Implications of Neuronal Plasticity for Structural and Functional Chains in the Brain

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4th Nov 2020 Nursing Essay Reference this

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Theme: discuss the concept of neuronal plasticity and its implications for structural and functional changes in the brain in adulthood

Question: is there an obvious connection between neural plasticity and epilepsy and what are the strategies for neural plasticity as a potential treatment for epilepsy?

Introduction

Epilepsy is a neural disease that has been affecting individuals since before the 19th century, with almost five people in every one thousand people in North American and Europe alone are found to be diagnosed with epilepsy (Speed et al., 2014). Epilepsy is a highly heterogenous condition, passing from generation to generation, it is also able to encompass clinical subtypes. It can be defined through the use of an electroencephalogram (EEG), specific seizure types, and also with brain imaging techniques (Speed et al., 2014). It is an illness that is characterised and identified by the experience of two or more unprovoked seizure within the time span of two years (Alarcón, 2012). With the term unprovoked referring to the absence of underlying acute conditions that are able to induce seizure in individuals who would not otherwise experience seizures (Alarcón, 2012). It was believed to be related to bad omens and possessions back when there was a lack of understanding of how the brain worked. They believed that the seizure was related to a demon or a bad spirit leaving the body. This was until the 19th century where they saw the development of an understanding for the concept of functional localisation in the brain (Alarcón, 2012). Seizure manifestations are believed to come from dysfunction in the cerebral cortex of the brain, with the cerebral cortex being the structure that is responsible for complex brain structures, it is believed that during seizures the cerebral cortex functions abnormally (Alarcón, 2012). As mentioned before, the EEG scanner can be used to define epilepsy, this is in addition to being able to identify and also diagnose epilepsy in individuals. However, due to there being an inadequate history and misinterpretation through an EEG, it allows for 4-25% of people tested, to be misdiagnosed (Baxter, 2006). The reason being for the difficulty in accurately diagnosing epilepsy in individuals is the lack of a reliable and easy test, with many people believing that the EEG is a suitable diagnostic without realising the limitations that come with it (Baxter, 2006). Trough studies people have found techniques to make this more reliable, such as a video-EEG recording. The clinical events may occur during the routine recording, but occasionally prolonged recording and provocation methods are needed. Provocation methods that can be used can include sleep deprivation, hyperventilation, and reflex stimuli if appropriate, but the effects of this methodology on the accuracy of diagnosing epilepsy is unclear (Baxter, 2006). Non-EEG methods of diagnosing epilepsy could be witness reports, home videos of epileptic events, and the history of the individual. As epilepsy is most prevalent in countries that lack comprehensive health services, history can be considered one of the most important diagnostic tools for diagnosing epilepsy (Baxter, 2006). With epilepsy proving to be one of the best examples of plasticity, there is a significant connection between the two (Scharfman, 2002). Brain or neural plasticity is a life-long process and can involve both Hebbian and non-Hebbian synaptic plasticity (Caverzasio, 2018). There are 2 kinds of synaptic modulation, Hebbian plasticity which occurs over a short period of time, and also non-Hebbian plasticity, which is occurring over a long period of time (Caverzasio, 2018). A synapse that has Hebbian plasticity is known to increase in strength if experiencing coincident pre-synaptic and post-synaptic synaptic neural plasticity (Seel, 2012).

This phenomenon of plasticity is focused around proving that experience is able to leave a trace on the neuronal network, potentially modifying the effectiveness of the transfer of information (Ansermet & Magistretti, 2007). Meaning that what is acquired during experience, is permanently modifying the connections among neurons in the brain. Plasticity introduces a new dialectic in regard to the organism, it is able to imply and suggest diversity and singularity (Ansermet & Magistretti, 2007). Plasticity in epilepsy has mostly been studied in the hippocampus, this is due to the hippocampus being quite susceptible to seizures and many types of epilepsy involving the hippocampus (Scharfman, 2002). Most studies regarding plasticity and epilepsy has been conducted on rodents, though this has proven to give useful information. The changes that occurred in the hippocampus of the rodents after seizures are able to serve as a model for plasticity in humans with epilepsy (Scharfman, 2002).

Current research

As mentioned in the previous paragraph, most of the studies that have been conducted regarding plasticity and epilepsy have been done on animals, mostly rodents. However, most of the human studies that have been done are found to be based on data taken from tissue specimens during surgery (Scharfman, 2002). A researcher by the name of Helen Scharfman found studies that have been conducted on rodents relating to their hippocampus have shown results that can be applied to other species, they also appear to be generalisable to other areas in the brain (Scharfman, 2002). Scharfman also found that all of the changes that occur in the dentate gyrus after the events of a seizure can be used to clarify epileptogenesis.

Another study done in 2005 by a researcher named Jacobs looked into the effects of lesions on the brain on epilepsy. However due to what was most likely ethical issues, animal models were used rather than human participants. The study used two models, the undercut model and the micro-gyrus model (Jacobs et al., 2005). The undercut model focuses on epilepsy that is a result from penetrating brain injuries, this has been modelled through the formation of chronic neocortical partial isolations, or “undercuts”, with intact blood supply (Jacobs et al., 2005). Differing from the micro-gyrus model which regards lesions that have occurred during cortical development, thus, resulting in a more serious cellular pathology (Jacobs et al., 2005). The general results that were gathered from this research showed that there are three general ways in which injury may lead to hyperexcitability. The first finding regarding direct injury to cortical neurons, which can result in a change to the membrane ion channels that allow for cells to be more responsive to excitatory inputs. Consequently, impacting the way that these cells would respond to these excitatory inputs, potentially weakening them. The second finding concerning the connectivity of the cortical circuit, this is also highly impacted after injury to the brain. This is due to the potential enhancement of excitatory connections which may increase reoccurring excitatory loops within the epileptogenic areas of the brain (Jacobs et al., 2005). The third and final way in which injury can lead to hyperexcitability is due to focal injury being able to produce widespread changes, this can be in glutamate receptors, as well as the developing brain in general (Jacobs et al., 2005). All of which are proven factors contributing to epileptogenesis.

In the year 2002, three researchers worked together to uncover the consequences that epilepsy can have on the developing brain, as well as discussing the potential for epilepsy to be managed through surgical methods. The researchers found that the developing brain is highly susceptible to seizures, this can be confirmed by previous studies that have been done on both animals and humans (Strafstrom et al., 2000). Evidence has been found through the use of numerous animal models to suggest that early seizures have the potential to cause structural physiological changes in the development of neural circuits. This is then able to damage the balance between excitatory and inhibitory neurons, ultimately leading to increased susceptibility to seizures (Strafstrom et al., 2000). This research found that the same principles that govern brain plasticity, are potential contributors to an increased vulnerability to epilepsy. It showed that there are similarities in the studies done regarding epilepsy and brain development, some animal studies associate with studies done on simple and complex neural circuits, with both types of studies demonstrating common principles (Strafstrom et al., 2000). Thus, supporting the concept that many of the neural functions that are observed during lab models testing epilepsy are relevant to epilepsy in human brains. The research that was done for this article found that the influence of neuronal activity on a wide variety of developmental cellular processes implies that there is intense neural activity occurring during seizures. This can consequently lead to profound developmental effects (Strafstrom et al., 2000). Another researcher by the name of Thomas Sutula conducted research in the year of 2004 regarding the effects of the progression of epilepsy on neuroplasticity. Sutula found that there are recent longitudinal studies which show a substantial number of individuals with epilepsy also undergo brain atrophy. This is the breakdown of tissues and also involves apoptosis which is essentially programmed cell death (Sutula, 2004). Sutula also found that long-term seizure induced plasticity in neural circuits is bi-directional. Including the progressive damage, as well as the development of resistance to additional damage. Though there is a correlation between plasticity and epilepsy, it is a highly heterogenous disease, hence not all cases of epilepsy are the result of seizure induced plasticity (Sutula, 2004).

In the aforementioned research that was done by Scharfman, there were suggestions for future research, leading to better understanding which could ultimately lead to better treatment strategies for the future. Such as studying which changes that occur during brain plasticity are adaptive and which are maladaptive (Scharfman, 2002). Scharfman also states that to gain a better understanding of brain plasticity and epilepsy will require a collection of expertise, such as neuroscientists, clinicians, epilepsy researchers etc (Scharfman, 2002). As well as information from the 2002 study suggesting that more research should be done regarding the use of surgery, whether surgical treatment done early into the individual’s life will alter the long-term diagnosis favourably (Strafstrom et al., 2000). As for more recent studies, there have not been many that have specifically covered the grounds of testing to determine whether there is an obvious connection between neural plasticity and epilepsy. Though few studies have suggested that epilepsy is one of the best examples of neural plasticity, there is a lack of studies specifying on the two (Scharfman, 2002). Another key factor to take into account for future research into brain plasticity and epilepsy, is the use of a different animal model. Most studies feature rodent brains when studying epilepsy and brain plasticity, however, there may be advantages in using larger animal models, where there is a clear presence of white matter content in the brain structure. This would then be able to represent the human brain more accurately (Semple et al., 2013).

It has been proven that there is an obvious connection between seizure activity and cognitive dysfunction, with most finding relation between the hippocampus an epilepsy. Some experimental models focused on primates show that the removal or deletion of epileptic centres has the potential to improve cognitive function (Reid et al., 1997). There are different forms of synaptic plasticity, one that is important to epilepsy and brain function as well as memory, one of those being long-term potentiation (LTP). This can be demonstrated artificially through the stimulation of pathways in the brain at high frequencies. Research has shown that there is a connection between electro-convulsions and the hippocampus of rodents. To determine whether there is a connection between the LTP and electro-convulsive seizures (ECS), a researcher by the name of Reid worked with the effects of spaced electrical seizure induction, which he then compared with single seizure induction and a controlled condition (Reid et al., 1997). Results from this concluded that ECS altered plasticity in the hippocampus through the induction of LTP, such that the capacity for any further synaptic potentiation was consumed gradually. Electrically induced seizure activity is proven to have a profound effect on hippocampal plasticity in rodents (Reid et al., 1997).

Discussion

As mentioned previously, there has been a lack of specific studies regarding neuroplasticity and epilepsy, as well as a lack in recent studies done. Though this does restrain the accuracy, as well as reliability of the studies that have been discussed in the previous section.  Due to majority of the research discussed being conducted before the year of 2010, there is potential for the research to be outdated. More recent studies might have more advantage as there may be a better understanding of the concept of neural plasticity through more advanced technology or research. With the same applying to the understanding of epilepsy, there may be a different understanding compared to when the research previously discussed was conducted. Therefore, more current research would prove more accurate and reliable due to the better understanding, and more research to allow for a better understanding of both neural plasticity and epilepsy. Though the research could be considered outdated, the research has been conducted by reliable researchers and has been published through credible journals.

Due to ethical reasons, majority of the research regarding epilepsy and neural/brain plasticity has been conducted on animal models, with most studies using rodents for their participants. As we are two completely different species, there may be some challenge in connecting the results from the rodent studies to epilepsy in the human species. There have been several pre-clinical models that have been developed which utilise rodents of various ages, though there is an obvious species difference in the timing of some key development and maturation events. Therefore, it may hinder the scientific comparison between the two species, making it more difficult to interpret and understand (Semple et al., 2013). Below is table 1, showcasing the different areas and milestones of development occurring in the brain, this can range from the development of the immune system to the brain reaching most of its adult weight. It highlights the differences in the development of the brain at different stages of life, the further into life they move the more experience they have allowing their brain to adapt and develop further. It can be seen there is a significant difference in the rates at which human and rodent brains develop (Semple et al., 2013). This then has the potential to hinder the quality of the research and also the results that have been gathered through the research.  

Table 1, Developmental Milestones in Human and Rodent Development, (Semple et al., 2013), page 3.

Human

Rodent

Developmental milestones

23 to 32-week gestation (pre-term infant)

 Rodent post-natal day 1–3

Oligodendrocyte maturation state changes—pre- dominance of mitotically active pre-OLsa. Immune system development.
Establishment of the blood-brain barrier.

36 to 40-week gestation (term infant)

Post-natal day 7–10

Peak brain growth spurt.
Peak in gliogenesis.
Increasing axonal and dendritic density.

Oligodendrocyte maturation state changes–switch to a pre-dominance of immature OLs. Consolidation of the immune system.

2 to 3-year-old

Post-natal day 20–21

Brain reaches 90–95% of adult weight.

Peak in synaptic density at 50% > adult levels. Peak in myelination rate.
Neurotransmitter and receptor changes.

4 to 11-year-old

Post-natal day 25–35

Fractionation/specialization of prefrontal cortex neural networks (structural maturation). Maximum volume of grey matter and
cortical thickness.

12 to 18-year-old

Post-natal day 35–49

Reduced synapse density, reaching a plateau at adult levels.
Refinement of cognitive-dependent circuitry. Ongoing myelination; increasing white matter volume and fractional anisotropy.

20 years +

Post-natal day 60+

Adult levels of neurotransmitters.
Adult levels of synaptic density.
Ongoing myelination and declining grey matter.

As mentioned in previous sections, there are numerous things that can be done to improve the research that is being done on brain plasticity and its connection with epilepsy. This is including more recent studies, using larger animal models to more accurately represent the human brain, enhancing the accuracy of results, as well as determining which of the many changes that occur during brain plasticity are adaptive and maladaptive. Leading to more understanding of how brain/neural plasticity connects with the neural disease of epilepsy.

Though no researcher has yet to uncover whether the changes that occur during brain plasticity can be used to assist with potential treatment strategies for epilepsy. The research that is currently being done regarding plasticity has shown that plasticity in areas such as the hippocampus in the rodent brain significantly correlates with the onset of epilepsy and seizures, however, there is a lack when it comes to connecting plasticity in other areas of the brain. As neural plasticity regards the brain adapting to experience in life, there is no clear understanding whether it is a malfunction/hindrance during adaptation that is responsible for epilepsy. More research regarding these two concepts is required to gain further understanding and insight, though brain plasticity and epilepsy are obviously connected, further understanding is able to help with future treatment potentials and even more understanding to how the changes and adaptations made in the brain connect with epilepsy.

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