A second measure that has been widely used in studies of schizophrenia patients is the Continuous Performance Test (CPT). The CPT measures sustained vigilance, a phenomenon that first became of interest to psychologists during the Second World War, when the Royal Air Force commissioned a series of experiments to discover the optimal length of time that a radar operator could function effectively when on anti-submarine patrol.14 To a person tested on the CPT, the experience is a bit like watching a radar display. Letters are briefly presented on a computer screen, usually at the rate of one every second or so. The participant has to press a button immediately after seeing particular targets, which may be simple (e.g. the letter ‘T’) or complex (e.g. the letter ‘X’ but only when it follows the letter ‘T’). When ordinary people are administered the test, their performance usually decreases over a relatively short period of time as their attention fades. Many studies, such as those conducted by Keith Nuechterlein and his colleagues at the University of California at Los Angeles Clinical Research Center for the Study of Schizophrenia, have shown that this performance decrement is greater in psychotic patients than in normal people.15 By studying the effects of varying some of the characteristics of the CPT, for example the complexity of the target and how clearly it is presented on the screen, Nuechterlein and his colleagues have been able to study more precisely the attentional difficulties experienced by their patients. For example, they observed that patients with predominantly negative symptoms performed very poorly on ‘high load’ (difficult) versions of the test.16
A third test which we will consider here measures the very earliest processes involved in perception, and is best described in the words of Michael Foster Green, who also works at the UCLA Clinical Research Center:
Imagine that you are seated in front of a screen and an experimenter is presenting letters to you one at a time with a type of projector. Although the duration of each letter is very brief (perhaps 10 msec.), you can easily identify each letter with perfect accuracy. The experimenter pauses and tells you that he/she will continue to show you letters at the same duration, but there will be one difference: after you are shown each letter, the screen will go blank for a short time and some crossed lines will appear where the letter had been. Your job is only to report the letter and ignore the crossed lines. The task probably sounds quite easy because you had no difficulty identifying the letters before, and the duration of the letters will not change. However, when the stimuli are presented, you might find that you can seethe crossed lines, but no letter at all. This is the backward masking effect.17
The backward masking effect occurs because visual information is briefly held in a sensory store (sometimes called the iconic memory) prior to being passed on to later brain centres for more detailed processing. If the ‘mask’ of crossed lines is presented very soon after the initial letter, it displaces the information about the letter from the sensory store before it can be passed on. As the later processing is required for us to be aware of the letter, we are unable to identify it.
By varying the interval between the presentation of the letters and the mask until the letters can be seen, it is possible to measure the amount of time the sensory store requires to pass on the letter for later processing. In 1981, Dennis Saccuzzo and David Braff, two researchers at the University of California at San Diego, showed that this interval was longer for schizophrenia patients than for normal controls, indicating that the speed with which the visual information was being passed on was slower for the patients.18 It was later observed that unmedicated patients’ performance on the test improved after they had been given anti-psychotic drugs.19
In this short space it has been difficult to do justice to the large volume of research on the performance of psychotic patients on attentional tests, and the attempts that have been made to account for these findings. Of the many models of attentional dysfunction that have been proposed I will mention just one, developed over a number of years by Keith Nuechterlein and his colleagues at UCLA.20 On the basis of a detailed theory of the processes involved in normal attention, they have argued that the patterns of results observed in their patients can best be explained in terms of two separate types of abnormality.
First, they argue that poor performance on the backward masking task and on certain versions of the CPT (especially versions in which the stimuli are blurred and difficult to identify) is caused by deficits in the very earliest and most automatic stages of information processing. Interestingly, these deficits seem to be present in patients who are enjoying a remission of their symptoms, and Nuechterlein and his colleagues therefore argue that the deficits are enduring psychological characteristics that cause people to be vulnerable to breakdown under times of stress.
Second, they argue that poor performance on other versions of the CPT (especially versions in which complex targets are employed) and also on the DSDT is best explained by an inability to use active memory to guide the selection of information. When we try to focus on some types of stimuli to the exclusion of others, we have to hold a representation of the target stimuli in an active ‘on-line’ memory store (the same memory system that you use when performing mental calculations). The content of this store – sometimes known as working memory – therefore exerts control over our voluntary attention. Nuechterlein and his colleagues argue that the poor performance of patients on the complex versions of the CPT is caused by a failure of this kind of control, probably caused by some kind of deficit in the working memory system. As performance on the complex versions of the CPT is usually worst during periods of active illness, and usually improves during remission, Nuechterlein and his colleagues argue that this type of deficit is directly involved in the onset of symptoms.
Impressive though this work has been, it suffers from three important limitations. First, the reader will not be surprised when I question the specificity of the findings. Although much less effort has been made to study cognitive deficits in bipolar patients than in patients with a diagnosis of schizophrenia, when those efforts have been made, similarities between schizophrenia and bipolar patients have been more apparent than differences. For example, bipolar patients have been found to perform poorly on the DSDT,21 the backward masking task,22 and on other measures of working memory and attention.23 Poor performance on the CPT has been found, not only in bipolar patients24 but also in unipolar depressed patients who are experiencing psychotic symptoms.25
Second, gross cognitive deficits appear to be only tenuously linked to the behaviours and experiences that most people would regard as prototypical of psychosis. In a recent review of the relevant evidence, Michael Foster Green has pointed out that poor scores on most deficit measures seem to be unrelated to positive symptoms (see Figure 8.1)!26 Although most patients perform poorly, little difference is observed between those with hallucinations and delusions and those with other symptoms or–on many tests–even between patients who are currently ill and those who are in remission. In contrast, performance on neuropsychological and cognitive deficit measures seems to be a much better predictor of patients’ social and occupational functioning. Patients with severe deficits generally fare less well when living in the community, are poor at dealing with social problems, and experience very great difficulty when attempting to learn new skills.
Green’s response to this paradoxical lack of association between positive symptoms and deficits is surprising. Evoking Bleuler’s distinction between primary and secondary symptoms of schizophrenia, he has concluded that cognitive deficits are the core of schizophrenia, and that positive symptoms are peripheral features. To put this proposal another way, he has suggested that we redraw the boundaries of the disorder to put deficits in the centre, so that positive symptoms are no
Figure 8.1 Relationship between cognitive deficits, drug treatment, symptoms and social functioning (functional outcome) according to Michael Foster Green and Keith Nuechterlein (‘Should schizophrenia be treated as a neurocognitive disorder?’, Schizophrenia Bulletin, 25:
309–19, 1989). The strength of causal relationships is indicated by the type of arrows shown.
longer attributed much importance. Of course, even if we were to accept this proposal, it would still be necessary to identify those processes that, in addition to cognitive deficits, are responsible for delusions and hallucinations. After all, it is usually these symptoms, however peripheral, that drive patients and their families to seek psychiatric help.
A final limitation of the research we have reviewed concerns the type of mental functions studied. Most psychologists have chosen to focus on gross mental functions, especially perception and attention, and have employed stimuli that have been essentially meaningless (for example, strings of numbers in the DSDT, sequentially presented letters in the CPT, and abstract patterns in the WSCT). Because they knew that performance on psychological tests is influenced by the content of the test materials, early test designers regarded meaning as a dangerous complication. This was not an entirely senseless attitude, as the poor performance of patients on attentional measures is presumably telling us something quite important. However, it should be obvious that these tests do not measure the kinds of tasks that the human mind performs in ordinary life. We are likely to get a more complete picture of the psychological mechanisms involved in psychosis if we focus not only on raw deficits but also on those processes that are known to be important in everyday functioning. In the remainder of this chapter, I will briefly review some of these processes, particularly those which will prove important when we come to look more closely at symptoms in later chapters.
The Social Brain
So far as the brain is concerned, any stimulus is not the same as any other. Its operations are content-specific, which is to say that the brain processes different kinds of information in different ways. This preference for certain kinds of stimuli in contrast to others is a requirement for intentionality (the ‘aboutness’ that connects the contents of our thoughts to the external world) and underlies the cognitive biases which, we will see in later chapters, play an important role in symptoms.
Recent studies have shown that the normal brain has specialized to deal with one particular class of stimuli above all others. These stimuli are the most complex and demanding objects in our everyday environment, namely other human beings. Unless you are a Nobel-prize-winning rocket scientist, the problems that demand most of your attention, in all likelihood, involve your relationships with others, a fact that is reflected in popular culture, from songs and novels to films and television soap operas. (The characters of Neighbours, Friends and Coronation Street are constantly falling out with each other, making up, finding new lovers or losing old ones. We almost never see them sweating over some intractable problem at work, or struggling to complete their tax returns.)
The idea that the human mind has evolved to preferentially process social information is sometimes called the social brain hypothesis. Considerable evidence in its favour can be found in both the biological and the psychological literature. Let us begin by considering anatomical comparisons of human beings and other species. Compared with other vertebrates, we have a disproportionately sized cerebral cortex. Across the vertebrate species, brain volume increases on average as a two-thirds power of body mass (in other words, in proportion to the surface area of the body), reflecting the increased processing capacity needed by big organisms with large numbers of sensory receptors and muscle fibres.27 However, when this relationship is taken into account, it is evident that some species have brains that are larger than would be expected from their body size, a phenomenon known as encephalization. The most encephalized species is, of course, ourselves, with other primates following closely behind. The evolutionary pressures responsible for encephalization remain a matter of some controversy. Robin Dunbar, an evolutionary psychologist working at the University of Liverpool, has suggested that group size made an important contribution to this process. The members of each species relate to each other in groups of characteristic size, and Dunbar has shown that this size correlates reasonably well with encephalization. Larger groups, according to this hypothesis, demand larger brains, and so our own brains have evolved to cope with social systems that are more complex than those of any other species. If Dunbar’s theory is correct, the majority of our brain’s ‘computing power’ is dedicated to processing social information.28
Leslie Brothers, a psychiatrist working at the University of California in Los Angeles, has argued that neurophysiological investigations provide a second important strand of evidence about the social brain. In studies carried out mainly on monkeys, Brothers and her colleagues have recorded the responses of specific neurones following the presentation of different kinds of stimuli. In these experiments, some neurones have been found to be specifically responsive to social information. For example, neurones have been identified which fire only when the animal sees a hand, a face, eye movements or other bodies walking. These are mostly located in the temporal lobes, in areas such as the inferotemporal cortex and the amygdala. Brothers has suggested that these structures function as an ‘editor’, which highlights social information for preferential processing by other areas of the brain, thereby determining which stimuli are personally signifi-cant.29 (Interestingly, other researchers have argued that the amygdala plays an important role in emotion, a proposal that is consistent with Brothers’ theory, as emotional responses are most often elicited when we encounter social problems.)30
A third source of evidence about the social brain comes from psychological studies of ordinary human beings. If the human brain has evolved to deal with social stimuli, we should find tasks that employ these stimuli easier to perform than tasks that do not. There is an abundance of evidence supporting this prediction (much of which was collected before the social brain hypothesis was first proposed) but there is only space enough in these pages to describe one example, taken from the field of child psychology. In the 1950s, the famous Swiss child psychologist Jean Piaget reported a series of studies that appeared to demonstrate that young children are unable to ‘decentre’ their imagination from their experience.31 In some of these studies, children were shown a model of three mountains, and a doll was placed on one corner of the model. When children below the age of 9 were asked to choose a picture that showed how the mountains looked from the position of the doll they almost always failed, the younger children typically choosing a picture taken from their own perspective. At first sight, this seems to be powerful evidence in favour of Piaget’s account of the cognitive limitations of young children. However, British child psychologist Martin Hughes later carried out a similar study in which much younger children seemed to perform better than Piaget’s 7- and 8-year-olds. In this task, two toy policemen were placed on a table, divided by two intersecting walls. When asked to place a third doll in a position where it could not be seen by either policeman, children were able to do this with 90 per cent accuracy, implying that they could simultaneously think about the perspectives of both policemen. Margaret Donaldson, a psychologist at the University of Edinburgh, has accounted for this apparent discrepancy with Piaget’s work by pointing to the socially realistic nature of Hughes’s task.32 Young children know what it is like to be naughty and to hide from adults. The motives and the intentions of the characters in Hughes’s task were therefore comprehensible to them. For this reason, they were able to complete the task successfully, unlike the older children confronted with the more abstract task devised by Piaget.
A final source of evidence about the social brain concerns the impairments seen in some neuropsychological disorders. If the brain has evolved specific mechanisms for dealing with social information, it would not be surprising if some conditions turned out to be the consequence of the loss of or inability to develop specific kinds of social reasoning. Autism is a disorder that seems to reflect this kind of problem. The main features of the condition, which usually become evident within the first few years of life, are an inability to engage in imaginative play, impaired devel
opment of language and a failure to form even rudimentary relationships.33 In many cases, these difficulties are so severe that the autistic person requires lifelong care. Although the causes of the disorder are poorly understood, a high proportion of autistic children have demonstrable brain damage, suggesting that some kind of disruption of specific neural circuits may be implicated.
Psychological research conducted over the last two decades has suggested that the inability to understand the mental states of other people may be a core feature of autism, and that the symptoms that lead to its diagnosis may be a consequence of this deficit.34 The ability to guess what people think, and to anticipate what they might do (in other words, to use folk psychology effectively), is a vital ingredient of normal social life. In adulthood, it enables us to recognize our friends and enemies, and to predict what will happen when we try to interact with them. When talking to another person, it allows us to adjust our speech to match the perceived needs of the listener. Children who acquire this ability are often said to possess a theory of mind* (for this reason, psychologists sometimes speak of people having ToM skills), a term which has been rightly described as ‘a daft expression because it [misleadingly] suggests that a child theorizes about the nature of feelings, wishes, beliefs, intentions, and so on’.35 It might be more correct to say that we can ‘mentalize’.
Madness Explained Page 23
