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Biomedical subjects

A Mayes

Publications and source records attributed to A Mayes.

16 recordsLinked to original sources
PubMed2000

Convergent neuroanatomical and behavioural evidence of an amygdala hypothesis of autism.

In this study we report a convergence of behavioural and neuroanatomical evidence in support of an amygdala hypothesis of autism. We find that people with high-functioning autism (HFA) show neuropsychological profiles characteristic of the effects of amygdala damage, in particular selective impairment in the recognition of facial expressions of fear, perception of eye-gaze direction, and recognition memory for faces. Using quantitative magnetic resonance (MR) image analysis techniques, we find that the same individuals also show abnormalities of medial temporal lobe (MTL) brain structure, notably bilaterally enlarged amygdala volumes. These results combine to suggest that developmental malformation of the amygdala may underlie the social-cognitive impairments characteristic of HFA. This malformation may reflect incomplete neuronal pruning in early development.

Adolescent↗
PubMed1995

Automatic registration of SPECT images as an alternative to immobilization in neuroactivation studies.

Subtraction of the two components (baseline and stimulation) of a neuroactivation study using 99Tcm HMPAO SPECT requires accurate registration of the two images. Immobilization of the subject during and between the two components of the study can prove difficult and degrades signal to noise ratio. The use of an automated image registration technique for registering the two components of the test can, even in the case where the subject is removed from the scanner, produce significantly better registration than immobilization.

Algorithms↗
PubMed1995

Life preservers.

Explore the source record for details and available documents.

Domestic Violence↗
PubMed1990

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.

Adult↗
PubMed1981

A similarity between weak normal memory and amnesia with two and eight choice word recognition: a signal detection analysis.

Two and eight choice recognition memory was compared in a group of normal individuals shortly after learning a list of words and seven days later. In addition to selecting the correct response, subjects were required to indicate the confidence of their choices. The results showed that eight choice recognition performance was differentially worse than two choice recognition at delayed compared to immediate test. These results were similar to some reported by Miller (1977) in which he compared recognition in dementing amnesics and controls at immediate test. While Miller interpreted his data in terms of a selective retrieval deficit in amnesics, our data suggests that both sets of results arise because Signal Detection Theory is applicable to recognition memory data. An additional result was that subjects felt they guessed correctly selected words more frequently after a delay.

Adult↗
PubMed1981

How similar is the effect of cueing in amnesics and in normal subjects following forgetting?

Verbal recognition and cued recall were compared in normal subjects after intervals of 15 minutes, one week and six weeks. When given cues subjects were encouraged to produce as many appropriate words as possible in a 30 second period and rate the words for familiarity. Guessing controls were used and subjects' skill at generating words without a memory component was also assessed. The results confirmed others in showing that cued recall declines more slowly over time than recognition. Further, although subjects cued well at six weeks they did not feel correctly cued words to be familiar. A similar effect has been noted with amnesic cueing. Also, at the six week interval, correct words tended to be generated later than after the shorter intervals, and there was a correlation between cued recall and cueing skill in general. These findings suggest that normal subjects who have largely forgotten and, probably, also amnesics use cues differently from normal subjects who are tested immediately after learning.

Adolescent↗
PubMed1980

Is amnesia caused by an activational deficit? A preliminary electrophysiological investigation of acquisition in amnesics.

Six alcoholic amnesics were compared with 6 matched controls in a task involving visual presentation of words under 'learn', 'repeat' and 'passive' instructions whilst their EEG was recorded from the vertex. Although the amnesics' N2-P3 component to word stimuli was similar to that of controls, their word-elicited N1-P2 component was of greater amplitude and their EEG showed an overall reduction in power in the period immediately following word offset. The group difference for N1-P2 was similar in all instructional conditions, but the EEG power difference was greater in the learn condition. It was argued that the N1-P2 enhancement may reflect an attempt by the amnesics to compensate for an unspecified activational impairment indicated by their reduced post-word EEG power.

Alcoholism↗
PubMed1980

Amnesia is not caused by cognitive slowness.

It has been suggested that the memory disorder in human organic amnesia might be caused by the slow processing of information. Such slowness might be differentially greater for semantic tasks, and/or for tasks requiring the extraction of multiple features of stimuli, or it might simply be a non-specific slowing. These possibilities were tested in a group of alcoholic amnesics and matched normal controls by presenting subjects with a series of words and requiring them to identify one specified word or one of two specified words, or membership of a specified category or one of two specified categories. Although amnesics' reaction times were slightly slower than controls' the effect was insignificant, and there was no hint of differential slowing in the semantic or multiple processing tasks. It was concluded from these results and a consideration of the reaction time literature that cognitive slowness is unrelated to the main cause of amnesia.

Alcohol Amnestic Disorder↗