Human Brain Plasticity - Essay Example

?TMA1-3 by 0 ANSWERS TO QUESTION 1 Plasti Plasti is like the ability of the brain to change because of a particular situation that the person undergoes. Because of a different experience or sensation, the brain neurons form new connections and break some old ones. This is plasticity and if the brain does not exhibit such a characteristic, then it must be fixed. In mental health, plasticity is of a particular significance because it is through plasticity that mental illnesses occur. Circumstances in the environment, personal traumatic experiences and certain chemicals have an effect on the brain and such effects cause changes in it that will result in mental illnesses. If the brain did not have plasticity as one of its characteristics, then it would not give rise to long-term changes in its structure so as to result in a mental illness. Moreover, plasticity has implications in therapy, for it is the role of the medicine to cause changes in the brain so as to cure the mental illness. If the brain did not have the quality of plasticity, then no cure would ever take place and treatment of mental illnesses would not be possible since every mental illness is permanent. Consequently, if the brain were not plastic, then psychiatry would lose its significance. Examples of plasticity include the effect of oxytocin on the brain of the baby, and since the brain is plastic, oxytocin changes the structures of the neural connections so that the baby develops an attachment to the mother while breastfeeding (Book 1, 2010, p. 76). Moreover, the stimulation of the brain of the child through oxytocin becomes permanent and even beneficial to the baby because the changes brought about by oxytocin to the brain help in the development of the brain and other biological structures related to this organ. If the brain did not exhibit plasticity, these things would not be possible (Book 1, 2010, p.77). Another example of brain plasticity is when the hormone serotonin would flood the brain. Brains of depressed people who committed suicide have an “abnormally high numbers of serotonin receptors in their prefrontal cortex” (Book 2, 2010, p. 61). If there were no plasticity in this particular area of the brain and if the brain did not exhibit plasticity at all, then this part of the brain would get as much serotonin as it can yet there would be no effect on the behavior or the effect simply wears off. However, with plasticity, just like in this example, there are corresponding and even permanent changes in one’s brain such as a strong desire to change one’s behavior. Worse, the new connections in the brain will transform the brain permanently and will change a person’s thoughts from normal to suicidal. Still, another simple example of brain plasticity is the repairs that brain cells undergo with the application of certain chemicals like BDNF. Damaged neural networks in the brain are repaired by BDNF in order to make them function properly again. If the brain did not exhibit plasticity, then no repairs would be made in it by BDNF. Moreover, the effects of BDNF on plasticity vary according to the area of the brain that it affects because BDNF has an antidepressant effect in the hippocampus while a social withdrawal effect on the mesolimbic dopamine pathway (Book 2, 2010, p. 68). 1.2 Questions about the Study (i) In the study, the two factors that appear to have been controlled include the age and the level of educational attainment of the participants. This is so because according to the author, there has been no significant difference in these two factors. Besides, even by inspection, there is but a very small gap between 38 years for the MBSR group and 39 years for the control group, and similarly, a very small gap exists between 17.7 years of education for the MBSR group and 17.3 years for the control group. (ii) Yes, MBSR training made a difference to mindfulness. According to the abstract, “The density of neuronal matter had increased significantly in [various] brain areas…in those who participated in an 8-week mindfulness-based stress-reduction course.” The mere phrase “had increased significantly” is already an indicator of the difference that MBSR training had made to mindfulness. Although the author does not present evidence, we understand this statement of the result to be substantial. (iii) Based on the account above, MBSR training did not make any measurable difference to the brain. Apart from the statement that MBSR training had made a significant increase in the density of neuronal matter, the study did not show exact numerical data for the quantities. Moreover, it was only a questionnaire that the researchers used to obtain data about mindfulness and it does not state exactly whether or not MRI was used to confirm the results from the questionnaires. Moreover, there is no mention of a sort of definite comparison of brains from the MBSR group and from the control group in terms of performance that can be measured through quantitative data. (iv) We cannot be sure that any changes to the brain were caused by the practice of mindfulness meditation. The response that the participants of the MBSR training showed was measured only through a questionnaire, and there was no mention of an MRI confirming whether the results had anatomical evidence or not. Moreover, even if the MRI had confirmed these changes, there is still a problem whether these changes were actually caused by the MBSR training or whether these participants were already predisposed to such changes. In short, no strong conclusions can be formed without a replication of the study. 1.3 The Hippocampus Increase in the density of cells in the hippocampus will have some significant effects on a person. The hippocampus has the unique characteristic of developing neurogenesis and is therefore associated with the occurrence of depression or the effects of antidepressant treatment (Book 2, 2010, p. 64). Antidepressants increase neurogenesis in the hippocampus and therefore counter the effect of stress which is to decrease neurogenesis in the same area, and this is confirmed by an experiment on rats to which antidepressants were administered everyday for several weeks (Book 2, 2010, p. 65). Moreover, serotonin levels increase as antidepressants are administered and so it increases the number of BDNF molecules, thus resulting also in increased neurogenesis. Nevertheless, there is no clear evidence that “a lack of neurogenesis causes depression” (Book 2, 2010, p. 66). BDNF, however, boosts neurogenesis in the hippocampus and it has corresponding antidepressant actions in that area (Book 2, 2010, p. 68). By virtue of this evidence, neurogenesis in the hippocampus will most likely cause happiness or elation in a person, as it seems to be a cure for depression. 2.0 A BIOPSYCHOSOCIAL APPROACH TO EXPLAINING THE DIFFERENCE BETWEEN TWO PEOPLE IN A STRESSFUL SITUATION One of the two people develops depression in the same stressful situation. Although the cause could be threefold in nature, one possible reason could be some physical or biological factors that predisposed him to depression. It could be a physiology that had already been altered by a history of drug abuse or substance abuse like alcohol. Perhaps, this person already used to experience mental problems when he was younger and perhaps dealt with it through alcohol or illicit drugs (Book 1, 2010, p. 15). Perhaps, he was able to stop this gradually on his own but he did not know that his brain was partly damaged during that time. Therefore, the situation may have stimulated the brain damage, which in turn helped trigger the depression. Moreover, as the biological state is interdependent with the psychological and the social, then perhaps what aggravated his possible brain damage was the idea that his alcoholism may have altered his psychological state and changed his beliefs. When he changed his beliefs, he may have also encountered people of the same negative mental state, and thus unconsciously put himself in the social context of a depressed individual. Furthermore, his biological state may have been inherited from a parent and perhaps he did not have a parent who underwent depression himself or one who experienced a mental disorder in his lifetime (Book 1, 2010, p. 18). A second possible reason may concern the person’s psychological state, and this particular person who ended up in depression may have already been harboring hostile and depressing thoughts, or perhaps an overall pessimistic or nihilistic philosophy similar to that of an angry, resentful person (Book 1, 2010, p. 16). This person therefore has a mentality that may automatically interpret situations negatively and he may have already been used to looking at almost all things and situations negatively. Moreover, as previously stated, he may have taken drugs and substances before that altered not only his physical brain but his overall consciousness and may have even helped him develop his negative beliefs about life. As one’s biology and psychology are interdependent, his psychological state may have helped trigger the production of hormones in his brain that eventually gave him depression. A third possible reason concerns the social context in which the person lives. Perhaps, this person may have just undergone a recent traumatic experience concerning his family or perhaps his lover (Book 1, 2010, p. 18). As the social context is interdependent with the biological and the psychological, such experience may then have caused either the production of hormones that triggered depression or the formation of negative psychological beliefs that eventually led to the same depressing state, or perhaps both. Perhaps, this person just broke up with his girlfriend or he may have had a major fight with her, with a friend or with a parent. He may then have interpreted these events as something that had a negative “meaning” (Book 1, 2010, p. 18). According to Book 1, “For one person, a partner walking out would be felt as the end of the world, whereas for another, it might be greeted with indifference or even relief” (Book 1, 2010, p. 18). Although we would not be able to exactly know what really happened to this person, one thing is relatively more certain than the others – he may have approached the social changes around him as he would “the end of the world” or something close to that. In short, the person’s biological, psychological and social state all helped trigger in him a state of depression. The other person did not experience depression perhaps also because of biological, psychological and social factors. Although the stressful situation to which this second person was exposed may have been severe, this man may not have experienced alcoholism or any form of substance abuse in his past. Thus, his brain was not altered and so perhaps there was nothing that interfered in the normal or regular production of hormones in him, and so he did not end up in depression. With his psychological state, perhaps it was more like he inherited the genes of positive attitude from his parents and that neither of his parents had a history of substance abuse or mental disorder (Book 1, 2010, p. 18). Moreover, perhaps he had a healthy relationship not only with his family, friends and lover but perhaps also with his finances. Thus all these things may have developed in him a healthy and positive psychological state that somehow served as a shield against any stressful situation (Book 1, 2010, p. 16). As to his social state, and as what was previously stated, perhaps work, family and relationships as well as finances were all working well at the moment that he was exposed to the stressful situation (Book 1, 2010, p. 18). The positivity of his environment may then have neutralized the negativity of the stressful situation. 3.0 ANSWERS TO QUESTION 3 Research Methods Strand Part 2: Evaluating experimental design Title of article: A controlled trial of the Litebook light-emitting diode (LED) light therapy device for treatment of Seasonal Affective Disorder (SAD) What was the aim or objective of the study? Describe how this was converted to an experimental measure (Book 1, Box 1.1) 4 marks This particular research study aims to “conduct a randomized placebo-controlled trial to test the efficacy of a white LED device whose light emission was relatively concentrated in shorter wavelengths” (Desan et al., 2007). In short, the study wants to know whether light therapy using light-emitting diodes or LEDs is effective against Seasonal Affective Disorder or SAD. What was the experimental hypothesis? (Book 1, Box 2.1) 2 marks Light therapy using LEDs can effectively treat SAD. What was the null hypothesis? (Book 1, Box 2.1) 2 marks There will be no difference after light therapy using LEDs is applied to patients with SAD. What was the independent variable? (Book 1, Box 2.1; Book 2, Box 2.2) 2 marks 1. Time of treatment (1, 2, 3, or 4 weeks) 2. Source of light: Litebook LED treatment device or an placebo inactivated negative ion generator What was the dependent variable? (Book 1, Box 2.1; Book 2, Box 2.2) 2 marks Severity of the depressive symptoms Which criteria, if any, were used in the selection of participants? (Book 1, Box 2.2) 2 marks Participants were required to be from age 18 to 65, should be diagnosed with SAD, and should have a SIGH-SAD score of 20 or greater. What type of design was used (was it between or within participants)? What problems might arise using this choice of design? (Book 1, Boxes 2.2 and 3.1) 4 marks A between-participants design was used because there were separate groups of people, one for the control group and one for the experimental group. What were the conditions (e.g. experimental and control)? (Book 1, Boxes 2.1 and 2.2; Book 2, Box 2.2) 2 marks Experimental conditions: patients with Litebook treatment device producing 1350 lux of light at 20 inches for 30 minutes each morning Control conditions: patients with negative ion generator producing no negative ions at 20 inches for 30 minutes each morning How did the researchers prevent or reduce confounding variables? (Book 2, Box 2.2) 2 marks The confounding variables were prevented by asking the patients to maintain a more or less stable or constant schedule of sleep and to avoid other forms of treatment. This was to avoid the factor of sleep or of other forms of treatment. They were also asked not to tell the blinded clinician which device they were using. This was to avoid bias in clinical evaluation. Does the study have external validity? Explain your answer. (Book 2, Box 3.1) 2 marks The study indeed has external validity because its results are relevant to everyone with SAD and everyone who is seeking treatment for their SAD through light therapy. In this way, through the results of the study, they are encouraged to use LEDs. Are the results reliable? Explain your answer. (Book 1, Section 4.2.4; Book 2, Box 3.1) 2 marks The results are reliable since they used a tried and tested statistical technique for measuring symptoms of depression (SIGH-SAD). How are the results presented (what descriptive statistics are used)? (Book 2, Box 1.3) 2 marks The results are presented using tables displaying SIGH-SAD scores, and mean SIGH-SAD scores are used. ANOVA analyses of the SIGH-SAD scores were also presented. Can you think of an improvement to the design? Explain why this would be an improvement. 2 marks The gender of the participants should have been considered, as well as a comparison between LEDs and fluorescent/incandescent light sources. Although there was no previous theory regarding gender differences as to the effect of light therapy in the treatment of SAD, a possible difference in terms of gender would serve as a basis for a new theory. As for the type of light source, the authors themselves underlined the difference between LEDs and fluorescent/incandescent light sources in the Background section of the study. Lastly, if light intensity can be varied, it would also be an interesting variable since effectiveness of treatment may also depend not on the type of device but only on the intensity of light produced. Read More