Meiosis and Sexual Life Cycles
Even while epileptic patients experience seizures, the converse should never be considered true, especially for those patients that experience seizures because of disturbances in brain metabolism. According to Dingledine, Varvel & Dudek (2014), metabolic disorders result in seizures in three different approaches. The first one occurs through the alteration of the intracellular osmolality, the second is the accumulation of intracellular toxins, and the last is the depletion of the respiratory substrates that could be important for membrane functionality. Seizures, therefore, have an effect in the death of neurons, which explains their contribution to the development of epilepsy (Dingledine, Varvel & Dudek, 2014). Isolated short-lived seizures are not probable agents of neuron death, but repetitive and severe seizures are a cause. The fact that status epilepticus kills the neurons in addition to causing chronic epilepsy, neurological death is widely considered a fundamental element of an acquired epileptogenesis. Even while some studies indicate that neurological death is not a necessary agent for acquired epileptogenesis, recent studies rule out this notion through indicating that the death of neurons is fundamental for the condition (Dingledine, Varvel & Dudek, 2014).
Molecular Basis of Inheritance
Epilepsy refers to neurological condition that is common and reflecting a hyperexcitability of the neurons that arises from largely unknown molecular and cellular mechanisms. In generalized epilepsy that has an autosomal epilepsy syndrome that is dominant and febrile seizures, there has been an identification of mutations in three genes that code the voltage-gated sodium channels that are also called the beta 1 or alpha subunits (SCN1B, SCN2A, and SCN1A) as well as a single GABA receptor subunit gene, the GABRG2 (Lossin et al., 2002). It is also noted that SCN1A mutations affect the channel inactivation, which causes a persistent sodium current that flows inwards. Such a gain-of-function anomaly will probably boost excitability of the membranes of the neurons through a prolonged depolarization of the neurons, which explains a plausible underlying mechanism that describes the inherited epilepsy in humans from a biophysical standpoint.
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Cell Communication and Cell Cycle
As noted, epilepsy is defined by repeated instances of electrical activity bursts within specific regions of the brain, which are referred to as seizures. The outcome in behavioral terms of the seizure activities relies fundamentally on the regions of the brain that have been affected by the over-reactivity activities. A review of the signaling pathways among the neurological cells entailed in the creation of seizures within epileptogenic regions is useful (Bozzi, Dunleavy & Henshall, 2011). The pathways the modulatory neurotransmitters such as serotonin, norepinephrine, and dopine activate entailing the activation kinases related to extracellular activities as well as an induction of immediate early genes has a special connection to the epileptic seizures (Bozzi, Dunleavy & Henshall, 2011). In this case, the immediate early genes have been identified by extant literature to be the leading causes for long-term behavioral and molecular responses that the acute seizures induce. Another focus of the studies on this subject suggest that the deleterious effects of activities of seizures that focus on the contribution of apoptosis-related pathways of signaling results in the progression of the illness. Therefore, it is suggested that a comprehensive comprehension of the pathways of signaling entailed in both long-term and acute seizure responses is a fundamental approach to the unravelling the foundations of epilepsy and its ultimate cure as well as therapeutic mechanisms (Bozzi, Dunleavy & Henshall, 2011).
Photosynthesis and Epilepsy
In approximately three percent of the people that live with epilepsy, an exposure to flashing lights that flash at specific intensities or to specific patterns that are visible could induce seizures, a condition that is referred to as photosensitive epilepsy (Epilepsy Foundation, 2017). It is imperative understanding that this condition is more prevalent among adolescents and children than it is among other age groups. Seizures in individuals that are photosensitive could be induced through an exposure to any of the situations described subsequently. Epileptic individuals could experience epilepsy when they become exposed to computer monitors and television screens because of the rolling or flickering images, specific video games, or television broadcasts that entail a rapid flashing as well as alternating coloring patterns, and an exposure to intense strobe lighting such as visual fire alarms. Other conditions may include an exposure to natural light that may include sunlight that shimmers off water, flickering through slats on the Venetian blinds, and through trees (Epilepsy Foundation, 2017). The condition might also be caused through an exposure to certain visible patters of coloring such as stripes that contain contrasting colors. Therefore, understanding the contribution of photosensitivity to the inducement of epileptic seizures is critical to caring for individuals that have the illness.
Cellular Respiration and Fermentation
Extant literature indicates that glycolysis rises during seizures and that lactic acid that results from the process could be used as the source of energy (Yang, 2013). Nevertheless, the manner in which lactic acid provisions the energy during seizures and the manner in which it can take part in the termination of such seizures remains unclear (Yang, 2013). Studies also suggest that lactic acid is involved in the activation of seizures as well as the provision of energy during the early stages of the attack. While the seizure advances, the levels of lactic acid reduces the tissue pH while inducing metabolic acidosis that resultantly terminates it.
Epilepsy and Metabolism
Epileptic encephalopathy could be triggered by metabolic defects that are inborn and, which could be rare on an individual basis but overall represent a fundamental clinical proportion of child neurology (Yu & Pearl, 2013). Such cases may present alongside different phenotypes of epilepsy that include refractory neonatal seizures among others. Whatever the case, as described within a preceding section of this work, metabolism disorders has a direct relationship with epileptic seizures since it alters the communication pathways of the neurons. Specifically, within conditions of normal physiology, almost the whole of the energy that the brain uses for normal functioning is a derivative of an aerobic glucose oxidation (). It should also be noted that glucose metabolism and uptake increases at the time of epileptic seizures compared to any other form of brain activity. It is also notable that the lactate levels of the brain also increase at the time of seizure, which is a reflection of the repaid increases in the glycolytic respiration than the normal oxygen metabolism. In this case, the rate of production of pyruvate dehydrogenase fails to match the required rate of its conversion to acetyl-CoA. Therefore, lactate dehydrogenase transforms the pyruvate produced during glycolysis to lactate when there are periods of a deprivation of glucose, which further suggests that further glucose metabolism would happen during epilepsy.
Cell Biology and Membranes in Epilepsy
A disrupted balance between cerebral inhibition and excitation that results in unprovoked and recurrent convulsions defines epilepsy. Studies are being conducted to create a comprehension of the underlying mechanisms of epileptic seizures with the objective of bettering the strategies of treatment. For this case, research on the tissues of the brain membranes gains importance for the creation of activities related to epilepsy. It is reported that epileptic seizures trigger variations in molecular organization of lipids forming the membranes with the potential to affect the structures relating to the functionalities of membrane proteins (Turker et al., 2014). Therefore, it is noted that epilepsy is associated with a disruption in the functionalities of the membranes of the neurons through altering their composition.
The Importance of Researching Epilepsy
The fact that epilepsy is such a devastating disease affecting the brain suggests the very need for research concerning the causes, diagnosis, and treatment of the ailment. Therefore, this research is a critical milestone in understanding the causes, especially thru understanding brain functioning during epilepsy. However, as much as the study provides an understanding of brain functioning, including communication pathways and metabolism during epilepsy, it fails to describe the most appropriate diagnostic and treatment procedures to be followed in dealing with epilepsy.
References
Bozzi, Y., Dunleavy, M., & Henshall, D. C. (2011). Cell signaling underlying epileptic behavior. Frontiers in behavioral neuroscience , 5 .
Dingledine, R., Varvel, N. H., & Dudek, F. E. (2014). When and how do seizures kill neurons, and is cell death relevant to epileptogenesis?. In Issues in clinical epileptology: a view from the bench (pp. 109-122). Springer Netherlands.
Epilepsy Foundation (2017). Photosensitivity and Seizures . Retrieved 23 December 2017, from https://www.epilepsy.com/learn/triggers-seizures/photosensitivity-and-seizures
Lossin, C., Wang, D. W., Rhodes, T. H., Vanoye, C. G., & George, A. L. (2002). Molecular basis of an inherited epilepsy. Neuron , 34 (6), 877-884.
Turker, S., Severcan, M., Ilbay, G., & Severcan, F. (2014). Epileptic seizures induce structural and functional alterations on brain tissue membranes. Biochimica et Biophysica Acta (BBA)-Biomembranes , 1838 (12), 3088-3096.
Yang, H., Wu, J., Guo, R., Peng, Y., Zheng, W., Liu, D., & Song, Z. (2013). Glycolysis in energy metabolism during seizures. Neural regeneration research , 8 (14), 1316.
Yu, J. Y., & Pearl, P. L. (2013). Metabolic causes of epileptic encephalopathy. Epilepsy research and treatment , 2013 .
