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Post-Brain Injury Recovery and Plasticity Essay

Executive Summary

The human body system is highly complex. Most important, it adapts to meet various body needs through various functional systems. The nervous system, for instance, has some specialized functions. However, these functions are impaired when the system is injured. The purpose of this biological essay was to demonstrate how the human body system, specifically the nervous system, could enhance recovery after the brain injury as most neuroscience researchers have shown. After TBI or stroke, notable molecular, cellular, and network structures undergo regeneration to support and allow undamaged sections of the brain to reorganize and support impaired functions. These processes illustrate the adaptive and resilient nature of the human body system. There are recovery events that demonstrate plasticity of the brain, for instance. It is, however, imperative to note that adaptive could be beneficial or detrimental based on neurorehabilitative conditions (inhibiting or facilitating conditions). Today, neuroanatomical and neurophysiological alterations in the motor system triggered after an injury now offer novel ways to understand post-injury plasticity, as well as opportunities for therapeutic interventions for injured patients.


The human body system has changed over time to transform itself into a complex ecosystem made up of complicated web of smaller sub-systems, each focused on meeting specific body requirements, individually and as an integrated unit. Generally, the system works without human cognition or intervention. However, any disruption of balance and power of the human body has some advance effects. The nervous system, as component of the body system, is constituted in a manner that allows for vital recovery and resilience after critical functions are affected by injuries in an adult brain. For instance, following stroke, the most striking and sudden recovery in a motor activity takes place in less than 30 days, although case of moderate and critical stroke may last for about 90 days (Dancause and Nudo 273). The recovery patterns following focal traumatic brain insult are the same, but diffused insults usually need elongated periods. The neural bases responsible for the recovery, specifically when certain rehabilitative therapies are not available, have interested researchers and clinicians for several years (Nudo 887). In the last 25 years, for instance, contemporary neuroscience studies, including neuroanatomical, neurophysiological, and neuroimaging have greatly concentrated on this issue, resulting in amazing findings based on the extent of structural and functional plasticity of the central nervous system. The purpose of this biological essay is to demonstrate how human body system, specifically the nervous system, can enhance recovery after the brain injury.

Theoretical Perspectives

Some theoretical aspects have been fronted to explain the recovery in the absence of rehabilitation – a case referred to as spontaneous recovery. Three basic theoretical explanations have been proposed. First, during the diaschisis when the remote components linked to the area of the insult normally experience temporary reduced metabolism and blood supply, it is generally observed that the recovery process could be responsible for this phenomenon. Second, alteration in muscle and joint kinematic activities are noted after the cortical damage, and compensatory activities are usually introduced to perform roles in either restrained or critically various ways. Finally, the nervous system is subjected to a recovery process involving local and distant regeneration. While it is acknowledged that the process is adaptive, cases of maladaptive plasticity may also take place. Research activities focused on post-injury adaptive plasticity using “long-term potentiation, long-term depression, unmasking, synaptogenesis, dendritogenesis, and functional map plasticity” (Dancause and Nudo 273) have increased over the past years and are perhaps the most exhilarating aspects in the area of neuroscience because of their suggestions for comprehending and handling insult-related functional shortfalls.

The theory of vicariation has been advanced to explain different plasticity means responsible for functional recovery. That is, the ability of a given section of the brain to temporarily intervene for another. Given that the current views of brain structures appreciate the cerebral cortex as distributed in hierarchical manner, vicariation does not essentially need a completely unrelated feature to take over functions lost after the insult. Instead, other linked distributed components of the brain support functions of the impaired parts. In fact, it is demonstrated that the motor cortex of fully-grown mammals alters its functional patterns as a reaction to cortical insults (Dancause and Nudo 273).

Plasticity and Resilience

Resilience reflects the dynamic ability involving positive adaptation following a critical adversity. Implied within this idea are two major factors: (1) exposure to a severe adversity of threat; and (2) the realization of positive adaptation irrespective of the extent of the insult (Luthar, Cicchetti and Becker 543). Hence, these studies demonstrate the resilience nature of the human body system through brain plasticity after some adverse events. Years of research in the cerebral cortex have shown multiple physiological and anatomical instances of cortical plasticity. In fact, most cortical areas have demonstrated such plasticity, including the motor cortex and somatosensory cortex. These areas are extremely imperative for comprehending motor recovery processes after brain insults. These processes related to plasticity result from multiple endogenous and exogenous factors, but behavioral experience is noted as extremely critical. Behavioral needs are responsible for influencing budding features of every cortical area. Major activities noted are mainly replication and sequential coincidence. For instance, skilled motor functions that need the exact sequential coordination of muscles and joints have to be developed through repetitive processes. Repetitive processes are believed to facilitate the development of distinct modules in which the conjoint function is represented as a whole.

Possible explanations for brain plasticity in adults are currently available in neuroscience studies. It is observed that brain development involving guidance cues depends on activity-dependent axonal sprouting (Nudo 887). Two notable stages have been observed in development of thalamocortical joints. During the initial stage, the axonal regulation molecules are responsible for leading “thalamocortical axons to their respective destinations” (Nudo 887). These processes could be driven by spontaneous neural process. In the second stage, cortical function controls “axonal development found in the cerebral cortex, influencing topological connectivity outcomes” (Nudo 887). Further, postnatal axonal division features located in the cerebral cortex have some links with the sensory affiliated stimulus function maybe by starting molecular retrograde signals (Dancause and Nudo 273). Brain insults have shown the availability of long-range axonal sprouting once believed to be absent in adult mammals. Today, however, available evidence has shown the relevance of cortical activities for axonal developing in adult brain after injuries. It is observed that variations in post-infarct behavioral experiences could affect the specific neuron preferred for local and detached developing axons by separately activating function-specific cortical parts.

It is imperative to recognize that content-based reinforcement is vital for the required brain plasticity to take place in cortical neurons of fully developed mammals. Specifically, limited contacts with sensory stimuli result in slight or no prolonged alteration in receptive area features.

Many broad approaches involving motor map composition have been shown, and they are assumed to influence the motor cortex capabilities to encode motor skills. First, motor maps are viewed as subdivided with several, intersecting movement representations. Second, the nearest features located in cortical motor maps are extremely interlinked through a compact network of fibers of intracortical (Nishibe et al. 2221). Finally, motor maps are highly changeable and may be altered by multiple inherent and external factors. Overall, these elements offer a basis through which the development of new muscle synergies by alterations in the intracortical connectivity of specific movement representations may occur.

Since 1980s, major scientific discoveries have changed and shaped thinking regarding cortical plasticity. Specifically, neurophysiological research focused on the somatosensory cortex is responsible for current knowledge. Previously, it was widely recognized that functional plasticity took place in the cerebral cortex of growing animals. Current studies have shown that the topographic arrangement of the depiction of skin surfaces found in the somatosensory cortex of a mature monkey usually changes after peripheral nerve damages, behavioral training, or disuse. These findings support the concept of vicariation, and they are drivers of further research in neurophysiological and neuroanatomical plasticity in damaged and typical cerebral cortex. Afterwards, other studies were done in other areas of the sensory involving the cerebral cortex and the motor cortex in both humans and animals (Dancause and Nudo 273). All findings indicated stronger support for the concept that plasticity of cortical maps is a common factor of the cerebral cortex even in full-grown animals, and the principle of temporal coincidence and behavioral factor are responsible for budding features of cortical units irrespective of their distinct cortical area.

Supposing that plasticity and behavioral traits are interconnected, as it seems, then these findings are vital for comprehending recovery processes after injuries involving peripheral and central nervous system injuries. It is possible to trace the development of topographic maps in animals and, hence, it can serve as a biological marker for nerve recovery after injuries. In addition, by analyzing cellular and molecular relations of map alterations, it could be possible to more explicitly comprehend neural processes involving neuroplasticity, and finally manage these processes for effective rehabilitation of injured persons.

Injury Plasticity in the Motor Cortex

In most neurological diseases, deficiencies in motor functions are common. Nevertheless, it is observed that a fully developed CNS of adults can retain a significant ability to recuperate and adjust after serious insults to the brain.

The spontaneous recovery takes place once a person suffers an injury involving the CNS (Nudo 887). Hence, it is imperative to comprehend primary mechanisms involved in natural recuperation of functions as the first phase toward the creation of effective change interventions that could enhance the pace of recovery and full restoration of functions. It is observed that insults restricted to a specific part of the motor take place only in distinct “middle cerebral artery (MCA) strokes and focal traumatic brain injury or neurosurgical resections” (Nudo 887). However, some data obtained from animal models have shown that they can be used to demonstrate mechanisms involved in the motor recovery after the central nervous system injury.

Although recovery on different outcome measures takes place naturally following the insult, some aspects of the recovery may be realized because of behavioral compensation. For instance, it is a well-established fact that in human stroke compensatory movements of the trunk are used to compensate for reaching. Factors, such as enhanced disuse of impaired parts alongside elevated use of proximal may explain changes in a map topography. In the case of a rat model, for instance, the area of the caudal forelimb sustained injuries, but when natural recovery or rehabilitative training was not available, behavioral performance to determine ability to reach some pellets was conducted, and it improved with time. Nevertheless, after five weeks post-injury, it was observed that the rat still had some vital deficiencies. During this period, the rat had rostral forelimb area with the regular size as the forelimb. However, experimental maps showed the redistribution of features of the forelimb. For instance, there were reduced digits, but elongated proximal features. Therefore, when behavioral training is not available, the plasticity found in the normal parts of the motor will take place spontaneously, which largely shows the progress of compensatory motor structure, instead of an actual recovery of the original kinematic structure (Hara 4).

The advancement of the recovery itself can be viewed as a process of learning and restoration of impaired function, as well as adaptation and reparation of secured, remaining functions (Nudo 887). These recovery processes, learning and restoration depict resilience of the nervous system after injuries. Therefore, it demonstrates that the neurophysiological processes that promote learning in the unharmed cortex should facilitate motor relearning and adaptation once the brain is injured (Nudo 887). Overall, as several research findings demonstrate, there is an obvious role of the neural plasticity, which ensures both natural and directed functional recoveries following an injury of the nervous system.

Opportunities to Advance Neuroplasticity Principles after an Injury

As previously observed, after an injury to the nervous system that affects the brain through stroke or trauma, successive molecular and cellular activities are set into action in nearby tissues, which result in impermanent or enduring alterations in the anatomy and physiology of the involved components. Most of these changes are pathological outcomes of the insult, such as edema, and they could have possibly adverse outcomes (Nudo 887). However, most these adaptive developments could start early after the injury has occurred, result in low rates of pathophysiological activities, or cause neuroplastic alteration resulting in some forms of function restoration. While there is no in-depth comprehension of these events at the molecular, cellular and network points because of the emerging nature of the field, adequate information is now found to assist in evaluating various hypotheses regarding influences of certain post-injury interventions on the recovery of functions and their related neuroanatomical and neurophysiological foundation (Matteo et al. 11).

The experiment involving the altered mouse subgroups without Nogo receptor has demonstrated a great possibility for improving “neuroanatomical plasticity processes following nerve damage” (Nudo 887). Nogo is recognized as a protein that prevents the growth of axonal, and mice without receptor acquire their motor function after the injury effectively relative to controls.

Given the availability of massive evidence to support the claims of brain plasticity following neuronal injury and that behavioral accounts could change neuronal formations and function in normal and injured brains, it is now obvious and imperative to apply neuroplasticity principles as the basis for a broad range of therapeutic interventions to enhance recovery (Carmichael 895). It is however noted that timing and dose are necessary to ensure that effectual, evidence-based intervention systems are available to enhance recovery. Timing and dose should account for events at the molecular, cellular, and network stages (Nudo 887).

Relative to other drug-related interventions for brain injury, the behavioral training approach is also most effective at certain periods. Protein is generally the major element required for neural sprouting and control. Protein upregulation is usually observed shortly after the injury has occurred. Clinical studies have also shown that outcome measures could be revamped even several years after injuries, but the best period for improvement is associated with time during optimal reorganization initiated by the insult. For instance, it is observed that axonal development may start after three days, and it becomes fully developed within one month. Further, genes that enhance and inhibit neuronal are regulated during post-injury periods. It is also recognized that events that are responsible for neurogenesis only last for limited time. Hence, there is a vital need to comprehend how behavioral experience changes recovery processes in various way after a given period. Similarly, any harmful outcomes of behavioral therapies that could occur too early during treatment also require further analysis. Notably, specific type and motor activity event could be vital for controlling the neural environment and in influencing regenerative activities or neuronal loss cascades dominating during the initial phases after brain injuries.

As mentioned above, an optimal dose is an issue that is critical for behavioral experience. The issue is imperative for not only assessing and comprehending the extent of safety for acute cases, but also understanding the dose-reaction association for rehabilitation processes across various stages involved in post-stroke intervention time and recovery. From animal models, it is possible to determine what human individuals who have suffered stroke can endure.


The human body system is complex, and the nervous system is a vital component of the body system. In the event of an injury, such as stroke or TBI, vital sensory motor parts are adversely affected. In this case, recovery and resilience are often noted as a function of the human body system. In fact, following an injury to the cerebral cortex, a significant fraction of the brain is affected. Consequently, there are deficiencies in motor functions. However, considerable spontaneous or natural recovery takes place after few weeks or within a month following the injury. Efforts to understand how undamaged sensory motor components can support and enhance recovery of the affected functions have been a major area of interest for neurobiological studies. As such, in the past few decades, researchers have focused on understanding the underlying principles of neuroplasticity involved in recoveries after neurological insults. It is now widely proven that brain injuries, such as the ones experienced in stroke or TBI, usually start a cascade of regenerative processes few days after an injury. Researchers have linked plasticity following injury to cellular and other sub-system events that occur during regular brain growth. Evidence is obtained from both animal and human models to indicate possible novel strategies to therapeutic treatments. Behavioral experience now offers some important aspects related to brain plasticity, recent findings, and novel approaches to recovery in the nervous system.

Hence, the brain can be reshaped following an injury to adapt or fail to adapt based on the motor experiences. Overall, plasticity indicates the adaptive and resilience nature of the human body system.

Works Cited

Carmichael, S Thomas. “Emergent Properties of Neural Repair: Elemental Biology to Therapeutic Concepts.” Annals of Neurology 79.6 (2016): 895–906. Print.

Dancause, Numa, and Randolph J. Nudo. “Shaping Plasticity to Enhance Recovery After Injury.” Progress in Brain Research 192 (2011): 273–295. Print.

Hara, Yukihiro. “Brain Plasticity and Rehabilitation in Stroke Patients.” Journal of Nippon Medical School 82.1 (2015): 4-13. Print.

Luthar, Suniya S., Dante Cicchetti, and Bronwyn Becker. “The Construct of Resilience: A Critical Evaluation and Guidelines for Future Work.” Child Development 71.3 (2000): 543–562. Print.

Matteo, Barbara Maria, Barbara Vigano, Cesare Giuseppe Cerri and Cecilia Perin. “Visual Field Restorative Rehabilitation after Brain Injury.” Journal of Vision 16.9 (2016): 11. Print.

Nishibe, Mariko, Scott Barbay, David Guggenmos and Randolph J Nudo. “Reorganization of Motor Cortex after Controlled Cortical Impact in Rats and Implications for Functional Recovery.” Journal of Neurotrauma 27.12 (2010): 2221-32. Print.

Nudo, Randolph J. “Recovery After Brain Injury: Mechanisms and Principles.” Frontiers in Human Neuroscience 7 (2013): 887. Print.

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