Memory Disorders in Clinical Practice

Narinder Kapur

• Publisher: Psychology Press
• Year: 2017
• eBook ISBN: 9781317758716
• Topic: Psychology
• Subtopic: Cognitive Neuroscience & Neuropsychology
• Index: Psychology

This book has been specially designed to give practical help to those who have to deal with diagnosis and subsequent management of patients with memory dicturbance resulting from specific types of cerebral pathology. The author achieves this by organising his book on the basis of clinical aetiology. While anatomical and psychological perspectives are introduced, the emphasis is on approaches which will help clinicians in the management of patients with specific neurological diseases. For example, the essential topic of differential diagnosis is given prominence throughout: the principles of diagnositc assessment are discussed in a separate chapter, and specific diagnostic features are outlined in each of the chapters dealing with individual cerebral pathologies. The author draws on his own extensive experience as a practising clinical neuropsychologist to describe and evaluate the range of existing memory test procedures, and suggest additional procedures as appropriate. Full references are also given for those wishing to develop their own assessment of therapeutic procedures. Mainly intended for practising neurologists and clinical neuropsychologists, anyone whose work brings them into contact with patients suffering from memory disturbance will find this book invaluable.

Chapter 1
Assessment of memory functioning

Webster’s dictionary (1966) defines memory as the ‘conscious or unconscious evocation of things past’. As such, the term ‘memory’ can refer to a variety of learned behaviours, and it could be argued that many aspects of perception and language involve the use of certain memory systems. A number of authors have alluded to the range of possible human memory systems (e.g. Allport, 1985; Tulving, 1985; Warrington, 1986), but in the present context I will mainly be concerned with the more customary use of the term; i.e. the retention of specific information which has been acquired in the recent past. It is this aspect of memory which forms the basis of most of the memory symptoms reported by brain damaged patients (Kapur and Pearson, 1983), and which is the main focus of subsequent chapters. Difficulties at the level of identification of overlearned material, as occur in the various types of agnosia and as are found in some language disorders, will therefore be given relatively limited coverage.

Impaired memory functioning represents one of the most common cognitive symptoms and neuropsychological deficits found in neurological disease. In conditions with an insidious onset, memory difficulties are frequently one of the earliest features of cognitive deterioration; impaired memory functioning is also one of the most common residual deficits which form part of a patient’s permanent neurological disability. The early development of memory test procedures has been outlined elsewhere (Erickson and Scott, 1977). Many of the earlier tests of memory functioning were somewhat poorly designed, or were developed without any reference to experimental or theoretical insights into normal human memory. In recent years, this limitation has been partly rectified, with a greater interchange between research workers in the area of normal and abnormal memory function, and also between clinicians involved in the neuropsychological assessment of memory dysfunction and neuropsychologists who carry out research on memory disorders. Some of the most promising findings in recent research on memory disorders have been based on procedures originally developed by experimental psychologists. For a more detailed account of such procedures, the reader is referred to sources which have described research methods used to study normal memory (Puff, 1982; Underwood, 1983). Further sources which may be of use in selecting materials for memory test construction are indicated in Appendix 1.

Memory assessment in specific clinical conditions

Memory assessment in clinical practice may often be directed towards distinguishing between various forms of cerebral pathology, or between various sites in the brain which may be affected by a known pathology. The approach to such a clinical problem should, ideally, be framed in terms of the various diagnostic hypotheses which are tenable, and in terms of the features of memory functioning which may help to reject or confirm such hypotheses. The reader is referred to later chapters for information relating to distinctive features of memory functioning which may help in the diagnosis of specific clinical aetiologies, but for illustrative purposes I have designed a flowchart to exemplify this ‘hypothesis generation and testing’ approach (see Wood, 1984). This flowchart is shown in Figure 1.1 and represents, in a preliminary form, the prototype of a possible ‘expert system’ which could act as an aid to a clinician in the diagnosis of neurological conditions that may be accompanied by memory disorder. The following sections consider in more detail some of the common clinical conditions where memory assessment may be important for diagnostic purposes.

Distinguishing psychiatric from neurologically-based memory impairment

Symptoms of everyday memory difficulty and impaired performance on memory tests may be present in psychiatric patients in whom evidence of specific cerebral pathology cannot be established, and in this section I wil briefly review some of the features of memory disorders in psychiatric conditions which may distinguish such disorders from neurologically-based memory loss. The distinction between a ‘functional’ and an ‘organic’ disorder has in recent years become somewhat blurred, especially in view of the introduction of advanced imaging procedures which may indicate the presence of subtle cerebral metabolic or structural abnormalities in patients with psychiatric disorder (Gur, 1985). This overlap between psychiatric and neurological mechanisms for memory dysfunction is occasionally evident in patients with frontal lobe pathology, some of whom may show affective and volitional changes which contribute towards impaired performance on certain memory tasks. For most diagnostic purposes, any distinction between a psychiatric and a neurological basis to impaired memory should rely on a number of observations, preferably gathered over a period of time, since inconsistencies between sets of observations and across repeat assessments tend to occur more frequently in psychiatric conditions (see Zangwill, 1943). In the following sections, I will review some of the main psychiatric conditions in which memory symptoms may occur, and where evidence is available on similarities or differences with memory disorder in cerebral disease. The following sections will of necessity be tentative, since there are few ‘hard’ data available, and since many comparative studies of neuropsychological functioning in psychiatric and neurological patients have used heterogeneous or poorly defined groups for one or both sets of subjects (Heaton, Baade and Johnson, 1978).

Depression/marked anxiety

A significant proportion of patients with depression may include memory difficulties as part of their psychological symptomatology. In an individual case, it is important to be clear as to the specific differential diagnosis under consideration. The presence of depression itself is seldom at issue, but where this needs to be ascertained, then it may be useful to document symptoms such as weight loss, sleep disturbance, loss of libido, etc. Where memory deficits are not apparent over a range of memory tasks, especially difficult tasks which have, for example, a delayed recall or paired-associate learning component, then the question of further differentiation seldom arises, and it may be possible to indicate that depression/anxiety is likely to underlie the memory symptoms.

Where memory deficits are apparent, then the differential diagnosis may be one between memory impairment due to depression and that due to a specific cerebral pathology. In such cases, one can consider a number of features: Zangwill (1943) referred to inconsistencies in memory performance which may be evident across repeat assessments; inconsistencies between memory tests also support a psychiatric basis to any memory symptoms, especially where the two tests tend to be performed at an equivalent level by neurological patients with the condition which forms part of the differential diagnosis in question, or where the relative test scores are in the reverse direction to that which might be expected in a neurological condition. In addition, it may be useful to ask a patient, after he has performed at an average or above average level on a certain memory task, how well he feels he has done. If the patient thinks he has performed very poorly and could have done much better, this may often be an indication that high anxiety levels play a part in the patient’s complaint of everyday memory difficulties.

A further form of differentiation may relate to a patient with an established neurological condition, and where there is undoubted evidence of depression. The question may then be phrased in terms of evaluating the relative contribution of both aetiologies in determining the extent of any memory deficits. This type of clinical diagnosis is perhaps the most difficult of all, and it may be useful simply to list those features of memory symptoms and performance which tend to be associated with the particular neurological condition in question, and then to assess the extent to which they are present in the results of the memory assessment.

At the clinical level, features of the patient’s psychiatric history (e.g. past history of depression) and present condition (e.g. reports of depressed mood or anxiety) may help to distinguish patients whose memory impairment is secondary to depression (Rabins, Merchant and Nestadt, 1984). It is also important to gather information both on the general chronological occurrence of affective and memory symptoms, and the sequence of specific symptoms at a particular time (it may be useful to obtain information on this from a close observer of the patient, if one is available). Where the onset of memory difficulty has occurred some time after the onset of depression or some stressful life event, or where specific memory symptoms appear to occur only after a depressed mood state, then this is more likely to indicate a psychiatric rather than neurological basis to the patient’s memory difficulties. The number, recency, and unilateral versus bilateral nature of electroconvulsive therapy (ECT) should be taken into account, as should any possible side-effects of antidepressant medication on memory functioning.

The number and duration of memory symptoms may also, in some cases, help to identify memory disorder based mainly on anxiety or depression. If the patient admits to a large number of memory symptoms, in the context of only mild or moderate memory test impairment, or if the symptom duration is more than several years, in the context of few other cognitive or physical symptoms, then a psychiatric basis to the memory difficulties may be more likely (Kahn et al., 1975). Further, where the patient complains of marked memory difficulties, yet is able to give a

Figure 1.1 Flow chart to represent possible decision paths which may aid in the diagnosis of patients presenting with evidence of memory difficulties. Some important qualifications need to be borne in mind when adopting this type of conceptualization, and when considering an individual patient’s condition in relation to the flow chart. First, the decision criteria and end-diagnoses are based on relative probabilities, which in turn reflect both the writer’s personal clinical experience and his interpretation of published findings. A number of neurological patients will undoubtedly be found who represent examples of ‘mis-matches’ in relation to the flow chart. Second, the decision criteria relate primarily to aspects of memory functioning. Other aspects of cognitive functioning or other clinical features are not given as much weight for determining a particular diagnosis. This has been done purely for didactic purposes, and it is likely that higher levels of confidence for some diagnoses could be attained by considering other features of the patient’s condition. Third, this formulation does not make explicit allowance for the possibility of combined pathologies. This omission is also for didactic purposes, and it is recognized that such combined pathologies may often occur, especially in elderly patients. Fourth, the flow chart is mainly concerned with initial symptoms and test deficits in conditions in which there is uncertainty as to the clinical diagnosis. Residual memory deficits in conditions such as head injury pose less of a problem in this respect, and so are not indicated on the chart. Fifth, the decision paths are based on measures of memory functioning which are in relatively common use, and in most instances they can be fairly easily assessed. A higher probability of accurate diagnosis could probably accrue from the use of more fine-grained analyses of memory functioning, but for illustrative purposes these too have been omitted.

detailed account of his everyday memory symptoms and of their chronological development, then this may also be a pointer towards a non-organic basis to the symptoms. Behaviour during memory testing tends to be a less certain indicator of the basis of impaired memory functioning, although there is a tendency for depressed patients to give up more easily and to offer ‘don’t know’ responses rather than intrusion errors on particular test items.

Several studies have compared memory functioning in patients with depression and those with neurologically-based memory disorders. Cutting (1979) found that patients with ‘psychotic or retarded depression’ were impaired on a verbal paired-associate learning task and a visual pattern recognition memory test. From the group mean scores provided by Cutting, depressed patients performed better on the verbal learning task than patients with alcoholic Korsakoff’s syndrome and patients with primary degenerative dementia (although this latter group was diagnosed only on the basis of atrophy shown by pneumoencephalography). They performed worse on this task than patients with focal right hemisphere lesions. However, only the differences with respect to patients with Korsakoff’s syndrome and those with right hemisphere damage reached statistical significance. In the case of the pattern recognition memory test, depressed patients performed better than patients with right hemisphere lesions, with the first two of these differences reaching statistical significance. In terms of false-positive responses on the pattern memory task, depressed patients made more errors of this type than patients with dementia, Korsakoff’s syndrome or left hemisphere lesions, but none of these differences reached statistical significance. Taylor et al. (1986) observed impaired short-term memory performance in a group of patients with endogenous depression, and found that their test scores were significantly higher than those of a group of patients with Parkinson’s disease, some of whom also showed a significant degree of depression.

Using a group of patients with milder depression than those studied by Cutting (1979) or Taylor et al. (1986), Coughlan and Hollows (1984) also compared memory performance in depressed patients with that of neurological patients. The latter group was, however, somewhat heterogeneous, mainly comprising patients with severe head injury, but also including other cerebral pathologies. Depressed patients were psychiatric inpatients or day patients, and all were diagnosed by a psychiatrist as suffering from depression. Neurological patients performed worse than depressed patients on most verbal and non-verbal memory tests which were administered (see p. 43 for more information on these tests), and the most marked inferiority emerged on a forced-choice faces-recognition memory test (Warrington, 1984). Impaired performance on at least one memory test of each type (verbal/non-verbal) also distinguished depressed from neurological patients with a high level of confidence. A notable finding from the study by Coughlan and Hollows was that little relationship emerged between memory performance and self-rated depression in the group of psychiatric patients.

Schizophrenia

While several authors have commented on impaired memory functioning in schizophrenia (e.g. Cutting, 1985b; Kolakowska et al., 1985; Robertson and Taylor, 1985), few comparisons have been made of memory performance between such patients and those with specific neurological conditions. In most clinical settings, any memory difficulties present in schizophrenic patients will seldom represent an isolated deficit, and other features of the psychiatric condition will usually be more informative in any differential diagnosis relative to a possible neurological condition. In any such comparisons, it is important to take into account variables such as the chronic versus acute nature of the schizophrenic illness, and also the duration of medication, since both neuroleptic drugs (Famuyiwa et al., 1979), and anticholinergic medication used to treat the side-effects of such drugs (Tune et al., 1982), have been associated with impaired memory in schizophrenic patients.

Cutting (1985b) has referred to distinct patterns of memory deficits in acute and chronic schizophrenia. Acute schizophrenics tend to show more subtle memory deficits, evident in their use of mnemonic strategies and in their memory for certain material with an emotional content. On the other hand, chronic schizophrenics more commonly display marked memory impairment similar to that found in degenerative dementia. Cutting has argued that the memory deficits in acute schizophrenia ‘are consistent with a diminution of the right hemisphere’s contribution to memory’ (1985b), but he has not presented strong evidence in favour of such a hypothesis.

In the study by Cutting (1979), the memory performance of both acute and chronic schizophrenics was compared to that of neurological patients. On a verbal paired-associate learning test, chronic schizophrenics showed impaired performance compared to normal control subjects and to patients with right hemisphere lesions. Their level of impairment was similar to that shown by patients with dementia, and slightly better than those with Korsakoff’s syndrome. On the visual pattern memory task, they were impaired relative to control subjects and patients with left hemisphere lesions, but performed better than patients with Korsakoff’s syndrome or patients with dementia. In the case of patients with acute schizophrenia, Cutting found that they were impaired relative to control subjects only on the verbal paired-associate learning task, performing significantly better on this test than patients with Korsakoff’s syndrome. On the test of visual pattern memory, they performed better than patients with dementia, Korsakoff’s syndrome or right hemisphere lesions. Both acute and chronic schizophrenics made more false positive responses than patients with Korsakoff’s syndrome or dementia on the pattern memory task, and chronic schizophrenic patients also made significantly more false positive errors than patients with left hemisphere lesions.

Hysterical and fugue states

In 1961, Lewis observed that ‘there is nothing in the known psychopathology of hysterical amnesia which has not been observed in the organic cerebral syndrome’. A number of reviews of fugue states and hysterical memory loss are available (Pratt, 1977; Zangwill, 1983), and the reader is referred to these for more detailed documentation of relevant studies. Pratt (1977) has described the wandering away from normal surroundings which characterizes the initial stages of fugue state, followed either by recovery of identity and an amnesic gap for the episode or by loss of personal identity and extensive retrograde amnesia. Loss of personal identity and other personal information, together with retrograde amnesia disproportionate to anterograde memory functioning, are usually the two main features which help in distinguishing hysterical memory loss from neurologically-based amnesia (although it should be remembered that relatively isolated retrograde amnesia can occur in neurological conditions such as transient global amnesia – e.g. Roman-Campos, Poser and Wood, 1980). Other factors include the abrupt termination of the amnesia found in hysterical memory loss compared to the more gradual return of normal memory in conditions such as transient global amnesia, and the hysterical patient’s relative indifference to his memory disorder compared to the perplexed state usually associated with transient global amnesia (Croft, Heathfield and Swash, 1973). Furthe...

Table of contents

• Cover
• Half Title
• Dedication
• Title
• Copyright
• Preface
• Acknowledgements
• Terminology used in text
• Contents
• 1 Assessment of memory functioning in clinical practice
• 2 Cerebrovascular disease
• 3 Cerebral tumours
• 4 Penetrating head injury
• 5 Blunt head injury
• 6 Degenerative, demyelinating and hydrocephalic dementias
• 7 Infectious, metabolic and related diseases
• 8 Toxic and deficiency states
• 9 Epilepsy
• 10 Ablation/disconnection of cerebral tissue
• Appendix 1 Sources for materials which may be of use in designing memory tests for the assessment of neurological patients
• Appendix 2 Sources for information/materials relating to the remediation of memory disorders
• References
• Author index
• Index