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  1. 1. 1 NAME : Muniroh Hanafiah NIM : 070100392 GROUP :J6 FACILITATOR: dr.RR SUZY INDHARTY, M.Kes, Sp.BS
  2. 2. 2 DEPARTMENT OF NEUROSURGERY FACULTY OF MEDICINE ACMS-USU JULY 2012Introduction An adult brain was thought to be a rather static organ in the past, on the other handtoday it has been proven that the brain is able to reorganize and change itself in order to adaptto 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 yearsago by an American psychologist and philosopher, William James, in his book “Principle ofPsychology”. However the first to mention the term neuralplasticity was by a PolishNeuroscientist, Jerzy Konorksi in 1948.Konorski suggested that over time neurons that areactivated by the surrounding neurons may form new pathway which affects the plasticity ofthe brain. ( is Neuroplasticity? Neuroplasticity is defined as the ability of the brain to reorganizes neural pathway inthe brain in order to accommodate the new information and ability attained. Neuroplasticitycan occur in two ways; either by learning new things or the brain is adapting in order toadjust itself to the new situation for example when a person experience an accident and isunable to use his or her right hand then in order to cope the brain has to adapt by formingnew neural pathway and learn how to use the left hand instead. ( of NeuroplasticityHistology of Central Nervous systemNeuron
  3. 3. 3 In order to understand how neuroplasticity occurs, it is important to understand thebasic structure of the nervous system. The main histological components of the centralnervous 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. Aneuron is made out of a gel like structure and is prone to trauma. The neuron structure isstrengthened by the presence of neurofilament or neurofibril which acts as the cytoskeleton.The neurofilament also as the microtubule which transport metabolites good and regulatesneurotransmitter. In the central nervous system the neurons are surrounded by myelin sheathwhich are formed by the oligodendrocyte. The myelin plays an important role in isolating theneurons from affecting other neuron nearby. (Wibowo, D.S, 2008) In general neuron consists of three parts dendrite which plays a role in receiving thestimuli from the surrounding; cell body or perikaryon which act as the main centre of a singleneurons and the axon which is a bump like structure which either generates new impulses orcarry 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 theneuron can be classified as the following (1) multipolar neuron, which has more than has oneaxon 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 tothe periphery and the other to the spinal cord. According to the function neurons can be classified into motoric (efferent) whichcontrols the target organ such as muscle fiber, exocrine gland and endocrine gland; and thesensoric neuron (afferent) which involves receving sensoric stimulus from the environment.(Wibowo, D.S,2008) Fig.1. The different types of NeuronsGlia Cell Neuroglia or glia cell is a group of cell that made up 10% of the total neuron which isfound in the central nervous system. Glia cells are non-neuronal cells, their role mainly
  4. 4. 4involves them maintaining honeostasis, supplying nutrients, fixing the damaged tissues,protection and support as well as acting as the phagocytes. Other types of Glia cells includeastrocyte, oligodendrocyte, microglia and ependymal cell. (Wibowo D.S,2008) Astrocyte binds the neuron to the capillary and pia matter. A single astrocyte cellforms expanded end feet which is connected to the endothelial cell through a junctionalcomplex which forms a barrier between the central nervous system and the blood vessel. Thisappears to be the component of blood brain barrier. On its surface the astrocye cells have afew receptors and cells which releases metabolites substance and molecule which can eitherstimulate or inhibits the neuron function. Astrocyte also plays an important role inmaintaining the optimal condition in order for the neurons to function properly. In cases oftrauma 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 cellproduces myelin sheath which acts as an electrical insulator for the axon in the centralnervous system. The oligodendrocyte cells is similar to that of the Schwann cell in theperipheral nervous sytem, the only difference is that oligodendrocyte can surround a fewmyelin 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 ina small number in the substatia grisea and substatia alba. Microglia cells originate from themesoderm 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 reactionas well as repairing the damage that occurs to the central nervous system after an injury. Inpatient with multiple sclerosis the microglia cell will cause the degradation of the myelinsurrounding 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 ina few regions of the brain these cell modified themselves into epithelial choroidal cell andproduce cerebrospinal fluid. (Wibowo D.S,2008)Histology of Brain The brain consists of cerebrum, cerebellum and brain stem. The brain does not haveconnective tissues, the organ has a gel like structure and appears to form a complex structurewhich 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 layerstructures that each has their own function. Some part of the cortex region receives afferentimpulses while other region produces impulses to control the voluntary movement. There aremany types of important cell in the cerebral cortex such as the pyramidal cell which connectsthe cortex with the other brain parts. Cerebral cortex can be divided into the neocortex andallocortex. Neocortex has six layers of cell and is far more developed compare to allocortexwhich has only three layers of cell. The thickest layer of the neocortex layer is located at the
  5. 5. 5Brodmann area 4 due to the giant Betz cell. In the allocortex layer the hippocampus can befound. (Wibowo, D.S, 2008) The cerebellum also contains lots of folds within its structure and is arranged inlayers. The cerebellum plays a very important role in controlling the motoric function of themuscle movement. The cortex of the cerebellum consist of three layer starting with amolecular layer on the outside, purkinje cell and the granular layer on the inside. Purkinjefiber 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 thehistology of the medulla spinalis and the brain is the position of the substantia grisea and thesubstantia alba. In the medulla spinalis the subtantia alba surrounds the substantia griseawhereas 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 isinterlinked by the commisura substansia grisea. The sensory neuron has cell body outside ofthe medulla spinalis within the dorsal radix ganglion and ends at the posterior cornusubstantia grisea where it will form synapse with interneuron. The interneuron cell willintegrate the sensory impulse which it receives and sends the impulses to the brain. The brainwill 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 madeup of more than 100 billion nerves that communicate in trillions of connections calledsynapses.The brain is made up of many specialized areas that work together. The cortex is theoutermost layer of brain cells. Thinking and voluntary movements begin in the cortex. Thebrain stem is between the spinal cord and the rest of the brain. Basic functions like breathingand sleep are controlled here. The basal ganglia are a cluster of structures in the center of thebrain. The basal ganglia coordinate messages between multiple other brain areas. Thecerebellum is at the base and the back of the brain. The cerebellum is responsible forcoordination and balance. .(Wibowo, D.S,2008) The brain is also divided into several lobes; the frontal lobes are responsible forproblem 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 brains visual processing system. The brain is surrounded by a
  6. 6. 6layer 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, thereis active production of new neurons, astrocytes, glia, and other neural lineages fromundifferentiated neural progenitor or stem cells. Neurogenesis is considered a rather inactiveprocess in most areas of the adult brain. ( In the past, it was believed that a human adult nervous system does not have theability to regenerate itself partly because an adult brain contain neurons with complexstructure and highly differentiated. As a result of this it was assumed that the neuron is unableto re-enter the cell cycle and further differentiate. Another reason is because if an adultneurons were able to divide itself how would the new cell with the new dendrites, axon andsynapse 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 anadult brain new neurons are continually being created, the two predominant area include thesub ventricular zone which lines the lateral ventricle, where the neural stem cell and theprogenitor generate neuroblast that migrate to the olfactory bulb via the rostral migratorystream; and the subgranular zone which is part of the denate gyrus of the hippocampus. Thefirst evidence of neurogenesis in the cerebral cortex of an adult mammalian was discoveredby Joseph Altman in 1962 followed by the demonstration of adult neurogenesis in the dentategyrus of the hippocampus in 1963. In 1969 he discovered and named the rostral migratorystream. Unfortunately these discovery was ignored until later on in the 1990 when ademonstration was done proving hippocampal neurogenesis in humans and non primate.(Gage, F.H, 2002)
  7. 7. 7 Even thought there has been a lot of research being done on the functional relevanceof adult neurogenesis; the results still shows uncertainty, but there is some evidence thathippocampal adult neurogenesis is important for learning and memory. (Gage, F.H, 2002) Multiple mechanisms for the relationship between increased neurogenesis andimproved cognition have been suggested, including theories to demonstrate that new neuronsincrease memory capacity, and reduce interference between memories or add informationabout time to memories Experiments aimed at ablating neurogenesis have proveninconclusive, but several studies have proposed neurogenic-dependence in some types oflearning, and others seeing no effect. Studies have demonstrated that the act of learning itselfis associated with increased neuronal survival. However, the overall findings that adultneurogenesis 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 cellproducts. Such mechanisms may include generation of new neurons, glia, axons, myelin, orsynapses. Neuroregeneration in the peripheral nervous system is different in comparison withthat of the central nervous system; by the functional mechanism, the extent and speed. Whenan axon is damaged, the distal segment undergoes Wallerian degeneration, losingits myelin sheath. The proximal segment can either die by apoptosis or undergo thechromatolytic reaction, which is an attempt to repair the axon. In the CNS, synaptic strippingoccurs 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 thesame as the regeneration of the peripheral nervous system. After an injury occurs to thecentral nervous system it is not followed by extensive regeneration. It is limited by theinhibitory influences of the glial and extracellular environment. The hostile, non-permissiblegrowth environment is, in part, created by the migration of myelin-associated inhibitors,astrocytes, oligodendrocytes, oligodendrocyte precursors, and microglia. The environmentwithin 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 peripheralnervous system also contributes to the inhibitory environment because inhibitory myelin andaxonal debris are not cleared away as quickly. All these factors contribute to the formation ofwhat is known as a glial scar, which axons cannot grow across. The proximal segmentattempts to regenerate after injury, but its growth is hindered by the environment. It isimportant to note that central nervous system axons have been proven to regrow inpermissible environments; therefore, the primary problem to central nervous system axonalregeneration is crossing or eliminating the inhibitory lesion site. (Recknor J.B, S.K.Mallapragda, 2006)
  8. 8. 8 Glial scar formation is induced following damage to the nervous system. In the centralnervous system, this glial scar formation significantly inhibits nerve regeneration, whichleads to a loss of function. Several families of molecules are released that promote and driveglial scar formation. Transforming growth factors B-1 and -2, interleukins, and cytokines allplay a role in the initiation of scar formation. The inhibition of nerve regeneration is a resultof the accumulation of reactive astrocytes at the site of injury and the up regulation ofmolecules that are inhibitory to neurite extension outgrowth. The up-regulated molecules alterthe composition of the extracellular matrix in a way that has been shown to inhibit neuriteoutgrowth extension. This scar formation involves contributions from several cell types andfamilies of molecules. In response to scar-inducing factors, astrocytes up regulate theproduction ofchondroitin sulfate proteoglycans. Astrocytes are a predominant type of glialcell in the central nervous system that provide many functions including damage mitigation,repair, and glial scar formation. Chondroitin sulfate proteoglycans (CSPGs) have been shownto be up regulated in the central nervous system (CNS) following injury. (Recknor J.B, S.K.Mallapragda, 2006)Brain injuryThe brain injury mechanism is summarized in the diagram below:
  9. 9. 9(National Institute of Neurological disorder and stroke, 2003)Factors affecting Brain Plasticity By using Golgi-staining procedures, various investigators have shown that housinganimals in complex versus simple environments produces widespread differences in thenumber of synapses in specific brain regions. In general, such experiments show thatparticular experiences embellish circuitry, whereas the absence of those experiences fails todo so (e.g., Greenough & Chang, 1989). Until recently, the impact of theseneuropsychological experiments was surprisingly limited, in part because the environmentaltreatments were perceived as extreme and thus not characteristic of events experienced by thenormal brain. It has become clear, however, not only that synaptic organization is changed byexperience, but also that the scope of factors that can do this is much more extensive thananyone had anticipated. Factors that are now known to affect neuronal structure and behaviorinclude 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)
  10. 10. 10 • 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 diseaseTwo examples of the effect are described below:Early Experience It is generally assumed that experiences early in life have different effects on behaviorthan 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 beingplaced in complex environments either as juveniles, in adulthood, or in senescence (Kolb,Gibb, & Gorny, 2003). The result expected was that there would be quantitative differencesin the effects of experience on synaptic organization, however it was also a qualitativedifferences was found in the result. And like many investigators before, it was also found thatthe length of dendrites and the density of synapses were increased in neurons in the motorand 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 asjuveniles showed an increase in dendritic length but a decrease in spine density. In otherwords, the same environmental manipulation had qualitatively different effects on theorganization of neuronal circuitry in juveniles than in adults. To pursue this finding, an infant animals was given 45 min of daily tactile stimulationwith a little paintbrush (15 min three times per day) for the first 3 weeks of life. Thebehavioral studies results showed that this seemingly benign early experience enhancedmotor and cognitive skills in adulthood. The anatomical studies showed, in addition, that inthese animals there was a decrease in spine density but no change in dendritic length incortical neurons; yet another pattern of experience-dependent neuronal change. The result ofthe studies showed that experience can uniquely affect the developing brain which leads towonder if the injured infant brain might be repaired by environmental treatments. It was notsurprising when it was found that post injury experience, such as tactile stroking, couldmodify both brain plasticity and behavior because it has been proven that such experienceswere powerful modulators of brain development (Kolb, Gibb, & Gorny, 2000). What wassurprising, however, was that prenatal experience, such as housing the pregnant mother in acomplex environment, could affect how the brain responded to an injury that it would notreceive until after birth. In other words, prenatal experience altered the brain’s response toinjury later in life. This type of study has profound implications for preemptive treatments ofchildren at risk for a variety of neurological disorders. (Kolb B, Gibb R, Robinson, T, 2003)Psychoactive Drugs
  11. 11. 11 Many people who take stimulant drugs like nicotine, amphetamine, or cocaine do sofor their potent psychoactive effects. The long-term behavioral consequences of abusing suchpsychoactive drugs are now well documented, but much less is known about how repeatedexposure to these drugs alters the nervous system. One experimental demonstration of a verypersistent 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 smallincrease in motor activity (e.g., locomotion, rearing). When the rat is given the same dose onsubsequent occasions, however, the increase in motor activity increases, or sensitizes, and theanimal may remain sensitized for weeks, months, or even years, even if drug treatment isdiscontinued. Changes in behavior that occur as a consequence of past experience, and can persistfor months or years, like memories, are thought to be due to changes in patterns of synapticorganization. The parallels between drug-induced sensitization and memory led to thequestion whether the neurons of animals sensitized to drugs of abuse exhibit long-lastingchanges similar to those associated with memory (e.g., Robinson & Kolb, 1999). Acomparison of the effects of amphetamine and saline treatments on the structure of neurons ina brain region known as the nucleus accumbens, which mediates the psychomotor activatingeffects of amphetamine, showed that neurons in the amphetamine-treated brains had greaterdendritic material, as well as more densely organized spines. These plastic changes were notfound throughout the brain, however, but rather were localized to regions such as theprefrontal cortex and nucleus accumbens, both of which are thought to play a role in therewarding properties of these drugs. Later studies have shown that these drug-inducedchanges are found not only when animals are given injections by an experimenter, but alsowhen animals are trained to self-administer drugs, leading us to speculate that similar changesin 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 twoexamples that have just been discussed. For instance, brain injury disrupts the synapticorganization of the brain, and when there is functional improvement after the injury, there is acorrelated reorganization of neural circuits (e.g., Kolb, 1995). But not all factors act the sameway across the brain. For instance, estrogen stimulates synapse formation in some structuresbut 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 producesan enduring change in behavior leaves an anatomical footprint in the brain. (Kolb B, Gibb R,Robinson, T, 2003)Applications and ExamplesTreatment of brain damage
  12. 12. 12 A surprising consequence of neuroplasticity is that the brain activity associated with agiven function can move to a different location; this can result from normal experience andalso occurs in the process of recovery from brain injury. Neuroplasticity is the fundamentalissue that supports the scientific basis for treatment of acquired brain injury with goal-directed experiential therapeutic programs in the context of rehabilitation approaches to thefunctional consequences of the injury. The adult brain is not "hard-wired" with fixed neuronal circuits. There are manyinstances of cortical and subcortical rewiring of neuronal circuits in response to training aswell 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. Theevidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, butcurrent research has revealed that other parts of the brain, including the cerebellum, may beinvolved 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 structuresincluding the cerebral cortex. The specific details of how this process occurs at the molecularlevels and are still an active topic in neuroscience research. The manner in which experiencecan influence the synaptic organization of the brain is also the basis for a number of theoriesof brain function including the general theory of mind and epistemology referred to as NeuralDarwinism and was developed by immunologis Gerald Edelman. The concept ofneuroplasticity is also central to theories of memory and learning that are associated withexperience-driven alteration of synaptic structure and function in studies of classicalconditioning in invertebrate animal. Paul Bach-y-Rita, deceased in 2006, was the "father of sensory substitution and brainplasticity.” In working with a patient whose vestibular system had been damaged hedeveloped BrainPort, a machine that "replaces the vestibular apparatus and send balancesignals to the brain from the tongue."] After the machine was used for some time it was nolonger necessary, as the patient then regained the ability to function normally. Plasticity is the major explanation for the phenomenon. Because the patient’svestibular system was "disorganized" and sending random rather than coherent signals, theapparatus found new pathways around the damaged or blocked neural pathways, helping toreinforce the signals that were sent by remaining healthy tissues. Bach-y-Rita explainedplasticity by saying, "If you are driving from here to Milwaukee and the main bridge goesout, first you are paralyzed. Then you take old secondary roads through the farmland. Thenyou use these roads more; you find shorter paths to use to get where you want to go, and youstart to get there faster. These "secondary" neural pathways are "unmasked" or exposed andstrengthened as they are used. The "unmasking" process is generally thought to be one of theprincipal ways in which the plastic brain reorganizes itself." (Colota V.A, Rita P.B, 2002) Randy Nudos group found that if a small stroke (an infarction) is induced byobstruction of blood flow to a portion of a monkey’s motor cortex, the part of the body that
  13. 13. 13responds by movement will move when areas adjacent to the damaged brain area arestimulated. Understanding of interaction between the damaged and undamaged areas provides abasis for better treatment plans in stroke patients. Current research includes the tracking ofchanges 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 alsoinvolved in studying the treatment plans that may enhance recovery from strokes, such asphysiotherapy, 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, explainsimprovements in functional outcomes with physical therapy post stroke. Rehabilitationtechniques that have evidence to suggest cortical reorganization as the mechanism of changeinclude Constraint-induced movement therapy, functional electrical stimulation, treadmilltraining with body weight support, and virtual reality therapy. Robot assisted therapy is anemerging technique, which is also hypothesized to work by way of neuroplasticity, thoughthere is currently insufficient evidence to determine the exact mechanisms of change whenusing this method. Jon Kaas, a professor at Vanderbilt University, has been able to show "howsomatosensory area 3b and ventroposterior nucleus of the thalamus are affected by longstanding unilateral dorsal column lesions at cervical levels in macaque monkeys. Adult brainshave the ability to change as a result of injury but the extent of the reorganization depends onthe extent of the injury. His recent research focuses on the somatosensory system, whichinvolves a sense of the body and its movements using many senses. Usually when peopledamage the somatosensory cortex, impairment of the body perceptions are experienced. He istrying to see how these systems (somatosensory, cognitive, motor systems) are plastic as aresult of injury. (Young J.A, Tolentino, M., 2011)Meditation A number of studies have linked meditation practice to differences in corticalthickness or density of gray matter. One of the most well-known studies to demonstrate thiswas led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientistat the University of Wisconsin, has led experiments in cooperation with the Dalai Lama oneffects of meditation on the brain. His results suggest that long-term, or short-term practice ofmeditation results in different levels of activity in brain regions associated with such qualitiesas 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 mayhave been previously injured, yet are otherwise currently healthy. This phenomenon is relatedto neuroplasticity due to a maladaptive reorganization of nervous system, both peripherallyand centrally. During the period of tissue damage, noxious stimuli and inflammation cause an
  14. 14. 14elevation of nociceptive input from the periphery to the central nervous system. Prolongednociception from periphery will then elicit a neuroplastic response at the cortical level tochange its somatotopic organization for the painful site, inducing central sensitization. Forinstance, individuals experiencing complex regional pain syndrome demonstrate a diminishedcortical somatotopic representation of the hand contralaterally as well as a decreased spacingbetween the hand and the mouth. Additionally, chronic pain has been reported to significantlyreduce the volume of grey matter in the brain globally, and more specifically at the prefrontalcortex and right thalamus. However, following treatment, these abnormalities in corticalreorganization and grey matter volume are resolved, as well as their symptoms. Similarresults have been reported for phantom limb pain, chronic low back pain and carpal tunnelsyndrome. ( The structure of the brain is constantly changing in response to an unexpectedly widerange of experiential factors. Understanding how the brain changes and the rules governingthese changes are important not only for understanding both normal and abnormal behavior,but also for designing treatments for behavioral and psychological disorders ranging fromaddiction to stroke. Although much is now known about brain plasticity and behavior, manytheoretical issues remain. Knowing that a wide variety of experiences and agents can altersynaptic organization and behavior is important, but leads to a new question: How does thishappen? This is not an easy question to answer, and it is certain that there is more than oneanswer. 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 canchange? 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 rulesgoverning when one or the other might occur? This question leads to another, which iswhether 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 skilllike playing the piano? Consider, too, the issue of the permanence of plastic changes. If aperson stops smoking, how long do the nicotine-induced plastic changes persist, and do theyaffect 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 goodthing, it is reasonable to wonder if plastic changes might also be the basis of pathologicalbehavior. Less is known about this possibility, but it does seem likely. For example, drugaddicts often show cognitive deficits, and it seems reasonable to propose that at least some ofthese deficits could arise from abnormal circuitry, especially in the frontal lobe. (Kolb B,Gibb R, Robinson, T, 2003)
  15. 15. 15 Bibliography 1. Colota, V.A, Rita. PB, Shepherd Ivory Franz: His Contribution to neuropsychology and rehabilitation. Cognitive Affective and Behavioral Neuroscience 2002, 2(2), 141- 148 2. Davidson, R.J, Lutz Antoine, Buddha’s Brain: Neuroplasticity and Meditation, January 2008 3. Frost, S. B., Barbay, S, Friel K. M. et el, Reorganization of Remote Cortical Regions After Ischemic Brain Injury A Potential Substrate for Stroke Recovery : J Neurophysiol 89: 2003, 3205–3214,
  16. 16. 16 4. Gage, F.H, Neurogenesis In The Adult Brain. Journal of Neuroscience. Feb 1st 2002, 22(3) 612-613 5. Kandel, Schwatz, Principle of Neural Science, Mcgrawhill Medical ed 4th, January 2000, Chapter 55 6. Kolb B, Gibb R, Robinson, T, Brain plasticity and behavior, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Alberta, Canada (B.K., RG.), and Department of Psychology, University of Michigan, Ann Arbor, Michigan (T.R.), 2003 7. National Institute of Neurological Disorders and Stroke, 2003 8. Wibowo D.S, Neuroanatomi Untuk Mahasiswa Kedokteran, Bayumedia Publishing Malang, Juli 2008 9. www. 10. www.whatisneuroplasticity .com, last updated 2010 11. 12. Young, J. A., & Tolentino, M. (2011). Neuroplasticity and its Applications for Rehabilitation. American Journal of Therapeutics. 18, 70-80.