Children, Research And Policy

Basil Bernstein, Julia Brannen

• Publisher: Routledge
• Year: 2013
• Print ISBN: 9780748404056
• eBook ISBN: 9781135347697
• Edition: 1
• Topic: Medicina
• Subtopic: Prestazione di assistenza sanitaria

First Published in 1996. Research on childhood is a growing area of interest in social policy. Covering both familial and institutional settings, this book explores relevant issues, including the female workforce and changing family forms.

Part I

Research

Chapter 1

Specificity of Brain-Behavioural Relationships Revisited: From Epileptic Personality to Behavioural Phenotypes

Michael Rutter and William Yule

An important early phase in Barbara Tizard’s career was concerned with research in the field of epilepsy. Her key review of the concept of a characteristic epileptic personality, together with her systematic appraisal of the relevant empirical evidence, did much both to clarify the issues and to cast doubt on the stereotypes that prevailed at the time. Although it is now more than three decades since her review, the paper continues to be cited as marking a significant turning point in the way the topic was thought about (see e.g. Taylor and Eminson, 1994). In her review, Barbara Tizard highlighted five main issues (Tizard, 1962). First, there was the question of whether psycho-pathological disorders were more frequent among epileptic subjects than in the general population. The evidence at that time was fragmentary and inconclusive but Tizard suggested that there might be a true increase. Second, there was the rather different question of whether such psychological disturbances took a characteristic form in people suffering from epilepsy. Tizard noted the unsatisfactory quality of much of the evidence but concluded that the disturbances were quite varied in type and there was no indication that there was such a thing as a characteristic epileptic personality. Accordingly, there was a need for research to identify the variables – whether they be psychosocial, neurophysiological or structural – that accounted for the heterogeneity. Third, she considered the possibility that there might be either different levels of psychiatric risk, or different forms of psychopathology, associated with the type of epilepsy, the location of an epileptic focus or the presence of organic brain pathology. She concluded that there might well be associations of this kind but the evidence was insufficient to lead to any kind of firm conclusion. Fourth, she drew attention to the inadequacy of the measuring instruments available to assess either levels of psychopathology or (most especially) specific types of psychological dysfunction. Finally, Tizard underlined the problems of inferences based on selected clinic samples. She urged the need for good epidemiological data using discriminating and well-validated measures.

During the thirty-four years that have passed since Barbara Tizard’s review of epileptic personality, considerably better evidence has become available. It has broadly confirmed all the main conclusions she drew in 1962, but it has also served to open up new avenues of research and has led to the development of a number of new concepts. In this chapter we briefly review some of these developments, with particular reference to epidemiological data on the psychiatric risks associated with epilepsy and with other forms of neurological dysfunction; the findings on differences in specificity of psychological sequelae according to the age of the individual at the time of brain injury; the evidence on the validity of highly specific behavioural syndromes (with special reference to autism); and the concept of behavioural phenotypes.

Psychiatric risk and neuro-epileptic disorders

Systematic epidemiological data on the psychiatric risks associated with epilepsy and with neurological disorders in childhood were first provided by the Isle of Wight surveys undertaken during the 1960s (Rutter, Graham and Yule, 1970a; Rutter, Tizard and Whitmore, 1970b). A range of multiple screening measures was used to detect all cases of epilepsy or neurological disorder in children aged five to fifteen years who were resident on the Isle of Wight. Children with neuro-epileptic disorders were compared with those who had physical disorders not involving the brain (such as diabetes, heart disease, asthma, or peripheral sensory deficits) and a random sample of the general population. The whole population was assessed using parent and teacher questionnaires of demonstrated reliability and validity (see Elander and Rutter, 1996). Parents and children were also interviewed using investigator-based standardized assessments of psychopathology; individual psychological testing of the children was undertaken and information was sought from teachers. The results showed convincingly for the first time that the rate of psychiatric disorder was substantially higher in children with brain disorders than in children who were free of physical problems or in children whose physical disorders did not involve the brain. Specific reading difficulties were also more frequent in the neuro-epileptic sample. Because the study was based on epidemiological coverage of the total population, rather than a clinic sample, the strong association between brain disorders and psychopathology cannot have been due to a referral bias. The fact that disorders of the brain carried a much higher psychiatric risk than other physical disorders also strongly suggested that the psychiatric risk derived from brain pathology rather than from non-specific effects that might accompany physical handicap or from having a stigmatizing disorder. Part of the risk seemed to derive from the cognitive impairment that was also more common in the brain disorder group but the psychiatric risk was still much increased even after account had been taken of lower IQ. The inference that it was brain pathology per se that led to the increased psychopathological risk was confirmed in a further study undertaken in London (Seidel, Chadwick and Rutter, 1975) in which children with cerebral disorders were compared with a matched group of children whose neurological disorders stem from lesions below the brain stem (such as poliomyelitis). The children with brain disorders were twice as likely to have psychiatric problems, despite the fact that the two groups were similar in both social background and visible crippling, and despite the fact that children with an IQ below seventy were excluded.

In both these epidemiological studies, the brain lesions had been present from infancy or early childhood and it was not possible to examine the effects on psychopathology of a newly acquired brain disorder. Accordingly, a further prospective study of a representative sample of children who acquired a severe head injury was undertaken (Rutter, Chadwick and Schaffer, 1983a); the group was compared, during the course of a follow-up lasting over two years, with a similar sample of children with mild head injuries and a group of children with orthopaedic injuries not involving either loss of consciousness or damage to the head. Data on the children’s behaviour before injury were obtained very shortly after the accident and before the sequelae could be evident. The results were clear-cut in showing a much increased rate of psychopathology in the case of severe head injuries but not in the case of mild ones. In parallel with the stereotype of the epileptic personality, effectively contradicted by the findings reviewed by Tizard (1962) in the 1960s, there was the notion that there was a distinctive and characteristic behavioural response to brain injury in childhood (Bakwin and Bakwin, 1967). This was usually equated with some variant of the hyperkinetic syndrome and it was broadened and extrapolated so that the presence of hyperactivity, attention deficits and the like was used to infer ‘minimal cerebral dysfunction’ (MBD) (Kalverboer, van Praag and Mendlewicz, 1978). So called ‘soft signs’ was also used to infer organic brain pathology (Yule and Taylor, 1987). Empirical findings showed that the concept of MBD was no better validated than that of the epileptic personality. Not only was it found that children with definite organic brain pathology showed a most heterogenous range of psychiatric disorders but also most children with hyperkinetic disorders lacked unequivocal evidence of neurological dysfunction. The stereotype of MBD stood up to empirical testing no better than the epileptic personality (Rutter, 1982a) and it too has come to be abandoned by most researchers and clinicians.

The next question concerns the factors within the group of children with neuro-epileptic disorders that created an increased psychopathological risk. The question is an important one because some two-thirds of the children did not show psychiatric disorder and hence the mere fact of brain injury was clearly not sufficient in itself to give rise to a psychiatric condition. The Isle of Wight study findings showed that structural disorders of the brain (such as cerebral palsy) carried a higher psychopathological risk than did uncomplicated epilepsy. On the other hand, psychiatric disorders were more common among children whose structural brain disorders also involved epilepsy than among those where the brain disorder was not associated with epileptic attacks. Among the children with uncomplicated epilepsy, the rate of psychiatric disorder was highest in those with psychomotor attacks but otherwise the type of epilepsy was not a good predictor of psychiatric risk. Several studies have sought to determine whether the localization of epileptic foci is of psychiatric significance but the findings are contradictory and inconclusive. The inconsistency of findings probably partly derives from the fact the EEG findings on epileptic foci tend to vary over time and over repeated testing (Kaufman, Harris and Schaffer, 1980), in part because the EEG data have been of variable quality and usually non-blind and non-standardized, and partly because few of the samples have been epidemiological. Certainly, it cannot be concluded that either the nature of the epilepsy or the localization of the epileptic focus are irrelevant for the development of psychopathology but, equally, there is no good evidence that either are crucial, with the possible exception of a higher psychiatric risk associated with psychomotor attacks or temporal lobe epilepsy (Goodman, 1994a).

The possible importance of the localization of acquired brain lesions was investigated through a systematic study, using standardized methods of assessment of proven reliability and validity, in a group of children with localized brain lesions confirmed through neurosurgery (Shaffer, Chadwick and Rutter, 1975). No substantial associations were found. On the other hand, the investigation was undertaken before the availability of modern methods of brain imaging and, in their absence, it was not possible to be sure that the observed brain lesion was the only one that was present. The matter remains open. What is much needed is an epidemiological study using high quality standardized imaging methods, and good EEG data, as well as standardized assessments of psychopathology.

A further issue of considerable theoretical, as well as practical, importance is the extent to which non-neurological factors affect psychiatric risk. All the evidence indicates that they play a substantial role (Rutter, Graham and Yule, 1970a; Rutter, Chadwick and Schachar, 1983b; Hermann and Seidenberg, 1989). Thus, serious psychosocial adversity much increases the likelihood of significant psychopathology. It might be thought likely that brain abnormalities and psychosocial risk would act synergistically. That is, it might be supposed that the presence of brain dysfunction would act, in part, through increasing the child’s susceptibility to the ordinary run of psychosocial stressors and adversity. The evidence to date of any such interaction remains weak and inconclusive and remarkably little is known on the precise mechanisms by which organic brain dysfunction predisposes to psychiatric disorder.

Age effects on the sequelae of brain lesions

In adult life, there is good evidence that the lateralization of brain injuries makes an important difference to the pattern of cognitive sequelae (Newcombe, 1969; McFie, 1975). Thus, lesions of the dominant hemisphere, but not of the non-dominant one, are associated with loss of language and aphasic-type language abnormalities, together with verbal deficits on cognitive tests. By sharp contrast, this has not been found in relation to brain lesions incurred prenatally or in the infancy or early childhood period. Thus, in Chadwick et al.’s (1981) study of localized brain lesions, there was no evidence that the pattern of cognitive deficits was affected by which hemisphere was damaged. Similarly, in their study of children with hemiplegic cerebral palsy, Vargha-Khadem et al. (1992) found no differences in cognitive pattern according to whether the left or right hemisphere was involved. Cognitive impairment was substantially greater in the case of individuals with epilepsy as well as cerebral palsy, but the side of the hemiplegia appeared irrelevant. Similarly, lesions of the dominant hemisphere in early childhood do not lead to aphasia in the way that comparable lesions in later child or adult life do (Woods and Carey, 1979). Also, hemispherectomy in children with severe unilateral brain lesions does not have the effects that would be expected on the basis of findings in adults (Heywood and Canavan, 1987). It should not be supposed that these findings mean that brain lesions in early life are less functionally damaging. Neuronal regrowth may be more possible but this can lead to harmful misconnections as well as restoration of prior functioning (Schneider, 1979; Rutter, 1982b, 1993a; Goodman, 1994b).

The precise mechanisms involved in plasticity remain uncertain. In some way or other, it seems that either transfer of functions from one hemisphere to the other occurs more readily in the immature brain or, alternatively, there is greater plasticity in the take-up of functions. On the face of...

Table of contents

• Cover Page
• Half Title page
• Title Page
• Copyright Page
• Dedication
• Contents
• Acknowledgments
• Introduction
• An Interview with Barbara Tizard
• 1 Research
• 2 Research and Policy
• List of contributors
• Index