Amnesia
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Knowlton, B. J., Mangels, J. A., & Squire, L. R. (1996). A neostriatal habit learning system in humans. ''Science, 273''(5280), 1399-1402. | Knowlton, B. J., Mangels, J. A., & Squire, L. R. (1996). A neostriatal habit learning system in humans. ''Science, 273''(5280), 1399-1402. | ||
Stirling, J. (2002). ''Introducing neuropsychology.'' New York: Psychology Press. | Stirling, J. (2002). ''Introducing neuropsychology.'' New York: Psychology Press. | ||
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Ogden, J. A. (2005). ''Fractured minds.'' New York: Oxford University Press. | Ogden, J. A. (2005). ''Fractured minds.'' New York: Oxford University Press. |
Revision as of 04:41, 22 April 2008
Amnesia is a memory deficit, resulting from brain damage, disease, or injury. Memory loss may be selective or generalized, temporary or permanent, and it may affect short-term memory, long-term memory, or both. Research for amnesia is does not have the ability to be experimentally manipulated. Therefore, amnesia information is reliant on amnesic individuals who volunteer for research.
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Diencephalic Amnesia
Damage to the diencephalic structues also has the ability to lead to memory impairments. Cases of diencephalic amnesia were used in a study by Knowlton et. al. hypothesizing separate but parallel learning systems. In patients with amnesia, either with damage to the hippocampal formation or diencephalic midline, participants performed normally on a probabilistic classification task. However, scores for a declarative memory task were poor. The results were opposite for participants with Parkinson's disease. These results demonstrate declarative memory is dependent on the medial temporal lobe or diencephalon, but not on the neostriatum. The opposite is the case for probabilistic classification learning.
A 'pure' case of diencephalic amnesia comes in the form of NA. After suffering a freak accident involving a fencing foil, NA had damage to his left dorsal thalamus, his mamillary bodies (bi-laterally), and his mamillo-thalamic tract. He showed normal short-term memory, but was severely impaired in declarative long-term memory, particularly for verbal material.
Global Amnesia
Global amnesia is usually a result of bilateral damage to structures on the internal aspects of the cerebral hemispheres. It is characterized by an inability to learn/retain new information, including verbal, nonverbal, visual, or auditory, as well as a period of retrograde amnesia. Those suffering from Korsakoff's disease as well as patients who survive herpes simplex encephalitis may demonstrate global amnesia.
Frontal Amnesia
Frontal amnesia is characterized as memory deficits resulting from frontal lobe damage. Typically, the patient is impaired in learning and recalling new information.
Korsakoff's Syndrome
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Concussion Amnesia
Concussion-induced amnesia almost always results in temporary memory impairment, unless there was organic damage to the brain. A typical case may include both anterograde (after on-set) amnesia and retrograde (before accident) amnesia. A unique feature of concussion amnesia is that memory loss usually is partially recovered with time, although there is nearly always some permanent loss. There may be impairments in the consolidation of new information from short-term to long-term memory.
ECT-Induced Amnesia
Electroconvulsive therapy involves the induction of epileptic seizures by electric current. ECT-induced amnesia resembles that of concussion amnesia. There is both anterograde and retrograde amnesia, but also shrinkage over time.
References
Knowlton, B. J., Mangels, J. A., & Squire, L. R. (1996). A neostriatal habit learning system in humans. Science, 273(5280), 1399-1402. Stirling, J. (2002). Introducing neuropsychology. New York: Psychology Press.
Ogden, J. A. (2005). Fractured minds. New York: Oxford University Press.