MEMORY CONSOLIDATION AND HIPPOCAMPUS | ALCOHOLIC KORSAKOFF’S SYNDROME AND DIENCEPHALIC AMNESIA

MEMORY CONSOLIDATION AND HIPPOCAMPUS | ALCOHOLIC KORSAKOFF’S SYNDROME AND DIENCEPHALIC AMNESIA

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According to an old concept of how the long-term memory develops after initial acquisition is referred to as consolidation. However, from a cognitive neuroscience perspective, consolidation is conceived of as biological changes that underlie the long-term retention of learned information, and we can ask what brain structures and systems support this process.

 

Because damage to the medial temporal lobe does not wipe out most of the declarative memories formed over a lifetime, we know that the hippocampus is not the storehouse of stored knowledge. Rather, the medial temporal lobe appears to support the process of forming new memories; that is, the hippocampal region is critical for the consolidation of information in long term memory. The strongest evidence that the hippocampus is involved in consolidation comes from the fact that amnesics have retrograde amnesia for memories from one to a few years prior to the damage to the medial temporal lobe or diencephalon, a pattern that does not support a storage role but rather a role in consolidation.

 


What might consolidation involve at the neural level? One idea is that consolidation strengthens the associations between multiple stimulus inputs and activations of previously stored information. The hippocampus is hypothesised to coordinate this strengthening, but the effects are believed to take place in the neocortex. The idea is that once consolidation is complete, the hippocampus is no longer required for storage or retrieval. Nonetheless, keep in mind that although the memories are stored in the neocortex, the hippocampus is crucial for consolidation.

 

Alcoholic Korsakoff’s Syndrome and Diencephalic Amnesia

The medial temporal lobe is not the only area of interest in human memory. Amnesia emerges from brain damage in other regions too. For example, damage to midline structures of the diencephalon of the brain causes amnesia. The prime structures are the dorsomedial nucleus of the thalamus and the mammillary bodies. Damage to these midline subcortical regions can be caused by stroke, tumors, and metabolic problems like those brought on by chronic alcoholism as well as by trauma.

 

In the last half of the nineteenth century, the Russian psychiatrist Sergei Korsakoff reported an anterograde and retrograde amnesia associated with alcoholism. Long term alcohol abuse can lead to vitamin deficiencies that cause brain damage. Patients suffering from alcoholic Korsakoff’s syndrome have degeneration in the diencephalon, especially the dorsomedial nucleus of the thalamus and the mammillary bodies. It remains unclear whether the dorsomedial thalamic nucleus, the mammillary bodies, or both are necessary for the patients’ amnesia. Yet, damage to the diencephalon can produce amnesia.

 

References:

 Gazzaniga, M.S., Ivry, R., & Mangun, G.R. (2002). Cognitive Neuroscience: The Biology of the Mind. New York: W.W. Norton.

Gleitman, L. R., Liberman, M., & Osherson, D. N. (Eds.)(2000). An Invitation to Cognitive Science, 2nd Ed. Cambridge, MA: MIT Press.

Levinthal, C.F. (1990). Introduction to Physiological Psychology. New Jersey: Prentice Hall.

Sternberg, R.J. (2009). Applied Cognitive Psychology: Perceiving, Learning, and Remembering. London: Cengage


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