In Experiment 1 participants gave 3 successive free recalls of items learned either individually or in pairwise collaboration. The first and third recalls were performed individually, the second alone or in collaboration. Collaborative recall led to an inhibitory effect after individual learning but not after collaborative learning, in which partners had similar retrieval strategies. Consistent with a retrieval locus for collaborative inhibition, non-recalled items reappeared in subsequent individual recall. Experiment 2 showed that collaborative inhibition was eliminated when a separate retrieval cue was given for each item. Experiments 2 and 3 also showed that when participants learned items in the same order, their retrieval strategies were more similar and they showed less collaborative inhibition. It is concluded that mutual interference in collaborative recall is due to the mutual disruption of individual retrieval strategies.
When people collaborate over their recall of a shared experience, it might be expected that they could "cross-cue" each other so as to produce new memories not available to either member of the pair on their own. In a previous series of experiments (Meudell et al., 1992), we found that pairs of people always recalled more than one person, but we failed to show that social interaction facilitated performance so as to produce such "emergent" new memories. However, a phenomenon akin to cross-cuing was employed by Tulving and Pearlstone (1966) in their classic study of the availability and accessibility of memories; accordingly, in this study, we repeated Tulving and Pearlstone's work directly in a social context. So as to assess whether new memories emerged in collaborating pairs, a sequential design was employed. People learned categorized lists of words, and then all the subjects recalled the items strictly on their own. Subjects then recalled again in pairs (collaboratively) or once more on their own. The results showed that even when the opportunity for cross-cuing was directly manipulated through the provision of categorized lists, no additional new memories emerged in the collaborating groups. Possible mechanisms for the results are considered.
The hypothesis that two people collaborating in recall would remember more than a single person was examined in a series of four experiments. All the experiments used variations on the same 'sequential' design where, in social conditions, people recalled alone initially and then recalled jointly in pairs: as a control for reminiscence, some people recalled alone on two separate occasions. On the second recall in all of the experiments two people always recalled more than one, but this was simply due to the independent statistical summation of two people's memories: no evidence whatsoever was found for the pairs of people generating new information that was not available to either member of the pair. This surprising result was not attributable to artefacts linked to the complexity or familiarity of stimulus material, nor was it linked to variations in people's cognitive perspectives. No evidence of social facilitation of memories was therefore found: two people recalling together certainly pool their separate memories so as to outperform individuals but the social interaction does not appear to generate previously unavailable memories.
Psychometric and neuropathological findings on two Korsakoff amnesics are described. Both patients showed anterograde and retrograde amnesia, poor performance on the Peterson short-term memory task, on the Wisconsin card sort test and on certain visuo-spatial tasks. Patient J.W. performed consistently worse on tests of anterograde, but not retrograde amnesia, whereas patient B.C. showed more perseverative difficulties and, unlike J.W., his measured intelligence seemed to have declined from its premorbid level. Both patients showed marked neuronal loss from the medial mammillary bodies and a narrow band of gliosis in the medial thalamus, adjacent to the wall of the third ventricle, a region known as the paratenial nucleus. Only B.C. showed visible signs of cortical atrophy. Morphometric measures did, however, reveal reduced nucleolar volumes in layers III and V of the frontal cortex, with B.C. also showing more marked neuronal loss from these layers. B.C. also showed neuronal loss from the CA1 region of the hippocampus and reduced nucleolar volumes in the septum. Significantly, both patients had normal neuronal numbers and nucleolar volumes in the nucleus basalis of Meynert. J.W. only showed greater dysfunction than B.C. in one region: the locus caeruleus. This finding was related to his more severe amnesia.
Groups of amnesics with aetiologies that included chronic alcoholism, encephalitis and ruptured anterior communicating artery aneurysm (ACoAA) were examined on the Cognitive Estimation Test (CET), FAS Word Fluency Test (FAS) and the full and Nelson (1976) versions of the Wisconsin Card Sorting Test (WCST). The alcoholic amnesics were impaired on all four tests, whereas the post-encephalitic amnesics were impaired on the FAS and CET but performed normally on both versions of the WCST. The ACoAA amnesics were impaired on both the FAS and the CET, and scored at a level in between the other amnesic subgroups on the WCST.
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