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Neuroplasticity

 

Neuroplasticity

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

Neuroplasticity, also known as brain plasticity, is an

  • Neuroplasticity at the US National Library of Medicine Medical Subject Headings (MeSH)
  • Neuro Myths: Separating Fact and Fiction in Brain-Based Learning by Sara Bernard

External links

  • Chorost, Michael (2005). Rebuilt: how becoming part computer made me more human. Boston: Houghton Mifflin.  
Other readings
  • Ramachandran. Phantom Limb Syndrome.  about consciousness, mirror neurons, and phantom limb syndrome
Videos
  • Pinaud, Raphael; Tremere, Liisa A.; De Weerd, Peter, eds. (2006). Plasticity in the visual system: from genes to circuits. New York: Springer.  
  • Pinaud, Raphael; Tremere, Liisa A., eds. (2006). Immediate early genes in sensory processing, cognitive performance and neurological disorders. New York: Springer.  
  • Begley, Sharon (5 November 2004). "Scans of Monks' Brains Show Meditation Alters Structure, Functioning". The Wall Street Journal (Washington D.C.). p. B1. Archived from the original on 2008-02-02. 
  • Donoghue, John P. (2002). "Connecting cortex to machines: recent advances in brain interfaces" (PDF). Nature Neuroscience 5: 1085–1088.  
  • Flor, H. (July 2002). "Phantom-limb pain: characteristics, causes, and treatment". The Lancet Neurology (Elsevier) 1 (3): 182–189.  
  •  
  • Cohen, Wendy; Hodson, Ann; O'Hare, Anne; Boyle, James; Durrani, Tariq; McCartney, Elspeth; Mattey, Mike; Naftalin, Lionel; Watson, Jocelynne (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 (3): 715–729.  
  • Giszter, Simon F. (January 2008). "SCI: Present and Future Therapeutic Devices and Prostheses". Neurotherapeutics (Elsevier) 5 (1): 147–162.  
  • Mahncke, Henry W.; Connor, Bonnie B.; Appelman, Jed; Ahsanuddin, Omar N.; Hardy, Joseph L.; Wood, Richard A.; Joyce, Nicholas M.; Boniske, Tania; et al. (15 August 2006). "Memory enhancement in healthy older adults using a brain plasticity-based training program: A randomized, controlled study". Proceedings of the National Academy of Sciences of the United States of America 103 (33): 12523–12528.  
  • 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.  
  • Nudo, Randolph J.; Milliken, Garrett W. (1996). "Reorganization of Movement Representations in Primary Motor Cortex Following Focal Ischemic Infarct in Adult Squirrel Monkeys". Journal of Neurophysiology 75 (5): 2144–149.  
  • Wieloch, Tadeusz; Nikolich, Karoly (June 2006). "Mechanisms of neural plasticity following brain injury". Current Opinion in Neurobiology 16 (3): 258–264.  

Further reading

  1. ^ Pascual-Leone A., Freitas C., Oberman L., Horvath J. C., Halko M., Eldaief M.; et al. (2011). "Characterizing brain cortical plasticity and network dynamics across the age-span in health and disease with TMS-EEG and TMS-fMRI". Brain Topography 24: 302–315.  
  2. ^ Pascual-Leone A., Amedi A., Fregni F., Merabet L. B. (2005). "The plastic human brain cortex". Annual Review of Neuroscience 28: 377–401.  
  3. ^ a b Rakic, P. (January 2002). "Neurogenesis in adult primate neocortex: an evaluation of the evidence". Nature Reviews Neuroscience 3 (1): 65–71.  
  4. ^ Hubel, D.H.; Wiesel, T.N. (1 February 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; Reh, Thomas A. (2008). Reh, Thomas A., ed. "Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits". PLoS ONE 3 (6): e2366.  
  6. ^ Chaney, Warren, Dynamic Mind, 2007, Las Vegas, Houghton-Brace Publishing, pp 33–35, ISBN 0-9793392-0-0 [4]
  7. ^ Chaney, Warren, Workbook for a Dynamic Mind, 2006, Las Vegas, Houghton-Brace Publishing, page 44, ISBN 0-9793392-1-9 [5]
  8. ^ a b Bos, I; De Boever, P; Int Panis, L; Meeusen, R (August 2014). "Physical Activity, Air Pollution and the Brain". Sports Medicine.  
  9. ^ Buonomano, Dean V.;  
  10. ^ Merzenich, M.M.; Nelson, R.J.; Stryker, M.P.;  
  11. ^ 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.  
  12. ^ a b c d e f g h i j k Doidge, Norman (2007).  
  13. ^ Interview with Merzenich, 2004
  14. ^ Draganski et al. "Temporal and Spatial Dynamics of Brain Structure Changes during Extensive Learning" The Journal of Neuroscience, 7 June 2006, 26(23):6314–6317
  15. ^ "Remembering Leaders in the Field of Blindness and Visual Impairment." National Center for Leadership in Visual Impairment. Salus University. 20 November 2008
  16. ^ "BrainPort, Dr. Paul Bach-y-Rita, and ... - Mind States - tribe.net". Mindstates.tribe.net. 30 March 2005. Retrieved 12 June 2010. 
  17. ^ "Wisconsin Alumni Association – Balancing Act". Uwalumni.com. Archived from the original on 2011-07-06. Retrieved 12 June 2010. 
  18. ^ a b 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" (PDF).  
  19. ^ Young J. A., Tolentino M.; Tolentino (2011). "Neuroplasticity and its Applications for Rehabilitation". American Journal of Therapeutics 18 (1): 70–80.  
  20. ^ a b Jain, Neeraj; Qi, HX; Collins, CE; Kaas, JH (22 October 2008). "Large-Scale Reorganization in the Somatosensory Cortex and Thalamus after Sensory Loss in Macaque Monkeys". The Journal of Neuroscience 28 (43): 11042–11060.  
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  22. ^ a b c Stein, Donald. "Plasticity." Personal interview. Alyssa Walz. 19 November 2008.
  23. ^ Traumatic Brain Injury (a story of TBI and the results of ProTECT using progesterone treatments) Emory University News Archives
  24. ^ 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.  
  25. ^ a b Cutler, Sarah M.; Cekic, Milos; Miller, Darren M.; Wali, Bushra; VanLandingham, Jacob W.; Stein, Donald G. (24 September 2007). "Progesterone Improves Acute Recovery after Traumatic Brain Injury in the Aged Rats". Journal of Neurotrauma 24 (9): 1475–1486.  
  26. ^ Progesterone offers no significant benefit in traumatic brain injury clinical trial, Emory University, Atlanta, GA
  27. ^ Dominick M. Maino: Neuroplasticity: Teaching an Old Brain New Tricks, Review of Optometry, January 2009
  28. ^ Indu Vedamurthy; Samuel J. Huang; Dennis M. Levi; Daphne Bavelier; David C. Knill (27 December 2012). "Recovery of stereopsis in adults through training in a virtual reality task". Journal of Vision 12 (14).   Article 53
  29. ^ Robert F. Hess; Benjamin Thompson (February 2013). "New insights into amblyopia: binocular therapy and noninvasive brain stimulation". Journal of AAPOS 17 (1). pp. 89–93.  
  30. ^ Marshall, Abigail (August 18, 2013). The Everything Parent's Guide to Children with Dyslexia. Adams Media; Second Edition edition (August 18, 2013). p. 136.  
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  32. ^ Kral A, Sharma A; Sharma (2012). "Developmental Neuroplasticity after Cochlear Implantation". Trends Neurosci 35 (2): 111–122.  
  33. ^ Kral A, O'Donoghue GM (2010). "Profound Deafness in Childhood". New England J Medicine 363: 1438–50.  
  34. ^ 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.  
  35. ^ Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N; Elbert; Knecht; Wienbruch; Pantev; Birbaumer; Larbig; Taub; et al. (1995). "Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation". Nature 375 (6531): 482–484.  
  36. ^ Flor H, Cortical Reorganization And Chronic Pain: Implications For Rehabilitation, J Rehabil Med, 2003, Suppl.41:66–72
  37. ^ Moseley, Brugger, Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb, PNAS, 16 September 2009,[6]
  38. ^ Seifert F., Maihöfner C. (2011). "Functional and structural imaging of pain-induced neuroplasticity". Current Opinion in Anaesthesiology 24: 515–523.  
  39. ^ Maihöfner C., Handwerker H.O., Neundorfer B., Birklein F. (2003). "Patterns of cortical reorganization in complex regional pain syndrome". Neurology 61: 1707–1715.  
  40. ^ Apkarian A.V., Sosa Y., Sonty S; Sosa; Sonty; Levy; Harden; Parrish; Gitelman; et al. (2004). "Chronic back pain is associated with decreased prefrontal and thalamic gray matter density". J Neurosci 24 (46): 10410–10415.  
  41. ^ Karl A., Birbaumer N., Lutzenberger W.; Birbaumer; Lutzenberger; Cohen; Flor; et al. (2001). "Reorganization of motor and somatosensory cortex in upper extremity amputees with phantom limb pain". J Neurosci 21 (10): 3609–18.  
  42. ^ Flor H., Braun C., Elbert T.; et al. (1997). "Extensive reorganization of primary somatosensory cortex in chronic back pain patients". Neurosci Lett 224: 5–8.  
  43. ^ Napadow V., Kettner N., Ryan A.; Kettner; Ryan; Kwong; Audette; Hui; et al. (2006). "Somatosensory cortical plasticity in carpal tunnel syndrome: a cross-sectional fMRI evaluation". Neuroimage 31 (2): 520–530.  
  44. ^ Pagnoni, Giuseppe; Cekic, Milos (28 July 2007). "Age effects on gray matter volume and attentional performance in Zen meditation.". Neurobiology of Aging 28 (10): 1623–1627.  
  45. ^ Vestergaard-Poulsen, Peter; van Beek, Martijn; Skewes, Joshua; Bjarkam, Carsten R; Stubberup, Michael; Bertelsen, Jes; Roepstorff, Andreas (28 January 2009). "Long-term meditation is associated with increased gray matter density in the brain stem.". NeuroReport 20 (2): 170–174.  
  46. ^ Luders, Eileen; Toga, Arthur W.; Lepore, Natasha; Gaser, Christian (14 January 2009). "The underlying anatomical correlates of long-term meditation: larger hippocampal and frontal volumes of gray matter.". Neuroimage 45 (3): 672–678.  
  47. ^ Lazar, S.; Kerr, C.; Wasserman, R.; Gray, J.; Greve, D.; Treadway, Michael T.; McGarvey, Metta; Quinn, Brian T.; et al. (28 November 2005). "Meditation experience is associated with increased cortical thickness". NeuroReport 16 (17): 1893–97.  
  48. ^ Lutz, A.; Greischar, L.L.; Rawlings, N.B.; Ricard, M.; Davidson, R. J. (16 November 2004). "Long-term meditators self-induce high-amplitude gamma synchrony during mental practice". PNAS 101 (46): 16369–73.  
  49. ^ Sharon Begley (20 January 2007). "How Thinking Can Change the Brain". http://www.dalailama.com. 
  50. ^ Davidson, Richard; Lutz, Antoine (January 2008). "Buddha's Brain: Neuroplasticity and Meditation" (PDF). IEEE Signal Processing Magazine. 
  51. ^ Chris Frith (17 February 2007). "Stop meditating, start interacting".  
  52. ^ 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.  
  53. ^ Gretchen Reynolds (16 September 2009). "Phys Ed: What Sort of Exercise Can Make You Smarter?".  
  54. ^ "Human Echolocation". Journal of Vision 10 (7): 1050. 2010.  
  55. ^ "Neural Correlates of Natural Human Echolocation in Early and Late Blind Echolocation Experts". PLOS ONE 6: e20162. 2011.  
  56. ^ Thaler, L; Arnot, S.R.; Goodale, M.A (2011). "Neural correlates of natural human echolocation in early and late blind echolocation experts". Public Library of Science 6 (5). 
  57. ^ a b c Parry D.M.; et al. (1997). "Immunocytochemical localization of GnRH precursor in the hypothalamus of European starlings during sexual maturation and photorefractoriness". J. Neuroendocrinol 9: 235–243.  
  58. ^ a b c D.M. Parry, A.R. Goldsmith Ultrastructural evidence for changes in synaptic input to the hypothalamic luteinizing hormone-releasing hormone neurons in photosensitive and photorefractory starlings J. Neuroendocrinol., 5 (1993), pp. 387–395
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  67. ^ Anthony D. Tramontin, Eliot A. Brenowitz "Seasonal plasticity in the adult brain. Trends in Neurosciences, Volume 23, Issue 6, 1 June 2000, Pages 251–258
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  69. ^ LeDoux, Joseph E. (2002). Synaptic self: how our brains become who we are. New York, United States: Viking. p. 137.  
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  77. ^ Brain Science Podcast Episode #10, "Neuroplasticity"
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References

See also

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."[12]

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."[12] 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."[12]

Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London’s layout in local taxi drivers.[81][82][83] A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media world-wide.

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."[12] He found more evidence of this possible brain reorganization with Shepherd Ivory Franz's work.[79] 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)."[80] This notion has led to motivational rehabilitation programs that are used today.

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 the skin and its touch receptors could act as a retina (using one sense for another[78]). 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."[12]

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."[12] 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.[12]

A significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.[71][77]

In 1945, Stratton experiment,[75] and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder [e.g., see pp 260–62 Vol. I (1945), p 696 Vol. II (1950)].[74] He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.[76]

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.

Research and discovery

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.[72] 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.[68] The use of the word plasticity (neuroplasticity) to describe changes in the nervous system was coined and proposed by Jerzy Konorski in 1966.[73]

Until around the 1970s, an accepted idea across neuroscience, with some exceptions, 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.[71]

Proposal

History

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.[70]

Plasticity was first applied to behavior in 1890 by William James in The Principles of Psychology.[68] The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.[69]

Etymology

Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year.[63] Humans experience a change in the "size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it"[60] during the fall, when these parts are larger. In the spring, both reduce in size.[67]

The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain.[59] Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals.[60] In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.[62]

Within the class Aves, black-capped chickadees experience an increase in the volume of the hippocampus and strength of neural connections to the hippocampus during fall months.[64][65] This change in brain morphology for spatial memory within the hippocampus is not limited to birds, and affects some rodents and amphibians.[61] In songbirds, many song control nuclei in the brain increase in size during mating season.[61] Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common.[66] Gonadotropin-releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.[57][58]

Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals.[61] These changes can improve the chances of mating during breeding season.[57][58][59][61][62][63] Examples of seasonal brain morphology change can be found within many classes and species.

Seasonal brain changes

In a single lifespan, individuals in an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages.[57][58][59][60] Some changes occur seasonally in species to enhance or generate response behaviors.

In animals

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 [54] and 2011 [55] 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. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.[56]

Human echolocation

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.[53] Similar results have meanwhile been found for humans.[8]

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 mini-treadmills 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.[52]

Fitness and exercise

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter.[44][45][46] One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[47] 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.[48][49][50][51]

Meditation

[43].carpal tunnel syndrome and [42]chronic low back pain [41] 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 the nervous system, both peripherally and centrally. During the period of tissue damage,

Chronic pain

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.[37] 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."

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.[35] Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.[36] This phenomenon is sometimes referred to as maladaptive plasticity.

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.[34] 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.

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

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 [32] 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.[33]

Sensory prostheses

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.

Brain-machine interface (BMI) is a rapidly developing field of neuroscience. According to the results obtained by Mikhail Lebedev, Miguel Nicolelis and their colleagues,[31] 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.

During operation of brain-machine interfaces

Michael Merzenich developed a series of "plasticity-based computer programs known as Fast ForWord.[30] 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. After use of the ET program for 8–10 weeks, there was a "significant increase in task-specific performance." The data collected from the study indicated that a neuroplasticity-based program could notably improve cognitive function and memory in adults with ARCD.

Treatment of learning difficulties

After decades in which the assumption that binocular vision, in particular stereopsis, had to be achieved in early childhood lest it could never be gained, in recent years the successful improvements in persons with amblyopia, convergence insufficiency or stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.[27][28][29]

Vision

A study published in the New England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.[26]

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."[25] The promising results of progesterone treatments "could have a significant impact on the clinical management of TBI."[25] 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.

They developed a treatment that includes increased levels of progesterone injections to give to brain-injured patients. "Administration of progesterone after traumatic brain injury[23] (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhance spatial reference memory and sensory motor recovery."[24] 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.[22] 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.[22]

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)[21] 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.[22] 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.

[20]

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.[19]

pharmacotherapy, and electrical-stimulation therapy.

Plasticity is the major explanation for this 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."[12]

Paul Bach-y-Rita, deceased in 2006, was the "father of sensory substitution and brain plasticity."[15] In working with a patient whose vestibular system had been damaged he developed BrainPort,[16] a machine that "replaces her vestibular apparatus and [will] send balance signals to her brain from her tongue."[12] 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.[17]

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 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 followed from the ground-breaking work of another Nobel laureate, Eric Kandel, and his colleagues at Columbia University College of Physicians and Surgeons.

The adult brain is not entirely "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]

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.

Treatment of brain damage

Applications and example

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.[14]

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.[12][13]

[12] An interesting phenomenon involving cortical maps is the incidence of

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.

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, and Kevin Fox. 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.

In the late 1970s and early 1980s, several groups began exploring the impacts of removing portions of the sensory inputs. emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.[11]

Cortical organization, especially for the homunculus).

Cortical maps

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," summarizing Hebbian theory. 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.

Neurobiology

Contents

  • Neurobiology 1
    • Cortical maps 1.1
  • Applications and example 2
    • Treatment of brain damage 2.1
    • Vision 2.2
    • Treatment of learning difficulties 2.3
    • During operation of brain-machine interfaces 2.4
    • Sensory prostheses 2.5
    • Phantom limbs 2.6
    • Chronic pain 2.7
    • Meditation 2.8
    • Fitness and exercise 2.9
    • Human echolocation 2.10
    • In animals 2.11
      • Seasonal brain changes 2.11.1
  • Etymology 3
  • History 4
    • Proposal 4.1
    • Research and discovery 4.2
  • See also 5
  • References 6
  • Further reading 7
  • External links 8

Decades of research[6] have 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 (physiology). As of 2014 neuroscientists are 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 in response to hitherto unsuspected stimuli.[7][8]

Hubel and Wiesel had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, remained largely immutable after the critical period in development.[4] Researchers also studied critical periods 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 in other parts of the brain, including in the cerebellum.[5]

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, neuroscientists maintained a scientific consensus that brain structure was 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]

[2]

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