Neurophysiological Basis of Amnesia - Essay Example

? Neurophysiological Basis of Amnesia Within the spectrum of memory and cognitive disorders, there can be both organic and psychological causes. The lines between the two can blur easily. There are dissociative disorders in which medical testing is required to rule out neurophysiological factors that can mimic the effects of deeper, organic dysfunction. Key distinguishing factors are coming to light due to new research, and the post-mortem study of affected brains. While simple brain trauma or disease-states can cause the loss of memory, there are organic/medical conditions that may also impede new memories. The classic form of 'soap-opera' amnesia seems to close off personal information, allowing a fresh start upon which new plot-twists can be written. States similar to this can be termed psychogenic, or dissociative. While the loss of identifying information can result from emotional-psychological or medical causes, the latter may result in an inability to progress beyond the point of initial neuropathology. PSYCHOLOGICAL FACTORS Psychogenic, or what is now known as Dissociative amnesia, is one of several conditions called dissociative disorders, in some cases related to dissociative identity disorders. These disorders are mental illnesses in which failure and disruptions occurs in the patient's conscious self. This includes anomalies in memory, identity, and perception of the world or themselves. The dissociative symptoms themselves are the result of a plurality of these symptoms. This family of conditions causes profound disruption of the patient's normal ability to function socially. With consequences for relationships and vocation. Psychogenic/Dissociative amnesia occurs when certain information is blocked from the mind, most likely in conjunction with a particular neurological or psychological trauma - from which the individual feels a desperate instinct to retreat or hide from. But this break from reality impedes one's ability to remember vital personal details and necessary information. This lapse leaves the individual with gaps far of far greater severity than simple 'locked-my-keys-in-the-car' absent-mindedness borne of unfocused distraction. In order to block the emotional trauma, extensive stretches of time must be excised from conscious recollection, with all the social consequences therein. Dissociative amnesia occurs more often in females than males, (Web MD) and it is linked to stress and emotional trauma. Disruptions in society due to crisis or violence make these conditions more likely, such as situations of war or disaster. ORGANIC FACTORS Brain injuries can result in essentially two discrete patterns of memory loss; Anterograde and Retrograde amnesia. Anterograde amnesia is characterized by an inability to form new memories of events preceding the initial brain trauma. Past events, and those from childhood may be well recalled; but the ability to record new, factual information concerning items and facts since the accident will be impeded. The patient may be – stuck – in time, without realizing it. Short-term memory may be preserved; thus it is possible to engage the patient in normal conversation, during which they will be able to respond naturally, and may seem relatively normal for the duration of the stimuli. Interruption, or simply the passage of time will impede these memories. Knowledge is accumulated, and then ‘dumped’ from short-term memory, without the safety-net of long-term memory acquisition and association. With damage to the structures governing more permanent memory tracing and formation, it is ‘out of sight, out of mind’, and the specific details of the interaction will no longer be accessible to the patient. (Myers, 2006) , (Winocur, 2001) In this case, there may be trauma to the basal forebrain, which contains regions responsible for the production of acetylcholine, strongly suspected as being crucial towards the formation of new memories. (Myers, 2006) Damage to the artery system supplying this region with blood can also induce trauma leading to similar consequences. Structures whose damage creates a proclivity to Anterograde amnesia include a deep, internal structure called the diencephalon, which includes the medial thalamic nuclei. (Myers, 2006) Meyers has documented that even when the ability to form new, factual memories of events is impeded, certain task-oriented instinctual memory formation may still be possible. “Thus, an individual with amnesia can be taught a new skill, such as how to play a game or how to write backwards. The next day, the amnesic individual will claim to have no memory of the prior session, but when asked to try executing the skill, can often perform quite well - indicating that some memories have been formed.” (Myers, 2006) The opposing condition, retrograde amnesia occurs – typically due to damage to the hippocampus, which damages older memories. The patient have no difficulty in acquiring new memories on into the future, but will be unable to recall events prior to the accident. In this eventuality, researchers have noted that recall may be contingent on proximity to the accident. Memories closer in time to the actual trauma may be unrecoverable, but some aspects of childhood memory may be extant. (Winocur et al. 2001) Winocur found during rat brain studies that food preferences acquired within two days of hippocampal surgery suffered memory impairment. But older memories appeared intact. The role of the hippocampus in amnesia and memory will be more fully described below. But the delineation between organic and psychological factors as listed above, is a priority towards our understanding of the acquisition of new memories. For years, neuropsychological tests involving functional brain imaging have suggested that the hippocampus does store an allocentric representation of actual spatial locations. (Burgess et al. 2001) Hassabis et al. (2006) conducted tests to determine whether a population of amnesic patients with primary damage to the hippocampus would be able to acquire novel imagined experiences upon hearing short, verbal descriptions corresponding to common occurrences from contemporary, daily life. This study revealed a significant deficiency compared with the control group in imagining new experiences. Evidence suggests that trauma to the hippocampus can leave patients with an inability to orient imagined objects within a spatial context. There is difficulty, it seems in organizing items to concoct a novel scenario due to an ambiguity in terms of environmental coherence, or stability. (Hassabis et al. 2006) Episodic memory and the mental flexibility needed for hypothetical imagining or extrapolation of events exhibit considerable similarities concerning the underlying psychological mechanisms associated with both. (Greenberg & Rubin, 2003.), (Conway & Pleydell-Pearce, 2000.) Here, we can putatively define episodic memory as the retrieval of the context of actual experienced events in a literal sense. (Burgess et al. 2001) These thought-constructs include imagery, access of semantic memory/knowledge, sentence-paragraph order and structure, and nuanced perspectives and details concerning remembered events. (Rubin et al. 2003), (Addis et al. 2004) In addition, episodic memory and imagination depend upon the relevant visualization of key elements in a structural/spatial context, apart from simply remembering what something looks like. (Burgess et al. 2001) Face and object recognition seems to involve different brain functions, and regions besides the hippocampus. (Rosenbaum et al. 2004), (Kosslyn et al. 2001) It's easy to hypothesize, at this point that the hippocampus is vital towards structural positioning in terms of strategic thinking. Without its proper functionality, contrived images become disjointed in space and are unbound to reality. By extension, one might project that the hippocampus allows the mnemonic reconstruction of places and events spatially. The hippocampal system is needed for retention/retrieval of detailed, autobiographical memories, regardless of how long ago they were acquired. (Moscovitch et al. 2005), (Maguire, 2001) It has been known for decades that damage to the hippocampus can - in the immediate sense, cause amnesia. Physical trauma therein may prevent the patient from reconstructing the past within the context of memory. Hinting at the role of the hippocampus in imagination and scenario generation are other observations that victims of organic, physically-traumatic, or hypoxic brain-damaged amnesia may have difficulty imagining themselves in the future. (Rosembaum et al. 2005), (Bayley et al. 2005), (Klein et al. 2002) Numerous studies have attempted to elucidate the exact role of the hippocampus functionally, with ambiguous results. The hippocampus has been characterized as a computational index for neocortical storage, and a time-sensitive long-term memory support structure, (Medial-temporal region) while the parietal lobes are involved with manipulation and re-imagining memory episodes. (Burgess et al. 2001), (Maguire et al, 2006) While there is general agreement that this brain region does support episodic memory is difficult to describe in terms of neurobiological mechanisms. Functional brain imaging has revealed that the hippocampus is concerned with memory, maintains long-term memory, and again - spatial memory. Division of labor within the medial temporal lobe seems to exist, but it is difficult to localize episodic or semantic memories to a particular fold of brain matter. (Squire et al. 2004), (Eichenbaum, 2004.), (McKenna & Gerhand, 2002), (Hartley et al. 2007) Semantic memories, on the other hand, benefit from hippocampal contribution for some time before they can be retrieved independently of the hippocampus. Even semantic memories can be comingled with episodic features dependent on the hippocampus. (Muscovitch et al. 2005) Researchers have reviewed and catalogued numerous aspects related to episodic memory in general, including the distinctions between, different forms of memory itself, and whether hippocampal injury/lesions have different influences on recent or distant memories. Still, other areas in which distinctions are not always clear would be the difference between episodic retrieval compared with read–out, recitation-based memory? In addition what causes the formation of – and the retrieval of a specific event memory in terms of the active neurophysiological mechanisms? Neural models of the medial-temporal and parietal regions for memory retrieval represent likely options by which to mechanistically address these questions. TESTING METHODOLOGY A vital tool in these investigations, once we have identified the role of the hippocampus is the elucidation of magnetic resonance imaging. In many neurological studies, the name and process is further refined as 'functional MRI', or fMRI. Functional MRI (fMRI) can measure signal/impulse changes in the brain that are due to changes neurological activity. The brain is initially scanned at a lower resolution but with a rapid frequency. Increases in neural activity cause subsequent increases in the Magnetic resonance signal. This effect can be referred to as the BOLD (blood-oxygen-level dependent) mechanism. Increased neural activity causes an increased demand for oxygen due to consumption, and the circulatory system not only meets the need, but can actually overcompensate for this condition, increasing the amount of oxygenated hemoglobin compared with deoxygenated hemoglobin. Because of the tendency of deoxygenated hemoglobin to attenuates the MR signal, the reaction of the circulatory system causes a signal increase in proportion to the neural activity. The precise mechanics of the correlation between neural-metabolic activity and the BOLD effect is a subject of ongoing research. And with greater oxygen consumption comes a greater need for glucose. Key to the fMRI technology is a tracer element, often a radiological marker that can be employed to identify not simply which brain areas 'light-up' in terms of electrical current, but actual metabolic utilization. Radiolabeled carbon-14 isotopes of deoxyglucose can be used to determine what brain regions are metabolizing glucose and what rate and time. The isotope of carbon will release neutrons that can be read via exposure to X-ray film. With this tracer in the bloodstream, an experimental animal's brain would pull glucose into the active brain regions exhibiting the highest energy/fuel consumption. (Filler, 2010) The synthetic glucose isotopic analog occupies the normal receptors for the molecule, blocking the normal glucose breakdown. This will cause the isotope tracer to accumulate inside the cell; the more active that cell, the greater the quantity detected. Thus, increased exposure on the X-ray film. (Filler, 2010), (Aggleton et al. 2005), (Maguire et al. 2005) DISCUSSIONS Researchers can demonstrate that amnesic patients with bilateral damage to the hippocampus were significantly impaired on tasks of visualization, recall, and the formation of new imaginary images. (Hassabis et al. 2006), (Spiers et al. 2001) Using questionaires and MRI techniques, it is possible to arrive at several, supportable conclusions: Initially, the literature supports the supposition that patients with hippocampal amnesia have a deficit in the rich-imagination of novel experiences. Also, these facts elucidate the true capacity of the hippocampus as it extends beyond only reliving past experiences, including not only concocted, realistic extrapolations related to the self, but this region controls the generation and construction of completely fictional episodes within the mind of the subject. Is there a possibility that the described dysfunctions in these brain-injured patients are due to simply wide-spread memory failure, due to amnesia once again, whereby ‘holes’ exist in the scenarios they should be able to construct? The process of memory retrieval is, quite obviously impeded in amnesiacs. Further research seeking to fully resolve such issues should focus upon testing patients in everyday tasks reinforced by numerous, non-episodic repetitions. From the available literature, as described above, it is plausible to label the hippocampus as a spatial-coherence center. This proposition underscores the patient deficits and could encompass the entirety of the dysfunctional findings. What scenarios patients did imagine were fractured, incoherent and lacking in the logical structure of vivid memories. The hippocampal-region may be said to make a critical contribution to the generation of novel experiences by granting the spatial dimensions, and environmental grounding without which the item/object details do not make rational sense. (Eichenbaum, 2004). With a close connection between imaginary experiences and actual, episodic memories, damage to this brain region can be said to fundamentally impede the ability to imagine or immerse one-self in what should be remembered events. For investigators and clinicians with an interest in the study and documentation of patients with amnesia, the flaws in normal performance could be generalized as simple memory impairment, especially for complex instructions requiring step-by-step execution. But, in the study described by Hassibis et al. 2006, there was verification with visual reminders during practical performance analyses, used to verify that the subjects did not actually forget the instructions. Despite ready reminders, an impairment of imagination was extant nonetheless – not only a problem with memory. This revealed the linkage between hypothetical imaginings and the ability to form real memories. The Hassibis study participants did not ask for clarification or explanation, as they would if they were truly aware of mental confusion. According to the establishment view of memory retrieval and formation, the function of the hippocampal-system in episodic memory creation is time-sensitive. Eventually? true long-term ‘storage’, will occur with relocation and consolidation to the neocortex in a gradual process. (Squire et al. 2004) In the traditional theories, the neocortex is said to hold representational forms that allow a framework of spatial reasoning, and placement during episodic extrapolations, as well as semantic, non-spatial memories. This older view would posit memory maintenance without support from the hippocampus. But often, it is in the breaking of something that its true value is revealed. Logically then, the neocortex would have the presumed ability to coordinate function in multiple regions in order to meet the needs of long-term memory and imagination. Disturbances and trauma to the hippocampus should make no difference for the projection of new scenarios via active imagination, yet research is finding that this is not the case. (Prabhakaran et al. 2000), (Moses & Ryan 2005). Older theories must give way to findings demonstrating the imagination impairment experienced by patients suffering trauma and lesions on the hippocampal region. Hassibis et al. instructed patients not to verbally recount an actual memory, in part or as a whole. Control groups had no difficulty replicating vivid memory recreations with minimal use of episodic memory. (Hassibis et al. 2006) The traditional views concerning amnesia, the neocortex, and the hippocampus should be subject to reevaluation, as should all scientific theories in principle. Findings above give support for the idea that the hippocampus plays a vital role in imagining experiences via the adaptive reconstruction of spatial context. This function may not be destined for shunting off into the neocortex. (Hannula et al. 2005), Lee et al. 2005). An interconnectedness exists between the process of pure imagination of new experiences and the ability to reminisce over the past. The hippocampus has a clear role both in future projections and past reminders It has been theorized that discrepancies between investigations of distant episodic memory in hippocampal-injury patients may have to do with limitations in the vividness, or fidelity of an immersive memory of the past. (Bayley et al. 2005) Further tests, and more comprehensive questionaires and scoring systems should be performed. Research by Levine, et al. found an age-based discrepancy that sheds light on the roles of different forms of memory. Question-protocols were scored according to a reliable system for categorizing episodic and non-episodic information. It was found that young adults heavily favored a strong recollection of episodic details reflecting events, locations, and perceptions, older adults preferentially responded to semantic details not limited in time or place specifically. This pattern continued after further probing for contextual details. (Levine et al. 2002) Here is an opportunity for further elucidation; what physical differences and progressions could be identified by age? Would an fMRI reveal a shifting pattern between youth and maturity? SUMMARY We have investigated the physiological underpinnings of amnesia, with discussion of both psychological, and medical-neurological causes. The primary focus of this study has been an identification of the organic workings in the case of amnesia, as a neuropathology. While the initial symptoms of both psychological and neurological amnesia are initially similar; key differences highlight the difference between mental dissociation and trauma: 1.) Localized damage to the Hippocampus. 2.) An inability to imagine the future. 3.) Diminished capacity to construct imaginary, physical scenarios in the present 4.) Dysfunction in episodic memories of specific places in the past. It was also necessary to describe the process by which most detailed scans of the activity of brain regions is measured. Magnetic resonance imaging, or MRI, or fMRI can detect metabolic activity in various brain regions. Techniques exist to measure the oxygen intake, glucose metabolism, and electrical output Radioisotopes of carbon can enter cells, bind the available receptors, and displace conventional carbon within glucose molecules. The emissions from these isotopes can be read via X-ray technology. In this manner, brain activity can be measured by the documentation of neural activity through metabolism. The more emissions detected, the more active the cells. In addition, we have demonstrated the evolution of thought within the fields of neurology by demonstrating challenges presented herein to older theories concerning the importance of the neocortex. It has been theorized that in order for long-term memory to form, there must be a migration of the associated brain activity from the hippocampus to the neocortex. But the amnesia caused by physical, and hypoxic trauma to the hippocampus entailed a memory pathology that proves compelling. The inability to form, and recollect spatial information due to damage is a vital revelation that promises to push neurophysiological research towards further discoveries. Throughout the discussion, the necessity, and opportunities for further research has been described. References Addis, D. R., Moscovitch, M., Crawley, A. P. and McAndrews, M. P. (2004), Recollective qualities modulate hippocampal activation during autobiographical memory retrieval. Hippocampus, 14: 752–762. doi: 10.1002/hipo.10215 Aggleton, JP. Vann, SD. Denby, C. Dix, S. Mayes, AR. Roberts, N. Yonelinas, AP. 2005. 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Anterograde and retrograde amnesia in rats with large hippocampal lesions. Hippocampus. 2001;11(1):18-26. Read More