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Memory Reconsolidation to Patients with PTSD - Research Paper Example

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The paper "Memory Reconsolidation to Patients with PTSD" focuses on the critical analysis of the memory reconsolidation to patients with Post-Traumatic Stress Disorder (PTSD). Neurobiology is the study of the cells of the nervous system and their alignment in their functions…
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Extract of sample "Memory Reconsolidation to Patients with PTSD"

Memory reconsolidation to patients with post traumatic stress disorder Name: Institution: Course: Lecturer: Date: Introduction Neurobiology is the study of the cells of the nervous system and their alignment in their functions which process the information in the brain hence the immediate response or behaviour. It is a combination of two components which are biology and neuroscience (Forcato, Rodrı`guez, Pedreira & Maldonado, 2010). The brain is the part that helps in the responsive part of our body from survival instincts, reflexive behaviour when faced with danger but at times when the brain is exposed to some distress or threat it results to dsyregulation in the brain. The chronic dsyregulation of the brain system can cause functional impairment hence the blockage in their brains which is called post traumatic stress disorder which simply means a person has been psychologically traumatized (Hardt, Einarsson & Nader, 2010). Discussion According to Jonathan (2013), Post Traumatic Stress Disorder (PTSD) may develop when a person encounters something they cannot fathom or contemplate for example extreme fear from death of a loved one to sexual assault cases etc but through recent researches scientists have come to understand that it is not only depend on the stress levels of the subject but also the individual characteristics (Forcato et al., 2010). The three symptoms of PTSD are firstly the reminders of the incident for example having flashbacks, the other one is when a patient more sensitive to their senses but now in the high levels like being impulsive, agitate, hyper arousal, insomnia since if they sleep they might have nightmares of the incident. and lastly the being non associative with the environment around them like withdrawing themselves from company, avoiding people etc A person is concluded to have the disorder if the symptoms persists for more than a month long. To relate the disease to the brain neuroscientists’ correlate the persons brain response in various pars to see their reaction hence the conclusion that the patient has PTSD (Jonathan, Sherin, Charles & Nemeroff, 2011). The brain regions that the scientist looks at include the endocrine systems which regulate the stress response of an individual and also the neurotransmitter pathways that detect fear when the patient is conscious or not. Through the research they have come up with findings that make people susceptible to the disorder which are said to be; physical injury (Traumatic Brain Injury), genetic susceptibility, gender especially female, prior trauma people have been faced with, but the factors contribute to the vulnerability of the subject not that it is a must a person to have it (Chan & LaPaglia, 2013). The neurobiological impact to the psychological trauma in the brain from a genetical, developmental and psychological perspective but first understanding the biology of the brain when faced with the PTSD. A summary of neurobiological features with identified abnormalities and functional implications in patients with post-traumatic stress disorder are different in various parts of the body. According to Jonathan et al., (2013) has written a good summary in the changes of the various regions. Also Studies using rodents has shown that as they learn to disassociate the shock (normally a number of electric shocks) within a particular context (e.g. after pressing a lever that normally provides food the fear diminishes (Garelick& Storm, 2005). What researchers haven’t concluded is the cause of the success of extinction with three key different theories; a) unlearning the context and fear association) new learning that masks the original association or c) habitual learning that can lead to response fatigue (Jovanovich & Ressler, 2010)). As a memory ages it becomes more stable and less sensitive to change however there is new research indicating that the anterior cingulate cortex (ACC) also has an important function in reconsolidating fear memories where consolidation does not occur every time it is retrieved (Einarsson& Nader, 2014). Einarsson and Nader infused the antagonist (Ro25-6981) in rats three days before the contextual fear conditioning of a foot shock and found they had far lower freezing rates (sign of fear) than the control group infused with saline. They further found that rats infused immediately after the fear condition had similar freezing rates to the control group 4 hours later however 24 hours later showed impaired freezing indicating impaired memory consolidation. Their overall results showed that contextual fear memory that is 3 days old can be impaired by inhibiting synthesis at the cellular level in the ACC .PTSD in part can be a deficiency in fear inhibition (Jovanivic, 2010). Jovanivic found that combat veterans suffering PTSD who were exposed to an unconditioned fear stimulus that was not related to their original traumatic experience (in this case a street sign that signaled danger) still showed a higher fear response using acoustic startle and skin measurements. This research suggesting if these same antagonists are injected into military personal who are about to be exposed to a traumatic incidents may help. However some might argue that the strength of fear training used (only 3-foot-shock, other studies use 8-foot) in the Frankland et al study were not adequate to show cellular reconsolidation. Throught the clinical trials that have been tried on rodents none has been proved to work as per now everything is on clinical basis. All those brain regions show the change but they are countered by some factors since some disorders or diseases share the same symptoms which can confuse people thus being given a different diagnosis. For example in the neuroendocrine the changes are also connected to a person who has suffered from a TBI making the diagnosis difficult for the conclusion of what the subject Is suffering from (Sutherland & Lehmann, 2011). Also some of the symptoms don’t correlate with other people who are said to have PTSD for example people who survive the Holocaust but they came to a conclusion that the reason was because the severity and timing of the psychological trauma are different. Memory reconsolidation is all about the retrieval of the past events and succumbing to the facts of what has happened and dealing with the issue. Researchers have tried various methods to memory retrieval but the most effective has been therapy that has helped people overcome their PTSD. Researchers have tried various ways to reconsolidate memories by also conducting clinical trials to test their theories. Sutherland & Lehmann, (2011), Pharmacological methods on the hippcompai of mice and showed that both recent and not remote memories (memories connected to a specific time in the past like a past birthday or significant event) were disrupted if the retrieval treatment was longer while briefer sessions only effected recent memories According to Jovanovich & Ressler (2010) the functional role of reconsolidation is to ensure that memories reflect the most current state of knowledge by updating old with new information. Therefore, the interpretation on the finding is that updating only occurs in conjunction with the violation of predictions based on prior experience. However, critics of the reconsolidation process argue that only rather new memories can be modified as it is asummed that they are presumably not fully consolidated (Soeter & Kindt, 2012). However, the old memories which are fully consolidated are not changeable through the process of reconsolidation. It is difficult to establish the exact moment at which a memory can be considered to be fully consolidated. Furthermore, if one assumes that strength declines over time because of forgetting, one might actually expect the opposite pattern that is, that more recent memories are less prone to modification than older ones. There is a time window for the interference to occur beyond a certain time, when reconsolidation is complete and the memory is safely stored, the opportunity to interfere is lost. Not any new information at the time of retrieval could modify the original memory. Therefore, memory reconsolidation should be viewed as an update mechanism. Memory is not a recording; memory is a construction.  To be useful to us in the present and future, that reconstruction must constantly change (Sederberg et al., 2011). Conclusion In conclusion PTSD is a disorder that is mostly brain related but mostly psychological but with good care of the subject them going to see the therapist to help them let go of what is disturbing them is better than just giving the patient drugs to cope, with anything the brain is a very powerful tool and if computed to a certain way by the it is how the brain will react no doubt since if you don’t want to remember you won’t remember what happened but with the help of the right people like support groups will help in overcoming the fear other than breaking down the barrier. By making it seem more of a disease than a disorder will bring more complications to the patient other than help since that is not something that you get forms a virus or bacteria or even it is not contagious but psychological. Recommendation Thus the recommendation I have to despite the need to want to know why the brain acts the way it acts let not forget that it is still a powerful tool that can do many things if just let to do it on its own since drugs are not also so good to our bodies they make us dependant on them despite them being a cure for most of our troubles it is not the best for all of the problems we have. Future research should be done to help people know how to deal with extreme fears so as not to undergo the PTSD despite some having success in memory reconsolidation but not all. Future research Future research should be done to see how to deal with the people suffering with PTSD and how to deal with memory reconsolidation not also in the medicine sector but also acupuncture or other various methods that bring calm to people and doesn’t revolve around taking drugs also by investing more in the therapy approach to overcome the disorder. References Chan and LaPaglia (2013) Impairing existing declarative memory in humans by disrupting reconsolidation.  PNAS http://www.pnas.org/content/early/2013/05/16/1218472110.abstract Jovanovich, T., PhD. & Ressler, Kerry J, M.D., PhD. (2010). How the neurocircuitry and genetics of fear inhibition may inform our understanding of PTSD.The American Journal of Psychiatry, 167(6), 648-62. Retrieved from http://search.proquest.com/docview/366580481?accountid=13380 Forcato, C., Rodrı`guez, M. L., Pedreira, M. E., & Maldonado, H. (2010). Reconsolidation in humans opens up declarative memory to the entrance of new information. Neurobiology of Learning and Memory, 93,77 – 84 Hardt, O., Einarsson, E., & Nader, K. (2010). A bridge over troubled water: reconsolidation as a link between cognitive and neuroscientific memory research traditions.Annual Review of Psychology, 61, 141 - 167 Jonathan E. Sherin, Charles B. & Nemeroff.(2011). Post-traumatic stress disorder: the neurobiological impact of psychological trauma. Dialogues Clin Neuroscience.; 13(3): 263–278. Sederberg, P. B., Gershman, S. J., Polyn, S. M., & Norman, K. A. (2011). Human memory reconsolidation can be explained using the temporal context model. Psychonomic Bulletin & Review, 18 , 455-468 Soeter, M., & Kindt, M. (2012). Stimulation of the noradrenergic system during memory formation impairs extinction learning but not the disruption of reconsolidation. Neuro psychopharmacology, 37 , 1204 – 1215 Sutherland, R.J., & Lehmann, H. (2011). Alternative conceptions of memory reconsolidation and the role of the hippocampus at the systems level in rodents. Current Opinion in Neurobiology 21(3), 446-451.doi:10.1016/j.conb.2011.04.007 Read More
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