Implicit Memory and Metacognition

By Lynne M. Reder | Go to book overview

we need better information on how "frontal" memory impairments (false recognition, confabulation, intrusions in cued recall, domain-specific deficits in recalling studied information, source amnesia) relate to one another, within individual patients. How many underlying dimensions of variation are there (cf. Goldman-Rakic, 1987; Schacter, 1987b; Shimamura, 1995)? Furthermore, how do these different memory impairments relate to other cognitive deficits (poor planning, perseveration) exhibited by frontal patients ( Stuss, Eskes, & Foster, 1994)? We also need more sophisticated ways of characterizing what neural circuits are disrupted by frontal damage. For example, ruptured anterior communicating artery aneurysms often disrupt connections between frontal cortex and midbrain structures involved in neuromodulation. In light of our earlier suggestion regarding neuromodulation and "focusing," we need to be able to characterize which neuromodulatory systems (if any) are most likely to have been disrupted by a particular frontal lesion.

These analyses of metamemorial processes and the frontal lobes should interact closely with ongoing research concerning implicit memory. Little is yet known about how frontal lobe lesions interact with implicit memory phenomena, such as priming (for an exception to this rule, see Shimamura, 1992). In the earlier discussion, we have focused on how metacognitive processes interact with (i.e., retrieve and interpret) coherent episodic traces. However, situations frequently arise (even outside of implicit memory experiments!) in which people fail to retrieve a full-blown episodic trace associated with a particular experience, yet they are still influenced in some way by that experience. In these situations, metacognitive processes implemented by the frontal lobes are given the job of interpreting isolated images, thoughts, or feelings ( Squire, in press). Jacoby and others (e.g., Kelley & Jacoby, 1990) have offered useful cognitive analyses of how metecognitive processes interpret subtle changes in processing brought on by prior exposure to stimuli. However, there are limits as to how well we can understand the mechanisms of metacognition without looking more directly (by means of functional brain imaging and studies of brain-damaged patients) at how the brain maps our present thoughts and feelings onto specific past episodes. It appears to us that the time is ripe to develop, in greater detail, a cognitive neuroscience perspective on the processes that allow us to take full, conscious possession of the past.


ACKNOWLEDGMENTS

The writing of this chapter was supported by a National Defense Science and Engineering Graduate Fellowship awarded to the first author, National Institute of Neurological Disorders and Stroke Grants POI NS27950 and NS26895, and National Institute on Aging Grant RO1 AG08441.

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