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Jackie Thill Physiological Psychology May 1, 2012 Final Paper Amnesia The human brain encodes, stores, and retrieves information; this process is what is referred to as one’s memory. Research has shown that memories are created, stored, and created in parts of the limbic system, especially the hippocampus (Carlson, 2010). There are three main types of memories sensory memory, short-term memory and long-term memory. Sensory memory is memory that takes less than a half of a second for one to be able to describe the item (Carlson, 2010). Short-term memory is the memory of the incident or the stimulus that last usually a few seconds and no more than a minute. Long-term memory is the storage of short-term memory and sensory memory that lasts for a greater length of time but not forever. Memories are one of the most important aspects of a person. Memories are how one remembers our childhoods, the faces of the one’s you love, and the moments that have changed your life making you the person you are today. What if you lost these precious memories or could not create new memories? “Amnesia refers to a deficit in memory that can be at the same time dense and yet circumscribed (Duff et. al, 2008).” In other words, amnesia is a condition in which a part of an individual’s memory is lost. There are many different types of amnesia and many different ways in which an individual can lose their memory. In this paper, there will be a focus on four types of amnesia, anterograde amnesia, retrograde amnesia, post-traumatic amnesia, and Korsakoff's syndrome and the research along with them. I personally chose this topic because my memories are the one thing I cannot imagine living without because my memories are the priceless. Anterograde Amnesia The first type of amnesia to look at is anterograde amnesia. Anterograde amnesia refers to the inability to learn new information after amnesia takes effect. Anterograde amnesia is one of the most studied and fascinating phenomena caused by brain damage usually a traumatic brain injury though there are other causes such as drugs, shock, or even illness (Carlson, 2010). Anterograde amnesia is the inability to create new long-term memories after the event of some sort of brain disturbance (Carlson, 2010). The likeliness of ‘pure’ retrograde amnesia is rare (Carlson, 2010). Normally patients with anterograde amnesia can create some new memories such as muscle memory. There has been a lot of research on anterograde especially because it is one of the hardest types of amnesia to cope with because the individual cannot learn anything new. Like many forms of amnesia, anterograde amnesia is not known to be caused by a specific location in the limbic system. Though, John Aggleton found that anterograde amnesia is regularly associated to the medial temporal lobe and the medial diencephalon (Aggleton, 2008). Looking through different studies, there is a different focus on each of the causes. Aggleton looked at a group of individuals with anterograde amnesia that was caused by fornix lesions and hippocampal lesions (Aggleton, 2008). Akira Midorikawa and Mitsuru Kawamura looked at a case study of a man who had his meningiomas, or tumors in the meninges, removed; after which he began to have seizures which then lead into anterograde amnesia (Midorikawa and Kawamura, 2007). Melissa Duff and others looked at a case study of an elderly woman who suffered from a closed head injury which then caused severe anterograde amnesia (Duff et. al, 2008). All studies show some of the different causes of anterograde amnesia. The article by Akira Midorikawa and Mitsuru Kawamura and the article by Melissa Duff both looked at how individual case studies dealt with their anterograde amnesia. Midorikawa and Kawamura looked at the effects of an antiepileptic drug (AED) on anterograde amnesia (Midorikawa and Kawamura, 2007). Antiepileptic drugs have been used to help prevent epileptic seizures and accelerated forgetting, but no studies have extensively shown the affects it has on anterograde amnesia (Midorikawa and Kawamura, 2007). Anterograde amnesia is such an extreme and powerful phenomenon that finding some kind of treatment is imperative. Midorikawa and Kawamura found that the AED had no effect on anterograde amnesia and that more than likely this type of amnesia is irreversible (Midorikawa and Kawamura, 2007). Duff, on the other hand, went a different way in her approach with treatment. In her case study, the older woman with anterograde amnesia was every bit as severe as the famous H.M. case (Duff et. al, 2008). impairments. Duff looked at ways to help individuals to cope with their memory It worked remarkably well, the patient developed real-world abilities (Duff et. al, 2008). This included breaking down tasks into smaller more practicable tasks and using lists/reminders to help her with responsibilities such as in the shower (Duff et. al, 2008). Though this also did not reverse the anterograde amnesia it made life more manageable and the patient was able to have a ‘successful’ life (Duff et. al, 2008). Retrograde Amnesia The second type of amnesia to look at is retrograde amnesia. retrograde amnesia to refer to the opposite of anterograde amnesia. Some believe Retrograde amnesia refers to the inability to recall old information after amnesia takes effect. Like anterograde amnesia, retrograde amnesia is caused by brain damage usually a traumatic brain injury or emotional trauma though there are other causes such as drugs or even illness (Carlson, 2010). Retrograde amnesia is a failure to access memories of events that happened, or information that was encoded, before the event of some sort of brain disturbance (Carlson, 2010). temporary. Retrograde amnesia is usually found to be Along with this, more new memories that are closer to the ‘brain disturbance’ are more likely to be elapsed than the memories farther away from the incident (Carlson, 2010). Narinder Kapur writes an analysis of the differences between the two types of retrograde amnesia, episodic amnesia and semantic amnesia (Kapur, 1999). Bernhard Sehm writes his findings on focal retrograde amnesia (FRA) (Sehm et. al, 2011). Episodic retrograde amnesia is described as forgetting personally experienced events or autobiographical information (Kapur, 1999). With episodic amnesia, the individual forgets things like their eleventh birthday or first day of school. Semantic retrograde amnesia is described as forgetting connections of knowledge or factual information (Kapur, 1999). With semantic amnesia, the individual forgets things such as geography or historical dates. FRA, also known as functional amnesia “is a rare neurocognitive disorder presenting with an isolated loss of retrograde memory (Sehm et. al, 2011).” Kapur found that “Extensive episodic and semantic retrograde amnesia generally entails lesions to a wide range of neocortical structures, particularly those in the temporal lobe (Kapur, 1999).” Along with that, Kapur also found that lesions to the frontal lobe and the thalamus can result in either of the two retrograde amnesias (semantic or episodic amnesia) though there is not a direct causation (Kapur, 1999). Sehm found that FRA was in the outcome of epileptic seizure (Sehm et. al, 2011). Andrei Miu looked at how high emotions can produce emotion-induced retrograde amnesia (ERA) (Miu et. al, 2005). Emotions play a huge role as a developmental factor and symptom of retrograde amnesia. Miu looked intently into how emotional arousal can enhance or severely harm one’s amnesia (Miu et. al, 2005). Miu showed this by giving participants emotionally arousing words which in turn produced either a positive or negative memory response (Miu et. al, 2005). Kapur found similar results saying that the emotional significant of the incident correlates with the severity of the retrograde amnesia (Kapur, 1999). Sehm found that patients with retrograde amnesia caused symptoms of emotional issues (Sehm et. al, 2011). Some symptoms included insecurity is social settings, because of fear of meeting people they should already know, anxiety of learning new things, and depression (Sehm et. al, 2011). Post-Traumatic Amnesia The third type of amnesia to look at is post-traumatic amnesia. Post-traumatic amnesia refers to a mixture of anterograde and retrograde amnesia that is caused by a traumatic brain injury (TBI); in addition individuals suffering from post-traumatic amnesia might not be able to remember specific people and the events around that person as well (Langhorn, et. al, 2010). Post-traumatic amnesia is caused by any TBI but usually from some sort of blow to the head. Statistics show that around seventy percent of TBIs patients will experience post-traumatic amnesia (Langhorn, et. al, 2010). Depending on the severity of the trauma correlates with the severity of the amnesia (De Monte, et. al, 2006). Veronica Eileen de Monte looked at the different effects of post-traumatic amnesia from a mild TBI on information processing (De Monte, et. al, 2006). It is important to look at the effects of mild traumatic brain injuries because that is most common brain injuries. De Monte “showed that patients with [mild traumatic brain injuries] in [post-traumatic amnesia] recalled fewer words after two presentations and after a delay and completed fewer symbols in 90 seconds on Digit Symbol than patients with [mild traumatic brain injuries] not in [post-traumatic amnesia] (De Monte, et. al, 2006).” With these results, De Monte concluded the patients with post- traumatic amnesia caused by mild traumatic brain injury have slower verbal memory and information processing (De Monte, et. al, 2006). Leanne Langhorn and E. Noé both looked at the rehabilitation of post-traumatic amnesia. Langhorn looked to understand if the fast medical personal started rehabilitation on individuals with post-traumatic amnesia the better affect the rehabilitation will have (Langhorn, et. al, 2010). Noé looked at how the apolipoprotein E genotype affects verbal memory recovery (Noé, et. al, 2010). Taking in the fact that the less severe the TBI is the easier the recovery it is; it is essential to look at the recovery especially of more extreme cases. Langhorn found that through literary analysis that there is not complete evidence to prove that either way the effect of early rehabilitation for individuals with post-traumatic amnesia (Langhorn, et. al, 2010). Noé found “APOE genotype seems to be associated with the trajectory of cognitive recovery after TBI, but does not play a determinant role in the efficacy of memory rehabilitation in this population (Noé, et. al, 2010).” Korsakoff's Syndrome The last type of amnesia that this paper will look at is Korsakoff’s syndrome. Korsakoff’s syndrome is defined as a more extreme case of anterograde amnesia referring to the inability to form any new memories but can recall all the old memories (Carlson, 2010). Patients can normally function, remember, and converse normally even though they have the inability to retain new information or events. Like the other amnesias, Korsakoff’s syndrome is caused by brain damage, in this case, from due to a vitamin B1 deficiency usually due to chronic alcohol abuse or malnutrition (Carlson, 2010). Roos Van Oort and Roy P. C. Kessels stressed the importance of executive deficits in individual’s with Korsakoff’s syndrome will greatly affect their daily living (Van Oort, R., Kessels, R. C. (2009). Van Oort and Kessels believed that a DSM-IV criterion does not fully encompass the how much Korsakoff’s syndrome affects the individual. In the end Van Oort and Kessels conclude that “Next to amnesia, executive deficits are a prominent characteristic of cognitive impairment in Korsakoff patients. It is argued that the new DSM criteria should consider incorporating executive dysfunction as an important feature of alcohol-induced persistent cognitive disorder (Van Oort, R., Kessels, R. C. (2009).” Maria de Fatima Alves Monteiro and Roy P. C. Kessels both looked at the how Korsakoff’s syndrome affect the individual and what steps can be taken toward helping the individuals. Kessels looked at how Korsakoff’s syndrome can produce fake memories (Kessels, et. al, 2008). Alves Monterio looked at how there are different rehabilitation. Kessels concluded after his studies, “There were deficits in source memory, in which patients incorrectly assigned previously learned words to an incorrect word list. Also, Korsakoff patients had extensive executive deficits, but no relationship between the severity of these deficits and the severity of confabulation or intrusions on a memory task was found (Kessels, et. al, 2008).” Alves Monterio found that individuals with Korsakoff’s syndrome respond positively were teaching individuals to be aware of their illness, find routine in life, and therapy for depression (Alves Monteiro, et. al, 2011). There are many other types of amnesia such as dissociative amnesia, Lacunar amnesia, and transient global amnesia. This paper talked about the four major types of amnesia and the research along with it. There is much research that still needs to be looked at so more options of rehabilitation and understanding of the different kinds of amnesia. Works Cited Aggleton, J. P. (2008). Understanding anterograde amnesia: Disconnections and hidden lesions. The Quarterly Journal Of Experimental Psychology, 61(10), 1441-1471. doi:10.1080/17470210802215335 Alves Monteiro, M., Prado Bolognani, S., Rivero, T., & Amodeo Bueno, O. (2011). Neuropsychological intervention in a case of Korsakoff's amnesia. Brain Impairment, 12(3), 231-238. doi:10.1375/brim.12.3.231 Carlson, N. R. (2010). Physiology of behavior. (10 ed., pp. 465-482). Boston: Allyn & Bacon. De Monte, V., Geffen, G., & Massavelli, B. (2006). The effects of post-traumatic amnesia on information processing following mild traumatic brain injury. Brain Injury, 20(13-14), 1345-1354. doi:10.1080/02699050601082073 Duff, M. C., Wszalek, T., Tranel, D., & Cohen, N. J. (2008). Successful life outcome and management of real-world memory demands despite profound anterograde amnesia. Journal Of Clinical And Experimental Neuropsychology, 30(8), 931-945. doi:10.1080/13803390801894681 Kapur, N. (1999). Syndromes of retrograde amnesia: A conceptual and empirical synthesis. Psychological Bulletin, 125(6), 800-825. doi:10.1037/00332909.125.6.800 Kessels, R. C., Kortrijk, H. E., Wester, A. J., & Nys, G. S. (2008). Confabulation behavior and false memories in Korsakoff's syndrome: Role of source memory and executive functioning. Psychiatry And Clinical Neurosciences, 62(2), 220-225. doi:10.1111/j.1440-1819.2008.01758.x Langhorn, L., Sorensen, J. C., & Pedersen, P. U. (2010). A critical review of the literature on early rehabilitation of patients with post-traumatic amnesia in acute care. Journal Of Clinical Nursing, 19(21-22), 2959-2969. doi:10.1111/j.13652702.2010.03330.x Midorikawa, A., & Kawamura, M. (2007). Recovery of long-term anterograde amnesia, but not retrograde amnesia, after initiation of an anti-epileptic drug in a case of transient epileptic amnesia. Neurocase, 13(5-6), 385-389. doi:10.1080/13554790701851536 Miu, A. C., Heilman, R. M., Opre, A., & Miclea, M. (2005). Emotion-Induced Retrograde Amnesia and Trait Anxiety. Journal Of Experimental Psychology: Learning, Memory, And Cognition, 31(6), 1250-1257. doi:10.1037/0278-7393.31.6.1250 Noé, E. E., Ferri, J. J., Colomer, C. C., Moliner, B. B., & Chirivella, J. J. (2010). APOE genotype and verbal memory recovery during and after emergence from posttraumatic amnesia. Brain Injury, 24(6), 886-892. doi:10.3109/02699051003724952 Sehm, B., Frisch, S., Thöne-Otto, A., Horstmann, A., Villringer, A., & Obrig, H. (2011). Focal retrograde amnesia: Voxel-based morphometry findings in a case without MRI lesions. Plos ONE, 6(10), doi:10.1371/journal.pone.0026538 Van Oort, R., & Kessels, R. C. (2009). Executive dysfunction in Korsakoff's syndrome: Time to revise the DSM criteria for alcohol-induced persisting amnestic disorder?. International Journal Of Psychiatry In Clinical Practice, 13(1), 78-81. doi:10.1080/13651500802308290