Enhancing Recovery of Function after Traumatic Brain Injury
Abstract:
Until recently, recovery of function after a traumatic brain injury (TBI) has been thought to be a vain pursuit; the neurological transformations were thought to be irreversible. However, the phenomenon known as plasticity allows brain tissue to grow and integrate with other tissue after trauma. Whereas a healthy brain maintains its plasticity, a brain after a TBI can only form new neural connections through constant stimulation and enriched environments, achieved through therapy (after spontaneous recovery occurs). Rehabilitation facilitates therapy and therapy directs dendrite growth, which can ultimately restore recovery of function after TBI. The current direction of rehabilitation, however, emphasizes compensation (e.g. functional remediation) for lost abilities rather than the restorative approach to rehabilitation. By looking at various conventional and future approaches to recovery of function, this document argues for the utilization and manipulation of the brain’s neuroplastic capabilities using the remediation approach to optimize person’s quality of life after TBI.
The brain holds within itself an amazing capacity to heal after trauma, allowing for some degree of recovery of function. New treatments and therapies can facilitate the brain’s natural healing capability and promote recovery of function of impairments following a traumatic brain injury (TBI). This area is an exciting, emerging field of interest, especially when considering its possible positive ramifications on the medical field and rehabilitation community—not to mention the lives of individuals who have sustained TBIs.
While physical rehabilitation is mostly concerned with compensation of losses, cognitive rehabilitation (CR) after brain injury remains relatively an untapped and unexplored dichotomy. While there are numerous scientific articles on the brain’s innate ability to achieve recovery of function through plasticity, there has been little, if no research implemented in the area of CR in relationship to recovery of function after TBI. The two CR techniques, the functional and restorative approaches are constantly debated for their practical rehabilitation benefits after brain injury. Unfortunately, a compromise has not yet been reached.
The purpose of this document is to discuss the scientific mechanisms of the brain’s ability for recovery of function and to advocate for the restorative approach to rehabilitation/ remediation after TBI. The neurologically based recovery of function phenomenon has enormous implications to an individual’s physical and cognitive recovery. This document gives an initial overview of the discovery of and two descriptive alternatives of the recovery of function phenomenon. It briefly examines present and future strategies to enhance recovery of function through the use of pharmacological approaches, genetic-based therapy and transplantation of neural/adult stem cells. Finally, a synopsis of the positive ramifications a neuroplastic-centered approach has on the cognitive aspects of recovery of function after TBI is presented.
History and Literature Review
Margaret Kennard is the American pioneer of the 1930s and early 40s who experimented with brain lesions in primates and introduced two important terms: sparing, “the absence of expected behavioral abnormalities” and recovery of function, “deficits that diminish in severity or disappear entirely” after injury to the brain (Finger S., 1999, 273). Although she was not the first person to study or to discover a law surrounding recovery of function, Finger notes that “[t]hanks to her efforts, growth and development became even more dynamic and important considerations to researchers and clinicians interested in the effects of brain damage” (1999, 280). Kennard believed that reorganization occurred within the damaged systems of the brain rather than in unrelated structures (Almli C. & Finger S., 1992). Her three most important ideas on recovery of function included:
The close relationship between normal growth and the reactive neural growth seen after injury
The notion that remaining elements within the same neural system are those most likely to account for improved performance
The belief that the capacity for functional reorganization diminishes as elements with in the system mature and become ‘committed’ to specific functions (Almli C. & Finger S., 1992, 73).
Kennard conclusively believed if neural reorganization does take place it is in spared parts of the damaged system. In her experiments with adult primates, significant sparing and recovery of function were exhibited over-time, especially if brain lesions were made in stages rather than all at once. Margaret Kennard was a major influence on the thinking surrounding recovery of function, helping to launch the modern era of research in this area.
Over the years, researchers have defined the term recovery of function in different ways. The present day definition of recovery of function following a TBI is described as enhancing the potential for functional recovery, involving two alternatives: “(1) to prevent nerves cells from dying (neuronal sparing) [emphasis added] and (2) to control subsequent growth of nerve cells that survive the injury (neuronal reorganization) [emphasis added]” (Almli C. & Finger S., 1992, 73).
The first recovery of function alternative promotes the prevention of nerve cell death, which is caused by a disruption of the blood supply to and within the brain damaged regions. This disruption of blood supply results in the death of additional nerve cells within the brain (tertiary death) (Almli C. & Finger S., 1992). This disruption of the blood supply may also cause healthy tissue surrounding the brain lesion to absorb excessive calcium to a toxic degree and can result in additional neuronal depletion (Almli C. & Finger S., 1992). Therefore, prevention of secondary brain damage is dependent upon the sufficient blood supply to the brain.
The second recovery of function alternative involves the growth of surviving cells. These nerve cells change in morphology and function, which is known as the neural reorganization phenomena. This alternative includes denervation supersensitivity, “an increase in neurotransmitter sensitivity by nerve cells following a loss of some of their inputs” (Almli C. & Finger S., 1992, 74). This increase in neurotransmitters can either result in the preservation of synoptic functioning, which can cause brain injury symptoms to disappear or it can exaggerate brain injury symptoms (Almli C. & Finger S., 1992). Therefore, the prevention of secondary damage after injury is also contingent on the growth of surviving brain cells.
The second alternative also involves the neural reorganization phenomenon, reactive synaptogenesis or otherwise known as axon collateral sprouting. Reactive synaptogenesis is “the growth and establishment of ‘new’ synapses at sites vacated by other axons that are degenerating or dying following brain injury” (Almli C. & Finger S., 1992, 75). This innate phenomenon of reactive synaptogenesis has enormous repercussions for the TBI rehabilitation community. However without further research on the possible rehabilitative implications of neural reorganization, it is still unknown whether or not these new synaptic connections contribute to the recovery of function, to additional TBI sequelae or are benign.
As documented above, it has be scientifically documented that neural reorganization and denervation supersensitivity and reactive synaptogenesis do occur following TBI. However, recovery of function still depends upon a number of unknown factors. Therefore, a tremendous amount of research is still needed to identify the brain chemicals (eg. nerve growth factors) that influence the consequent survival and growth of neural cells after TBI.
Brain Regeneration
It wasn’t until the discovery of neurotrophic factors (NTFs), a specific type of nerve growth factor that occurs naturally as proteins in the brain, which promote the growth, and survival of neurons during development and after trauma, that scientists believed brain cells could redevelop after TBI (Dixon, 2002). These neurotrophic compounds may help to stimulate synaptic regeneration, improve synaptic efficacy and enhance other neurocellular processes (National Institutes of Health [NIH], 2002). A neuron may acquire NTFs in one of three ways:
“(1) from its target tissue, neuronal or non-neuronal, (2) from neighboring neurons and other cells or (3) from itself.” (Lipton P. & Kalil R., 1995, ¶4).
NTFs play a role in promoting plasticity by helping adult neurons maintain and regenerate their processes (Society for Neuroscience, 1994). Scientists are looking at ways to harness NTFs to encourage the regrowth of damaged neurons and to improve neurological damage. NTFs play a key component in developing and keeping brain cells alive, while simultaneously supporting healthy adult neurons throughout (Society for Neuroscience, 1994). NTFs fit into neuron receptors much like a key fits into a lock (Society for Neuroscience, 1994). Physical exercise has also proven to increase the production of NTFs in the brain and therefore, is beneficial in augmenting recovery of function (Johnson D.A., Ruston S & Shaw J., 1996). Therefore, it is evident that NTFs play a vital role in sustaining normal brain functioning.
Recent research has shown that NTFs are: (1) present in early development of the nervous system and responsible for the initial growth and development of neurons in the peripheral and central nervous systems; (2) released by target tissue of growing neurons and determine whether a neuron reaches its target development (those that don’t reach the target die) and (3) capable of making damaged neurons regrow their processes in a test tube and in animal models (Society for Neuroscience, 1994). These three findings represent exciting possibilities for reversing devastating degenerative neurological disorders like TBI. The use of NTFs as therapeutic agents may be years away; however, continued research in this area holds tremendous promise.
Pharmacological approaches
Prevention of secondary or tertiary neuronal death using drugs is also an important current component for recovery of function after TBI. Post-acute administration of neurotransmitter agonists, “drugs that bind to receptor sites and stimulate receptors’ function” have shown to enhance synaptic functioning (Venes D., 2001, 58). This type of neurotransmitter replacement therapy is accomplished through increasing levels of absent or dormant neurotransmitters to supplement the rehabilitation process. Pharmacological strategies have been reported to improve recovery of function most consistently (Dixon C., 2002).
As previously mentioned, when healthy tissue in the region of the brain lesion takes on excessive calcium to the degree of being toxic, it can and can result in additional brain cell death (Almli C. & Finger S., 1992). However, the pharmacological drug knows as nimodipine can be administered post-injury and acts as a calcium blocker to prevent subsequent neuronal death (Almli C. & Finger S., 1992). This drug has shown considerable potential for reducing behavioral impairments subsequent to TBI. These ‘new’ drugs or pharmacological agents help to decrease neuronal depletion and also have potential to improve functional recovery in rehabilitation through: (1) reducing neurobehavioral deficits, (2) the remediation of post-concussional symptoms, (3) improving motor functioning and 4) improving cognitive functioning (Almli C. & Finger S., 1992).
Two of the most commonly used psychoactive, stimulating drugs that enhance or change synaptic function are Amantadine hydrochloride (amantadine) and methylphenidate. Both these drugs have been tested and found useful in promoting recovery of function (Dixon C., 2002). In several uncontrolled case studies, it was suggested that amantadine might also improve neurobehavioral deficits (Dixon C., 2002). Likewise, evidence has also been documented to
show that methylphenidate facilitates recovery in the domains such as: anger, attention, memory deficits and significantly increases positive behavioral changes (Dixon C., 2002). Pharmacological compounds can enhance the benefits of rehabilitation therapies through “psychoactive drugs that stimulate appropriate neurotransmitter pathways;” however, despite the increasing possibilities of pharmacological agents to enhance recovery of function after TBI, focus still needs to concentrate on the rehabilitative phase (NIH, 2002, ¶4).
Pharmacological agents also have the potential to enhance functional recovery in rehabilitation, especially when used in combination with behavioral and physical therapies.
Drugs that reduce a patient’s chronic pain and/or fatigue could be used in combination with exercise to enhance health benefits and promote recovery of function (NIH, 2002).
Genetic-Based Therapy
Future advances in brain injury rehabilitation include gene therapy, “the deliberate alteration of the genetic material of the body’s cells to prevent or treat disease” (Biotechnology Programme, 2001, ¶1). According to Dr. Kenneth L. Brigham, M.D., the director of the Center for Lung Research and Joe and Morris Werthan Professor of Investigative Medicine at
Vanderbilt University, gene therapy, he predicts, is that genetic-based therapy will be the major therapeutic advance in the next two decades (Vanderbilt University Medical Center, 1996, ¶3).
Somatic gene therapy is “a strategy in which a nucleic acid, typically in the form of DNA, is administered to alter the genetic repertoire to target cells for therapeutic purposes” (Helm G., 1999 35). Genetic-based therapy is achieved when “the defective gene is…replaced by a normal version of the gene” (Biotechnology Programme, 2001, ¶1). One such method of transfer can be done through a direct injection of “gene therapy vectors [agents used to introduce genetic material into a cell’s nucleus] into specific brain regions” (Helm G., 1999, 35). Neurogenetic therapy is possible with TBI because the injury allows for external agents to act upon the brain (Hayes, R.L, 1997). While intricately and medically involved, this contemporary therapy can access the genetic root of recovery of function after brain injury.
In fact, the discovery of neurotrophic factors, which promote the growth and survival of neurons during development and after trauma, has led to the genetic transfer known as ex vivo, cultured transplant of genetically modified tissue. This genetic transfer could be suitable for treatment in genetic therapy after brain injury. Although genetic therapy hold enormous implications for individuals with brain injury, before the gene therapy can be attempted at the ex vivo level, several gaps need to be bridged (Hayes, R.L, 1997).
Future applications of gene therapy could possibly improve neuronal plasticity and axonal regeneration (Helm G., 1999). An even greater benefit of gene therapy, however, is “the potential for growing nerve fibers that have been severed during initial injury” through the utilizing neurotrophic factors or by using gene therapy to “turn-off the effects of proteins” that inhibit nerve fiber growth (Helm G., 1999, 36). There is no doubt that gene therapy is a complex concept, but the bottom line is that gene therapy is advantageous when compared to standard pharmacological interventions. These advantages could be “utilized by neuroscientists and clinicians alike to improve brain function” (Helm G., 1999, 35). However, since there is with only superficial knowledge surrounding the mechanisms of gene therapy to restore or enhance nerve regeneration, further research is needed before human trials can commence.
Neural/Adult Stem Cells
Brain stem cells, which have the almost magical ability to make every other type of brain cell, including more of itself, have tremendous promise for potential treatment for brain injury (McDeavitt J. & Kanelos S., 1998). Enormous implications surround the use of brain stem cells to enhance recovery of function. The procedure for stem cell transplantation, in simple terms, is through the injection of brain stem cells into the “putamen area of the brain” and from there the stem cells miraculously migrate to damaged areas of the brain to “make healthy copies of the wrecked cells and correct the disorder” (Kotulak, 1999, A16). These processes of migration and self-repair occur naturally within the body. The stem and brain cells communicate with each other using a chemical language to heal the damage.
There are two possible approaches for utilizing stem cell repair. The first strategy is through a “cell replacement…to achieve structural brain repair” in which “stem cells are isolated from CNS tissue” and grafted into the brain (Peterson, 2002, 38). The second strategy and a more difficult procedure is to “recruit endogenous neural stem cells to proliferate, migrate and differentiate into appropriate functional neurons” thereby achieving self-repair (Peterson, 2002, 38). The key to stem cell repair is learning how to magnify a person’s stem cell production in order to replaced damaged brain cells (Kotulak, 1999).
Jack M. Parent, M.D., a neurologist and assistant professor of neurology at the University of Michigan is focusing his research on understanding how the “self-repair mechanism works [to] someday help physicians reduce brain damage” (University of Michigan, 2002, ¶1). Through experiments with rats, he discovered that epileptic seizures or strokes caused “neuroblasts—cells midway in development between a stem cell and a fully developed neuron—to multiply and form neural chains that [can migrate] across the brain to the site of injury”
(University of Michigan, 2002, ¶2). Parent is investigating common cues that activate neuroblasts’ development and growth. One such study involves growth factors or neurotrophic factors that stimulate the creation and migration of neuroblasts (University of Michigan, 2002). It has also been determined that migration of neuroblasts after brain injury “may not always be beneficial… [and] may lead to seizures” (University of Michigan, 2002, ¶10). The consequences could be harmful. Therefore, “many years of research at the molecular level and in animals will be necessary before human clinical trials could even be considered” (University of Michigan, 2002, ¶4). However, as scientific and medical communities’ understanding of neuroblasts evolve so will their understanding of the intricate functioning of neuroblasts’ relevance to recovery of function after TBI.
Plasticity, Rehabilitation and Environmental Enrichment
Recovery, in general, is typically enhanced with the exposure to enriched environments and rehabilitation, therefore, recovery is ultimately a re-learning process. However, fatigue often inhibits a patient’s level of effort, duration, endurance and quality of all activities. Physical exercise as a type of stimulation has proven to have “unequivocal benefits on [a person’s] physical and mental status” (Johnson D.A., Ruston S. & Shaw J., 1996, 248). The continuation of physical exercise is a important after brain injury.
“[M]any of the mechanisms that drive initial neuronal development reappear during regeneration and recovery” and are augmented through exposure to an enriched environment (NIH, 2002, ¶3). This reiterates why therapeutic exercise is of vital importance when used in conjunction with enriched environments—because it stimulates and regenerates neural pathways (NIH, 2002). Environmental feedback and stimulation are critical components in recovery of brain function (Perna R., 2002). “The more complex the task the greater the advantages” because environmental enrichment promotes a “variety of structural and functional changes in the brain” (Johnson D.A., Ruston S. & Shaw J., 1996, 249).
Plasticity is defined in the Taber’s Cyclopedic Medical Dictionary 19the Edition as “1) the ability to be molded; 2) the ability of tissues to grow or integrate with others during development, after trauma, or after an illness” (1674). Likewise, regeneration is a component of plasticity and is defined as “[r]epair, regrowth or restoration of a part such as tissue” (Venes, 2001, 1850). Therefore, the terms plasticity and regeneration are intimately connected and appear to be closely associated to the recovery of function principle. Until few years ago, it was previously believed that “younger, less mature tissue may display greater potential for growth” (McDeavitt J. & Kanelos S., 1998, 40). However, it has been discovered that “[t]he relationship between brain plasticity and age is simply not linear” (Perna R., 2002, 32). New neurons can be produced from adult stem cells (e.g., adult neurogenesis) and that stem cell regeneration also continues throughout life (University of Michigan, 2002). This discovery has “overturned the long-held dogma that neurons are formed exclusively before birth” (Peterson, 2002, 34). A healthy brain maintains a certain level of plasticity and functional reorganization throughout life. It can occur in four stages:
developmental plasticity—when the immature brain first begins to process sensory information
activity-dependent plasticity—when body changes affect the balance of sensory activity received by the brain
plasticity of learning and memory—when behavior is altered based on new sensory information
injury-induced plasticity—which occurs after brain trauma
(John F. Kennedy Center, 1999).
In order to develop interventions to overcome the sequelea of brain injury, it is extremely important to understand the underlying factors of brain plasticity because “recovery of function tends to be equated with plasticity” (Perna R., 2002, 32).
Another name for brain plasticity is neuroplasticity, “the ability of the brain to alter function and structure as a result of experience” (Gray D.S., 2002, 32). Neuroplasticity reinforces neuronal growth, function, structure and allows for change, which can be as beneficial as a surgeon’s knife (Gray D.S., 2002). Neuroplasticity is proof that the brain can “shift resources to meet a task at hand to at least some extent and perhaps more than previously expected: [recovery] can happen spontaneously or be influenced by experience—both in terms of enriched environment and specific therapies even late after injury” (Gray D.S., 2002, 42). This concept reiterates how beneficial rehabilitation is after TBI; it promotes dendrite growth and this growth is paramount in a patient’s level of recovery. New brain connections must be ‘trained’ and ‘retrained’ through continual repetition and interaction with a patient’s environment.
A patient’s pre-injury and post-injury experiences are vital in his/her degree of recovery. When discussing the level of neuroplasticity after TBI, one must take into consideration a patient’s pre-morbid level of brain activity. The more active a person’s brain is before injury, the better his/her chances for recovery due to existing pre-wired brain circuitry. “Good recovery is always correlated with enhanced connectivity, whereas poor recovery is correlated with an absence of reorganized connectivity” (Perna R., 2002, 33). Neuroplasticity is the guiding principle behind the recovery of function phenomena after brain injury.
Cognitive Rehabilitation
From the cumulative discussions addressed so far, concerning the amazing possibilities of neuroplasticity, it can be deduced that recovery of function is theoretically viable after TBI. Therefore, recovery of function in this sense not only encompasses the visible, physical aspects of lost functions, but it also encompasses those neurological functions invisible to the human eye, e.g. those involving cognitive deficits.
The techniques used in cognitive rehabilitation (CR) can be dated back to the times of the ancient Greeks, although it wasn’t until after World War II that CR was recommended as a method of intervention for soldiers who had sustained head injuries (Mickey D. & Stoll, J., Sindberg, H, Ross, R., Chiang, C., Dunlop, D, 1998.). In 1974, Michael Mahoney of Pennsylvania State University wrote, “[m]an is viewed as a complex organism capable of impressive adaptation” and that “[h]e is in a continuous reciprocity relationship with his environment” (145). Continuing the discussion on his fundamental philosophy concerning the cognitive learning model, Mahoney states that man’s behavioral changes are influenced by “the current physiological state of the organism, his past learning history, the existing environmental situation and a variety of interdependent cognitive processes” (145). Mahoney asserts that man’s “awesome complexity derives from his extensive evolutionary definition”, which can be witnessed through his three mutually dependent nervous systems: the central, somatic and autonomic (145). Thereby, the “[o]ne cardinal characteristic of the cognitive learning perspective is its view of man as an active element in his own growth and development” (146).
But what if man’s central nervous system was disrupted or in fact damaged by a TBI. Can Mahoney’s cognitive learning model, which capitalizes on man’s innate capacity for change actually be possible after TBI? If one considers the scientific principles surrounding recovery of function then yes, theoretically, cognitive remediation can and should be possible even after TBI. Ben-Yishay and Diller state, even though there has not been a clearly defined relationship between the neurological damage caused by TBI, recovery of brain function and CR techniques a relationship surely exists when investigating the recent studies of “neural plasticity an synaptic regeneration,…which point toward[s] a theoretical basis for brain injury rehabilitation” (1993, 206). However, the effectiveness of cognitive therapy in the treatment of patients with TBI has been a “controversial issue” (Jordan, B.D., 2000, 3123) because of the “[d]ifferences in conceptual/philosophical approaches to recovery of function after brain injury” (Ben-Yishay, Y. & Diller, L., 1993, 204). CR lacks scientific proof.
It has only been over the past 25 years that specialists in the field developed CR “techniques aimed at the restoration of cognitive skills and the training of functional abilities in persons with neurologically brain-base injury” (Rizzo, A.A. & Buckwalter, J.G., 1997, ¶5). It was not until a 1999 review that selective cognitive-behavioral rehabilitation techniques were in fact even recommended for effectively treating patients with TBI (Jordan, B.D., 2000).
Sohlberg and Mateer (1989) defined cognitive rehabilitation (CR) as a therapeutic process of increasing or improving a person’s capacity to process and use incoming information to increase functioning in everyday life. For an individual with brain injury, being able to function in everyday life includes being able to perform those unconscious routines used daily in life. CR is seen as:
as a means of remediation for disorders of perception, memory and language, (2) as the application of specific cueing systems for enhancing ability on specific functional tasks and (3) as systematic amelioration through intensive remedial training of interference in problem-solving ability in order to promote functional competence in a broader array of everyday life situations (Ben-Yishay, et al., 1993, 206).
Two CR methodologies are restorative and functional approaches. The recovery of cognitive function methods can be useful in retraining thinking abilities, which range from basic attention skills to higher logical functioning (Rizzo, et al., 1997). The aim of the restorative approach focuses on improving specific cognitive functions (NIH, 1998). The restoration process encourages the retraining of neurotransmitters in the brain, helping to establish new neural growth and reorganization, encouraging neuroplasticity. The goal of the second methodology, the functional approach, is to teach life skills that utilize existing abilities.
A list of general cognitive interventions has been formulated at the National Institutes of Health Consensus Development Conference. It encompasses a spectrum of viable possibilities for achieving recovery of function after TBI and includes: cognitive or academic exercises, computer-assisted training, compensatory technique training, use of external aids, communication skill training, psychotherapy, behavior modification, comprehensive interdisciplinary models, vocational rehabilitation, pharmacotherapy, physical exercise, physical therapy or aerobic training, art and music therapy, nutrition, spirituality [and] alternative or nontraditional therapies
(Jordan, B.D., 2000, 3124).
In addition, poetry therapy also seems to improve cognitive skills after TBI through the use of mnemonics, rhymes and mental imagery (Parent, R. & Anderson-Parente, J., Stapeton, M., 2001).
Alternative medicine or nontraditional therapies can include: meditation and/or relaxation therapy, myotherapy, music therapy, dance/movement therapy, Neuromuscular and Deep Tissue massage, chiropractic, acupuncture, nutritional support, homeopathy or holistic medicine. Virtual Reality (VR) technology, a relatively new technique has been found useful in retraining cognitive abilities after TBI. VR is “designed to simulate naturalistic environments” (Rizzo, A.A. & Schultheis, M., Kerns, K.A., Mateer, C., in press, ¶4). The future implications of VR technology for the rehabilitation of individuals with TBI are very promising because they offer “new opportunities for the development of innovative neuropsychological assessment and rehabilitation tools” that combines both the restorative and functional approaches to CR (Rizzo et al., in press, ¶1).
However, like most if not all neurologically based theories and techniques, the restorative and functional cognitive remediation approaches have criticisms, especially in regards to application and efficiency in the real world context. Criticism surrounding the restorative approach is that it relies too heavily on test materials or tasks that are artificial in any real world context, especially in the context of generating transferable, functional cognitive challenges. In this sense, the learning does not transfer or “generalize to performance outside the training environment” (Rizzo, et al., 1997, ¶6). The key criticism surrounding the functional approach is based on the generalized truth that the real world is not static. The functional approach uses route and stereotypical behaviors that do not transfer into real life situations—where daily circumstances and activities constantly change and are not routine, but rather individuals continually need to creatively modify behaviors in order to fit real-life events. Rizzo and Buckwalter have written that the restorative approach places its primary and more practical emphasis on teaching individuals “how to think”, while the objective of the functional approach teaches “individuals how to do” (1997, ¶8). However, to ultimately achieve recovery of function after brain injury an individual needs to utilize both the restorative and functional approaches. One approach can not be held in higher esteem than the other, but rather there needs to be an amalgamation of both approaches to ultimately benefit the individual with brain injury.
Despite the intrinsic difficulties in assessing CR and its “lack of rigorous scientific evaluation”, cognitive recovery is an essential part of the recovery process after TBI (Salazar, A.M. & Warden, D.L., 2000, 3075). Even though major limitations still exist within the field of rehabilitation due to its narrow focus of contemporary medical approaches that concentrate on the functional approach after brain injury (NIH, 1998), change is still possible. The philosophy of CR therapy now needs to turn towards including the restorative approach towards remediation after TBI. Rather than just focusing on enhancing an individual’s existing capabilities and learning to use compensatory strategies, the rehabilitation process after TBI should combine the restorative and functional approaches more effectively. In order to highlight the increasing possibilities of recovery of cognitive function after TBI, a combined philosophy of restorative and functional rehabilitation is needed to promote the individual’s short-term goals as well as his/her global (long term) outcomes (NIH, 2000).
Conclusion
Recovery of function has been defined, through the years, in different ways and likewise, there are various ways the brain can achieve recovery of function after a traumatic brain injury, both physically and cognitively. However, two definitions of recovery of function have been mainstreamed: neuronal reorganization and neuronal sparing. Neuronal reorganization or the rewiring of lost or damaged brain connections, neuroplasticity, has shown to have a positive effect on recovery of function and is associated with repetition of therapy and exposure to enriched environments.
A present strategy to enhance recovery of function is through the use of pharmacological drugs. Pharmacological compounds have proven successful in the increase of neuronal sparing when administered after a brain injury. This strategy not only increases neuronal sparing, but also helps to improve neurobehavioral deficits, motor functioning, recovery of cognitive functioning and remediation of post-concussional symptoms. Pharmacological agents have also promoted recovery of function when used in conjunction with rehabilitation and physical exercise. Environmental feedback and stimulation are also crucial aspects used to promote recovery of brain function.
Genetic-based therapies and stem cell transplantations are two flourishing and optimistic procedures to enhance recovery of function after TBIs—hopefully to be realized in the near future. Gene therapies have the potential to possibly improve: neuronal plasticity, axonal regeneration, growth of severed nerve fibers and the ability to turn-off the damaging effects of some proteins that inhibit nerve fiber growth. Stem cell transplantation is another vital alternative in recovery of function after TBI—with the potential to replace lost nerve cells and/or assists in reestablishing neural regeneration. Further research, however, is still needed before human trials can begin.
The future of brain injury research appears to be very promising in relation to recovery of function after TBI. However, regardless of future strategies, presently, children, adolescences and adults can still make extraordinary functional recoveries after TBI. Not only can recovery of function be achieved on a physical level, but it is also possible at the cognitive realm due to the brain’s remarkable plasticity.
Two techniques frame the process of CR after TBI, the restorative and functional approaches. Unfortunately, an amalgamation of both approaches has been implausible because of the practical value of each contrasting rehabilitative approach has been persistently disputed by its opposition. The criticism surrounding the restorative approach is that it is artificial and not realistic, while the criticism surrounding the functional approach is that it only teaches what to do and does not teach how to think.
However, despite this lack of compromise in CR techniques, the scientific proof of plasticity still exists. The brain is not a static organ. As a person grows older, the brain maintains its plasticity. It is clearly dynamic. As quoted by the afore mentioned Jack Parent, MD, “You don’t have to perfectly rebuild the brain to improve significantly the patient’s quality of life after a [TBI]… [i]f we could learn how to repair even half the damage, it may be enough”
(University of Michigan, 2002, ¶12). Parent’s sentiment reiterates the neuroplastic principle that if any level of recovery of function is attainable and can improve an individual’s life for the better after TBI, recovery of function is a worthwhile pursuit. Neuroplasticity is a viable opportunity still yet to be fully addressed, explored and embraced by the brain injury community.
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