Evaluating the Limitations of Post-traumatic Amnesia as a Severity Scale Traumatic brain injuries (TBI) account to a third (30.5%) of all injury-related deaths in the U.S. with an estimated 1.7 million individuals sustaining TBI each year (Center for Disease Control and Prevention, 2010). Classifications of brain injury (e.g., mild, moderate and severe) is mostly done using the Glasgow coma scale (GCS) which has gained broad acceptance for the assessment of the severity of brain damage (Bauer & Fritz, 2004). Recent studies suggest that almost all patients with moderate or severe TBI have a period of recovery during which they are responsive but confused. This state is commonly referred to as the post-traumatic amnesia. Post-traumatic amnesia (PTA) is defined as “a failure of continuous memory” (Artiola et al., 1980; p.377). PTA is often cited as the best method for codifying the degree, level of recovery and outcome after a closed head injury (e.g., Artieola et al., 1980; Tate, Pfaff, & Jurjevic, 2000). PTA duration is a better indicator of outcome than early injury scales such as the GCS score (Richardson et al., 2009).This analysis will examine the limitations of the general PTA assessment scale, and investigate the benefits and limitations of both retrospective and prospective methods used to measure the duration of PTA. There is a frequent assumption that coma depth and extent, and PTA are concomitant—reflecting different facets of common mechanism (Wilson, Teasdale, Hadley, Wiedmann, & Lang, 1993). Researchers contend that when PTA and coma have been juxtaposed, their correlation has substantiated to be only moderately closer. Furthermore, they assert that previous studies exploring PTA and coma as predictors of outcome ... ... middle of paper ... ...reliable is it? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC486693/pdf/jnnpsyc00001-0046.pdf McMillan, T.M., Jongen, E.L.M.M., Greenwood, and R.J. (1996). Assessment of post-traumatic amnesia after severe closed head injury: retrospective or prospective? Journal of Neurology, Neurosurgery, and Psychiatry, 60, 422-427 http://jnnp.bmj.com/content/60/4/422.full.pdf Tate, R. L., & Pfaff, A., Jurjevic, L. (2000)Resolution of disorientation and amnesia during post-traumatic amnesia. Journal of Neurology, Neurosurgery, and Psychiatry, 68, 178-185 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736763/pdf/v068p00178.pdf Wilson J.T.L., Teasdale, G.M., Hadley, D.M., & Wiedmann, K.D., Lang, D. (2012). Post-traumatic amnesia: still a valuable yardstick. Journal of Neurology, Neurosurgery, and Psychiatry, 56, 198-201 http://jnnp.bmj.com/content/57/2/198.full.pdf
A study done by Kylie Sutherland and Richard Bryant in 2007, highlights the importance of memory in PTSD symptoms. For their study, they took 20 PTSD victims who had either been involved in a non-sexual assault or a motor vehicle accident. They had the participants look at positive and negative cue words and asked them to point out a memory for each. They took five words for e...
Concussions are very common. In the United States alone 1.4 million people suffer from concussions annually (Schafer). Researchers studied fifty brains of people who have suffered from concussions t...
Chronic Traumatic Encephalopathy, previously referred to as dementia pugilistica, can be understood as a tauopathic, neurodegenerative and neuropsychiatric disease. While there is no neurobiological or neuropathological explanation as to why CTE occurs, the majority of researchers believe the disease is strongly related to previous head injuries. An individual suffering from CTE will most likely experience changes in their mood, behavior and cognition. Because this is a relatively new area of research, there are still a vast amount of unknowns pertaining to the disease’s symptoms, pathology, and natural course.
The authors of this article stated that “lesions restricted to the hippocampal formation and/or extend hippocampal system can disrupt conscious recollection in anterograde amnesia…” (Gilboa, Winocur, Rosenbaum, Poreh, Gao, Black, Westmacott and Moscovitch 2006). These authors believed that lesions that occurred in this area cause the patient to suffer from anterograde amnesia.
Yates, Keith, et al. “Longitudinal Trajectories of Postconcussive Symptoms in Children With Mild Traumatic Brain Injuries and Their Relationship to Acute Clinical Status.” Pediatrics. 123.3 (2009) : 735-743. Web. 11 Apr. 2014.
...l and cognitive function after severe traumatic brain injury. Journal Of Trauma & Acute Care Surgery, 73(2 Suppl 1), S165-72. doi:10.1097/TA.0b013e318260896a
Those who are in favor of retrieved memories state that these memories can be repressed and remain unattainable for years until an individual seeks therapy, where these memories can often be uncovered and trauma related to them can be treated (Freyd, 1994). On the other hand, some individuals have expressed concerns with the concept of repressed memories since, according to them, there is little scientific evidence that can support the theory (Patihis, Ho, Tingen, Lilienfeld & Loftus, 2014). In other words, cases where individuals experience traumatic events but often lack memories of these, often do not provide sufficient reliable evidence to make credible arguments. Memory research offers further insight into the controversial topic of “memory wars” by explaining if the notion of repressing memories and placing them into the unconscious is a feasible hypothesis. Furthermore, research presented in this brief will discuss the reliability and usefulness of using recovered memories as evidence in a court cases. Due to the controversial nature of recovered memories in judicial courts and scientific communities, it is important to consider research in the area to determine truthfulness in allegations involving recovered memories, as these have previously posed
Traumatic brain injuries, ingestion of toxic substances that alter the brain, emotional distress, and hypoxia/ anoxia serve as the most common causes for amnesia. Traumatic brain injuries occur because of damage to brain tissue, such as concussions, alteration, lesions, and destruction of tissue. Due to complex neural connections and pathways, the severing of any of them is irreplaceable. Toxic substances could include many drugs such as alcohol or other illegal concentrated substances. When the brain receives inadequate oxygen, it suffers hypoxia, and when the brain cannot receive any oxygen, it undergoes
Consequently, any major incidents that involve severe head injuries by force may cause retrograde amnesia. So, what is the significance of short and long-term memory storage in relation to amnesia? Through encoding and retrieval, we are able to experience external events; record them in our sensory memory; where they become encoded in our short-term memory; and then eventually encoded to our long-term memory—which is beneficial to our retrieving process. Again, imagine waking up one morning with a memory deficit, due to an incident that you have no idea occurred. How do you imagine you would react?
All of the disorders in the Dissociative Disorders category need to be distinguished from conditions which are due to a General Medical Condition or the use of a Substance. Moreover, Dissociative Amnesia is within the diagnostic criteria for Dissociative Fugue, Dissociative Identity Disorder, Posttraumatic Stress Disorder, Acute Stress Disorder and Somatization Disorder; hence, an additional diagnosis of Dissociate Amnesia is not given. Dissociative Amnesia must be differentiated from Age-Related Cognitive Decline and nonpathological forms of amnesia.
Humans’ memory involves three steps; encoding, storage, and retrieval. Different types of amnesia affect different parts of our memory. Anterograde amnesia (AA) is a type of memory loss that causes an individual’s storing ability to fail. A patient with anterograde amnesia is the one who is grossly deficient in the formation of new memories. (H. Markowitsch 155-183) This is an interesting effect, since it is very different from the common idea of memory loss. The individual will still be able to recall memories from before the amnesia, however. While the exact cause of AA is still unknown, there are many possible causes. It is most commonly acquired one of three ways. One cause is benzodiazepine drugs. These are psychoactive drugs that alter brain function, resulting in temporary changes to perception, mood, consciousness, and behavior. These drugs, if abused, can cause anterograde. The second cause is a brain injury, but only if the damage is done to the hippocampus or the surrounding area. Should the injury not cause death, it can cause amnesia. The third cause is illness. This cause is much rarer than the previous two, however. Amnesia will only occur if the illness causes inflammation of brain tissue. However, there is also a form of temporary AA called blackout. This most commonly happens when one gets drunk. The rise in blood alcohol concentration causes short term memories created during intoxication to be blocked from storage and later retrieval. This is only temporary, since long term memory creation is restored once the individual is sober. An example of AA in media would be the movie Memento, in which the main character retains his personality and old memories, but cannot form any new
...d disregard clues in a situation and fail to warn the person to use safety and caution (Pitman et al. 771). Research has shown that when affected by PTSD the hippocampal size has decreased between “0.0-0.5 which in percentage is 0-20%”, and that is a relatively large margin (Vilens and Sher 5). Vilens and Sher examined the reduction in the hippocampus by types of traumatic events and found that, “there seems a trend toward combat trauma resulting in larger changes, followed by childhood sexual abuse, accidents and interpersonal violence” (5). Studies on the amygdala have shown an increase in reaction to trauma related stimuli, and also play a role in the extent of the symptoms that one experiences (Pitman et al. 772). The prefrontal cortex, and corpus callosum both show lower volumes in people diagnosed with PTSD rather than those who are not (Vilens and Sher 5-6).
Normal memory function involves many parts of the brain, and any disease, injury or psychological problem can interfere with the brains function. Amnesia can result from damage to the brain structures that form the limbic system, which controls your emotions and memories. These structures include the thalamus and
While there are several classified types of amnesia I choose to focus on retrograde and anterograde amnesia, because these are most common. Retrograde amnesia refers to the inability to remember events before the brain damage occurs, and anterograde is the inability to remember events after the brain damage. (2). Okay, so now I know the difference. One you cannot remember your past. The other you cannot remember your present. Now, the question to be posed is how exactly do these two degrees differ in relation to the way the brain operates when confronted with the trauma?
Research has demonstrated the vast implications of false memories for eyewitness testimony and therapeutic recall. However, there is also great potential for positive applications of this research. The plasticity of memories could have significant therapeutic implications. Positive false memories could be created as well as neutralizing traumatic ones. Researchers in cognitive psychology and neuroscience are currently researching these possibilities. This paper will discuss the current state of research on therapeutic memory manipulation.