Do amnesics forget faces pathologically fast?

In 1978, Huppert and Piercy introduced a general method for comparing forgetting rates across groups differing in their baseline memory performance. The method has since become a standard for measuring rate of forgetting in amnesia. Using this method, amnesic subjects with presumed damage to midline diencephalic structures have consistently been reported to forget at a normal rate whereas patients with medial temporal lobe damage have sometimes been reported to forget pathologically fast. Conclusions about amnesic forgetting rates using Huppert and Piercy's procedure, however, are unsafe because the matching procedure results in the shortest mean item-presentation-to-test delay being longer in amnesics than control subjects. A further problem with previous work is that frequently the shortest delay at which performance is measured is 10 minutes. An alternative procedure to Huppert and Piercy's is outlined which eliminates the matching confound. An experiment was carried out using this procedure with face stimuli, and with amnesic and control performance matched immediately following study, and then tested at delays of 5, 12, and 30 minutes. Pathologically fast forgetting was observed in a group of 19 amnesics over the first 5 minutes, but between 12 and 30 minutes their controls forgot faster so that the two groups had forgotten the same amount after 30 minutes. A subgroup of nine Korsakoff patients, with probable damage to midline diencephalic structures, showed a similar abnormal forgetting pattern to the remaining 10 amnesics, some of whom had medial temporal lobe damage. A retroactive interference condition was also included for the 12 minute condition at which delay patient and control recognition was mildly and equivalently disrupted. For unknown reasons perhaps related to a storage abnormality, amnesics lose face recognition memory sooner in the first 30 minutes of forgetting than do normal people, who show accelerated forgetting later so as to match patients after 30 minutes delay.

Encoding ability is preserved in amnesia: evidence from a direct test of encoding.

The encoding ability of 17 amnesics of mixed aetiology and 17 matched normal controls was assessed directly using a novel procedure. On two separate occasions, subjects were shown 60 complex drawings each containing six pictures. On one occasion each drawing was shown for 6 sec, and on the other occasion it was shown for 25 sec. Immediately after presentation of each drawing subjects were asked a single unpredictable question about picture colours, location, size or semantic category. Amnesics performed normally in the 6-sec exposure condition indicating that all of the tested kinds of information were encoded at a normal rate. Performance in this condition correlated with short-term, but not long-term memory in the amnesics indicating that it depended largely on encoding and short-term memory. However, the amnesics were impaired in the 25-sec condition where performance should have depended on (long-term) memory abilities at which they were impaired. The results are inconsistent with available encoding deficit accounts of amnesia.

Disproportionate incidental spatial-memory and recall deficits in amnesia.

Seventeen amnesics, including patients with Korsakoff's disease, post-encephalitic amnesia and amnesia caused by rupture of an anterior communicating artery aneurysm, were compared with 17 matched control subjects on a task in which 16 nameable shapes were placed on different squares of a 49-square grid. One version of the task tapped free recall and recognition of the shapes and a second version tapped three forms of spatial memory. The patients were tested after more learning opportunity and shorter delays than were the controls so as to match their recognition levels. Under these conditions, the amnesics performed worse than the controls on free recall, location-to-target memory, target-to-location memory and possibly on non-associative spatial memory although this was less impaired than target-to-location memory. Each of the main aetiological subgroups showed these disproportionate deficits to an apparently similar degree. The disproportionate free recall deficit was unrelated to the spatial memory deficits and overall severity of amnesia, and was associated with ageing and signs of frontal lobe dysfunction. The disproportionate spatial memory deficits were unrelated to frontal lobe dysfunction, but the target-to-location memory measure was associated with impairments of recognition and recall of target material. The results are broadly consistent with the context-memory deficit hypothesis of amnesia.

Performance on tests sensitive to frontal lobe lesions by patients with organic amnesia: Leng & Parkin revisited.

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.

Spatiotemporal memory and rate of forgetting in acute schizophrenics.

Some schizophrenics show anomalies in the frontal and temporal lobes. It is uncertain whether the cognitive deficits shown by Type I schizophrenics are caused directly by such anomalies, or by a deficit in the exertion of attentional effort. In this study, 16 acute schizophrenics, who broadly fitted the Type I characterization and their controls were given a battery of cognitive tests. The patients were impaired on effort-demanding tasks such as the Wisconsin Card Sorting Test, a verbal fluency test and the WAIS, which are susceptible in varying degrees to frontal, temporal and parietal lobe lesions. Patients were not disproportionately impaired, however, on a test of temporal memory and another of spatial memory, an impairment pattern that selectively reflects frontal and medial temporal lobe lesions respectively, nor were they impaired on a rate of forgetting task sensitive to medial temporal lobe lesions. These tasks were chosen not only because performance on them is selectively sensitive to frontotemporal lobe lesions, but also because it seems to depend on exerting minimum amounts of attentional effort. It is tentatively concluded that the cognitive deficits shown by Type I schizophrenics are caused by a problem in exerting attentional effort of unknown origin.