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Neuroplasticity challenges the idea that brain functions are fixed in certain locations.

Neuroplasticity (also referred to as brain plasticity, cortical plasticity or cortical re-mapping) is the changing of neurons, the organization of their networks, and their function via new experiences. This idea was first proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected for the next fifty years.[1] The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.[2]

The brain consists of nerve cells (or "neurons") and glial cells which are interconnected, and learning may happen through change in the strength of the connections, by adding or removing connections, or by adding new cells. "Plasticity" relates to learning by adding or removing connections, or adding cells. During the 20th century, the consensus was that lower brain and neocortical areas were immutable in structure after childhood, meaning learning only happens by changing of connection strength, 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. This belief is being challenged by new findings, suggesting all areas of the brain are plastic even after childhood. [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 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 (anatomy) and functional organization (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.

Contents

Neurobiology

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. If there are two nearby neurones that often produce an impulse simultaneously, their cortical maps may become one. This idea also works in the opposite way, ie that neurones which do not regularly produce simultaneous impulses will form different maps.

Cortical maps

Cortical organization, especially for the sensory systems, is often described in terms of maps.[6] 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 and 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. 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 emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.[7].

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 (see Ramachandran for review). This is most commonly described in people that have undergone amputations in hands, arms, and legs, but it is not limited to extremities. The phantom limb feeling, which is thought[8] to result from disorganization in the brain map and the inability to receive input from the targeted area, may be annoying or painful. 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.

The concept of plasticity can be applied to molecular as well as to environmental events[9][10] 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. Plasticity in more recent writing is frequently described as a property of the central nervous system with the term reorganization used to introduce the specific types of changes observed including axonal sprouting, long-term potentiation or the expression of plasticity related genomic responses Pinaud.

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 neurotransmitters 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[8][11].

A 2005 study found that the effects of neuroplasticity were 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.[12].

History

Proposal

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 neurones to develop after birth.[13]

The idea that the brain and its functions are not fixed throughout adulthood was first proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected.[1]

Research and discovery

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.[13][14]

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.”[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 (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]

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 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).”[15] 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 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 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.”[5]

Applications and examples

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 approaches to the functional consequences of the injury.

The adult brain is not "hard-wired" with fixed and immutable 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, the formation of new nerve 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.”[12] In working with a patient whose vestibular system had been damaged he developed 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 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]

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.

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]

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) 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.

They developed a treatment that includes increased levels of progesterone injections to give to brain injured patients. “Administration of progesterone after 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.”[16] 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.

Treatment of learning difficulties

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 brain plasticity-based program could notably improve cognitive function and memory in adults with ARCD.

Brain plasticity during operation of brain-machine interfaces

Brain-machine interface (BMI) is a rapidly developing field of neuroscience. According to the results obtained by Mikhail Lebedev, Miguel Nicolelis and their colleagues (Lebedev et al. 2005), 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.

Phantom limbs

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.

Phantom limbs are phenomena in which a person continues to feel pain or sensation within a part of their body which has been amputated. 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. Pain is often experienced due to the association of this area with the pain that may have been experienced by the limb before it was amputated. Much of this was discovered by neuroscientist Vilayanur S. Ramachandran, who also developed a method of treatment for it called a mirror box, again using neuroplasticity to remove the association of the limb with the surrounding cortex by providing visual feedback to make it appear that the limb is responding.[17]

Meditation

Richard Davidson is a Harvard-trained neuroscientist at the University of Wisconsin–Madison's W.M. Keck Laboratory for Functional Brain Imaging and Behavior. He has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest "alterations in patterns of brain function assessed with functional magnetic resonance imaging (fMRI), changes in the cortical evoked response to visual stimuli that reflect the impact of meditation on attention, and alterations in amplitude and synchrony of high-frequency oscillations that probably play an important role in connectivity among widespread circuitry in the brain."[18][19][20]

See also

References

  1. ^ a b "The Principles of Psychology", William James 1890, Chapter IV, Habits http://psychclassics.yorku.ca/James/Principles/prin4.htm
  2. ^ LeDoux, Joseph E. (2002). Synaptic self: how our brains become who we are. New York: Viking. p. 137. ISBN 0670030287. 
  3. ^ a b "Neurogenesis in adult primate neocortex: an evaluation of the evidence" Nature Reviews Neuroscience 3, 65-71 January 2002
  4. ^ Hubel, D.H.; Wiesel, T.N. (February 1, 1970). "The period of susceptibility to the physiological effects of unilateral eye closure in kittens". The Journal of Physiology 206 (2): 419-436. 
  5. ^ a b Ponti, Giovanna; Peretto, Paolo; Bonfanti, Luca (2008). "Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits". PLoS ONE 3 (6). doi:10.1371/journal.pone.0002366. 
  6. ^ Buonomano, Dean V.; Merzenich, Michael M. (March 1998). "CORTICAL PLASTICITY: From Synapses to Maps". Annual Review of Neuroscience 21: 149-186. doi:10.1146/annurev.neuro.21.1.149. 
  7. ^ Wall, J.T.; Xu, J.; Wang, X. (September 2002). "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 Research Reviews (Elsevier Science B.V.) 39 (2-3): 181-215. doi:10.1016/S0165-0173(02)00192-3. PMID 12423766. 
  8. ^ a b Doidge, Norman. The Brain that Changes Itself. Viking, 2007
  9. ^ 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
  10. ^ 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
  11. ^ [1] Interview with Merzenich in 2004
  12. ^ 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
  13. ^ a b Meghan O'Rourke Train Your Brain April 25, 2007
  14. ^ Brain Science Podcast Episode #10, "Neuroplasticity"
  15. ^ Colotla, Victor A.; Bach-y-Rita, Paul (2002). "Shepherd Ivory Franz: His contributions to neuropsychology and rehabilitation". Cognitive, Affective & Behavioral Neuroscience 2 (2): 141-148. http://htpprints.yorku.ca/archive/00000236/01/Colotla_Bach-y-Rita_2002.pdf. 
  16. ^ Cutler, Sarah M.; Cekic, Milos; Miller, Darren M.; Wali, Bushra; VanLandingham, Jacob W.; Stein, Donald G. (September 24, 2007). "Progesterone Improves Acute Recovery after Traumatic Brain Injury in the Aged Rats". Journal of Neurotrauma 24 (9): 1475-1486. doi:10.1089/neu.2007.0294. 
  17. ^ Ramachandran, Vilayanur S.; Hirstein, William (1998). "The perception of phantom limbs. The D. O. Hebb lecture" (PDF). Brain 121: 1603-1630. PMID 9762952. http://brain.oxfordjournals.org/cgi/reprint/121/9/1603.pdf. Retrieved 2010-01-31. 
  18. ^ Lutz, A.; Greischar, L.L.; Rawlings, N.B.; Ricard, M.; Davidson, R. J. (2004-11-16), "Long-term meditators self-induce high-amplitude gamma synchrony during mental practice", PNAS 101 (46): 16369–73, doi:10.1073/pnas.0407401101, http://www.pnas.org/cgi/content/full/101/46/16369, retrieved 2007-07-08 
  19. ^ The Dalai Lama. “How Thinking Can Change the Brain".
  20. ^ Davidson, Richard; Lutz, Antoine (January 2008), "Buddha’s Brain: Neuroplasticity and Meditation", IEEE Signal Processing Magazine, http://brainimaging.waisman.wisc.edu/publications/2008/DavidsonBuddhaIEEE.pdf 

REFERS TO SECTION ON APPLICATIONS OF NEUROPLASTICITY

3. Cohen, Wendy; Hodson, Ann; O'Hare, Anne; Boyle, James; Durrani, Tariq; McCartney, Elspeth; Mattey, Mike; Naftalin, Lionel et al. (June 2005). "Effects of Computer-Based Intervention Through Acoustically Modified Speech (Fast ForWord) in Severe Mixed Receptive-Expressive Language Impairment: Outcomes From a Randomized Controlled Trial". Journal of Speech, Language, and Hearing Research 48: 715-729. doi:10.1044/1092-4388(2005/049). 

4. Cutler, Sarah M.; Hoffman, Stuart W.; Pettus, Edward H.; Stein, Donald G. (October 2005). "Tapered progesterone withdrawal enhances behavioral and molecular recovery after traumatic brain injury". Experimental Neurology (Elsevier) 195 (2): 423-429. doi:10.1016/j.expneurol.2005.06.003. 

5. Doidge, Norman (2007). The Brain That Changes Itself: Stories of Personal Triumph from the frontiers of brain science. New York: Viking. ISBN 9780670038305. 

6. Frost, S.B.; Barbay, S.; Friel, K.M.; Plautz, E.J.; Nudo, R.J. (2003). "Reorganization of Remote Cortical Regions After Ischemic Brain Injury: A Potential Substrate for Stroke Recovery". Journal of Neurophysiology 89: 3205–3214. doi:10.1152/jn.01143.2002. http://jn.physiology.org/cgi/reprint/89/6/3205.pdf. 

7. Giszter, Simon F. (January 2008). "Spinal Cord Injury: Present and Future Therapeutic Devices and Prostheses". Neurotherapeutics (Elsevier) 5 (1): 147-162. doi:10.1016/j.nurt.2007.10.062. 

8. Kaas, Jon H. (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. doi:10.1523/JNEUROSCI.2334-08.2008. 

9. Mahncke, Henry W.; Connor, Bonnie B.; Appelman, Jed; Ahsanuddin, Omar N.; Hardy, Joseph L.; Wood, Richard A.; Joyce, Nicholas M.; Boniske, Tania et al. (August 15, 2006). "Memory enhancement in healthy older adults using a brain plasticity-based training program: a randomized, controlled study". Proceedings of the National Academy of Sciences of the USA 103 (33): 12523–12528. doi:10.1073/pnas.0605194103. PMID 16888038. 

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.

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.; Hoffman, Stuart W. (July/August 2003). "Concepts of CNS Plasticity in the Context of Brain Damage and Repair". Journal of Head Trauma Rehabilitation 18 (4): 317-341. http://journals.lww.com/headtraumarehab/Fulltext/2003/07000/Concepts_of_CNS_Plasticity_in_the_Context_of_Brain.4.aspx. 

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

15. Wieloch, Tadeusz; Nikolich, Karoly (June 2006). "Mechanisms of neural plasticity following brain injury". Current Opinion in Neurobiology 16 (3): 258-264. doi:10.1016/j.conb.2006.05.011. PMID 16713245. 

Further reading

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 readings

External links








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