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Biomedical subjects

A R Mayes

Publications and source records attributed to A R Mayes.

At least 73 records · Page 4Linked to original sources
PubMed1989

Amnesia and memory for modality information.

In this study, lists of words were used in a mixed-modality fashion (some read aloud by the subject, others read only by the experimenter). They were presented in this format to both Korsakoff amnesics and matched controls, with subjects only told to remember the words themselves. Controls and amnesics were matched on item-memory (forced-choice recognition) by using longer lists, tested at longer delays, for the controls. Despite this, however, the controls performed significantly better than the amnesics at modality-identification judgements about the items chosen during recognition. Whether the reported result reflects the memory deficit which causes amnesia, or whether it is more properly attributed to additional (frontal lobe) pathology present in only certain amnesics, is discussed.

Adult↗
PubMed1989

Enhancement of word completion priming in amnesics by cueing with previously novel associates.

Seventeen amnesics of mixed aetiology were given a new association word completion task to determine what factors cause variation among amnesics in the extent of such priming. As a group, the patients failed to show new association word completion although several individual amnesics had scores in the normal range. The extent of new association word completion correlated with word fluency as measured by the FAS test and with cued recall in the priming task. It correlated weakly with some measures of amnesic severity, but not with intelligence. Word completion unassisted by new associations did not correlate with any other variable.

Adult↗
PubMed1989

Why are amnesic judgements of recency and frequency made in a qualitatively different way from those of normal people?

The Huppert and Piercy (1978) test of recency and frequency judgements was given to a group of 12 non-Korsakoff amnesics of mixed aetiology and to four non-amnesic patients with selective frontal lobe lesions. The results confirmed that non-Korsakoff amnesics show a significant tendency to base their recency and frequency judgements on memory strength and that amnesics with medial temporal lobe damage show this tendency at least with recency judgements. The patients with frontal lobe lesions performed like normal subjects. Patients who were dysexecutive or impaired in cognitive resources were less likely to base recency judgements on trace strength. Such a recency bias was not however, correlated with measures of amnesic severity. The tendency to base frequency judgements on memory strength was not related to either degree of amnesia or reduction of cognitive resources.

Adult↗
PubMed1988

Location of lesions in Korsakoff's syndrome: neuropsychological and neuropathological data on two patients.

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.

Aged↗
PubMed1988

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.

Adult↗
PubMed1987

Neural correlates of encoding in an incidental learning paradigm.

Event-related brain potentials (ERPs) were recorded during an incidental learning paradigm. Recall and recognition were better for words initially presented in tasks requiring semantic decisions (i.e., 'is it living?' or 'is it edible?') than for words in tasks requiring non-semantic decisions. ERPs elicited during performance of these tasks were predictive of subsequent memory performance. A late positive ERP elicited by words later recalled or recognized was larger than that elicited by words later forgotten. This enhanced positivity for to-be-remembered words could be accounted for, in part, by the fact that words in semantic tasks were remembered better and elicited larger ERPs than did words in non-semantic tasks. Similarly, words followed by affirmative rather than negative decisions were associated both with better recognition and with larger ERPs. However, ERPs were sensitive to processes that influenced later memory performance even within an individual semantic task and within the affirmative decision condition. In addition, results showed that the ERP differences based on later memory performance did not necessarily arise from amplitude variation in P3 waves that occurred at the same time.

Adolescent↗
PubMed1987

Amnesic sensitivity to proactive interference: its relationship to priming and the causes of amnesia.

A group of alcoholic amnesics was compared with a group of controls on an A-B, A-C word pairs interference paradigm. With memory instructions the amnesics needed 5 presentation trials to their controls' single trials to match the groups on A-B cued recall. Under these conditions they still showed more proactive interference on the A-C list. When both groups were given five presentation trials for each list and 'free association' instructions, then they both showed this level of interference. This suggested that the amnesic interference effect only occurs because priming is not modulated by conscious memory, i.e. it is an effect of poor conscious memory. This interpretation was further supported by the finding that amnesics forgot the A-B list faster over 2 hr than their controls, when memory instructions were given.

Aged↗
PubMed1986

Learning and memory disorders and their assessment.

Brain lesions cause memory to break down in several distinct ways in people. First, cortical lesions cause disturbances in short-term memory. Second, other cortical lesions disturb the retrieval of previously well-established semantic and episodic memories. Third, frontal cortex dysfunction seems to be related to a memory syndrome caused by a breakdown in the ability to plan and carry out elaborative processing. Fourth, and most explored, is the amnesic syndrome(s), caused by limbic system or diencephalic lesions. Other less-studied forms of memory breakdown almost certainly exist and some memory syndromes are compounded from these more basic deficits. Appropriate assessment of memory disorders must take this heterogeneity and complexity into account, and is important not only for clinical purposes but also to gain further insight into the precise nature of the different kinds of breakdown. The major theoretical and clinical requirements that such assessment procedures must meet are outlined.

Alzheimer Disease↗
PubMed1985

Recency and frequency judgements in alcoholic amnesics and normal people with poor memory.

Alcoholic amnesics have been reported to confuse when an event occurred with how frequently it occurred and conversely, how frequently something took place with when it happened. This lack of independence of recency and frequency judgements, shown by these amnesics (but not shown by normal people) has been interpreted as reflecting a selective amnesic failure in memory for contextual information; this failure, in turn, leading to poor recall and recognition memory. The effect is replicated on another group of Korsakoff patients and, by manipulations of retention intervals and of learning opportunity, it is also shown that normal people with memory that is as poor overall as that of amnesics still have specific contextual memory with which to make temporal judgements independently of frequency of presentation and (somewhat less obviously) frequency judgements independently of recency of presentation. The qualitative differences between amnesic and normal people cannot therefore be an artefact of testing generally poor memory in amnesics. While it is possible that the unavailability or inaccessibility of contextual information may cause amnesia, an alternative hypothesis, that poor contextual knowledge is an incidental feature in alcoholic amnesia (related to frontal lobe dysfunction), is also considered.

Alcohol Amnestic Disorder↗
PubMed1985

Is organic amnesia caused by a selective deficit in remembering contextual information?

An influential view of amnesia is that the recognition and recall failure is a consequence of a selective loss of memory for contextual, rather than target, information. The various forms of this viewpoint are outlined and one is considered in more detail. This hypothesis claims that amnesics suffer from a selective inability to remember background context i.e. spatiotemporal or extrinsic context. The evidence cited in support of this hypothesis is then critically reviewed and assessed in relation to two methodological problems. The first problem shows that when weak amnesic memory is compared with good normal memory qualitative differences in contextual memory may arise artefactually. The second problem is that contextual memory deficits, found in amnesics, may be incidental consequences of frontal cortex damage rather than essential to the core memory deficit. In the light of these problems it is concluded that currently there is no convincing support for the contextual memory deficit hypothesis of amnesia. Finally, guidelines are laid down which should enable the hypothesis to be more appropriately assessed, and an alternative kind of hypothesis is briefly outlined.

Alcoholism↗
PubMed1984

Patterns of confidence loss in the cued recall of normal people with attenuated recognition memory: their relevance to a similar amnesic phenomenon.

Amnesics show relatively good cued recall (but very poor recognition memory) yet display little confidence in the accuracy of their cued recall responses. In the two studies reported here a similar pattern of results was found in normal subjects who were either tested after a long retention interval or after being given inadequate time to learn target words, i.e. cued recall was relatively unaffected whereas both yes/no recognition of words and confidence in cued recall were much impaired. The finding of equivalent impairment in recognition and confidence in cued recall suggests that these forms of memory are mediated by common memory mechanisms. These mechanisms must be impaired in amnesics and, in normal subjects, are very sensitive to delay and learning exposure manipulations. In contrast, cued recall depends largely on a different form of memory spared in amnesics, and which in normal subjects is less susceptible than recognition memory to delay and brief exposure manipulations.

Adolescent↗
PubMed1978

Asymmetry in EEG alpha coherence and power: effects of task and sex.

Male and female subjects performed two spatial and two verbal tasks while EEG was recorded from right and left temporal and parietal sites. Measures of alpha band power asymmetry, coherence and phase angle were derived. Spatial tasks produced increased coherence within the right hemisphere. Interhemispheric coherence was higher for females, and at parietal than at temporal sites. Power asymmetry effects confirmed previous findings, reflected upon sex differences in cerebral lateralisation and upon strategies associated with functional cerebral organisation for task performance. The relation to performance studies and the value of the method in investigating dynamic functional organisation are discussed.

Alpha Rhythm↗