The Neuropsychology Of Schizophrenia

JOHN P CUTTING, Anthony David, JOHN P CUTTING, Anthony David

• Editore: Psychology Press
• Anno: 2019
• ISBN:
  9781317716204
• Edizione: 1
• Argomento: Psychology
• Categoria: Neuropsychology

Schizophrenia is being increasingly viewed as a neurological disorder. The Neuropsychology of Schizophrenia addresses the key questions in modern schizophrenia research. How do abnormalities of the brain produce the characteristic signs and symptoms of this most severe and mysterious mental malady? Where are these abnormalities? How do they develop? How can we detect them? What clinical and cognitive effects do they have?
This new book is the first of its kind to tackle these questions in a systematic way from a number of allied perspectives: from phenomenology to physiology, animal behaviour to metacognition and from PET scans to paper and pencil tests. A number of authors from the United Kingdom and the United States have made contributions; all are acknowledged experts in the field. The chapters each contain a concise review of the particular topic, empirical data and also a theoretical overview.
The Neuropsychology of Schizophrenia will be required reading for all serious students of schizophrenia from both medical and psychology backgrounds.

1 The Neuropsychology of Schizophrenia—Introduction and Overview

Anthony S. David

Department of Psychological Medicine, King’s College Hospital and the Institute of Psychiatry, London.

John C. Cutting

Institute of Psychiatry, London

The idea that there is a “neuropsychology of schizophrenia” is of relatively recent origin. Indeed, the term “neuropsychology” itself only dates back three or four decades. The concept to which it refers, however, is far from new.

The thrust of Kraepelin’s and most of his fin de siècle German contemporaries’ research into schizophrenia was towards elucidating the biological basis of the condition, which included questions such as whether particular parts of the brain were damaged more than others. The spate of higher-order neurological deficits uncovered in the last half of the nineteenth century—aphasia, agnosia, apraxia, alexia, etc.—led many psychiatrists to suppose that schizophrenia, like these other conditions, would turn out to have a specific link with some damaged brain site, e.g. Broca’s aphasia with a lesion in the left second and third frontal gyri. A minority of more neurologically-orientated physicians (e.g. Wernicke and Kleist) did, in fact, develop just such a detailed system (without any real neurobiological evidence, however). Kraepelin, although committed to this approach, was rigorous enough to realise that he could not as yet justify such schemes.

Bleuler’s incorporation of Freud’s and Jung’s psychodynamic explanations of psychiatric phenomena paved the way for a multitude of non-neuropsychological approaches—psychodynamic, social, existential, behavioural, and cognitive models—which persisted as the mainstream of thinking for over 70 years. All these merely adopted some current psychological model of mind (or non-mind in the case of behavioural) and schizophrenia was slotted into these in the most plausible way possible.

As late as the early 1980s, when one of us was contemplating a book on the matter, the title Neuropsychology of Schizophrenia was suggested to a publisher, who was enthusiastic about the title as anything to do with the brain was becoming a selling-point in the United States. By the time the literature had been reviewed, however, it was clear that, apart from Kraepelin’s, Wernicke’s, and Kleist’s modest beginnings, there was no corpus of work on the neuropsychology of schizophrenia, and the name was changed to The Psychology of Schizophrenia (Cutting, 1985). Ten years on, the situation is radically different. All the chapters in this book reflect this to a greater or lesser degree. Even those contributors who are still promoting what are essentially “preneuropsychological era” models, feel obliged to give their views some neuropsychological relevance.

Is there a common definition of the neuropsychology of schizophrenia? As already mentioned, neuropsychology per se is a new term, although its origin may have had psychiatric connections. Perhaps the first use of the word was in 1913, when Sir William Osler spoke at the opening of the Henry Phipps Psychiatric Clinic of the Johns Hopkins Hospital, Baltimore (Bruce, 1985). This was just 2 years after Bleuler’s description of The Schizophrenias (Bleuler, 1911–1950). The second landmark was the appointment of Karl Lashley as Research Professor of Neuropsychology at Harvard in 1937. However, Donald Hebb’s book, The Organisation of Behaviour: a Neuropsychological Theory, published in 1949, finally established neuropsychology on the intellectual map. Coming more up to date, the first journal devoted to the topic was launched in 1963—Neuropsychologia, edited by Henry Hécaen.

One way to avoid the arbitrariness of definitions is to look at current usage. Unfortunately this takes us even further from consensus. A recent target article in the journal Behavioural and Brain Sciences by Gray et al. (1991) carried the same title of this book, and Hemsley (Chapter 6) summarises many of the underlying theoretical points made in that article. For Gray and colleagues, neuropsychology is any study of behaviour in relation to the hardware of the brain (see also Robbins, 1990). In this case the brain refers to any brain, including that of the rat. The “neuro” prefix comes in because of experimental manipulation of that organ, either through lesioning or pharmacological agents. The limitations and advantages of inferences about human behaviour derived from animal work have been much debated over the years. Clearly they have an important place in providing the foundation to human neuropsychological theories.

Another usage is the application of psychometric tests derived from studies on populations with known brain lesions, to psychiatric patients. This is perhaps the most traditional form of psychiatric neuropsychology (David, 1989). It can be subdivided into the use of broad test batteries, which show patterns of deficits in, for example, visual-spatial or linguistic skills, which in turn may be interpreted in terms of right and left hemisphere problems (e.g. Flor-Henry & Gruzelier, 1983; see also Liddle, Chapter 3), and the use of more specific, custom-built tests intended to examine in detail a single psychological function or brain area, e.g. the use of the Tower of London and Wisconsin Card Sort test (WCST) (Shallice et al., 1991), or chimeric faces, a right posterior hemisphere test, (David & Cutting, 1990; see also Ellis and de Pauw, Chapter 18; Pantelis and Nelson, Chapter 13; Cutting, Chapter 14). This approach is, in essence, argument by analogy; the analogy may hold at a number of levels. For instance, at the behavioural level, the apathy and amotivation of the frontal-lobe-patient may resemble that of the chronic schizophrenic, as well as at the neuropsychological level, when there may be frequent perseverative errors on the WCST in both patient groups. Dunkley and Rogers (Chapter 11) go as far as to say that dementia praecox is as much a dementia as that of the Alzheimer type.

There is no reason why the neuropsychologist should be wedded to psychiatric nosology and indeed this may lead research into blind alleys. O’Carroll (1992) in a recent review showed how neuropsychology could act at different clinical levels from the diagnostic, e.g. schizophrenia (Dunkley and Rogers, Chapter 11; Pantelis and Nelson, Chapter 13), through the syndromic or subsyndromic, e.g. positive syndrome (Hemsley, Chapter 6), negative syndrome (Frith, Chapter 9), the “reality distortion” of Liddle (Chapter 3) to the symptom level, e.g. delusions (Bentall, Chapter 19), delusional misidentification (Ellis and de Pauw, Chapter 19), and hallucinations (Slade, Chapter 15; David, Chapter 17).

Fortunately, advances in neuroscience and neuroimaging have allowed these analogies, particularly with respect to brain localisation, to be tested. The structure of the brain region of interest may be examined with the detailed morphometry of the psychoneuropathologist or through CT and magnetic resonance brain imaging. Similarly, functional imaging utilising metabolism or cerebral blood flow (Early et al., Chapter 2; Liddle, Chapter 3) may serve not only to test the pattern of activation at rest or in response to a cognitive challenge (Weinberger et al., 1986; see also Nuechterlein et al., Chapter 4; Fleming et al., Chapter 12), but also the assumptions about the regional specificity of the test in question, based on patient data and crude clinicopathological correlations, which often turn out to be spurious. Also, the power of pharmacological agents to modify and produce abnormal psychological phenomena requires localisation in terms of neurotransmitter sites as well as functionally specific anatomical regions (Early et al., Chapter 2).

Early and colleagues report two separate findings in non-medicated schizophrenics: (1) an increase in blood flow (relative to the rest of the brain) in a subcortical region on the left; and (2) a tendency to ignore stimuli presented in the right visual field. Although this is in support of some lateralized deficit—neurobiological and psychological—in schizophrenia, it is somewhat idiosyncratic. The neurobiological finding is in line with several studies showing left hemisphere overactivity and right hemisphere underactivity in the condition. The psychological finding is curious, however, because visual neglect in subjects with focal lateralised brain damage is virtually always restricted to the left visual field, unless there is anomalous lateralisation of the search control mechanism. Moreover, right hemisphere damage also impairs search in the right visual field more than does left hemisphere damage in that (right) field.

Liddle (Chapter 3) reports different patterns of blood flow in different subtypes of schizophrenia. Patients with predominantly poverty of speech, flat affect, and decreased spontaneous movement exhibited reduced left-sided dorsolateral frontal perfusion. Patients with predominantly thought disorder and inappropriate affect exhibited decreased right-sided ventral frontal perfusion. One patient with catatonia resembled the former group.

It is not surprising that different symptom clusters in schizophrenia are associated with different blood flow patterns. Different mental activities provoke different blood flow patterns in normals, of course. Liddle’s results, however, are intriguing because they go some way towards mapping the cerebral dysfunction in different subtypes, though whether they reflect an end-stage cerebral dysfunction or some primary problem is not clear. The patients were all medicated.

As mentioned earlier, neuropsychology owes its distinctiveness from the rest of psychology by virtue of its reference to the brain. However, this has led to an obsession with brain localisation. While the location of schizophrenic disturbances to a cortical area would be a valuable achievement, the story would not end there. In fact this would provide but one link in a complete neuropsychology of schizophrenia chain, which would stretch from neural ultrastructure and chemical transmission to the most abstract of phenomenal experiences. Neuropsychology can justifiably regard as its legitimate domain the intervening steps between the abstract levels of representation—hallucinations, delusions, etc. and “pure” psychological phenomena, e.g. memory and attention. No direct reference may be made to the brain provided two underlying assumptions are held, namely, that these psychological processes may become distorted by dysfunction at a lower level—in the brain—and that schizophrenia is the manifestation of just such a distortion. In other words, cognitive psychology may be applied usefully to the study of schizophrenia but some reference to the biological underpinnings to cognition must be made eventually (Fleminger, Chapter 20; Bentall, Chapter 19; Slade, Chapter 15). This is the chief difference between the work done in the 1980s and earlier work. Much of the earlier endeavour may be described as “preneuropsychological” only insofar as neural bases for such phenomena as described by Green and Nuechterlein (Chapter 5) have yet to be elucidated fully. Green and Nuechterlein report abnormalities in processing visual information in schizophrenia, measured by a technique known as “backward masking”, in which two stimuli are presented for recognition, at different interstimulus intervals, with the purpose of evaluating the potency of the “sensory register” or “icon”; manics were equally impaired. This study illustrates the typical “preneuropsychology of schizophrenia methodology” amongst psychological studies on schizophrenia, and is included as an excellent example of its kind. Green and Nuechterlein attempt a bold integration of their findings (personal communication). They suggest that the interruption of information from a target involves the interaction of transient and sustained visual channels, which do not appear to interact before the level of the primary visual cortical area. The deficit observed may be an example of a general sensory gating deficit, which involves the failure to attenuate the second of two paired stimuli (in this case the mask). Gating is believed to involve mesolimbic dopamine pathways in the brain.

McKenna and colleagues (Chapter 10) adopt the traditional approach to the psychology of schizophrenia: examining one mental function—memory—and comparing its potency in schizophrenics and normals. What gives this chapter a neuropsychological slant is the choice of memory, as this is conventionally regarded as relatively intact in schizophrenics, but impaired if brain damage is present. McKenna et al. find gross memory deficits in their schizophrenics, especially in the realm of semantic memory. This has less in common with the everyday concept of memory but refers to a store of knowledge about the world. McKenna et al. speculate that access to this store may be unreliable, giving rise not only to deficit but also to “productive” symptoms such as illogicality and delusions. This has some resemblance to Cutting’s theory regarding impaired real-world knowledge and schizophrenia. Cutting (Chapter 14) puts forward a strong case for this to be the result of right hemisphere dysfunction, having first outlined the ground rules for such an inference (see also Cutting, 1990).

Fleming et al. (Chapter 12) propose that the memory deficit in schizophrenia is a result of some higher-order control-mechanism disorder, which is itself a consequence of frontal lobe dysfunction. This chapter conforms to the newer neuropsychological approach of trying to relate some psychological deficit in schizophrenia to a comparable psychological deficit in subjects with known brain disease. It is theoretical, but draws on data from such diverse sources as twin studies and cerebral blood flow conducted at the United States’ National Institute of Mental Health.

Pantelis and Nelson (Chapter 13) set out to examine theoretical formulations, such as those of Fleming et al., by administering recognised frontal lobe tests to schizophrenics. The authors find evidence for frontal lobe dysfunction in schizophrenia but extend this anatomical localisation to subcortical connections. The “frontal lobe hypothesis” of schizophrenia is fashionable at the moment and, although not all neurobiological procedures confirm it, certainly has to be taken seriously on the evidence of results such as these.

In the case of Frith’s work on the theory of mind (Chapter 9), there has been very little time to examine brain–cognition relationships in detail. Frith approaches the problem of the psychological deficit in schizophrenia from two relatively novel angles. The first relies on new findings on the nature of cognitive development in infants. The second incorporates the tendency in experimental psychological research to talk in terms of metapsychological entities, i.e. to go beyond the base mental functions (attention, perception, memory, etc.) and examine how the person’s whole mind tackles complex problems, including how it monitors and evaluates its own activity. The chapter is a theoretical discussion of how differe...