ABSTRACT
Behaviour disorders in both adults and children may be of epileptic origin . . . a child may commit anti social acts without purpose-set fires, steal, run away, display temper tantrums or have fits of screaming, crying or breath-holding to the point of unconsciousness. The question must be asked: How does Bennett know that behaviour disorder represents disguised epilepsy if the patient never displays epilepsy? His chain of reasoning seems to be: This individual displays behaviour disorder. He has an EEG similar to that displayed by some epileptics. Therefore he is an epileptic and the epilepsy has caused the behaviour disorder. (Bennett does not in fact say whether an EEG was taken in the cases cited in the quotation above.) This chain of reasoning is fallacious, and cannot provide any logical proof for Bennett’s assumptions. The only possible grounds for hypothesizing an epileptic equivalent seem to be where a patient displays an EEG pattern during disturbed behaviour similar to that which he displays during an epileptic attack. The only behaviour which has been subjected to this kind of test are the night terrors, fears, and anxiety attacks discussed above.Bennett repeats his assertions about temporal lobe epilepsy in a further paper (1965), making the same generalization with the same kind of evidence, and he asserts that ‘Many horrible crimes are attributable to epilepsy’.Pond (1963) suggested that the temporal lobe epileptic may display a withdrawal of interest and motivation as a basic personality pattern. Pond admitted that this view was reminiscent of some of the older writers on the epileptic personality. No case histories or methods of investigation are provided in support of this view, although animal evidence is cited that motivation falls as a result of rhinencephalic lesions (i.e. those associated with temporal lobe epilepsy). Pond suggests that the hyperkinetic child, although over-active in childhood, becomes apathetic after adolescence.Juul-Jensen (1964) found that 60 per cent of the temporal lobe epileptics he studied (221 cases) had difficulties in social adjustment, compared with 35 per cent of the remaining 694 cases of other types of epilepsy. He suggested that an intervening variable in this association was the failure of anticonvulsants to check temporal lobe epilepsy, in comparison with other types of epilepsy, since when the temporal lobe group was compared with a group matched for severity and frequency of attacks, no differences in the incidence of social adjustment could be found.Whitmore (1964), generalizing from material available from school medical officers, estimated that 1 in 3 children with temporal lobe epilepsy had behaviour disorder, and they tended to display the
symptoms of tensions, lack of toleration, quickness to quarrel, aggressiveness, moodiness and temper tantrums.Krych and his seven co-workers (1964) studied in great detail clinical and other factors in fourteen Polish children with temporal lobe epilepsy. The cases were compared according to the presence or absence of behaviour disorder. The only neurological feature associated with behaviour disorder was the existence of EEG lateralization in the dominant hemisphere. They concluded: ‘The occurrence of character disorders clearly correlates with unfavourable environmental conditions. Disturbed family situation and a rejecting attitude towards the child seem to be of a particular detrimental influence.’ The small number of cases involved did not permit significance testing of the different incidence of the extra-clinical factors.Serafetinides (1965) studied 100 temporal lobe epileptics at the Maudsley Hospital in whom a well-localized epileptogenic lesion allowed a unilaterial operation on the temporal lobe. These patients were specially referred to the Maudsley Hospital because of their psychiatric characteristics, and the most common picture of disturbed behaviour was that of aggression, 36 of the 100 patients displaying aggression. The aggressive group were more likely to be male, and to have an earlier onset of fits.A number of social factors were studied (normal home, broken home, family strife, unhappy childhood, step-parents, illegitimacy, mental illness in parents). In contrast to the study of Krych et al. (1965), no excess of environmental pathology could be found in the aggressive cases: in fact, there was a trend in the opposite direction: 11 per cent of the non-aggressive cases came from a broken home, and none of the aggressive cases; 20-5 per cent of the non-aggressive cases had a maladjusted father, compared with 5*5 per cent of the aggressive cases. The findings were in accord with Krych’s study for the factor of lateralization, in that in most of the aggressive cases the focus was on the dominant side of the brain (i.e. the left side for most subjects, who are righthanded). The success of the surgical removal of the epileptogenic area of the temporal lobe in reducing the aggressive behaviour leads Serafitinides to suggest that this behaviour is organic in origin. The majority of the patients in this study were aged 19 or less, the modal age being 3 to 9 years.Small et al. (1966) compared fifty subjects with temporal lobe epilepsy with fifty matched controls having other types of epilepsy. The incidence of the ‘sociopathic’ personality sometimes attributed to the temporal lobe epileptic (e.g. Hill, 1952) was found to be the same in both the temporal lobe cases and the controls.Stevens (1966) studied 100 consecutive adult patients referred to an epilepsy clinic. Fifty-four of the cases had psychomotor epilepsy with a temporal lobe location. Stevens concluded that the increased
risk of psychiatric hospitalization of this group, compared with the other types of epilepsy, could be adequately explained by the coincidence of temporal lobe epilepsy with an age cohort particularly susceptible to mental illness. Controlling the age factor indicated that there was no difference in psychiatric abnormality between temporal lobe and other types of epilepsy.Ounsted et al. (1966) studied ‘biological factors in temporal lobe epilepsy’ in a series of 100 children, selected from a much larger population of epileptic children in Oxford because of the unequivocal electrical evidence of temporal lobe epilepsy. The children were studied for a period of 10 years. Thirty-five had clear evidence of an ‘aetiological organic cerebral insult’, with 7 more cases having a suspicion of brain injury at birth. In the organic insult group, the incidence of epilepsy in siblings was 2 per cent; in a group having no insult, but status epilepticus, the sibling risk was 30 per cent; in the group with neither insult nor status, the sibling risk was 9-3 per cent. These differences were highly significant. The authors suggest that early status, caused by a genetic predisposition to epilepsy, causes damage to Ammon’s horn. Sclerosis follows, and an epileptogenic lesion arises. The early onset of epilepsy in the status group supports this view.The IQ of the cerebral insult group (N = 35) and the status group (N = 32) was significantly lower than that of the remaining children, with neither insult nor status (N = 28). The earlier the insult or the status, the greater the intellectual loss.Hyperkinesis, as described by Ounsted (1955), was present in 26 of the 100 children. Hyperkinesis was significantly associated with cerebral insult, status, low intelligence and male sex, and early onset of epilepsy. Only 3 of the hyperkinetic children did not have a history of cerebral insult or status. This fact, and the fact that hyperkinesis occurs in children with brain damage but without epilepsy, suggests (the authors conclude) that brain damage rather than epilepsy is the significant aetiological factor in these cases.Thirty-six of the children were found to display ‘catastrophic rage’—that is, outbursts of extreme rage and anger apparently out of proportion to the stimuli which provoked this behaviour. This rage had the effect of making schooling and social relationships for the child particularly difficult. The significant associations with these rage outbursts were a history of cerebral insult or status. However, although hyperkinesis and rage were often associated, they also occurred independently. Only in girls was catastrophic rage associated with low IQ and early onset of epilepsy, an enigmaticfinding. Children who had never had grand mal fits were free from rages.The home of the epileptic child was considered to be ‘disordered’
if one or more of the following five factors was present: (1) gross poverty; (2) death of mother at an early age; (3) grossly aggressive father; (4) psychosis in one or both parents; (5) gross chronic neurotic illness in one or both parents. There was a significant association between a ‘disordered’ home and the existence of catastrophic rage in the epileptic child. The data suggest the possibility that hyperkinesis has an organic origin, but rage can occur in those hyperkinetic cases which have a poor environment. The finding that has been made by other writers, of a notably high incidence of psychopathy or disturbed behaviour in the parents of the children, again occurred in this study. It will be noted that the authors merge diverse factors, such as poverty, with other factors with which they have only a loose conceptual relation, such as aggression of the child’s father.The careful observation of the children over a ten-year period indicated that only in 15 was there no personality abnormality. The pictures observed were: hyperkinesis plus rage; hyperkinesis plus a milder aggression; neurotic reactions, usually of a mixed form; general psychological problems arising for the first time at adolescence; and, in middle and late ’teens, schizophrenia and severe aggressive psychopathy.One interesting case report is of a 7-year-old boy who developed hyperkinesis after the successful control of fits. This case is reminiscent of those cases in which disturbed behaviour shows an inverse relationship to the occurrence of fits.This carefully conducted study, in which the population and methods of study were carefully specified, is in contrast to the many poorly conducted studies of temporal lobe epilepsy reported in earlier literature. The study has the merit that it does not overgeneralize about cause, leaving ‘residual areas’ open to further investigation. The obvious areas suggested are a fuller investigation of the neurotic pictures, and a more detailed investigation of environment and interaction between parents and children.Aird et al. (1967) studied the antecedents of temporal lobe epilepsy in 193 patients. They found that the epilepsy had an onset earlier than was previously suspected-42 per cent of cases had an onset in the first decade and 75 per cent in the first two decades. Comparison with normal controls showed that the temporal lobe group had a significantly higher percentage of anoxia, more abnormalities of development, behaviour problems of childhood, andunusual nocturnal phenomena. The authors suggest: ‘These findings suggest that serious dysfunction of the CNS had long antedated the final development of an overt form of temporal lobe epilepsy in approximately 50 per cent of the 156 patients with an onset of epilepsy after the age of 10’. The authors suggest that the same under-
lying dysfunction of the central nervous system creates a continuum of disturbance, ranging from abnormal behaviour to frank convulsions. However, some doubt must be cast on this conclusion, in view of the fact that the authors did not consider other possible factors which precipitate behaviour disorder, such as abnormal family environment or abnormal personality in the parents. These variables were not measured for subjects or controls. WHO (1957) has in fact indicated findings that in temporal lobe epilepsy there is often a marked picture of abnormal personality in the family members of the patient.
