Word production and comprehension in Alzheimer's diseáse: The breakdown of semantic knowledge

A previous study (Baddeley et al., 1986) explored the hypothesis that patients suffering from dementia of the Alzheimer type (AD) are particularly impaired in the functioning of the central executive component of working memory. It showed that, when patients are required to perform 2 concurrent tasks simultaneously, the AD patients are particularly impaired, even when level of performance on the individual tasks is equated with that of age-matched controls. Although the results were clear, interpretation was still complicated by 2 issues: first, the question of comparability of performance on the separate tests between AD and control patients; secondly, the question of whether our results could be interpreted simply in terms of a limited general processing capacity being more taxed by more difficult dual tasks than by the individual tasks performed alone. The present study followed up the AD and control patients after 6 and 12 mths. We were able to allow for the problem of comparability of performance by using patients as their own control. Under these conditions, there is a very clear tendency for dual task performance to deteriorate while single task performance is maintained. A second experiment varied difficulty within a single task in which patients and controls were required to categorize words as belonging to 1, 2 or 4 semantic categories. There was a clear effect of number of categories on performance and a systematic decline in performance over time. There was, however, no interaction between task difficulty as measured by number of alternatives and rate of deterioration, suggesting that the progressive deterioration in performance shown by AD patients is a function of whether single or dual task performance is required, and is not dependent on simple level of task difficulty. Implications for the analysis of the central executive component of working memory are discussed.

The decline of working memory in Alzheimer's disease : A longitudinal study

Cholinergic function and intellectual decline in Alzheimer's disease.

This paper examines three methodological issues concerning the measurement of semantic memory impairment in brain-damaged patients. Ten carefully selected patients with dementia of Alzheimer's type (DAT) and anomia were studied. A battery of perceptual tests and direct tests of semantic memory led to the conclusion that these patients represented a homogeneous group having a prominent deterioration of their semantic memory store without visual perceptual deficits. The first issue addressed in this patient group was whether verbal fluency impairment accurately reflected the loss of semantic memory. It was found that verbal fluency (generation of semantic category lists) was impaired due to two major constraints: deterioration of semantic memory store, and variable difficulties in semantic search. Verbal fluency, therefore, reflects semantic memory loss to some degree, but is not a direct test of semantic memory store in DAT. The second issue was whether semantic memory impairment in our patients conformed to the 'semantic storage disorder' syndrome hypothesized by Shallice (1987). It was shown that, consistent with this hypothesis, the patients demonstrated co-occurrence of consistency of errors, loss of semantic cueing, and preserved superordinate knowledge with loss of detailed knowledge of concept items. The third issue was whether semantic cueing and semantic priming are altered in a similar manner in DAT. It demonstrated that semantic cueing and semantic priming, using the same words whose concepts were degraded in semantic memory, yielded an entirely different pattern of results. Cueing and priming therefore may not be used interchangeably in the study of semantic loss after brain damage.

Semantic memory loss in dementia of Alzheimer's type. What do various measures measure?

A study of language functioning in Alzheimer patients

Evidence is presented to show that patients with Alzheimer's disease owe their memory disturbance to both an impairment in short-term memory and an additional difficulty in establishing new material in long-term storage. These findings are particularly discussed in relation to the notion that, since the pathological changes in Alzheimer's disease are particularly manifest in the hippocampal region, then this involvement of the hippocampus might explain the memory disorder. The present experiment, which is similar to one previously reported using subjects with bilateral hippocampal lesions, shows the two types of memory disorder resulting from bilateral hippocampal damage and Alzheimer's disease to be qualitatively different. Some outstanding problems with regard to obtaining a complete understanding of the nature of the amnesic phenomena in Alzheimer's disease are discussed.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S003329170004856X

Short- and long-term memory in patients with presenile dementia (Alzheimer's disease).

Two experiments concerned with the statistical characteristics of speech in presenile dementia are described. Apart from a lowered rate of production of words under certain conditions no speech abnormalities were detected on the variables examined.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0033291700056610

Some characteristics of verbal behaviour in presenile dementia.

Efficiency of coding and the short-term memory defect in presenile dementia.

The conventional view would appear to define hysterical symptoms (whether so-called conversion symptoms or hysterical dissociation) in terms of a number of features. The first is the occurrence of a symptom which, if taken at face value, would be an indication of some underlying pathological process; yet no pathology of a conventional kind can be elicited, and the presence of such pathology (whether physical or in the form of a formal psychiatric disorder) seems highly unlikely. An example of something meeting this criterion is a sensory impairment that does not match any recognized anatomical distribution and/or, where evidence can be obtained that the sensory system must be functioning very much better than the patient's claimed symptomatology would suggest (as in the cases reported by Grosz & Zimmerman, 1965; Miller, 1986). This seems to be the central and essential criterion and it is widely accepted that patients meeting this criterion are encountered from time to time. There are three other common criteria and all raise problems. It is usually assumed that there must be some secondary gain from the symptom. The difficulty here is that all disorders or illnesses can give rise to some secondary gain (e.g. people feel under an obligation to be especially considerate to those who are ill). Secondary gain therefore raises problems as one of the defining criteria of hysteria since it does not readily distinguish hysteria from true illnesses. A second, classical feature is the alleged presence of' la belle indifference' although again this must be regarded as a rather unreliable sign. What evidence there is about anxiety in hysterical patients tends to indicate that levels of general anxiety are, if anything, raised in those with so-called 'conversion hysteria' (Lader & Sartorius, 1968). Many authorities on hysteria would probably accept that secondary gain and '/a belle indifference' are unreliable as signs of hysteria. The final criterion is more central to most views of hysteria. It is that the patient is regarded as experiencing the symptom as ' real' and is not consciously aware that the symptom is being produced and maintained by means other than those of conventional pathological mechanisms. Thus, the hysterical patient with paralysis really is unable to move his paralyzed limbs. It is this latter criterion which distinguishes the hysteric from the malingerer who consciously simulates symptoms. (There can also be a problem in distinguishing hysterical symptoms from hypochondriacal complaints but this is not an issue of such great relevance to present concerns.) This discussion is principally concerned with the last of the above criteria for hysterical symptoms; that of the subjective reality of the symptom from the point of view of the patient. The use of this criterion raises a number of difficulties. It entails a judgment about whether or not the patient is aware of the status of the symptom. This is necessarily an unreliable and unsatisfactory judgment because no examiner has access to the content of any patient's consciousness. To maintain this criterion also biases explanations of hysteria towards those that involve unconscious mental mechanisms (as in the psychoanalytic tradition) or which, following Janet (1907), use the concept of dissociation. A model of the mind has to be postulated which involves some mental structure operating outside the realms of normal consciousness which can be used to create the symptom (or the processes underlying it). Not only are such structural models of the mind open to dispute on philosophical grounds (e.g. Ryle, 1949; White, 1967), but they are not amenable to empirical test in any critical way. Of course, verifiable predictions can be derived from such models but not of a kind that would challenge the fundamental basis of the model itself.

Defining hysterical symptoms.

The psychomotor performance of patients with presenile dementia was investigated in two experiments. It was found that motor retardation in dementia was due more to impaired effector processes rather than slowness in deciding when and where to move.

Edgar Miller

Papers

Short- and long-term memory in patients with presenile dementia (Alzheimer's disease).

Some characteristics of verbal behaviour in presenile dementia.

Efficiency of coding and the short-term memory defect in presenile dementia.

Defining hysterical symptoms.

Psychomotor performance in presenile dementia.