated with movements of the animal's own limb.
 
Active laboratory groups include those of [[John Donoghue (neuroscientist)|John Donoghue]] at Brown, [[Richard Andersen]] at Caltech, [[Krishna Shenoy]] at Stanford, [[Nicholas Hatsopoulos]] of University of Chicago, [[Andy Schwartz]] at [[University of Pittsburgh]], [[Sandro Mussa-Ivaldi]] at Northwestern and [[Miguel Nicolelis]] at Duke. Donoghue and Nicolelis' groups have independently shown that animals can control external interfaces in tasks requiring feedback, with models based on activity of cortical neurons, and that animals can adaptively change their minds to make the models work better. Donoghue's group took the implants from Richard Normann's lab at Utah (the "Utah" array), and improved it by changing the insulation from polyimide to parylene-c, and commercialized it through the company [[Cyberkinetics]]. These efforts are the leading candidate for the first human trials on a broad scale for motor cortical implants to help quadriplegic or trapped patients communicate with the outside world.
 
   
 
==See also==
 
==See also==
Line 77: Line 78:
 
* [[Arrowsmith School]]
 
* [[Arrowsmith School]]
 
* [[Brain fitness]]
 
* [[Brain fitness]]
* [[Edward Taub]]
 
 
* [[Environmental enrichment (neural)]]
 
* [[Environmental enrichment (neural)]]
 
* [[Homeostatic plasticity]]
 
* [[Homeostatic plasticity]]
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* [[Neuroconstructivism]]
 
* [[Neuroconstructivism]]
 
* [[Neuroplastic effects of pollution]]
 
* [[Neuroplastic effects of pollution]]
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* [[Non-synaptic plasticity]]
 
* [[Postactivation potentials]]
 
* [[Postactivation potentials]]
 
* [[Receptive fields]]
 
* [[Receptive fields]]
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* [[Vision restoration therapy]]
 
* [[Vision restoration therapy]]
   
==Other workers of interest==
 
* [[William Newsome]]
 
* [[Michael M. Merzenich]]
 
   
 
==Notes==
 
==Notes==

Latest revision as of 19:26, December 29, 2012

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Brain 2

Contrary to common ideas as expressed in this diagram, brain functions are not confined to certain fixed locations.

Neuroplasticity (from neural - pertaining to the nerves and/or brain and plastic - moldable or changeable in structure), also known as brain plasticity, refers to changes in neural pathways and synapses which are due to changes in behavior, environment and neural processes, as well as changes resulting from bodily injury.[1] Neuroplasticity has replaced the formerly-held position that the brain is a physiologically static organ, and explores how - and in which ways - the brain changes throughout life.[2]

Neuroplasticity occurs on a variety of levels, ranging from cellular changes due to learning, to large-scale changes involved in cortical remapping in response to injury. The role of neuroplasticity is widely recognized in healthy development, learning, memory, and recovery from brain damage. During most of the 20th century, the general consensus among neuroscientists was that brain structure is relatively immutable after a critical period during early childhood. This belief has been challenged by findings revealing that many aspects of the brain remain plastic even into adulthood.[3]

Hubel and Wiesel had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, were largely immutable after the critical period in development.[4] Critical periods also were studied with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and other parts of the brain, including the cerebellum.[5]

Decades of research[6] have now shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. Neuroscientific research indicates that experience can actually change both the brain's physical structure (anatomy) and functional organization (physiology). Neuroscientists are currently engaged in a reconciliation of critical period studies demonstrating the immutability of the brain after development with the more recent research showing how the brain can, and does, change.[7]

Neurobiology Edit

One of the fundamental principles of how neuroplasticity functions is linked to the concept of synaptic pruning, the idea that individual connections within the brain are constantly being removed or recreated, largely dependent upon how they are used. This concept is captured in the aphorism, "neurons that fire together, wire together"/"neurons that fire apart, wire apart." If there are two nearby neurons that often produce an impulse simultaneously, their cortical maps may become one. This idea also works in the opposite way, i.e. that neurons which do not regularly produce simultaneous impulses will form different maps.

Cortical maps Edit

Cortical organization, especially for the sensory systems, is often described in terms of maps.[8] For example, sensory information from the foot projects to one cortical site and the projections from the hand target in another site. As the result of this somatotopic organization of sensory inputs to the cortex, cortical representation of the body resembles a map (or homunculus).

In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the sensory inputs. Michael Merzenich, Jon Kaas and Doug Rasmusson used the cortical map as their dependent variable. They found—and this has been since corroborated by a wide range of labs—that if the cortical map is deprived of its input it will become activated at a later time in response to other, usually adjacent inputs. Merzenich’s (1984) study involved the mapping of owl monkey hands before and after amputation of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third digit, the area in the cortical map formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation.[9] This study demonstrates that only those regions bordering a certain area will invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. 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.[10]

Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, Kevin Fox and great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. However, the rodent studies were poorly focused on the behavioral end, and Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.

Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1–2 days at the time at which a new sensory motor behavior is first acquired, and changes are largely finished within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, and are strongest for the stimuli that are associated with reward, and occur with equal ease in operant and classical conditioning behaviors.

An interesting phenomenon involving cortical maps is the incidence of phantom limbs. Phantom limbs are experienced by people that have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limbs is still not entirely understood it is believed that cortical reorganization plays an important role.[11]

Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". Changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury which could kill nerve cells, would have to be considered "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.[11][12]

A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students' brains were imaged during the period when they were studying for their exams. In a matter of months, the students' gray matter increased significantly in the posterior and lateral parietal cortex.[13]

Applications and examples Edit

Treatment of brain damage Edit

A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move 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.

The adult brain is not "hard-wired" with fixed neuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury. There is solid evidence that neurogenesis (birth of brain cells) occurs in the adult, mammalian brain—and such changes can persist well into old age.[3] The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well.[5]

In the rest of the brain, neurons can die, but they cannot be created. However, there is now ample evidence for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural levels are topics of active neuroscience research. The manner in which 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 epistemology referred to as Neural Darwinism and developed by immunologist Nobel laureate Gerald Edelman. 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. This latter program of neuroscience research has emanated from the ground-breaking work of another Nobel laureate, Eric Kandel, and his colleagues at Columbia University College of Physicians and Surgeons.

Paul Bach-y-Rita, deceased in 2006, was the "father of sensory substitution and brain plasticity."[14] In working with a patient whose vestibular system had been damaged he developed BrainPort,[15] a machine that "replaces her vestibular apparatus and [will] send balance signals to her brain from her tongue."[11] After she had used this machine for some time it was no longer necessary, as she regained the ability to function normally. Her balancing act days were over.[16]

Plasticity is the major explanation for the phenomenon. Because her vestibular system was "disorganized" and sending random rather than coherent signals, the apparatus found new pathways around the damaged or blocked neural pathways, helping to reinforce the signals that were sent by remaining healthy tissues. Bach-y-Rita explained plasticity by saying, "If you are driving from here to Milwaukee and the main bridge goes out, first you are paralyzed. Then you take old secondary roads through the farmland. Then you use these roads more; you find shorter paths to use to get where you want to go, and you start to get there faster. These "secondary" neural pathways are "unmasked" or exposed and strengthened as they are used. The "unmasking" process is generally thought to be one of the principal ways in which the plastic brain reorganizes itself."[11]

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 will move 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.[17] With respect to the distal forelimb representation, "postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex."[17] 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.

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 have evidence to suggest cortical reorganization as the mechanism of change include Constraint-induced movement therapy, functional electrical stimulation, treadmill training with body weight support, and virtual reality therapy. Robot assisted therapy is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.[18]

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 long standing unilateral dorsal column lesions at cervical levels in macaque monkeys."[19] 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 when people damage the somatosensory cortex, impairment of the body perceptions are experienced. He is trying to see how these systems (somatosensory, cognitive, motor systems) are plastic as a result of injury.[19]

One of the most recent applications of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein (who has been in the field for over three decades)[20] and Dr. 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.[21] Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice. Also in females, he noticed that at certain points in the estrus cycle females recovered even more. After lots of research, they attributed this difference due to the levels of progesterone. The highest level of progesterone present led to the fastest recovery of brain injury in these mice.

They developed a treatment that includes increased levels of progesterone injections to give to brain injured patients. "Administration of progesterone after traumatic brain injury[22] (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhance spatial reference memory and sensory motor recovery."[23] In their clinical trials, they had a group of severely injured patients that after the three days of progesterone injections had a 60% reduction in mortality.[21] Sam* was in a horrific car accident that left him with marginal brain activity; according to the doctors, he was one point away from being brain dead. His parents decided to have him participate in Dr. Stein’s clinical trial and he was given the three-day progesterone treatment. Three years after the accident, he had achieved an inspiring recovery with no brain complications and the ability to live a healthy, normal life.[21]

Stein has done some studies in which beneficial effects have been seen to be similar in aged rats to those seen in youthful rats. As there are physiological differences in the two age groups, the model was tweaked for the elderly animals by reducing their stress levels with increased physical contact. During surgery, anesthesia was kept at a higher oxygen level with lower overall isoflurane percentage and "the aged animals were given subcutaneous lactated ringers solution post-surgery to replace fluids lost through increased bleeding."[24] The promising results of progesterone treatments "could have a significant impact on the clinical management of TBI."[24] These treatments have been shown to work on human patients who receive treatment soon after the TBI. However, Dr. Stein now focuses his research on those persons who have longstanding traumatic brain injury in order to determine if progesterone treatments will assist them in the recovery of lost functions as well.

Treatment of learning difficulties Edit

Michael Merzenich developed a series of "plasticity-based computer programs known as Fast ForWord." FastForWord offers seven brain exercises to help with the language and learning deficits of dyslexia. In a recent study, experimental training was done in adults to see if it would help to counteract the negative plasticity that results from age-related cognitive decline (ARCD). The ET design included six exercises designed to reverse the dysfunctions caused by ARCD in cognition, memory, motor control, and so on [9]. After use of the ET program for 8–10 weeks, there was a "significant increase in task-specific performance."[9] The data collected from the study indicated that a neuroplasticity-based program could notably improve cognitive function and memory in adults with ARCD.

Neuroplasticity during operation of brain-machine interfaces Edit

Brain-machine interface (BMI) is a rapidly developing field of neuroscience. According to the results obtained by Mikhail Lebedev, Miguel Nicolelis and their colleagues,[25] operation of BMIs results in incorporation of artificial actuators into brain representations. The scientists showed that modifications in neuronal representation of the monkey's hand and the actuator that was controlled by the monkey brain occurred in multiple cortical areas while the monkey operated a BMI. In these single day experiments, monkeys initially moved the actuator by pushing a joystick. After mapping out the motor neuron ensembles, control of the actuator was switched to the model of the ensembles so that the brain activity, and not the hand, directly controlled the actuator. The activity of individual neurons and neuronal populations became less representative of the animal's hand movements while representing the movements of the actuator. Presumably as a result of this adaptation, the animals could eventually stop moving their hands yet continue to operate the actuator. Thus, during BMI control, cortical ensembles plastically adapt, within tens of minutes, to represent behaviorally significant motor parameters, even if these are not associated with movements of the animal's own limb.

Active laboratory groups include those of John Donoghue at Brown, Richard Andersen at Caltech, Krishna Shenoy at Stanford, Nicholas Hatsopoulos of University of Chicago, Andy Schwartz at University of Pittsburgh, Sandro Mussa-Ivaldi at Northwestern and Miguel Nicolelis at Duke. Donoghue and Nicolelis' groups have independently shown that animals can control external interfaces in tasks requiring feedback, with models based on activity of cortical neurons, and that animals can adaptively change their minds to make the models work better. Donoghue's group took the implants from Richard Normann's lab at Utah (the "Utah" array), and improved it by changing the insulation from polyimide to parylene-c, and commercialized it through the company Cyberkinetics. These efforts are the leading candidate for the first human trials on a broad scale for motor cortical implants to help quadriplegic or locked-in patients communicate with the outside world.

Sensory prosthesesEdit

Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, 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 [26] 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 to learn mother language and acquire acoustic communication.[27]

Phantom limbsEdit

File:Mirror-box-comic.jpg
Main article: Phantom limb

The experience of Phantom limbs is a phenomenon in which a person continues to feel pain or sensation within a part of their body which has been amputated. This is strangely common, occurring in 60-80% of amputees.[28] An explanation for this refers to 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 limbs and neuroplasticity is a complex one. In the early 1990s V.S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Herta Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.[29] Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.[30] This phenomenon is sometimes referred to as maladaptive plasticity.

In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible 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.[31] 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 PainEdit

Main article: Chronic pain

Individuals who suffer from 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 nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from periphery will then elicit a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.[32] For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth.[33] Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus.[34] However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain,[35] chronic low back pain[36] and carpal tunnel syndrome.[37]

MeditationEdit

Main article: Research on meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[38] Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.[39][40][41][42]

Fitness and exerciseEdit

In a 2009 study, scientists made two groups of mice swim a water maze, and then in a separate trial subjected them to an unpleasant stimulus to see how quickly they would learn to move away from it. Then, over the next four weeks they allowed one group of mice to run inside their rodent wheels, an activity most mice enjoy, while they forced the other group to work harder on minitreadmills at a speed and duration controlled by the scientists. They then tested both groups again to track their learning skills and memory. Both groups of mice improved their performances in the water maze from the earlier trial. But only the extra-worked treadmill runners were better in the avoidance task, a skill that, according to neuroscientists, demands a more complicated cognitive response.[43]

The mice who were forced to run on the treadmills showed evidence of molecular changes in several portions of their brains when viewed under a microscope, while the voluntary wheel-runners had changes in only one area. "Our results support the notion that different forms of exercise induce neuroplasticity changes in different brain regions," Chauying J. Jen, a professor of physiology and an author of the study, said.[44]

Human echolocationEdit

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 [45] and 2011 [46] using Functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation.

EtymologyEdit

Plasticity was first applied to behavior in 1890 by William James in The Principles of Psychology,[47] though the idea was largely neglected for the next fifty years[citation needed]. The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.[48]

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.[49]

History Edit

Proposal Edit

Until around the 1970s, an accepted idea across neuroscience was that the nervous system was essentially fixed throughout adulthood, both in terms of brain functions, as well as the idea that it was impossible for new neurons to develop after birth.[50]

In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But, these findings were eventually forgotten.[51] The idea that the brain and its functions are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected.[47]

Research and discovery Edit

In 1923, Karl Lashley conducted experiments on rhesus monkeys which demonstrated changes in neuronal pathways, which he concluded to be evidence of plasticity, although despite this, as well as further examples of research suggesting this, the idea of neuroplasticity was not widely accepted by neuroscientists. However, more significant evidence began to be 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.[50][52]

In the 1960s, Paul Bach-y-Rita invented a device that allowed blind people to read, perceive shadows, and distinguish between close and distant objects. This "machine was one of the first and boldest applications of neuroplasticity."[11] The patient sat in an electrically stimulated chair that had a large camera behind it which scanned the area, sending electrical signals of the image to four hundred vibrating stimulators on the chair against the patient’s skin. The six subjects of the experiment were eventually able to recognize a picture of the supermodel Twiggy.[11]

It must be emphasized that these people were congenitally blind and had previously not been able to see. Bach-y-Rita believed in sensory substitution; if one sense is damaged, your other senses can sometimes take over. He thought skin and its touch receptors could act as a retina (using one sense for another[53]). In order for the brain to interpret tactile information and convert it into visual information, it has to learn something new and adapt to the new signals. The brain's capacity to adapt implied that it possessed plasticity. He thought, "We see with our brains, not with our eyes."[11]

A tragic stroke that left his father paralyzed inspired Bach-y-Rita to study brain rehabilitation. His brother, a physician, worked tirelessly to develop therapeutic measures which were so successful that the father recovered complete functionality by age 68 and was able to live a normal, active life which even included mountain climbing. "His father’s story was firsthand evidence that a ‘late recovery’ could occur even with a massive lesion in an elderly person."[11] He found more evidence of this possible brain reorganization with Shepherd Ivory Franz's work.[54] One study involved stroke patients who were able to recover through the use of brain stimulating exercises after having been paralyzed for years. "Franz understood the importance of interesting, motivating rehabilitation: ‘Under conditions of interest, such as that of competition, the resulting movement may be much more efficiently carried out than in the dull, routine training in the laboratory’(Franz, 1921, pg.93)."[55] This notion has led to motivational rehabilitation programs that are used today.

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 the field - that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia - that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning - how we learn, think, perceive, and remember are possible even in the elderly."[11] Merzenich’s work was affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten’s brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was"… as though the brain didn’t want to waste any ‘cortical real estate’ and had found a way to rewire itself."[11]

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 was 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."[11]

Other workers of interestEdit


See alsoEdit


NotesEdit

  1. Cite error: Invalid <ref> tag; no text was provided for refs named Pascual-Leone_et_al._2011
  2. Cite error: Invalid <ref> tag; no text was provided for refs named Pascual-Leone_et_al._2005
  3. Cite error: Invalid <ref> tag; no text was provided for refs named Rakic_2002
  4. Cite error: Invalid <ref> tag; no text was provided for refs named Hubel_et_al_1970
  5. Cite error: Invalid <ref> tag; no text was provided for refs named Ponti_et_al_2008
  6. Chaney, Warren, Dynamic Mind, 2007, Las Vegas, Houghton-Brace Publishing, pp 33-35, ISBN 0-9793392-0-0 [1]
  7. Chaney, Warren, Workbook for a Dynamic Mind, 2006, Las Vegas, Houghton-Brace Publishing, page 44, ISBN 00979339219 [2]
  8. Cite error: Invalid <ref> tag; no text was provided for refs named Buonomano_et_al_1998
  9. Cite error: Invalid <ref> tag; no text was provided for refs named Merzenich_et_al_1984
  10. Cite error: Invalid <ref> tag; no text was provided for refs named Wall_et_al_2002
  11. Cite error: Invalid <ref> tag; no text was provided for refs named Doidge_2007
  12. Interview with Merzenich, 2004
  13. Draganski et al. "Temporal and Spatial Dynamics of Brain Structure Changes during Extensive Learning" The Journal of Neuroscience, June 7, 2006, 26(23):6314-6317
  14. "Remembering Leaders in the Field of Blindness and Visual Impairment." National Center for Leadership in Visual Impairment. Salus University. 20 Nov. 2008
  15. BrainPort, Dr. Paul Bach-y-Rita, and ... - Mind States - tribe.net. Mindstates.tribe.net. URL accessed on 2010-06-12.
  16. Wisconsin Alumni Association - Balancing Act. Uwalumni.com. URL accessed on 2010-06-12.
  17. 17.0 17.1 (2003). Reorganization of Remote Cortical Regions After Ischemic Brain Injury: A Potential Substrate for Stroke Recovery. Journal of Neurophysiology 89 (6): 3205–3214.
  18. Young J. A., Tolentino M. (2011). Neuroplasticity and its Applications for Rehabilitation. American Journal of Therapeutics 18: 70–80.
  19. 19.0 19.1 Jain, Neeraj (October 22, 2008). Large-Scale Reorganization in the Somatosensory Cortex and Thalamus after Sensory Loss in Macaque Monkeys. The Journal of Neuroscience 28 (43): 11042–11060.
  20. Coulter Department of Biomedical Engineering: BME Faculty. Bme.gatech.edu. URL accessed on 2010-06-12.
  21. 21.0 21.1 21.2 Stein, Donald. "Plasticity." Personal interview. Alyssa Walz. 19 Nov. 2008.
  22. Traumatic Brain Injury (a story of TBI and the results of ProTECT using progesterone treatments) Emory University News Archives
  23. (October 2005). Tapered progesterone withdrawal enhances behavioral and molecular recovery after traumatic brain injury. Experimental Neurology 195 (2): 423–429.
  24. 24.0 24.1 (September 24, 2007) Progesterone Improves Acute Recovery after Traumatic Brain Injury in the Aged Rats. Journal of Neurotrauma 24 (9): 1475–1486.
  25. (May 11, 2005)Cortical Ensemble Adaptation to Represent Velocity of an Artificial Actuator Controlled by a Brain-Machine Interface. The Journal of Neuroscience 25 (19): 4681–4693.
  26. Kral A, Sharma A (2012). Developmental Neuroplasticity after Cochlear Implantation. Trends Neurosci 35 (2): 111–122.
  27. Kral A, O'Donoghue GM. Profound Deafness in Childhood. New England J Medicine 2010: 363; 1438-50
  28. Beaumont, Geneviève, Mercier, Pierre-Emmanuel, Malouin, Jackson (2011). Decreasing phantom limb pain through observation of action and imagery: A case series. Pain Medicine 12 (2): 289–299.
  29. Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N et al. (1995). Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation. Nature 375: 482–484.
  30. Flor H, Cortical Reorganization And Chronic Pain: Implications For Rehabilitation, J Rehabil Med, 2003, Suppl.41:66-72
  31. Moseley, Brugger, Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb, PNAS, Sept 16, 2009,[3]
  32. Seifert, F. & Maihöfner, C. Functional and structural imaging of pain-induced neuroplasticity. Current Opinion in Anaesthesiology 2011; 24: 515–523.
  33. Maihöfner C., Handwerker H.O., Neundorfer B., Birklein F. Patterns of cortical reorganization in complex regional pain syndrome" Neurology 2003; 61:1707–1715.
  34. Apkarian A.V., Sosa Y., Sonty S et al. (2004). Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. J Neurosci 24: 10410–10415.
  35. Karl A., Birbaumer N., Lutzenberger W. et al. (2001). Reorganization of motor and somatosensory cortex in upper extremity amputees with phantom limb pain. J Neurosci 21: 3609–18.
  36. Flor H., Braun C., Elbert T., et al. Extensive reorganization of primary somatosensory cortex in chronic back pain patients. Neurosci Lett 1997;224:5–8.
  37. Napadow V., Kettner N., Ryan A. et al. (2006). Somatosensory cortical plasticity in carpal tunnel syndrome: a cross-sectional fMRI evaluation. Neuroimage 31: 520–530.
  38. (2005-11-28) Meditation experience is associated with increased cortical thickness. NeuroReport 16 (17): 1893–97.
  39. (2004-11-16)Long-term meditators self-induce high-amplitude gamma synchrony during mental practice. PNAS 101 (46): 16369–73.
  40. includeonly>Sharon Begley. "How Thinking Can Change the Brain", Wall Street Journal, 20 Jan 2007.
  41. (January 2008). Buddha's Brain: Neuroplasticity and Meditation. IEEE Signal Processing Magazine.
  42. includeonly>Chris Frith. "Stop meditating, start interacting", 17 February 2007.
  43. Liu Yu-Fan, Chen Hsuin-ing, Wul Chao-Liang, Kuol Yu-Min, Yu Lung, Huang A-Min, Wu Fong-Sen, Chuang Jih-Ing, Jen Chauying J. et al. (2009). Differential effects of treadmill running and wheel running on spatial or aversive learning and memory: Roles of amygdalar brain-derived neurotrophic factor and synaptotagmin I.. Journal of Physiology 587 (13): 3221–3231.
  44. Cite error: Invalid <ref> tag; no text was provided for refs named Reynolds_2009
  45. Human Echolocation, Journal of Vision August 13, 2010 vol. 10 no. 7 article 1050 http://www.journalofvision.org/content/10/7/1050.abstract
  46. Neural Correlates of Natural Human Echolocation in Early and Late Blind Echolocation Experts,PLoS One, May 25, 2011, DOI:10.1371/journal.pone.0020162 , http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0020162
  47. Cite error: Invalid <ref> tag; no text was provided for refs named James_1890
  48. Cite error: Invalid <ref> tag; no text was provided for refs named LeDoux_2002
  49. Cite error: Invalid <ref> tag; no text was provided for refs named Shaw_2001
  50. 50.0 50.1 Meghan O'Rourke Train Your Brain April 25, 2007
  51. (1996). Aspects of the search for neural mechanisms of memory. Annual Review of Psychology 47: 1–32.
  52. Brain Science Podcast Episode #10, "Neuroplasticity"
  53. Wired Science . Video: Mixed Feelings. PBS. URL accessed on 2010-06-12.
  54. Shepherd Ivory Franz. Rkthomas.myweb.uga.edu. URL accessed on 2010-06-12.
  55. (2002). Shepherd Ivory Franz: His contributions to neuropsychology and rehabilitation. Cognitive, Affective & Behavioral Neuroscience 2 (2): 141–148.

ReferencesEdit

REFERS TO SECTION ON APPLICATIONS OF NEUROPLASTICITY

1. Cekic, Milos, Sarah M. Cutler, Donald G. Stein, and Bushra Wali. "Progesterone Improves Acute Recovery after Traumatic Brian Injury in the Aged Rats." Journal of Neurotrauma 24 (2007): 1475-486.

2. Colotla, Victor A., and Paul Bach-y-Rita. "Shepherd Ivory Franz: His contributions to neuropsychology and rehabilitation." Cognitive, Affective, & Behavioral Neuroscience 2 (2002): 141-48.

3. Cohen, Wendy, Ann Hodson, Anne O'Hare, James Boyle, et al. "Effects of Computer-Based Intervention Through Acoustically Modified Speech (Fast ForWord) in Severe Mixed Receptive-Expressive Language Impairment: Outcomes From a Randomized Controlled Trial. " Journal of Speech, Language, and Hearing Research 48.3 (2005): 715-29. Research Library. ProQuest. Georgia Institute of Technology, Atlanta, Ga. 1 Dec. 2008 <http://www.proquest.com/>

4. Cutler, Sarah M., Stuart W. Hoffman, Edward H. Pettus, and Donald G. Stein. "Tapered Progesterone Withdrawal Enhances Behavioral and Molecular Recovery After Traumatic Brain Injury." Experimental Neurology 195 (2005): 423-29.

5. Doidge, Norman. The Brain That Changes Itself : Stories of Personal Triumph from the Frontiers of Brain Science. New York: Penguin Group (USA) Incorporated, 2007.

6. Frost, SB, S. Barbay, K.M Friel, E.J Plautz, and R.J Nudo. "Reorganization of Remote Cortical Regions After Ischemic Brain Injury:A Potential Substrate for Stroke Recovery." Journal of Neurophysiology 89 (2003): 3205-214.

7. Giszter, Simon F. "Spinal Cord Injury: Present and Future Therapeutic Devices and Prostheses." Neurotherapeutics: The Journal of the American Society for Experimental NeuroTherapeutics 5 (2008): 147-62.

8. Jain, Neeraj, Hui-Xin Qi, Christine D. Collins, and Jon H. Kaas. "Large-Scale Reorganization in the Somatosensory Cortex and Thalamus after Sensory Loss in Macaque Monkeys." The Journal of Neuroscience 28 (2008): 11042-1060.

9. Mahncke, Henry W., and Michael M. Merzenich. "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 (2006): 12523-2528.

10. Nudo, Randolph J., and Garrett W. Milliken. "Reorganization of Movement Representations in Primary Motor Cortex Following Focal Ischemic Infarct in Adult Squirrel Monkeys." Journal of Neurophysiology 75 (1996): 2144-149.

11. Ramachandran, VS, and W. Hirstein. "The Perception of Phantom Limbs: The D.O. Hebb Lecture." Brain 121 (1998): 1603-630.

12. "Remembering Leaders in the Field of Blindness and Visual Impairment." National Center for Leadership in Visual Impairment. Salus University. 20 Nov. 2008 <http://www.salus.edu/nclvi/honoring/bach_y_rita.htm>.

13. Stein, Donald G., and Stuart W. Hoffman. "Concepts of CNS Plasticity in the Context of Brain Damage and Repair." J Head Trauma Rehabilitation 18 (2003): 317-41.

14. Stein, Donald. "Plasticity." Personal interview. Alyssa Walz. 19 Nov. 2008.

15. Wieloch, Tadeusz, and Karoly Nikolich. "Mechanisms of Neural Plasticity Following Brain Injury." Rev. of Current Opinion in Neurobiology. 2006: 258-64. 18 May 2006. Science Direct. Georgia Institute of Technology, Atlanta. 24 Oct. 2008 <www.sciencedirect.com>.

Further readingEdit


Useful Videos

^Limb Syndrome (a talk given by Ramachandran about consciousness, mirror neurons, and phantom limb syndrome)

^^Traumatic Brain Injury (a story of TBI and the results of ProTECT using progesterone treatments) Emory University News Archives

Other Interesting Readings

Micheal Chorost How Becoming Part Computer Made Me More Human

Norman Doidge Brain That Changes Itself

Donald Stein Brain Injury and Recovery

External linksEdit


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