PubMed · 5071908
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D L Scarborough. 1972. Stimulus modality effects on forgetting in short-term memory.. https://doi.org/10.1037/h0033667
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Memory is sometimes a troublemaker. Schacter has classified memory's transgressions into seven fundamental 'sins': transience, absent-mindedness, blocking, misattribution, suggestibility, bias and persistence. This paper focuses on one memory sin, misattribution, that is implicated in false or illusory recognition of episodes that never occurred. We present data from cognitive, neuropsychological and neuroimaging studies that illuminate aspects of misattribution and false recognition. We first discuss cognitive research examining possible mechanisms of misattribution associated with false recognition. We also consider ways in which false recognition can be reduced or avoided, focusing in particular on the role of distinctive information. We next turn to neuropsychological research concerning patients with amnesia and Alzheimer's disease that reveals conditions under which such patients are less susceptible to false recognition than are healthy controls, thus providing clues about the brain mechanisms that drive false recognition. We then consider neuroimaging studies concerned with the neural correlates of true and false recognition, examining when the two forms of recognition can and cannot be distinguished on the basis of brain activity. Finally, we argue that even though misattribution and other memory sins are annoying and even dangerous, they can also be viewed as by-products of adaptive features of memory.
Two strategies used to uncover neural systems for episodic-like memory in animals are discussed: (i) an attribute of episodic memory (what? when? where?) is examined in order to reveal the neuronal interactions supporting that component of memory; and (ii) the connections of a structure thought to be central to episodic memory in humans are studied at a level of detail not feasible in humans. By focusing on spatial memory (where?) and the hippocampus, it has proved possible to bring the strategies together. A review of lesion, disconnection and immediate early-gene studies in animals reveals the importance of interactions between the hippocampus and specific nuclei in the diencephalon (most notably the anterior thalamic nuclei) for spatial memory. Other parts of this extended hippocampal system include the mammillary bodies and the posterior cingulate (retrosplenial) cortex. Furthermore, by combining lesion and immediate early-gene studies it is possible to show how the loss of one component structure or tract can influence the remaining regions in this group of structures. The validity of this convergent approach is supported by new findings showing that the same set of regions is implicated in anterograde amnesia in humans.
The dearth of studies on amnesia in children has led to the assumption that when damage to the medial temporal lobe system occurs early in life, the compensatory capacity of the immature brain rescues memory functions. An alternative view is that such damage so interferes with the development of learning and memory that it results not in selective cognitive impairments but in general mental retardation. Data will be presented to counter both of these arguments. Results obtained from a series of 11 amnesic patients with a history of hypoxic ischaemic damage sustained perinatally or during childhood indicate that regardless of age at onset of hippocampal pathology, there is a pronounced dissociation between episodic memory, which is severely impaired, and semantic memory, which is relatively preserved. A second dissociation is characterized by markedly impaired recall and relatively spared recognition leading to a distinction between recollection-based versus familiarity-based judgements. These findings are discussed in terms of the locus and extent of neuropathology associated with hypoxic ischaemic damage, the neural basis of 'remembering' versus 'knowing', and a hierarchical model of cognitive memory.