Neuroplasticity

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NAME : Muniroh Hanafiah

NIM : 070100392

GROUP :J6

FACILITATOR: dr.RR SUZY INDHARTY, M.Kes, Sp.BS

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DEPARTMENT OF NEUROSURGERY

FACULTY OF MEDICINE ACMS-USU

JULY 2012

Introduction

An adult brain was thought to be a rather static organ in the past, on the other hand
today it has been proven that the brain is able to reorganize and change itself in order to adapt
to new situation such as learning a new dance step or in order to recover from an injury.
(Kolb B, Gibb R, Robinson, T, 2003)

The theory of neuroplasticity was believed to have been introduced about 120 years
ago by an American psychologist and philosopher, William James, in his book “Principle of
Psychology”. However the first to mention the term neuralplasticity was by a Polish
Neuroscientist, Jerzy Konorksi in 1948.Konorski suggested that over time neurons that are
activated by the surrounding neurons may form new pathway which affects the plasticity of
the brain. ( www.whatisneuroplasticity.com)

What is Neuroplasticity?

Neuroplasticity is defined as the ability of the brain to reorganizes neural pathway in
the brain in order to accommodate the new information and ability attained. Neuroplasticity
can occur in two ways; either by learning new things or the brain is adapting in order to
adjust itself to the new situation for example when a person experience an accident and is
unable to use his or her right hand then in order to cope the brain has to adapt by forming
new neural pathway and learn how to use the left hand instead. (www.spineuniversity.com)

Nature of Neuroplasticity

Histology of Central Nervous system

Neuron

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In order to understand how neuroplasticity occurs, it is important to understand the
basic structure of the nervous system. The main histological components of the central
nervous system are the neurons. (Wibowo, D.S,2008)

Neurons are nerve cell that are responsible for the chemical reaction, transmission,
sensing the stimuli, activating certain cell in response and releasing neurotransmitter. A
neuron is made out of a gel like structure and is prone to trauma. The neuron structure is
strengthened by the presence of neurofilament or neurofibril which acts as the cytoskeleton.
The neurofilament also as the microtubule which transport metabolites good and regulates
neurotransmitter. In the central nervous system the neurons are surrounded by myelin sheath
which are formed by the oligodendrocyte. The myelin plays an important role in isolating the
neurons from affecting other neuron nearby. (Wibowo, D.S, 2008)

In general neuron consists of three parts dendrite which plays a role in receiving the
stimuli from the surrounding; cell body or perikaryon which act as the main centre of a single
neurons and the axon which is a bump like structure which either generates new impulses or
carry impulse from one cell to the next. (Wibowo, D.S, 2008)

Neurons can be classified either by its structure or by its function. According to structure the
neuron can be classified as the following (1) multipolar neuron, which has more than has one
axon and many dendrites;(2) bipolar neuron which has one dendrite and one axon;(3)
pseudounipolar which contains an axon that has split into two branches; one branch runs to
the periphery and the other to the spinal cord.

According to the function neurons can be classified into motoric (efferent) which
controls the target organ such as muscle fiber, exocrine gland and endocrine gland; and the
sensoric neuron (afferent) which involves receving sensoric stimulus from the environment.
(Wibowo, D.S,2008)

Fig.1. The different types of Neurons

Glia Cell

Neuroglia or glia cell is a group of cell that made up 10% of the total neuron which is
found in the central nervous system. Glia cells are non-neuronal cells, their role mainly

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involves them maintaining honeostasis, supplying nutrients, fixing the damaged tissues,
protection and support as well as acting as the phagocytes. Other types of Glia cells include
astrocyte, oligodendrocyte, microglia and ependymal cell. (Wibowo D.S,2008)

Astrocyte binds the neuron to the capillary and pia matter. A single astrocyte cell
forms expanded end feet which is connected to the endothelial cell through a junctional
complex which forms a barrier between the central nervous system and the blood vessel. This
appears to be the component of blood brain barrier. On its surface the astrocye cells have a
few receptors and cells which releases metabolites substance and molecule which can either
stimulate or inhibits the neuron function. Astrocyte also plays an important role in
maintaining the optimal condition in order for the neurons to function properly. In cases of
trauma or injury to the brain astrocyte cell proliferate to form scar tissue on the glial cell.
(Wibowo D.S,2008)

Oligodendrocyte is found in the substantia grisea and substatia alba, these cell
produces myelin sheath which acts as an electrical insulator for the axon in the central
nervous system. The oligodendrocyte cells is similar to that of the Schwann cell in the
peripheral nervous sytem, the only difference is that oligodendrocyte can surround a few
myelin axon at the same time. (Wibowo D.S,2008)

Microglia cell is small and oval in shaped with a few short bumps and is only found in
a small number in the substatia grisea and substatia alba. Microglia cells originate from the
mesoderm layer and migrated to the neuroectoderm layer at the of the embryonic phase.
These cells acts similar to that of the phagocyte cell and is involved in inflammation reaction
as well as repairing the damage that occurs to the central nervous system after an injury. In
patient with multiple sclerosis the microglia cell will cause the degradation of the myelin
surrounding the axon in the central nervous system. (Wibowo D.S,2008)

Empydemal cell is a cylindrical shaped cell and acts as a fluid transporting cell and in
a few regions of the brain these cell modified themselves into epithelial choroidal cell and
produce cerebrospinal fluid. (Wibowo D.S,2008)

Histology of Brain

The brain consists of cerebrum, cerebellum and brain stem. The brain does not have
connective tissues, the organ has a gel like structure and appears to form a complex structure
which consist of layered structure and non layered structure. (Wibowo, D.S, 2008)

The cerebral cortex is a structure with lots of fold and has a few regions with layer
structures that each has their own function. Some part of the cortex region receives afferent
impulses while other region produces impulses to control the voluntary movement. There are
many types of important cell in the cerebral cortex such as the pyramidal cell which connects
the cortex with the other brain parts. Cerebral cortex can be divided into the neocortex and
allocortex. Neocortex has six layers of cell and is far more developed compare to allocortex
which has only three layers of cell. The thickest layer of the neocortex layer is located at the

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Brodmann area 4 due to the giant Betz cell. In the allocortex layer the hippocampus can be
found. (Wibowo, D.S, 2008)

The cerebellum also contains lots of folds within its structure and is arranged in
layers. The cerebellum plays a very important role in controlling the motoric function of the
muscle movement. The cortex of the cerebellum consist of three layer starting with a
molecular layer on the outside, purkinje cell and the granular layer on the inside. Purkinje
fiber has a large body cell with lots of branches on its dendrites. (Wibowo, D.S, 2008)

Histology of Medulla Spinalis

Medulla spinalis is a continuity of the brain stem which is divided into a few segment.
Each segment is linked with the left and right spinal nerve. The main difference between the
histology of the medulla spinalis and the brain is the position of the substantia grisea and the
substantia alba. In the medulla spinalis the subtantia alba surrounds the substantia grisea
whereas in the brain it occurs the other way round. (Wibowo, D.S, 2008)

Substansia grisea contain neuron cell body with its dendrite , axon and glial cell.
Substansia grisea is divided into two cornu dorsalis and two cornu ventralis which is
interlinked by the commisura substansia grisea. The sensory neuron has cell body outside of
the medulla spinalis within the dorsal radix ganglion and ends at the posterior cornu
substantia grisea where it will form synapse with interneuron. The interneuron cell will
integrate the sensory impulse which it receives and sends the impulses to the brain. The brain
will send the impulse back along the interneuron cell which is then send to the peripheral.
(Wibowo, D.S,2008)

Anatomy of the brain

The brain is one of the largest and most complex organs in the human body. It is made
up of more than 100 billion nerves that communicate in trillions of connections called
synapses.
The brain is made up of many specialized areas that work together. The cortex is the
outermost layer of brain cells. Thinking and voluntary movements begin in the cortex. The
brain stem is between the spinal cord and the rest of the brain. Basic functions like breathing
and sleep are controlled here. The basal ganglia are a cluster of structures in the center of the
brain. The basal ganglia coordinate messages between multiple other brain areas. The
cerebellum is at the base and the back of the brain. The cerebellum is responsible for
coordination and balance. .(Wibowo, D.S,2008)

The brain is also divided into several lobes; the frontal lobes are responsible for
problem solving and judgment and motor function. The parietal lobes manage sensation,
handwriting, and body position. The temporal lobes are involved with memory and hearing.
The occipital lobes contain the brain's visual processing system. The brain is surrounded by a

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layer of tissue called the meninges. The skull (cranium) helps protect the brain from injury. .
(Wibowo, D.S,2008)

The picture below shows the brain cross section area.

Fig.2 Cross section of the brain
anatomy

Neurogenesis

Neurogensis is a process where new nerve cells are generated. In neurogenesis, there
is active production of new neurons, astrocytes, glia, and other neural lineages from
undifferentiated neural progenitor or stem cells. Neurogenesis is considered a rather inactive
process in most areas of the adult brain. (www.medterm.com)

In the past, it was believed that a human adult nervous system does not have the
ability to regenerate itself partly because an adult brain contain neurons with complex
structure and highly differentiated. As a result of this it was assumed that the neuron is unable
to re-enter the cell cycle and further differentiate. Another reason is because if an adult
neurons were able to divide itself how would the new cell with the new dendrites, axon and
synapse function without disrupting the existing circuits. (Gage, F.H, 2002)

Several discoveries over the past few years had shown that there is an area within an
adult brain new neurons are continually being created, the two predominant area include the
sub ventricular zone which lines the lateral ventricle, where the neural stem cell and the
progenitor generate neuroblast that migrate to the olfactory bulb via the rostral migratory
stream; and the subgranular zone which is part of the denate gyrus of the hippocampus. The
first evidence of neurogenesis in the cerebral cortex of an adult mammalian was discovered
by Joseph Altman in 1962 followed by the demonstration of adult neurogenesis in the dentate
gyrus of the hippocampus in 1963. In 1969 he discovered and named the rostral migratory
stream. Unfortunately these discovery was ignored until later on in the 1990 when a
demonstration was done proving hippocampal neurogenesis in humans and non primate.
(Gage, F.H, 2002)

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Even thought there has been a lot of research being done on the functional relevance
of adult neurogenesis; the results still shows uncertainty, but there is some evidence that
hippocampal adult neurogenesis is important for learning and memory. (Gage, F.H, 2002)

Multiple mechanisms for the relationship between increased neurogenesis and
improved cognition have been suggested, including theories to demonstrate that new neurons
increase memory capacity, and reduce interference between memories or add information
about time to memories Experiments aimed at ablating neurogenesis have proven
inconclusive, but several studies have proposed neurogenic-dependence in some types of
learning, and others seeing no effect. Studies have demonstrated that the act of learning itself
is associated with increased neuronal survival. However, the overall findings that adult
neurogenesis is important for any kind of learning are still very vague. (Gage, F.H, 2002)

Neuroregeneration

Neuroregeneration refers to the regrowth or repair of nervous tissues cells or cell
products. Such mechanisms may include generation of new neurons, glia, axons, myelin, or
synapses. Neuroregeneration in the peripheral nervous system is different in comparison with
that of the central nervous system; by the functional mechanism, the extent and speed. When
an axon is damaged, the distal segment undergoes Wallerian degeneration, losing
its myelin sheath. The proximal segment can either die by apoptosis or undergo the
chromatolytic reaction, which is an attempt to repair the axon. In the CNS, synaptic stripping
occurs as glia foot processes invade the dead synapse. (Kandel, Schwartz, 2005)

Central Nervous system Regeneration

The regeneration of neuron in the central nervous system after an injury is not the
same as the regeneration of the peripheral nervous system. After an injury occurs to the
central nervous system it is not followed by extensive regeneration. It is limited by the
inhibitory influences of the glial and extracellular environment. The hostile, non-permissible
growth environment is, in part, created by the migration of myelin-associated inhibitors,
astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environment
within the CNS, especially following trauma, counteracts the repair of myelin and neurons.
(Recknor J.B, S.K. Mallapragda, 2006)
Slower degeneration of the distal segment than that which occurs in the peripheral
nervous system also contributes to the inhibitory environment because inhibitory myelin and
axonal debris are not cleared away as quickly. All these factors contribute to the formation of
what is known as a glial scar, which axons cannot grow across. The proximal segment
attempts to regenerate after injury, but its growth is hindered by the environment. It is
important to note that central nervous system axons have been proven to regrow in
permissible environments; therefore, the primary problem to central nervous system axonal
regeneration is crossing or eliminating the inhibitory lesion site. (Recknor J.B, S.K.
Mallapragda, 2006)

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Glial scar formation is induced following damage to the nervous system. In the central
nervous system, this glial scar formation significantly inhibits nerve regeneration, which
leads to a loss of function. Several families of molecules are released that promote and drive
glial scar formation. Transforming growth factors B-1 and -2, interleukins, and cytokines all
play a role in the initiation of scar formation. The inhibition of nerve regeneration is a result
of the accumulation of reactive astrocytes at the site of injury and the up regulation of
molecules that are inhibitory to neurite extension outgrowth. The up-regulated molecules alter
the composition of the extracellular matrix in a way that has been shown to inhibit neurite
outgrowth extension. This scar formation involves contributions from several cell types and
families of molecules. In response to scar-inducing factors, astrocytes up regulate the
production ofchondroitin sulfate proteoglycans. Astrocytes are a predominant type of glial
cell in the central nervous system that provide many functions including damage mitigation,
repair, and glial scar formation. Chondroitin sulfate proteoglycans (CSPGs) have been shown
to be up regulated in the central nervous system (CNS) following injury. (Recknor J.B, S.K.
Mallapragda, 2006)

Brain injury

The brain injury mechanism is summarized in the diagram below:

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(National Institute of Neurological disorder and stroke, 2003)

Factors affecting Brain Plasticity

By using Golgi-staining procedures, various investigators have shown that housing
animals in complex versus simple environments produces widespread differences in the
number of synapses in specific brain regions. In general, such experiments show that
particular experiences embellish circuitry, whereas the absence of those experiences fails to
do so (e.g., Greenough & Chang, 1989). Until recently, the impact of these
neuropsychological experiments was surprisingly limited, in part because the environmental
treatments were perceived as extreme and thus not characteristic of events experienced by the
normal brain. It has become clear, however, not only that synaptic organization is changed by
experience, but also that the scope of factors that can do this is much more extensive than
anyone had anticipated. Factors that are now known to affect neuronal structure and behavior
include the following:

• Experience (both pre- and postnatal)
• Psychoactive drugs (e.g., amphetamine, morphine)
• Gonadal hormones (e.g., estrogen, testosterone)
• Anti-inflammatory agents (e.g., COX-2 inhibitors)

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• Growth factors (e.g., nerve growth factor)
• Dietary factors (e.g., vitamin and mineral supplements)
• Genetic factors (e.g., strain differences, genetically modified mice)
• Disease (e.g., Parkinson’s disease, schizophrenia, epilepsy, stroke)
• Stress
• Brain injury and disease

Two examples of the effect are described below:

Early Experience

It is generally assumed that experiences early in life have different effects on behavior
than similar experiences later in life. The reason for this difference is not understood,
however. To investigate this question, an experiment was carried out with an animals being
placed in complex environments either as juveniles, in adulthood, or in senescence (Kolb,
Gibb, & Gorny, 2003). The result expected was that there would be quantitative differences
in the effects of experience on synaptic organization, however it was also a qualitative
differences was found in the result. And like many investigators before, it was also found that
the length of dendrites and the density of synapses were increased in neurons in the motor
and sensory cortical regions in adult and aged animals housed in a complex environment
(relative to a standard lab cage). In contrast, animals placed in the same environment as
juveniles showed an increase in dendritic length but a decrease in spine density. In other
words, the same environmental manipulation had qualitatively different effects on the
organization of neuronal circuitry in juveniles than in adults.
To pursue this finding, an infant animals was given 45 min of daily tactile stimulation
with a little paintbrush (15 min three times per day) for the first 3 weeks of life. The
behavioral studies results showed that this seemingly benign early experience enhanced
motor and cognitive skills in adulthood. The anatomical studies showed, in addition, that in
these animals there was a decrease in spine density but no change in dendritic length in
cortical neurons; yet another pattern of experience-dependent neuronal change. The result of
the studies showed that experience can uniquely affect the developing brain which leads to
wonder if the injured infant brain might be repaired by environmental treatments. It was not
surprising when it was found that post injury experience, such as tactile stroking, could
modify both brain plasticity and behavior because it has been proven that such experiences
were powerful modulators of brain development (Kolb, Gibb, & Gorny, 2000). What was
surprising, however, was that prenatal experience, such as housing the pregnant mother in a
complex environment, could affect how the brain responded to an injury that it would not
receive until after birth. In other words, prenatal experience altered the brain’s response to
injury later in life. This type of study has profound implications for preemptive treatments of
children at risk for a variety of neurological disorders. (Kolb B, Gibb R, Robinson, T, 2003)

Psychoactive Drugs

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Many people who take stimulant drugs like nicotine, amphetamine, or cocaine do so
for their potent psychoactive effects. The long-term behavioral consequences of abusing such
psychoactive drugs are now well documented, but much less is known about how repeated
exposure to these drugs alters the nervous system. One experimental demonstration of a very
persistent form of drug experience-dependent plasticity is known as behavioral sensitization.
For example, if a rat is given a small dose of amphetamine, it initially will show a small
increase in motor activity (e.g., locomotion, rearing). When the rat is given the same dose on
subsequent occasions, however, the increase in motor activity increases, or sensitizes, and the
animal may remain sensitized for weeks, months, or even years, even if drug treatment is
discontinued.
Changes in behavior that occur as a consequence of past experience, and can persist
for months or years, like memories, are thought to be due to changes in patterns of synaptic
organization. The parallels between drug-induced sensitization and memory led to the
question whether the neurons of animals sensitized to drugs of abuse exhibit long-lasting
changes similar to those associated with memory (e.g., Robinson & Kolb, 1999). A
comparison of the effects of amphetamine and saline treatments on the structure of neurons in
a brain region known as the nucleus accumbens, which mediates the psychomotor activating
effects of amphetamine, showed that neurons in the amphetamine-treated brains had greater
dendritic material, as well as more densely organized spines. These plastic changes were not
found throughout the brain, however, but rather were localized to regions such as the
prefrontal cortex and nucleus accumbens, both of which are thought to play a role in the
rewarding properties of these drugs. Later studies have shown that these drug-induced
changes are found not only when animals are given injections by an experimenter, but also
when animals are trained to self-administer drugs, leading us to speculate that similar changes
in synaptic organization be found in human drug addicts. (Kolb B, Gibb R, Robinson, T,
2003)

Other Factors

All of the factors outlined above have effects that are conceptually similar to the two
examples that have just been discussed. For instance, brain injury disrupts the synaptic
organization of the brain, and when there is functional improvement after the injury, there is a
correlated reorganization of neural circuits (e.g., Kolb, 1995). But not all factors act the same
way across the brain. For instance, estrogen stimulates synapse formation in some structures
but reduces synapse number in other structures (e.g., Kolb, Forgie, Gibb, Gorny, &
Rowntree, 1998), a pattern of change that can also be seen with some psychoactive drugs,
such as morphine. In summary, it now appears that virtually any manipulation that produces
an enduring change in behavior leaves an anatomical footprint in the brain. (Kolb B, Gibb R,
Robinson, T, 2003)

Applications and Examples

Treatment of brain damage

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A surprising consequence of neuroplasticity is that the brain activity associated with a
given function can move to a different location; this can result from normal experience and
also occurs in the process of recovery from brain injury. Neuroplasticity is the fundamental
issue that supports the scientific basis for treatment of acquired brain injury with goal-
directed experiential therapeutic programs in the context of rehabilitation approaches to the
functional consequences of the injury.
The adult brain is not "hard-wired" with fixed neuronal circuits. There are many
instances of cortical and subcortical rewiring of neuronal circuits in response to training as
well as in response to injury. There is solid evidence that neurogenesis (birth of brain cells)
occurs in the adult, mammalian brain—and such changes can persist well into old age. 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.
In the other areas of the brain, neurons can die, but they cannot be regenerated.
However, there are numerous amount of 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
levels and are still an active topic in 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 was developed by immunologis 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.
Paul Bach-y-Rita, deceased in 2006, was the "father of sensory substitution and brain
plasticity.” In working with a patient whose vestibular system had been damaged he
developed BrainPort, a machine that "replaces the vestibular apparatus and send balance
signals to the brain from the tongue."] After the machine was used for some time it was no
longer necessary, as the patient then regained the ability to function normally.
Plasticity is the major explanation for the phenomenon. Because the patient’s
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." (Colota V.A, Rita P.B, 2002)
Randy Nudo's group found that if a small stroke (an infarction) is induced by
obstruction of blood flow to a portion of a monkey’s motor cortex, the part of the body that

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responds by movement will move when areas adjacent to the damaged brain area are
stimulated.
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. (Frost S.B, Barbay S.,
Friel K.M, et el, February 2003)
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.
Jon Kaas, a professor at Vanderbilt University, has been able to show "how
somatosensory area 3b and ventroposterior nucleus of the thalamus are affected by long
standing unilateral dorsal column lesions at cervical levels in macaque monkeys. 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. (Young J.A, Tolentino, M., 2011)
Meditation
A number of studies have linked meditation practice to differences in cortical
thickness or density of gray matter. One of the most well-known studies to demonstrate this
was led by Sara Lazar, from Harvard University, in 2000. 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.
(Davidson, R. J, 2008)
Chronic Pain
Individuals who suffer from chronic pain experience prolonged pain at sites that may
have been previously injured, yet are otherwise currently healthy. This phenomenon is related
to neuroplasticity due to a maladaptive reorganization of nervous system, both peripherally
and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an

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elevation of nociceptive input from the periphery to the central nervous system. Prolonged
nociception from periphery will then elicit a neuroplastic response at the cortical level to
change its somatotopic organization for the painful site, inducing central sensitization. For
instance, individuals experiencing complex regional pain syndrome demonstrate a diminished
cortical somatotopic representation of the hand contralaterally as well as a decreased spacing
between the hand and the mouth. Additionally, chronic pain has been reported to significantly
reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal
cortex and right thalamus. However, following treatment, these abnormalities in cortical
reorganization and grey matter volume are resolved, as well as their symptoms. Similar
results have been reported for phantom limb pain, chronic low back pain and carpal tunnel
syndrome. (www.spineuniversity.com)

Conclusion

The structure of the brain is constantly changing in response to an unexpectedly wide
range of experiential factors. Understanding how the brain changes and the rules governing
these changes are important not only for understanding both normal and abnormal behavior,
but also for designing treatments for behavioral and psychological disorders ranging from
addiction to stroke. Although much is now known about brain plasticity and behavior, many
theoretical issues remain. Knowing that a wide variety of experiences and agents can alter
synaptic organization and behavior is important, but leads to a new question: How does this
happen? This is not an easy question to answer, and it is certain that there is more than one
answer.

Other issues revolve around the limits and permanence of plastic changes. After all,
people encounter and learn new information daily. Is there some limit to how much cells can
change? It seems unlikely that cells could continue to enlarge and add synapses indefinitely,
but what controls this? We saw in our studies of experience-dependent changes in infants,
juveniles, and adults that experience both adds and prunes synapses, but what are the rules
governing when one or the other might occur? This question leads to another, which is
whether plastic changes in response to different experiences might interact. For example,
does exposure to a drug like nicotine affect how the brain changes in learning a motor skill
like playing the piano? Consider, too, the issue of the permanence of plastic changes. If a
person stops smoking, how long do the nicotine-induced plastic changes persist, and do they
affect later changes?

One additional issue surrounds the role of plastic changes in disordered behavior.
Thus, although most studies of plasticity imply that remodeling neural circuitry is a good
thing, it is reasonable to wonder if plastic changes might also be the basis of pathological
behavior. Less is known about this possibility, but it does seem likely. For example, drug
addicts often show cognitive deficits, and it seems reasonable to propose that at least some of
these deficits could arise from abnormal circuitry, especially in the frontal lobe. (Kolb B,
Gibb R, Robinson, T, 2003)

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11. www.spineuniversity.com

12. Young, J. A., & Tolentino, M. (2011). Neuroplasticity and its Applications for
Rehabilitation. American Journal of Therapeutics. 18, 70-80.

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