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The ability of the brain to re-task a different area following brain damage to one area Research Paper


Introduction

The ability of the brain to change following an individual’s experience is referred to as neuroplasticity (Alamacos, Segura, & Borrel, 1998). This characteristic of the brain was discovered more recently and discredits the earlier belief that the brain could never change after a person has gone through the critical period of infancy. The brain is chiefly made up of nerve cells and glial cells which are usually linked.

Learning can be achieved through the alteration of the strength of these connections. In the last century, the common belief was that the lower brain and the neocortical areas could not be altered in structure after structure after childhood (Winship & murphy, 2009).

This belief has been challenged by the new revelations that indicate that all parts of the brain are plastic and can be altered even in older individuals. This paper seeks to identify the ability of the brain to re-task a different area to perform a function that has been affected by brain damage (Lazar, Kerr, & Wasserman, 2005).

Earlier studies

Previous studies done by Wiesel and Hubel showed that ocular dominance columns that are located in the lowest neocortical visual area were largely not changeable after one has passed the critical period in development (Black, Cianci, & Markokowitz, 2001).

These critical periods were also examined in respect to language development; the findings suggested that all the sensory pathways were permanent subsequent to the critical period (Kaeser, et al., 2010). However, the earlier brain studies had also shown that changes in the environment could result in change in behavior and cognition.

This change was linked to the alteration in neuronal connections and neurogenesis in specific parts of the brain such as the hippocampus (Boudrias, Mcpherson, Frost, & Cheney, 2010).

Decades of enduring research on the functions and structure of the brain indicate that alterations take place in the lowest neocortical processing areas and that the alterations could result in marked changes in the pattern of neuronal activation in response to experience (Kaeser, et al., 2010).

The resulting neuroplasticity theory asserts that experience can result in the modification of the brain’s physical structure and the functional organization (Alamacos, Segura, & Borrel, 1998).

Neurobiology and cortical maps

The idea of synaptic pruning forms one of the important aspects of neuroplasticity. Synaptic pruning explains that specific links in the brain are subjected to constant removal or recreation depending on how they are being used (Draganski, 2006).

The concept of synaptic pruning is best captured in the aphorism “which states that neurons that fire together, wire together/neurons that fire apart, wire apart” (Boudrias, Mcpherson, Frost, & Cheney, 2010, p. 8). This indicates that two neighboring neurons that concurrently produce an impulse can form one cortical map.

Cortical maps are used to explain cortical organization of, in most cases, the sensory system (Giovanna, Paolo, Luca, & Thomas, 2008). For instance, sensory impulses from the two arms are projected to different cortical sites in the brain.

Thus the cortical organization defined by the response to sensory inputs represents the human body in form of a map. Researchers Merzenich, Doug Rasmusson and Jon Kaas conducted studies on the cortical maps by removing sensory inputs (Cutler & Hoffman, 2005).

Their findings which have been supported by various other studies show that the removal of an input in the cortical map results in the rewiring of the impulse through adjacent inputs.

Treatment of brain damage as an application of neuroplasticity

Through neuroplasticity studies it has been found out that a brain activity that results into a certain function can be relocated to a different part of the brain. This may take place in the course of normal experience or may occur in the course recovery following brain damage (Draganski, 2006).

Neuroplasticity forms the basis on which the scientific explanation for the treatment of acquired brain injury is founded. The restoration of the lost functions through therapeutic programs in form of rehabilitation is achieved due to the plastic nature of the brain (Frost, Bury, Friel, Plautz, & Nudo, 2002).

Cortical tissue damage, as might occur following stroke, is usually known to affect the initiation and execution of muscular contraction in the extremities opposite the side of the injury (Winship & murphy, 2009). In addition the precise manipulative power and the ability to skillfully utilize the upper extremity are usually weakened.

Depending on the extent of the injury, some functions usually return in weeks or months, although full recovery is uncommon in human beings. There is increasing evidence which indicates that the return of function observed following “cortical injury is largely attributed to the adaptive plasticity in the remaining cortical and sub-cortical motor apparatus” (Black, Cianci, & Markokowitz, 2001).

For instance, the studies pneurophysiologic and neuroanatomic on animals and the neuroimaging and other non invasive stimulation research studies conducted on humans provide evidence to show that adaptive changes take place in the undamaged tissues that surround a cortical infarct (Lazar, Kerr, & Wasserman, 2005).

Contrary to the previous beliefs, the adult brain is not “hard wired” with fixed immutable neuronal circuits (Draganski, 2006). There are several instances through which the cortex and sub cortex can be rewired as a consequence of training or following an injury to the brain. This is supported by evidence that new brain cells can develop even in the adult mammal even at old age.

The research findings so far have shown that this mainly occurs in the hippocampus and the olfactory bulb, however, there is increasing evidence that indicates that other regions of the brain may undergo neurogenesis (Frost, Bury, Friel, Plautz, & Nudo, 2002). In most parts of the brain, dead neurons are not recreated but the specific functions are seen to be restored.

However, evidence on the active, “experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex is lacking” (Kaeser, et al., 2010, p. 13). The specific pathway through which the process takes place at the molecular level is subject to intense research.

Some theories have been advanced to explain how experience results in the synaptic organization of the brain, one of the theories include the general theory of the mind and epistemology referred to as Neural Darwinism which was developed by Gerald Edelman (Lazar, Kerr, & Wasserman, 2005).

Neuroplasticity also occupies a central point in the memory and learning theories that are characterized by changes in the structure and function of the synapses through experience (Lazar, Kerr, & Wasserman, 2005).

Sensory substitution and neuroplasticity is best remembered through the works of Paul Bach-y-Rita (Lazar, Kerr, & Wasserman, 2005). He came up with a brain port while working with a patient whose vestibular system had been injured. The “brain port machine would replace the patient’s vestibular apparatus by sending signals to her brain via the tongue” (Winship & murphy, 2009, p. 15).

The patient used the machine for a certain period of time and regained the normal function. Her experience is best explained through plasticity because her vestibular system was disorganized following prolonged gentamicin medication and thus was sending uncoordinated signals to the brain.

Using the machine developed by Paul bay her vestibular system was able determine new neural pathways that were instrumental in reinstating the lost function.

Paul Bach-y-Rita used the following analogy to explain the plasticity concept; “if one is driving from one place to another and the main bridge that connects the two places goes out, he will be paralyzed before deciding to take the old farmland roads that are definitely shorter” (Winship & murphy, 2009). By using these roads more, one will start getting wherever he wanted to go faster.

Thus the new established neural pathways become stronger with more use. The unmasking process of the new neural pathways is generally understood to one of the main principal ways through which the plastic brain reorganizes itself (Boudrias, Mcpherson, Frost, & Cheney, 2010).

Another group referred to as the Randy Nudo learned that if an infarction leads to the cutting of blood supply to a certain part of the motor cortex of a monkey, the part of the body that is stimulated by the affected brain portion will respond when adjacent areas are stimulated (Kaeser, et al., 2010).

In one of their studies, the intracortical microstimulation (ICMS) mapping techniques were applied on nine normal monkeys (Draganski, 2006). Some of the monkeys were subjected to ischemic infarction protocols. The monkeys that underwent ischemic infarction retained more finger flexion during food retrieval and after several months this deficit returned to the levels they were before the operation (Kaeser, et al., 2010).

In regard to the mapping conducted to represent the distal forelimb, it was shown that cortical representations of movements had undergone reorganization in the entire surrounding cortex that had not been damaged. Better understanding on how the normal and damaged cortical tissues interact has formed the basis for current therapeutical approach in the treatment of stroke patients (Frost, Bury, Friel, Plautz, & Nudo, 2002).

The Nudo group is currently taking part in studying the treatment approaches that may result in better management of stroke. Such approaches include “physiotherapy, pharmacotherapy and electrical stimulation therapy” (Cutler & Hoffman, 2005, p. 4).

A professor at the Vanderbilt University known as Jon Kaas has been able to reveal “how somatosensory area 3b and the ventroposterior (VP) nucleus of the thalamus are affected by long standing unilateral dorsal column lesions at cervical levels in macaque monkeys” (Kaeser, et al., 2010, p. 10).

This shows that the brains of an adult mammal can reorganize following brain damage or injury but the reorganization will be injury dependent. His more recent studies have been focused on somatosensory structure.

Normally when injury is inflicted on the somatosensory cortex, one experiences a dysfunction in the perception of some part of the body. Jon Kaas is currently trying to understand how these systems (somatosensory, cognitive, motor systems) are plastic as a result of injury (Frost, Bury, Friel, Plautz, & Nudo, 2002).

More recently, neuroplasticity was applied in the treatment of traumatic brain injuries. The treatment was done by a team of doctors and researchers at Emory University, particularly Dr. Donald Stein and Dr. David Wright (Cutler & Hoffman, 2005). This particular treatment was first of its kind to be applied in that it is affordable and does not show any side effects.

Dr. Stein had had earlier observed that female mice recovered better from brain injuries as compared to their male counterparts. In addition he realized that the female mice had a better recovery record in some stages of the estrus cycle. After intense research studies, the team attributed this phenomenon to the levels of progesterone (Cutler & Hoffman, 2005).

The higher the progesterone levels the better the recovery witnessed in the mice. Thus they developed a therapeutic approach that included enhanced levels of progesterone administration to patients with brain injuries.

It was shown that if progesterone administration was done following brain injury that result in “stroke there were fewer instances of edema, inflammation, and neuronal cell death, and enhanced spatial reference memory and sensory motor recovery” (Kaeser, et al., 2010, p. 7). Administration of progesterone on a group of severely brain injured patients showed a reduction in mortality rates by up to 60%.

Conclusion

This paper sought to use existing literature in academic sources to explain how a lost function due to brain injury or damage can be re-tasked to another part of the brain. The area concerned with this study is referred to as neuroplasticity which can be simply defined as the ability of the brain to change following an individual’s experience (Boudrias, Mcpherson, Frost, & Cheney, 2010).

Neuroplasticity has led to a major shift in the way the understanding of the human brain. Major studies have been carried out by researchers and doctors to understand how the brain is able to re-task different area following damage to one area. Though there is no conclusive evidence to show how this occurs at the molecular level, there has been a marked improvement in the understanding and therapeutical application.

References

Alamacos, M. C., Segura, G., & Borrel, J. (1998). Transfer function to a specific area of the cortex after induced recovery from brain damage. Eur J Neurosci, 5:853-863.

Black, P., Cianci, S., & Markokowitz, R. S. (2001). Question of transecallosal facilitation of motor recovery: Stroke implications. Trans Am Neurol , 95:207-210.

Boudrias, M., Mcpherson, R. L., Frost, S. B., & Cheney, P. (2010). Output Properties and organization of the forelimb Representation of Motor Areas on the Lateral Aspect of the Hemisphere in Rhesus Macaques. Cereb Cortex , 20(1):169- 186.

Cutler, S., & Hoffman, S. (2005). Tapered progesterone withdrawal enhances behavioral and moleculae recovery after traumatic brain injury. Experimental neurology , 195(2):423-429.

Draganski, B. (2006). Temporal and Spatial Dynamics of the brain structure changes during extensive learning. The journal of Neuroscience , 26(23):6314-6417.

Frost, S. B., Bury, S., Friel, M., Plautz, J., & Nudo, R. J. (2002). Reorganization of Remote Cortical Regions After Ischemic brain Injury: A potential Substrate for Stroke Recovery. J Neurophysiol , 89:32053214.

Giovanna, P., Paolo, P., Luca, B., & Thomas, R. (2008). Genesis of Neuronal and Glial progenitors in the cerebellar cortex of peripuberal and adult rabbits. journal pone , 12(4):345-7.

Kaeser, M., Alexander, F., Wyss, F., Bashir, S., Hamadjida, A., Liu, Y., et al. (2010). Effects of Unilateral Motor Cortex Lesion on Ipsilesional Hand’s Reach and Grasp Perfomance in Monkeys: Relationship With Recovery in the Contralesional Hand. J Neurophysiol , 103(3): 1630-1645.

Lazar, S., Kerr, C., & Wasserman, R. (2005). Meditation experience is associated with increased cortical thickness. neuroreport , 12(17)1893-97.

Winship, I. R., & murphy, T. H. (2009). Remapping the somatosensory cortex after Stroke: Insight from Imaging the Synapse to Network. Neuroscientist, 15(5):507-524.

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P., I. (2020, January 26). The ability of the brain to re-task a different area following brain damage to one area [Blog post]. Retrieved from https://ivypanda.com/essays/the-ability-of-the-brain-to-re-task-a-different-area-following-brain-damage-to-one-area-research-paper/

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P., Ibrahim. "The ability of the brain to re-task a different area following brain damage to one area." IvyPanda, 26 Jan. 2020, ivypanda.com/essays/the-ability-of-the-brain-to-re-task-a-different-area-following-brain-damage-to-one-area-research-paper/.

1. Ibrahim P. "The ability of the brain to re-task a different area following brain damage to one area." IvyPanda (blog), January 26, 2020. https://ivypanda.com/essays/the-ability-of-the-brain-to-re-task-a-different-area-following-brain-damage-to-one-area-research-paper/.


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P., Ibrahim. "The ability of the brain to re-task a different area following brain damage to one area." IvyPanda (blog), January 26, 2020. https://ivypanda.com/essays/the-ability-of-the-brain-to-re-task-a-different-area-following-brain-damage-to-one-area-research-paper/.

References

P., Ibrahim. 2020. "The ability of the brain to re-task a different area following brain damage to one area." IvyPanda (blog), January 26, 2020. https://ivypanda.com/essays/the-ability-of-the-brain-to-re-task-a-different-area-following-brain-damage-to-one-area-research-paper/.

References

P., I. (2020) 'The ability of the brain to re-task a different area following brain damage to one area'. IvyPanda, 26 January.

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