Brain Dysfunction - Coursework Example

Brain Dysfunction Table of Contents I. Introduction II. Discussion References I. Introduction This paper explores whether or not there is a correlation relationship or a causal relationship between the dysfunction of neurotransmitters on the one hand and anxiety, depression and other disorders on the other. In essence neurotransmitters are chemicals that effects the chemical stimulation of the bodys communication system via the nerves. In the brain, the function of neurotransmitters is to effect the communication within the brain and with the brain towards the rest of the human body. The way the communication takes effect is via the transmission of the chemicals from one neuron to the next, until the signal arrives at the destination, and a bodily process that is desired transpires. For instance, the movement of a human muscle is the product of the transmission of the chemicals from the brain to the muscle coded with information on how the muscle is to move. That, or the proper emotion is generated via the brain to that particular other region of the brain in charge of the emotions. In this sense the function of the neurotransmitter spans a wide gamut from maintaining overall wellness and health to the regulation of feelings etc. It is important to note that the human body sources its neurotransmitter chemicals from food, so that where imbalances in neurotransmitters are detected or suspected, then it is through the same ingettion pathways that neurotransmitter pathways are jammed, leading to imbalances in the chemicals, amino acids, and proteins that together are the building blocks of these neurotransmitters. Examples of substances that negatively impact neurotransmitter balance are drugs and alcohol. The literature on neurotransmitter imbalances induced by there substances point to a wide number of illnesses from such substances inciting imbalances in the bodys neurotransmitters (St. Gregory Retreat Center 2014). Other states of regulation and illnesses associated with neurotransmitter dysfunction are addiction, Alzheimers, obesity, phobias, depression, dysfunctional hormones, dysfunctions of the GABA, Crohns disease, Parkinsons, ADD, ADHD, syndrome of the restless leg, aggression that is out of place, pain of the chronic type, brain injury, and general dementia. Other conditions include low levels of drive for sex, poor control of the appetite, inability to sleep properly, and general dysfunctions of the adrenal systems. The question is whether the tie between neurotransmitter dysfunction and these disease states is one of correlation or causality (Stein 2013; National Treatment Centers for Environmental Disease 2014). II. Discussion The question is whether there is a correlation relationship or a causal relationship between neurotransmitter dysfunction and disorder states such as anxiety and depression, among others. There is evidence in the literature of a neurotransmitter basis to disease states, including for instance borderline personality disorder or BPD. The neurobiological foundation of such illnesses is established from a variety of perspectives, including assays, imaging studies, studies on the density of receptors, paradigms that challenge neuroendocrine systems, and those perspectives point to many neurotransmitter systems that have an association relationship with borderline personality disorder. In people with this disease, there is a disregulation of the systems of neurotransmitters. The thinking is that since neurotransmitter systems that are inherited along family lines can form the basis of the transmission of disease states through the generations of families is some indication that there is a causal relationship, though this is not conclusively determined, and it may be that both the existence of the dysfunctions in the neurotransmitter systems and the existence of the borderline personality disorder stem from some other cause, and that both meanwhile are correlative of each other (Gurvits et al. 2000). On the other hand, literature exists that suggests a causal relationship, not directly, but to be inferred from the way interventions for such aspects of Alzheimers and Parkinsons as dysfunction of the cognitive processes in patients with those diseases. Interventions for such cognitive dysfunction conditions include suggestions to tweak neurotransmitter mechanisms in certain parts of the brain, As the literature notes, there may be value in treating such dysfunctions in cognition by looking at the way some receptors can be changed in particular ways to tweak, so to speak, and correct the condition in such areas of the brain as the mesolimbic circuits nd the frontal-striatal parts of the brain and the neurotransmitter pathways in those regions, among others. The implicit assumption here is that there is a causal relationship between the dysfunction of the neurotransmitters in those regions on the one hand and the dysfunction in cognition in those persons afflicted by certain degenerative diseaeses like Alzheimers. This is so, because tweaks in the neurotransmitter systems in those brain parts are said to show promise in correcting the cognitive dysfunction and restoring sound cognition mechanisms in patients with brain disorders like Alzheimer;s (Xu et al. 2012). That said, the literature also suggests that while there is a suspicion that imbalances in neurotransmitters are symptomatic of people who are depressed, for instance, it is not clear whether it is the imbalance in the neurotramsmitters and the general dysfunction of the brain that is the cause of the depression, or whether the two are correlative and are caused by another set of factors that have nothing to do with brain dysfunction and neurotransmitter dysfunction at all. This is true, for instance, because depression and other conditions are traced not just to a single biological factor but to a host of factors, some environmental in nature, some genetic, and some psychological. This makes it difficult to pin down whether those factors in themselves cause brain dysfunction and depression, or whether it is the brain dysfunction from such factors that directly cause depression, or whether the two are tied by correlative factors rather than causal factors (National Institutes of Health n.d.). Elsewhere the literature goes only as far as saying that neurotransmitter systems are implicated in mechanisms that lead to depression, without saying exactly whether the implications are causal or correlative. Even the way the drugs that treat depression, which act on certain brain neurotransmitters, are said to not really pin down the correlative or the causal relationship between brain dysfunction and disease states either way. The discussion on brain neurotransmitters, particularly serotonin, dopamine and noriephrine do include discussions on the role that certain drugs play in suppressing the action of those neurotransmitters in the treatment of depressive states, but as to whether the dysfunctions in the neurotransmitters themselves are the cause of the depression and other mental disease states or not is something that is not conclusively determined. The problem is that where there are studies that support the neurotransmitter basis for depression, establishing a causal relationship, that relationship is not determined consistently in all studies, with other studies disproving the presence of a causal relationship altogether, for the same sets of conditions. Some people for instance, become depressed from low levels of a certain neurotransmitter, say norepinephrine, while others are not similarly affected by low levels of the same neurotransmitter in their bodies/brains. This suggests that the relationship is more complex, and is not just plainly causal as other studies suggest. If the relationship is really causal, then all studies must arrive at the same relationship. It is more that different people seem to react to various forms of brain and neurotransmitter dysfunction in different ways, which makes it difficult to pin down the relationship as causal or correlative with finality (CenterSite 2014). Meanwhile, there are other studies that seem to validate a causal relationship between brain dysfunction and neurotransmitter dysfunction in general and disease states in particular, though those are for physiologic rather than psychological conditions like anxiety and depression. This latter causal relationship is determined for hepatic encephalopathy, for instance, where the presence of the condition is said to be caused by changes in the neurotransmitter mechanisms in the body. These changes then induce liver failure. In this way, a causal link between brain dysfunction and the dysfunction of the neurotransmitter systems is established. In the case of liver failure, for instance, the heightened levels of certain chemicals, such as ammonia, in the brain, induce changes in the levels of some neurotransmitters, that are then directly tied to a causal relationship with the failure of the liver systems n the human body. The culprit brain chemicals can be said to cause the neurotransmitter changes, which in turn cause the liver to fail. This is how the causal relationship between physiologic disease states and brain and neurotransmitter dysfunction is established (Butterworth 2001). Also, there are more basic pieces of literature that establish the role of neurotransmitter depletion in the onset of various disease states, including anxiety and depression, and where the neurotransmitters are brought back to healthy levels via diet and food consumption, in the replenishment of the amino acids and proteins that are the building blocks of neurotransmitters of all kinds, then the physiologic basis of the disease states are addressed, and there are marked improvements in the conditions that afflict previous sufferers of the conditions. The thinking here is that with some conditions, then it is true that brain dysfunction and neurotransmitter dysfunction do have a causal relationship. This is to say that it is the dysfunction itself that causes the disease states, rather than some other cause or mechanism causing the neurotransmitter systems to go into dysfunctional routes. In this line of thinking it is brain physiologic dysfunction and the dysfunction of the neurotransmitter systems that are the fundamental causes of such conditions as depression and anxiety. This is the same as saying that depression and anxiety have biological bases, in the neurotransmitter systems and the physical brain. The physiologic hypothesis too goes to great lengths to prove this, and also in administering physiologic interventions that go to the root of the imbalances by prescribing replenishments of the building blocks of the neurotransmitters, the amino acids and proteins, through direct supplementation and dietary interventions. Here again is the reinforcement of the causal link established between depressive states and anxiety states on the one hand and neurotransmitter imbalances and dysfunctions on the other. In this line of thinking too a valid case can be made for viewing chronic brain dysfunctions and chronic imbalances in the brain chemistry and neurotransmitter makeup that cause chronic anxiety and depressive states, among many other conditions. Again, this does not take into consideration a host of other non-brain and non-neurotransmitter, non-physiologic foundations and bases, causes for certain disorders like anxiety (Kaslow 2013). Elsewhere in the literature there is a large body of literature that seem to support the assertion overall of a causal relationship between brain dysfunction and general dysfunctions in neurotransmitter systems and disease states, not just psychological states like depression and anxiety, but a host of other conditions, such as overall declines in cognition in the elderly. The hypothesis in this latter category too, is that the deterioration in the neurotransmitter systems in elderly people cause cognitive decline, with the implication that interventions to shore up these neurotransmitter systems can help improve mental cognition and delay or reverse overall levels of cognitive decline (Bartus et al. 1982). In mice, moreover it has been found that altering some receptors of neurotransmitters in the brains of those mice lead to the expression of genes that lead to Huntington disease, again indicating a causal relationship between neurotransmitter dysfunctions and disease states. Here again the finding is that physiologic disease states can result from dysfunctions in the neurotransmitter systems, and that the relationship is not correlative but direct causation (Cha et al. 1998). In similar vein, interventions to reverse disease states lie along the lines of correcting the dysfunctions in the neurotransmitter systems, by repairing receptors, allowing blocked neurotransmitter systems to do their work, suppressing certain neurotransmitter mechanisms, and the like (Yamamoto et al. 2000). In other studies, the deficiencies in neurotransmitters again are established to have direct causal relationships to the expression of certain disease states, corroborating the findings in the earlier cited studies in this paper. The conclusion is that the relationship between brain/neurotransmitter dysfunction and depression and other diseases is causal (Reynolds et al. 1999). References Bartus, R. et al. (1982). The Cholinergic Hypothesis of Geriatric Memory Dysfunction. Science 217 (30). 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Reversal of Neuropathology and Motor Dysfunction in a Conditional Model of Huntingtons Disease. Cell 101 (1). [Online] Available from: http://www.sciencedirect.com/science/article/pii/S0092867400806236 [Accessed 28 April 2014] Read More