In 1793, Italian anatomist Michele Vicenzo Malacarne performed an experiment where he took two animals, trained only one of them exhaustively for many years and then dissected both of them. He found that the cerebellum of the animal that he had trained was substantially larger. Sadly, these findings were not recognised for their importance and were forgotten. 
The term ‘plasticity’ was first used in terms of behaviour as far back as 1890 by William James (American philosopher, psychologist and physician) in his book The Principles of Psychology.  ‘Neural plasticity’ was first used by Jerzy Konorski, a Polish neuroscientist.
Today, the term ‘neuroplasticity’ is still not well defined. It remains an umbrella term, which covers both synaptic plasticity and non-synaptic plasticity. It refers to the way that changes in behaviour, external environment, the neural processes involved in thinking and emotions and bodily injury all create changes in neural pathways and synapses. 
For most of the 20th Century, neuroscientists agreed that brain structure was formed during a period of early childhood. It was almost impossible for scientists to receive funding for studying this because almost everyone agreed that brain structure was formed during early childhood and that no change was possible after ‘the critical period’.
The Critical Period
To developmental psychologists and developmental biologists, a critical period is a length of time during the life span when an organism has increased sensitivity to exogenous stimuli that are necessary for a particular skill to develop. If the organism does not get the required stimulus during this “critical period”, it was believed that it may be difficult or even impossible, for the organism to develop some functions later in life. 
This view was held up until the 1970s. It was also believed that each area of the brain had its’ own function which could not be changed.
Despite this long-held view, several pioneers (notably Paul Bach-y-Rita, Edward Taub, Michael Merzenich and Norman Doidge performed research and experiments which showed that it is possible for many areas of the brain to stay plastic (malleable and changeable) right up until full adult growth has been achieved  and even beyond that.
Thanks to continued research, we now understand that neuroplasticity ranges from the most basic changes in cells (caused by learning) to huge changes (cortical remapping) made by the brain in response to even catastrophic injury.
Studies of neuroplasticity have affected the understanding of cortical mapping, the treatment of acquired brain injury (internal and external), the treatment of chronic pain (including phantom limb pain), vision problems and help with learning deficits.
A Study in 1970 Changes Everything
A landmark study in 1970 by David Hubel and Torsten Wiesel, involved working with kittens.  They sutured one eye closed on each kitten and recorded their cortical brain maps, expecting to find that the closed eye not working. However, this was not the case and the results were groundbreaking. The part of the kitten’s brain which worked with the closed eye showed that it was processing visual information from the open eye. Hubel and Wiesel overturned long-held beliefs by showing that that ocular dominance columns in the lowest neocortical visual area, V1, were able to be changed after the ‘critical period’ of development.
The way that the cortex of the brain organises information, especially of the sensory systems, is called cortical mapping. The brain will receive sensory information from the foot via touch and will send that information to one site in the cortex. Similarly, information received from the hand will be sent to another cortical site. The end result of these somatotopic (point-for-point correspondence of a region of the body to a particular point on the central nervous system) sensory inputs to the cortex is a cortical representation of the body resembling a map.
Laboratory mice and rats are specialists in ‘whisker information’ rather than visual information. A large part of their brain processes sensory information received by their whiskers. For that reason, they have become ideal for neuroscientists studying sensory systems and cortical mapping.
In a whiskered mammal, information from the whisker travels to the brain through the trigeminal nerve. The information is then delivered to the brainstem. The areas most studied by neuroscientists are the pathways going through areas of the thalamus and then into the barrel cortex. A barrel is an anatomically distinguishable area in layer four of the somatosensory cortex. This is where somatosensory information from the contralateral side of the body arrive from the thalamus.
The ‘whisker barrel’ areas were discovered in a 1970 study by Woolsey and Van der Loos.  They hypothesized that “one barrel represents one vibrissae” – a single whisker. In 1973 they found further evidence for their hypothesis by damaging individual whiskers in newborn rodents. Brain analysis of these rates showed that a corresponding barrel for the missing whisker was not present.
Their hypothesis was again shown by studies in 1989  and 1991  by H.A. Swadlow.
Importance of the Barrel Cortex and the Cortical Column
The barrel cortex continues to play a large part in the understanding of neuroplasticity. Most of what neuroscientists know about corticothalamic processing comes from studies and research on the barrel cortex.
Researchers study the barrel cortex as a model of a cortical column. This column is a group of neurons found in the brain cortex and may be a minicolumn or hypercolumn. Minicolumns contain neurons which map similar features. A hypercolumn “denotes a unit containing a full set of values for any given set of receptive field parameters”. 
A cortical module may be used as an interchangeable term for a hypercolumn or it can mean many overlapping hypercolumns that form a block of tissue. The precise meaning of the term is still unclear. This is because no single corresponding structure has been found in the cortex. No cortical microcircuit has been found which corresponds to the column. As yet, no genetic information has been decoded for how to build a column. 
Despite all of this, the hypothesis of columnar organization is still the most widely used to demonstrate the processing of information in the cortex. 
Late 1970s and Early 1980s
At this time, researchers began to look at what would happen if parts of sensory inputs were removed. It was discovered that if the cortical map doesn’t get any sensory input, it will compensate by being activated later by other inputs – usually adjacent to the now dormant areas.
Mersenich’s Important 1984 Study 
Owl monkey hands were mapped and then their third digit was amputated. Before amputation the maps showed five regions, one for each digit of the hand. Sixty two days after the third digit was amputated, the subsequent cortical map showed that the area which had previously corresponded to the now missing digit had been taken over by the second and fourth digit regions – which were adjacent to the digit three region. The regions for the first and fifth digit were not adjacent to the third digit area and they remained unchanged. The study showed that only regions adjacent to an altered area will move in to change the cortical map.
An investigation in 2002 studied what happens to cause this plasticity. Wall and Xu  discovered that reorganisation doesn’t just occur at the cortical level, but at every level of processing. These multi-level changes give rise to the changes in mapping that are seen in the cerebral cortex.
Cortical plasticity caused by repeated experience parallels the acquisition of motor skills.
Repeated Experience Changes Cortical Mapping
In 1990, Xerri, Mersenich, Jenkins and Santucci  studied plasticity in the somatosensory system of owl and squirrel monkeys. The monkeys were trained to pick up pellets of food. The pellets were in five wells that differed in size. The monkeys were initially clumsy but quickly became more dextrous. Mapping showed that their spatial resolution doubled in just a few days. The study showed that even primary cortical sensory areas (in this case, the fingertips of the monkeys) may be changed by repeated experience. This study had important consequences for the understanding of learning and the acquisition of skills.
Reward Increases Plasticity
Merzenich and DT Blake performed studies in 2002, 2005 and 2006 using cortical implants to monitor the increase of plasticity in the somatosensory and auditory systems. They found that when a stimulus was combined with reward, the cortical map is stronger and larger. In some cases, they saw that when a new sensory motor behaviour is first gained, the cortical representation of that gain can double or treble in just one to two days. These changes finish in a few weeks. Sensory experience on its’ own was not enough to cause changes. It had to be combined with reward and be combined with conditioning behaviours.
Neuroplasticity Faster than Expected
A study in 2005  discovered that neuroplasticity in humans could take place in just a few months. Medical students studying for exams showed a significant increase of gray matter in both the posterior and lateral parietal cortex.
Negative and Positive Neuroplasticity
Norman Doidge (Canadian Psychiatrist, Psychoanalyst, and Author of The Brain That Changes Itself 2007 – a New York Times and international bestseller ) categorises examples of neuroplasticity as being positive or negative. An example of positive neuroplasticity would be an organism returning to normal after suffering a stroke. However, an excessive amount of neurones growing and causing a form of spasticity would obviously be negative.
The maladaptive rewiring of synapses that result in addictions and obsessive compulsive disorder would also be classed as negative.
Understanding of Neuroplasticity aids treatment of Acquired Brain Injury
We have seen how brain activity which corresponds to a particular function is able to move to an adjacent area and function there as it did in the original area. This happens during day-to-day living but it also happens during recovery from an internal or external acquired brain injury (ABI). This means that treatment of ABI can now be based on scientific knowledge. Therapy can now be tailored to how the injury has affected brain function. The outlook for patients who have suffered an ABI is now more positive as there is research based evidence that neurogenesis does happen in an adult, mammal brain. A 2002 study demonstrated that this doesn’t just happen in youth but can happen right through adult life and into old age. 
Evidence for neurogenesis was previously only found in the hippocampus and olfactory region but research in 2008 showed that it could also occur in the cerebellum as well as other regions of the brain. 
In the remainder of the brain, neurons may die but they cannot be made. Neuroscientists are actively researching how the brain is able to reorganise its’ synaptic networks using experiences.
This theory was expounded by the Nobel Prize winning Immunologist and Neuroscientist Gerald Edelman in his 1992 book ‘Bright Air, Brilliant Fire’  Edelman proposed that the ongoing process of selecting synapses which occurs in the brain may either strengthen or weaken the way grops of neurons connect. He argued that any successful output would modify brain activity so that selection based on experience would map occurances from all bodily systems into particular groups of neurons.
Edelman held that this choosing process is the same as Darwin’s Natural Selection. He argued that this method of plasticity was essential
Paul Bach-y-Rita’s BrainPort
Bach-y-Rita played a hugely important part in the understanding of neuroplasticity. He was referred to as the “father of sensory substitution and brain plasticity.” 
While working with a woman who had a damaged vestibular system (which caused her to be unable to balance) he created BrainPort. This machine “replaces her vestibular apparatus and [will] send balance signals to her brain from her tongue.”  After using BrainPort for some time, she was able to dispense with it as her brain had uncovered alternative pathways which became stronger the more they were used. This process is believed to be one of the main ways in which the plastic brain is able to organise itself in the face of ABI.
How Increased Knowledge of Neuroplasticity is Improving Functional Outcomes in Stroke Patients
In 2003 a study found that after inducing a small stroke in a monkey’s motor cortex, the area of the body that responds with movement would still move if areas adjacent to the region of damaged brain were stimulated. 
Ongoing research is looking at how to track changes in the cerebral cortex that are caused by a stroke. Once changes have been identified, the subsequent reorganisation of the brain may be further understood.
Stroke rehabilitation methods such as constraint-induced movement, electrical stimulation, treadmill work (with body weight support) and virtual reality therapy all have evidence that reorganisation of the cortex is the key method of change.
A very recent therapy is robot assisted. This is still a ‘work in progress’ but it is believed to work due to neuroplasticity. A review in 2011 found that there is not enough evidence yet to show the mechanics of change during this therapy. 
Attainable Level of Neuroplasty Depends on Extent of Brain Injury
Professor Jon Kaas has demonstrated “how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys.” 
In 2008, Kaas researched the somatosensory system. If a brain injury damages the somatosensory cortex, the person would experience and impaired perception of their body. Kaas wanted to see how plastic the involved systems (somatosensory, cognitive and motor) could be after brain injury. 
Progesterone Treatment for Traumatic Brain Injury
Recent research by Doctors at Emory University (particularly Dr Donal Stein and Dr David Wright) has lead to a groundbreaking treatment for traumatic brain injuries. This treatment has shown significant improvements in brain injured patients, has no known side effects and is inexpensive.
It was noted that female mice had a better recovery from brain injuries than males. Dr Stein realised that in that group of female mice, a subgroup of females who were at a particular time of their oestrus cycle had an even better recover. Following further research, this enhanced ability to recover was linked to the levels of progesterone in the female mile. The higher the level of progesterone, the faster and better the recovery.
As a result of this, a treatment was created that included giving injections of progesterone to patients who had suffered a brain injury. “Administration of progesterone after traumatic brain injury (TBI) and stroke reduces oedema, inflammation, and neuronal cell death, and enhance spatial reference memory and sensory motor recovery.”
In clinical trials, there was a 60% drop in mortality of brain injured patients who received progesterone injections.
Beneficial Effects Obtained in Both Young and Aged Rats
In 2007, a study demonstrated that progesterone could improve acute recovery after traumatic brain injury in not just young rats – but elderly ones as well. 
Because of physiological differences between young and older rats, the older rats received increased physical contact to lower their stress levels. While undergoing surgery, the older rats had a higher level of oxygen with their anaesthetic and they also received lactated ringers solution administered subcutaneously after surgery, to replace lost fluids. 
The exciting results with progesterone “could have a significant impact on the clinical management of TBI.”  Progesterone treatment has been demonstrated successfully on humans if they receive the progesterone soon after suffering a traumatic brain injury.
Dr Stein is now researching whether progesterone treatment can help patients with longstanding TBI to regain lost functions.
Neuroplasticity in the Treatment of Chronic Pain
It is noted that people who have a previous injury but who are otherwise in good health, may experience chronic, prolonged pain at the site of that injury. A study in 2011 demonstrated that this is due to a negative, maladaptive neuroplasticity. The nervous system has maladaptively reorganised peripherally and centrally.
At the time when the injury occurred, noxious stimuli and inflammation cause an increase in nociceptive input from peripheral regions to the central nervous system. If nociception from the periphery is prolonged, it will trigger a neuroplastic response. This cortical level response changes the somatotopic organisation of the painful area and induces central sensitisation. 
It has been shown that people with complex regional pain syndrome show a shorter spacing from hand to mouth but also have a lesser cortical somatotopic contralateral representation of their hand. 
Chronic Pain Lowers Volume of Grey Matter but This can be Cured
A 2004 study showed that chronic pain can significantly lower the volume of grey matter in all of the brain but specifically in the prefrontal cortex and the thalamus.  However, after treatment, this abnormality in reorganisation of the cortex and the decreased volume of grey matter – and the associated symptoms are all resolved.
These results have also been seen in studies of phantom limb pain, chronic back pain  and a 2006 study of carpal tunnel syndrome .
Maladaptive (Negative) Plasticity in Phantom Limb Pain
The experience of feeling pain or sensation in a limb which has been amputated is quite common in amputees. A 20011 study noted that 60 – 80% of amputees suffer from this phenomenon. 
The connection between the phantom limb phenomenon and neuroplasticity is complicated but it is believed to involve maladaptive neuroplasticity. In the early 1990s, V.S. Ramachandran hypothesised that the cortical maps of the amputated limb interacted with the region around them. This would result in activity in the region surrounding the cortex being ‘misread’ by the region of the cortex which previously corresponded to the now missing limb.
In a study in 1995, Herta Flor showed that cortical reorganisation and thus remapping only happens in people who experience phantom limb pain.  She demonstrated that referred sensations were not the trigger for reorganisation as previously thought. In a 2003 publication she cited that phantom limb pain was what triggered reorganisation in the cortex  – but this reorganisation was negative (maladaptive) rather than positive.
Patients Can Learn to Contort Missing Limbs
In 2009 a remarkable experiment was carried out by Lorimer Moseley and Peter Brugger. They used visual imagery to encourage patients who had lost an arm, to twist and contort their missing (phantom) limbs into physically impossible contortions.
The amazing results were that out of seven patients, four were able to make their phantom limbs move in a physically impossible way.
This experiment would suggest that the patients were able to modify their maladaptive cortical map regarding their phantom limbs. They were then able to create motor commands necessary to contort the missing limbs even with no feedback from their bodies. 
Moseley and Brugger stated “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.”
Knowledge of Neuroplasticity Brings Help for Vision Impaired and Blind Patients
For many years it was believed that if binocular vision (and in particular stereopsis) was not gained by early childhood, then it could never be achieved at all. However, in 2013, there were positive improvements in amblyopia, insufficiency of convergence and anomalies in stereo vision. Ongoing scientific and clinical research is taking place on improvements in binocular vision and recovery from stereopsis.   
Advances in Understanding How Blind People Compensate
It has been thought for years that blind people have been able to compensate for their lack of sight, by developing stronger senses in other areas. Recent studies have found that this is the case but how it occurs is unexpected.
Humans are able to use echolocation, just as bats do. Blind people are able to make a clicking noise and then use the resulting echo to understand their environment and navigate in safety. Studies performed in 2010  and 2011  with functional magnetic resonance imaging were able to demonstrate that blind people are able to adapt their brain to allow this new skill of echolocation to be learned.
Most interestingly, the findings showed that the click echoes that the blind patients heard were processed by areas of the brain that deal with vision and not with hearing. So the blind people were compensating but not by making one sense stronger than the missing one. 
Using Knowledge of Brain Plasticity to Correct Learning Difficulties and Deficits
Michael Mersenich (retired Professor of Neuroscience) has performed much research into neuroplasticity. He has many achievements in the field of brain plasticity and has contributed a large amount of new understanding to the field. In 2001, he was part of a research team who mapped out how sensory input could affect plasticity in the primary auditory cortex. 
While analysing the changes in brain maps of the primary somatosensory cortex in monkeys, he noted how cortical reorganisation occurred following changed schedules of activity from the skin.
He applied findings from several studies to the issues of children who had impairments or deficits in learning that was based on language. He performed studies of how training could be adapted by performing exercises on a computer. He was then able to design ways of improving the childrens’ temporal processing skills by creating games and tests that would require the use of multiple areas of the brain.
The results of these games and tests were used in the creation of a software program called FastForward which was developed in 1996. FastForward is educational software specifically developed to improve the cognitive skills of children who are suffering some form of learning deficit. It aims to help children to develop phonological awareness.
This is an auditory skill that develops as children learn to recognise how the sound of language is structured. Once they can recognise it, they can identify and use it. A study in 2010 demonstrated that this is why auditory skills develop before phonological awareness. 
This is why teachers of very young children aim to get their focus onto listening, distinguishing sounds of speech and external, environmental sounds.
It has long been known that children diagnosed with Autism, Asperger’s syndrome, Rett syndrome, Childhood Disintegrative Disorder or Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS, which is the most common and includes atypical autism) all have some level of impairment. This usually affects their use of language as a method of communication and as a method of socialisation and using their imagination for play. In many of these children the onset of these difficulties is before they turn three. Some of these children have difficulty in processing what they hear, especially if someone is talking to them and there is a lot of background noise.
FastForward was created to help children to improve their memory skills, attention span and the rate at which they process information. It has not only been able to help children with cognitive issues, it also led to further studies into the causes of autism and intellectual disability. A 2008 study demonstrated that children with autism exhibit monochannel perception. This is where behaviour is dominated by stimulus-driven mapping and weaker stimuli and almost completely ignored. 
A 2010 study concluded that computer-based auditory training programs had an impact on the biological processes of children with Autism Spectrum Disorder, bringing them some benefit. 
Neuroplasticity and Dyslexia
Another area where children can struggle due to deficits in phonological processing is developmental dyslexia. This is classically characterised by the child experiencing mild to severe difficulties when reading. Functional neuro imaging studies have shown that both children and adults with dyslexia show a deficit in the neural mechanisms required for phonological processing.
In a 2003 study , twenty children from ages eight to twelve undertook a remediation programme which concentrated on auditory processing and training in oral language. Functional MRI was performed on each child, before and after the remediation programme.
The training improved both language and reading in the dyslexic children. The post-training MRI’s showed a rise in activity in many areas of the brain. Increased activity in the left temporo-parietal cortex and the left inferior frontal gyrus brought the amount of brain activity in these areas much closer to what would be seen in children who could read normally.
The study concluded that in dyslexic children, the level of increased activation in the left cortex correlated with the level of improvement in the child’s ability with spoken language. The results suggested that when the language processing deficits of dyslexic children were remedied enough to improve their level of reading, the disrupted function in areas of the brain used for phonological processing was improved. Additionally, other regions of the brain created activation that compensated for the deficits in other areas.
How Understanding of Neuroplasticity is Changing how we View Fitness and Exercise
In a study in 2009, two groups of mice were made to swim a maze. In another trial, the mice were exposed to an unpleasant stimulus and the scientists recorded how long it took the mice to move away from it.
For the next four weeks, one group of mice were allowed to freely enjoy running in their exercise wheels. The other group were made to run faster in smaller wheels. The speed and length of time that they had to run was dictated by the scientists.
At the end of the four weeks, both groups of mice had their memory and learning abilities tested. Both groups of mice were able to swim the water maze better than they had in the first trial. However, only the mice that had been worked harder on the wheels performed better in the ‘avoiding unpleasant stimuli’ task, than they had the first time. This avoidance task required a more complicated cognitive response. 
The brains of both groups of mice were examined under a microscope. The mice who had been made to work harder had molecular changes in several areas of their brains. The mice who ran with free choice had changes in only one region of their brains.
In an interview in 2009 with The New York Times , one of the authors of the study, Professor Chuang Jih-Ing said “Our results support the notion that different forms of exercise induce neuroplasticity changes in different brain regions.”
Neuroplastic Effects of Pollution
An article published in Sports Medicine in August 2014 notes that people living in areas where pollution is high are likely to suffer long term effects on their health.  Growing up in these areas and spending adolescence there may lead to a lower mental capacity and a higher risk of damage to the brain.
All people, regardless of their age, living in highly polluted areas have a higher risk of suffering from a variety of neurological disorders.
It is known that both polluted air and pollution by heavy metals have negative effects on the functionality of the central nervous system. Pollutants are able to affect neurophysiology after the central nervous system has stabilised, due to negative neuroplasticity.
It is known that air pollution affects both small and large blood vessels and if pollution levels are high, people living in that area are at higher risk for having a stroke or a heart attack.
High levels of air pollution can have serious effects on neural functioning by permanently damaging vascular structures in the brain. The central nervous system can be damaged by pollution too. It can alter the blood brain barrier which can make neurons degenerate in the cerebral cortex, destroy glial cells in white matter and by creating neurofibrillary tangles which are a primary marker of Alzheimer’s Disease.
These changes caused by air pollution can change the structure of the brain and its chemistry – permanently. This can manifest in many disorders and impaired functions. It is not unusual for the effects of neural reorganisation to take a long time to show up.
The Effects of Air Pollution on Adults
The August 2014 article states that the effects of physical activity and the effects of air pollution on neuroplasticity counteract each other.
It is widely accepted that physical activity can enhance health, in particular the well being of the cardiovascular system. It has also been shown to enhance cognition, mental health and the processes involved in brain plasticity.
A neurotrophine – brain derived neurotrophic factor (BDNF) is believed to play a vital role in cognitive improvements triggered by exercise and bursts of physical exertion have been shown to raise levels of BDNF in serum. However, a study in 2013  on the effects of taking exercise in towns, showed that of rural and urban joggers undertaking an identical twelve week running training, only the rural joggers showed any improvement in cognitive function.
Air Pollution, Neuroplasticity and Alzheimer’s Disease
Neuron death can be caused by inflammatory processes slowing the growth of axons. These processes can also activate astrocytes which in turn create proteoglycans. Proteoglycans can only be place in the cortex and hippocampus of the brain and this may be why both of these regions show the most degeneration in people with Alzheimer’s.
In areas of high air pollution, metal particles carried in the air may travel through the nasal cavities and on to the blood brain barrier.
These occurrences, along with the known link between air pollution and neurofibrillary tangles, as well as subcortical vascular changes seen in dogs, would suggest that the negative, maladaptive effects of pollution could put people in polluted areas at a higher risk of developing Alzheimer’s Disease.
Thus, pollution could be a cause of early onset Alzheirmer’s via many mechanisms. It is accepted that the most general effect of air pollution on humans is higher levels of inflammation. Therefore, air pollution, along with negative neuroplasticity can contribute greatly to many neurological issues known to be caused by inflammatory processes.
1. Rosenzweig, Mark R. (1996). “Aspects of the search for neural mechanisms of memory”. Annual Review of Psychology 47: 1–32.
3. LeDoux, Joseph E. (2002).Synaptic self: how our brains become who we are. New York, United States: Viking. p.137. ISBN 0-670-03028-7
4. Shaw, Christopher; McEachern, Jill, eds. (2001). Toward a theory of neuroplasticity. London, England: Psychology Press. ISBN 978-1-84169-021-6
5. 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, October 2011, Volume 24, Issue 3-4, pp 302-315
6. Siegler, Robert (2006). How Children Develop, Exploring Child Develop Student Media Tool Kit & Scientific American Reader to Accompany How Children Develop. New York: Worth Publishers. ISBN 0-7167-6113-0.
7. Rakic, P. (January 2002). “Neurogenesis in adult primate neocortex: an evaluation of the evidence”.Nature Reviews Neuroscience 3 (1): 65–71.
8. 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.PMC 1348655. PMID 5498493.
9. Woosley, T.A., Van Der Loos, H. 1970. The structural organization of layer IV in the somatosensory region (SI) of mouse cerebral cortex: The description of a cortical field composed of discrete cytoarchitectonic units. Brain Research. 205-238.
10. Swadlow HA. Efferent neurons and suspected interneurons in S-1 vibrissa cortex of the awake rabbit: receptive fields and axonal properties. J Neurophysiol 62: 288–308, 1989
11. Swadlow HA. Efferent neurons and suspected interneurons in second somatosensory cortex of the awake rabbit: receptive fields and axonal properties. J Neurophysiol 66: 1392–1409, 1991
12. Horton JC, Adams DL (2005). “The cortical column: a structure without a function”. Philos. Trans. R. Soc. Lond., B, Biol. Sci. 360 (1456): 837–862.
13. Defelipe, Javier (2012). “The neocortical column”. Frontiers in Neuroanatomy 6.
14. Merzenich, M.M.; Nelson, R.J.; Stryker, M.P.; Cynader, M.S.; Schoppmann, A.; Zook, J.M. (1984). “Somatosensory Cortical Map Changes Following Digit Amputation in Adult Monkeys”.Journal of Comparative Neurology 224 (4): 591–605.
15. 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.
16. Christian Xerri, Michael M. Merzenich, William Jenkins and Stephen Santucci. “Representational Plasticity in Cortical Area 3b Paralleling Tactual-motor Skill Acquisition in Adult Monkeys.” Cereb. Cortex (1999) 9 (3): 264-276
17. 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
18. Doidge, Norman (2007). The Brain That Changes Itself: Stories of Personal Triumph from the frontiers of brain science. New York: Viking. ISBN 978-0-670-03830-5.
19. Rakic, P. (January 2002). “Neurogenesis in adult primate neocortex: an evaluation of the evidence”. Nature Reviews Neuroscience 3 (1): 65–71.
20. Ponti, Giovanna; Peretto, Paolo; Bonfanti, Luca; Reh, Thomas A. (2008). “Genesis of Neuronal and Glial Progenitors in the Cerebellar Cortex of Peripuberal and Adult Rabbits”. In Reh, Thomas A. PLoS ONE 3 (6): e2366.
21. Gerald Edelman, Bright Air, Brilliant Fire (Penguin, 1992), p.224
22. Remembering Leaders in the Field of Blindness and Visual Impairment.” National Center for Leadership in Visual Impairment. Salus University. 20 November 2008
23. 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 (6): 3205–3214.
24. Young J. A., Tolentino M.; Tolentino (2011). “Neuroplasticity and its Applications for Rehabilitation”. American Journal of Therapeutics 18(1): 70–80.
25. 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.
26. 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.
27. 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.
28. Seifert, F. & Maihöfner, C. Functional and structural imaging of pain-induced neuroplasticity. Current Opinion in Anaesthesiology 2011; 24: 515–523.
29. Maihöfner C., Handwerker H.O., Neundorfer B., Birklein F. Patterns of cortical reorganization in complex regional pain syndrome”
30. Apkarian A.V., Sosa Y., Sonty S et al.; Sosa; Sonty; Levy; Harden; Parrish; Gitelman (2004). “Chronic back pain is associated with decreased prefrontal and thalamic gray matter density”. J Neurosci 24(46): 10410–10415.
31. 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.
32. Napadow V., Kettner N., Ryan A. et al.; Kettner; Ryan; Kwong; Audette; Hui (2006). “Somatosensory cortical plasticity in carpal tunnel syndrome: a cross-sectional fMRI evaluation”. Neuroimage 31(2): 520–530.
33. 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.
34. Flor H, Elbert T, Knecht S, Wienbruch C, Pantev C, Birbaumer N et al.; Elbert; Knecht; Wienbruch; Pantev; Birbaumer; Larbig; Taub (1995). “Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation”. Nature 375 (6531): 482–484.
35. Flor H, Cortical Reorganization And Chronic Pain: Implications For Rehabilitation, J Rehabil Med, 2003, Suppl.41:66-72
36. Moseley, Brugger, Interdependence of movement and anatomy persists when amputees learn a physiologically impossible movement of their phantom limb, PNAS, 16 Sep 2009
37. Dominick M. Maino: Neuroplasticity: Teaching an Old Brain New Tricks, Review of Optometry, January 2009
38. 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
39. 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.
40. Human Echolocation, Journal of Vision 13 August 2010 vol. 10 no. 7 article 1050 http://www.journalofvision.org/content/10/7/1050.abstract
41. Neural Correlates of Natural Human Echolocation in Early and Late Blind Echolocation Experts, PLoS One, 25 May 2011,
42. 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).
43. Kilgard MP, Pandya PK, Vazquez J, Gehi A, Schreiner CE, Merzenich MM (2001). “Sensory input directs spatial and temporal plasticity in primary auditory cortex”. J. Neurophys. 86 (1): 326–38.
44. Kurtz, R. (2010). Phonemic awareness affects speech and literacy. Speech-Language-Development.
45. Bonneh YS, et al. (2008). “Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence”. Cogn Neuropsychol 25 (5): 635–52.
46. Russo, N.M., Hornickel, H., Nicol, T., Zecker, S., Kraus, N. (2010) Biological changes in auditory function following training in children with autism spectrum disorders. Behavioral and Brain Functions6(60), 1-8.
47.Temple, E., Deutsch, G. K., Poldrack, R. A., Miller, S.L., Tallal, P., Merzenich, M. M., & Gabrieli, J. D. E. (2003).Neural deficits in children with dyslexia ameliorated by behavioural remediation: Evidence from functional MRI. Proceedings of the National Academy of Sciences, 100(5), 2860-2865.
48. 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.
49. Gretchen Reynolds (16 September 2009). “Phys Ed: What Sort of Exercise Can Make You Smarter?”. New York Times.
50. Bos, I; Meeusen, R; Int Panis, L (August 2014). “Physical Activity, Air Pollution and the Brain”. Sports Medicine.
51. Bos, I.; De Boever, P.; Vanparijs, J.; Pattyn, N.; Int Panis, Luc; Meeusen, Romain (2013). “Subclinical effects of aerobic training in urban environment”. Medicine and Science in Sports and Exercise45 (3): 439–47.