Longterm Memory A Episodic Memory

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To many clinicians, an impairment in episodic memory, the inability to recall information or events within spatiotemporal contexts in the period of minutes, hours, or days, is the hallmark of AD. However, it should not be considered as a single distinguishing feature. Episodic memory impairment accounts for the loss of spatial or temporal orientation that can occur early on in AD. Formal testing of this type of memory almost always reveals substantial impairment across a range of tasks, for example, recalling lists of words, sentences, and stories or recognition memory for words, faces, and pictures. From a behavioral standpoint, memory loss has a distinct pattern as the dementia progresses. The following are the stages in the breakdown of memory function in AD.

Early AD: Mild memory lapses occur but cause only a few problems for the person. They are often falsely attributed to other factors, such as the effects of normal aging, stress, or depression. Examples are forgetting errands, failing to forward messages, and becoming disorientated in unfamiliar surroundings. Memory of episodes in the near distant past is poor, including memory of conversations with other people. These types of memory problems do not necessarily indicate a progressive neuropsychologi-cal impairment or dementing illness. Moderate AD: The memory impairment starts to have a very significant effect on daily living activities. Memory errors include becoming disorientated even in familiar surroundings, forgetting familiar people or friends, and confusing the time of day or day of week. The person becomes increasingly unable to keep track of daily events. Severe AD: Memory errors become more severe and can present safety problems for the person, such as those associated with wandering or forgetting to turn off the gas stove. Close relatives may be forgotten. Marked positive signs become apparent, such as confabulation and paramnesia.

The substantive impairment in episodic memory has been related to the pattern of neurodegeneration in AD. Studies of pure amnesia have implicated the mesial temporal lobe structures in memory functioning, including the hippocampus, the parahippocampal gyrus, and the perirhinal and entorhinal cortices. There is evidence that these structures are more heavily damaged early on in the time course of AD, including neurodegeneration of the hippocampus in which severe changes in the CA1 field are observed. Additionally, neurofibrillary tangles (NFTs) are found in large quantities in the entorhinal cortex (affecting layers II and IV). This structure receives projections from the perirhinal and parahippocampal cortices, which in turn project to association cortex including regions of the frontal, parietal, and temporal lobes. A hierarchical vulnerability of individual cytoarchitec-tural fields has been established through neuropatho-logical studies in which NFTs appear in highest densities first in the entorhinal cortex and then in the CA1 fields and the association and sensory cortices (Fig. 1). Structural magnetic resonance imaging (MRI) has also shown that loss ofvolume ofthe hippocampus is related to episodic memory loss rather than other aspects of cognition (e.g., language and constructional praxis). In addition to mesial temporal lobe involvement, there is evidence that damage to the diencepha-lon contributes to memory disorder. First, a feature of episodic memory impairment in AD is a lack of sensitivity to the context in which a memory is formed, similar to that found in amnesic patients with dience-phalic damage, such as occurs in Wernicke-Korsak-offs syndrome. Second, structural MRI has revealed an association between episodic memory loss and shrinkage of the diencephalic (thalamic) region.

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