Australian and New Zealand Journal of Psychiatry (1978) 12: 21

THE NEURAL BASIS OF AGGRESSION AND ITS TREATMENT BY PSYCHOSURGERY*

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by L. G. KILOH** and J. S. SMITH***

SYNOPSIS The limbic system and its connections provide the neural basis for aggressive behaviour. Violent individuals. may differ quantitively or qualitively from normal. Many of the latter suffer from epilepsy. In some the epileptiform discharges from the amygdala can only be recorded using depth electrodes. It can be taken that the control of abnormal degrees of violent behaviour is now possible. Should such operations be used? If so who should have them? What precautions need to be taken that such operations are not abused? How can informed consent be obtained? The development of new surgical techniques make these questions pertinent if not urgent.

There has been a great deal of argument whether aggression and its associated affect should be regarded as innate and instinctive, whether it is reactive, resulting from frustration as proposed by Durbin and Bowlby (1939) in their so called “reactive theory” or whether it is determined by the interplay of the problems and imperfections of our society (Wootton, 1959). To suggest that there is no innate element would certainly run counter to most observations, particularly those of the ethologists. On the other hand as Barnett (1967) has pointed out, the sharp distinction into fixed or instinctive behaviour and “learned” behaviour is no longer tenable. Certainly, within limits, both cultures and individuals can acquire the habit of aggression - though some appear to do so more easily than others.

“Men ought to know that . . . from the brain only arise out pleasures, joys, laughter and jests as well as our sorrows, pains, griefs and tears . . . I t is the same thing which makes us mad or delirious, inspires us with dread and fear, whether b y night or by day, brings sleeplessness, inopportune mistakes, aimless anxieties, absent mindedness and acts that are contrary to habit. . .” Hippocrates, “The Sacred Disease”

One can consider aggression in the same way that one regards anxiety or depression. In the majority of instances it is a dimensional problem. As a biologically advantageods characteristic it is distributed normally in the population with the inevitable result that a proportion of the population is endowed with an excess of the quality. Accepting that all behaviour reflects or is reflected in brain mechanisms it need occasion no surprise that in some cases - including the worst - the disturbance is a categorical one dependant on disturbance of these mechanisms by some form of lesion. The parallel with mental subnormality is close; the subcultural defectives are abnormal in a dimensional sense and the pathological group are categorical.

As with so many phenomena of psychiatric interest, aggression is impossible to define adequately. On the one hand the word may be used in its ordinary English sense of the habit of making unprovoked attacks on others, whilst again, it may be used - as is anxiety - to explain virtually the whole of human behaviour. I t is the motor counterpart of the affect of rage or anger. I t may be realistic or unrealistic, constructive or destructive, healthy or pathological.

*Presented at the 13th Annual Congress of the Australian and New Zealand College of Psychiatrists; Adelaide, October 1976 **.Professor of Psychiatry, University of New South Waies *** Director, Neuropsychiatric Institute, Rozelle, New South Wales

Aggression is likely to be subject to the same kind of rules as so many other human activities, in that the potential for such behaviour - dependent on the organization of the C.N.S. - interacts with a host of learning experiences, cultural and social factors, all capable of modifying brain function and indeed at a molecular level, brain structure (Eccles, 1973). There is now adequate evidence that the limbic system plays an important part in the experience and expression of emotion, including anger and rage but when considering the integration of “offensive” and “defensive” reactions, which are often so hard to separate behaviourally and experimentally, we have to look somewhat beyond this system. Subcortical structures are involved - to quote Delgado (1963) - “that extend almost continuously from

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THENEURAL BASISOF AGGRESSION

forebrain to brain stem and involve the ventral septum, preoptic area, amygdala, stria terminalis, anterior and posterior hypothalamus, postero-ventral nucleus of the thalamus, tectal area, central grey reticular substance and spinothalamic tracts”.

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In regard to the emotion of anger and its physical counterpart aggression, the amygdala appear to have especial importance. Each amygdaloid nucleus is an ovoid mass of grey matter about 2 cm in length situated medially in the anterior pole of the temporal lobe, extending from the cortex to the tip of the inferior horn of the lateral ventricle. Posteriorly it is related to the tail of the caudate nucleus. It consists of 12 or so subnuclei, commonly classified into: (a) an antero-medial o r cortico-medial group which are phylogenetically older and have olfactory connections; and (b) a baso-lateral group having close connections with the rest of the limbic system. The amygdala receive afferents from the temporal neocortex, the various sensory pathways, the dorsomedial nucleus of the thalamus, the septal area and the hypothalamus. They send efferents to the septum, preoptic region, the hypothalamus, the caudate nucleus and the midbrain reticular formation. They share similar circuits to the hippocampi, though their connections with the hypothalamus and orbitofrontal cortex are more intimate (Smythies, 1967). The connections are such as to ensure that the amygdala are subject to the influence of the neocortex. Alas, not only may the neocortex exert or attempt to exert control, but it provides the amygdala with the range and variability of expression so characteristic of man. One presumes that “learned” aggression is associated with defective or diminished neocortical control of the limbic system.

NEUROPHYSIOLOGY OF THE AMYGDALA AND ALLIED STRUCTURES IN ANIMALS Stimulation of the basolateral division of either amygdaloid nucleus produces attention (orienting response), fear and aggression (Kaada, Anderson and Jansen, 1954). Large numbers of experiments have now demonstrated that within the basolateral nuclei there are two zones yielding fear and rage responses respectively (Ursin, 1960). Romaniuk (1963; 1965) has shown that stimulation of the ventral subdivision of the medial hypothalamus also gives rise to aggressive behaviour and Delgado (1968) has demonstrated that in monkeys, aggression may be provoked by stimulation of the nucleus ventralis posterolateralis of the thalamus and of the central grey matter. In radio controlled monkeys Delgado (1968) has shown that the aggressive behaviour induced by stimulating the amygdala and these other structures is by no means stereotyped and indeed is indistinguishable from spontaneous aggression, constantly varying and adapted to the social situation in which the animal finds itself. In some experiments for example when the brain of a “boss”

monkey was stimulated, he would threaten, chase, corner and bite animals with which his normal relations were not overfriendly, whilst his particular friends were likely to escape. In a series of papers, Kluver and Bucy (1937, 1938 and 1939; also Kluver, 1958) described the effects of bilateral temporal lobectomy on rhesus monkeys. Of the various components of the Kluver-Bucy syndrome, the most obvious is tameness and placidity - which can be regarded as an unresponsiveness to fear and anger-provoking stimuli. Lesions restricted to the amygdala have a similar effect and have been demonstrated in a wide range of animals (Goddard, 1964). Amygdalectomized animals can still show normal aggression and fighting if the stimulus is strong enough. The effects of amygdaloidectomy on the social order of a colony of monkeys were reported by Rosvold, Mirsky and Pribram (1954). When the king or boss - a monkey named Dave - was operated upon, he was rapidly replaced by a younger aggressive animal, Zeke, and became submissive to all 7 members of the colony. Zeke was then operated upon and became submissive to all but Dave and the next lowest in the hierarchy. His place was taken by Riva originally third in the hierarchy. Next Riva had an operation but though the antero-medial nuclei were removed, the basolateral nuclei were spared. Riva’s position a t the top of the hierarchy remained unchanged. Destruction of those areas of the hypothalamus o r central grey matter from which aggressive responses are obtained abolishes any aggressive response obtained by stimulating the amygdala; destruction of the amygdala however, does not affect the stimulation response from the hypothalamus though it does abolish aggressive behaviour induced by removal of the septal area and subcallosal cortex (Brady and Nauta, 1953; King, 1958; Schwartsbaum et al., 1964). The limbic system thus appears to play animportant part in the experience of fear and anger and in initiating the associated patterns of behaviour. Egger and Flynn (1963; 1967) stress the fact that one of its important functions, and of the amygdala in particular, is to modulate the activity of other areas, especially the hypothalamus. Different areas may either suppress or facilitate various reactions mediated by the hypothalamus, particularly aggression, sexual activity, eating and drinking. As Magoun puts it the amygdala appear to set the bias on the central mechanisms concerned with the “consummatory phases of innate behaviour”. The limbic system receives signals from cortical and other centres concerned with the external environment and other signals indicating the state of the viscera or the internal environment. It is suitably placed to compute requirements and to initiate appropriate actions which will be subject to modification by previous learning experiences and, particularly in man, through the intervention of the frontal cortex and the dorsomedial nucleus of the thalamus (McLean, 1958) which permit predictions of the possible outcome of the proposed course of action. Thus in the case of a threat the information from the external environment is matched against visceral information, indicating the state of preparedness. Previous experience of personal capabilities and the appropriateness of retaliation is drawn upon and a rapid assessment is made of the consequences

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L.G. KILOHAND J.S. SMITH

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Figure 1. Bipolar recording showing spike activity in the amygdala (first eight channels). The spikes occur independently o n each side and are scarcely reflected in the surface leads (F3/C3 represents the left fronto-central, F4/C4 the right frontocentral and F3/F4 the mid-frontal electrode placements). both physical - and in the case of man - legal. The decision may be to fight or to run o r to smile and make friends and the appropriate coded instructions pass from the amygdala to the hypothalamus and motor areas (Smythies, 1966; 1967). It would be wrong to suggest that the idea of attacking originates in the amygdala; in the normal individual these structures appear to be adequately controlled or inhibited by influences from other areas. This of course is why the individual is normal! Some, alas, either because these extra-amygdaloid influences are inadequate or because the threshold at which the amygdala respond is set too low, react to what should be subthreshold environmental stimuli and over-react to what, for others, would be threshold stimuli. In man much of our information about the limbic system has been provided by the study of patients with temporal lobe epilepsy. In Bingley's (1958) patients anger with or without aggression proved to be the second commonest ictal emotion, anxiety of course being the first. He found that it occurred rarely with tumours and most commonly with sclerotic lesions especially when bilateral. Patients showing ictal aggression generally prove to have lesions involving the amygdala. Episodic attacks of rage and violence without clinical evidence of epilepsy are sometimes seen in patients with tumours or other lesions of one or both temporal lobes. A probable example is the well known case of Charles Whitman who shot 41 people in Austin, Texas, killing 17 of them. He had previously experienced a personality change

and forced thoughts of wanting to shoot people. At autopsy he was found to have a temporal lobe spongioblastoma (Mark and Ervin, 1970). Production of rage by stimulation of the amygdala in man has been achieved by a number of investigators usually in patients with temporal lobe epilepsy in whom amygdaloidotomy is being considered. In a 26 year old man studied at the Neuropsychiatric Institute (N.P.I.), Sydney, rage attacks occurred both as ictal and interictal phenomena. For five years prior to investigation at the N.P.I. he had suffered up to fivegrandma1 seizures weekly. Some were preceded by a n aura in which he experienced frontal headache, a rising epigastric sensation and less frequently nausea, dizziness, fatigue, excessive salivation and micropsia. H e could recall three episodes in which he remained aware of his environment but was unable to execute any movement. On five occasions he attempted to strangle people either prior to or immediately after a grand-ma1 seizure. At other times he had been involved in many assaults. Although the patient claimed that these assaultive outbursts were beyond his control and that he had no memory for the events, medical staff who had observed them believed that he was conscious and responsive to his environment and that his behaviour was calculated; they had variously labelled these episodes as attention seeking, histrionic or deliberately antisocial. On investigation, a large angioma was found situated beneath the orbital surface of the right frontal lobe. This was excised. During the next twelve months his seizures were less frequent but he assaulted eleven people,

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THENEURAL BASISOF AGGRESSION

four minutes during which time occasional spikes were observed in the right amygdaloid, both in the medial and lateral aspects, and intermittent high voltage delta wave activity was observed in the vicinity of both amygdala and in the right temporal surface E.E.G. During the next 21 minutes in which he gave a very detailed and accurate account of his aggressive outburst, the record was remarkable for repeated short bursts of high voltage delta wave activity. In the next 3 minutes the patient appeared confused and began to stutter and repeat himself. The recording showed long runs of high voltage delta wave activity in the medial and lateral aspects of both amygdala and a t the right surface electrode (Fig. 111). He was given 10 mg of diazepam intravenously. His behaviour quickly settled, his confusion cleared and the slow wave activity ceased.

inflicting extensive and severe facial injuries upon one patient.

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In order to investigate and treat the rage attacks sheaves of fine gold electrodes were implanted stereotactically into the media and lateral aspects of each amygdaloid nucleus (Fig. I). Recordings showed spike discharges occurring independently in both amygdaloid nuclei, particularly the right, most of the activity emanating from the medial aspects. Only rarely was this spike activity evident in the surface E.E.G. During one recording session, the patient was asked to describe his most recent attack on another patient and an argument he had had with a member of staff. During both these occasions a feeling of rage was associated with an increase in spike activity in the medial aspect of the right amygdaloid nucleus (Fig. 11).

Electrical stimulation was carried out using a bipolar current of 40 pulses per second with a 0.5 m sec pulse width passed between adjacent electrodes at 2V, 4V, 6V and 8V. The replicable responses obtained from stimulation in the region of the amygdala are depicted on a brain map (Fig. IV). Stimulation of the medial aspect of the right amygdaloid nucleus by passing a current between electrodes 2 and 3, repeatedly produced prolonged feelings of rage with a desire to break out of his restraints and to harm the people around him. Stimulation of the lateral aspect of the right amygdaloid nucleus produced a feeling of calm.

Following photic stimulation the patient experienced an unpleasant periumbilical sensation which became more intense and rose to the epigastrium at which stage he began to feel angry. He stated that the sensation was similar to that which preceded most of his assaultive behaviour. He then attempted to break away from his restraints saying that he wanted to kill the first member of staff who came into view.

O n the left side, stimulation between electrodes 18 and 19, which lay in the medial aspect of the amygdaloid nucleus,

It required a number of people to restrain him, and he shouted abuse a t all around him. H e remained enraged for

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Figure 2. Bipolar recording from the amygdala (first eight channels) and the scalp ( P 4 / 0 2 represents the right parietooccipital and P3/01 the left parieto-occipital electrode placements). The left side of the figure is a recording from the patient at rest. The right hand side shows high voltage spike activity elicited from the medial aspect of the right amygdaloid nucleus when the patient became enraged. The surface E.E.G. shows no change.

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Figure 3 . Bipolar recording from the amygdala (first eight channels) and surface (C4/P4 represents the right central-parietal and C3IP3 the left central-parietal electrode placements). The resting record is depicted on the left hand side. The right hand side shows high voltage slow wave activity in the amygdala after photic stimulation had elicited a rage attack. This activity is also evident on the surface in the right central-parietal region. repeatedly produced a transient feeling of increasing agitation which he described as similar to that he experienced before a seizure. Stimulation between electrodes 19 and 20 was associated with a transient feeling of rage. When the strength was increased to 6V an after discharge occurred associated with a psychomotor seizure which took the form of an absence which lasted one minute and 40 seconds. Stimulation between electrodes 10 and 11 which lay on the lateral aspect of the left amygdaloid nucleus repeatedly produced a feeling of calm and relaxation which lasted approximately one minute. Subsequently i t was found that a prolonged rage attack induced by stimulation of the medial aspect of the right amygdaloid nucleus could be aborted gradually by repeated stimulation of the lateral aspect of the contralateral amygdaloid nucleus or immediately by stimulation of the lateral aspect of the ipsilateral amygdaloid nucleus. A direct current of ImA was passed for 30 seconds with the anode in the vicinity of the amygdala and the cathode applied as a forearm cuff to determine the effects of "polarisation". Such a current is thought to block the function of axons in the vicinity of the electrode for a variable period without producing a lesion. The effects were usually the opposite to those obtained by stimulation so that polarisation of the left lateral amygdaloid nucleus (electrode 1 1 ) and the right lateral amygdaloid nucleus (electrodes 4 and 6) produced feelings of rage which lasted 10 minutes, 90 seconds and 3 minutes respectively, whilst polarisation of the left medial amygdaloid nucleus (electrodes 18, 19 and 20) and the right medial amygdaloid nucleus (electrodes 2 and 3) produced feelings of calm.

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Figure 4. Electrode placements in the vicinity of the amygdala (1-20). The left amygdaloid nucleus is in a plane (A-A) slightly anterior to that of the right nucleus (B-B). Stimulation between electrodes 4-5, 5-6 and 10-1 1 gave rise to a feeling of placidity; 2-3, rage; 18-19, a rising sensation with agitation and 19-20, to a psychomotor attack.

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THENEURAL BASISOF AGGRESSION

OPERATIONS FOR AGGRESSION

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Amygdaloidectomy - or amygdaloidotomy - has been practised fairly widely in recent years mainly for aggressive or hyperkinetic disorders. Few conclusions can be drawn from the early operations - open and time consuming but several of the accounts indicate that patients became quieter, less disturbed and less aggressive. In the series described by Narabayashi et a1 (1963), Heimberger et al (1966), Kiloh et al (1974) and Balasubramaniam and Kanaki (I 975) stereotactic procedures were used. The patients were heterogeneous epileptics and non-epileptics, severely subnormal and intellectually normal, self multilating and overtly aggressive. Sano (1962, 1966) produced lesions in the posterior part of the posterior hypothalamic nucleus (the ergotropic triangle). The appropriate area was identified by the sympathomimetic effects produced by stimulation. These stereotactic procedures appear to’be safe and relatively free from sequelae although some non-epileptic patients have had one or more fits afterwards. No sexual problems have occurred, memory remains undisturbed and the personality otherwise unaffected. In the studies with follow-up periods of 2 years or more, the success rate appears to be in the neighbourhood of 50-75%. The successful cases indeed became more effective and happier human beings. The literature concerning these operations has been reviewed by Kiloh (1974). Some at least of the failures are likely to be due to the imprecision of an acute surgical procedure, even though carried out stereotactically. to attack a complex structure with both excitatory and inhibitory functions. The use of chronically indwelling electrodes provides the opportunity for greater precision. In the NPI patient treatment commenced six weeks after the implantation of electrodes, a series of lesions being c;eated in the amygdala using suitable electrodes as anodes and a forearm cuff of lead as cathode. The effects were checked by stimulation and further lesions created as indicated. Following the creation of these lesions, no rage responses occurred when the medial aspect of either amygdaloid nucleus was stimulated. In the five weeks following the cessation of treatment the patient was more affable with the staff and fellow patients and exhibited no rage attacks or aggressive behaviour. Although he suffered three grandma1 seizures in this time, none was associated with aggressive behaviour, a fact considered remarkable by his long suffering relatives.*

DISCUSSION Clearly it is now within our power to modify aggressive behaviour in a reasonable number of cases and the probability is that with increasing knowledge and skill this proportion will rise.

Do we want to control aggression? Many maintain that aggression is essentially a moral problem for society to solve presumably by whatever means it ~~

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* This patient has now been followed up for mains free from rage attacks and aggression.

18 months

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favours at the time - by more penal or more permissive legislation, by reorganising society, by eliminating anomie, by abolishing poverty o r even by universal group therapy as Melanie Klein once suggested. Such views even if they possess some general validity overlook or deny the fact of human variability. Changes that may free one individual from the need to express his aggression may encourage its display in another. There is adequate evidence to show that social controls d o have some influence upon the majority of individuals look what happens when these are relaxed in wartime and in periods of famine; or distorted as in fascist Italy and Hitler’s Germany. Unfortunately, it is so much easier to legislate for controls than to persuade members of society to accept them; the sad history of prohibition in the U.S.A. is discouraging to say the least. Perhaps in the long-term, sociological and educational approaches may indeed exert significant control over aggression but whilst we explore these possibilities and await their effects, what of those individuals who continue to suffer and cause society to suffer because of uncontrolled o r uncontrollable aggression? And what of those with demonstrable lesions which are unlikely t o have been caused by - and are even less likely to respond - to social measures? It must be appreciated that many excessively aggressive individuals though unable to control their activities are well aware that their behaviour constitutes a disability and they are anxious to obtain help. Mark and Ervin (1970) point out that nearly a half of 150 aggressive individuals that they interviewed had attempted suicide in despair at what they had done. What have we to offer in the way of treatment to those whose anger is displayed so readily and who become aggressive with so little provocation that by any standard they must be regarded as abnormal? We can offer long-term hospitalization - a polite term for exclusion from society. This is unacceptable to patients and even more so to hospital staff; nor can one regard such “treatment” as curative. We can offer psychotherapy but results encourage no optimism. Claims have been made that behaviour therapy may be rather more effective. We can offer drugs. Unsubstantiated claims have been made for the effects of lithium and of antiandrogens but otherwise the only drugs likely to influence aggression are the major tranquillisers and the sedatives. In fact these have not proved particularly effective and the patients rarely have the will to continue taking such drugs for prolonged periods because of their unpleasant side effects. We can offer neurosurgery. Whatever the aetiology of the aggressive behaviour - whether it be dimensional or categorical in nature - this remains a rational approach if one accepts that environmental factors operate upon and are mediated through the brain, and that all behaviour is a resultant of a brain-environment interaction. There is adequate evidence that the remote environmental factors that help to mould our personalities - past experiences, or memories as they become - are represented by modifications of brain structure at a molecular and perhaps a synaptic level (Eccles, 1973). In other words the remote environment as far as the individual is concerned can no longer be regarded as a sociological event - it has either vanished without trace or it has become incorporated into brain structure, capable of modifying brain function in appropriate or inappropriate ways under appropriate or

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L.G. KILOHAND J.S. SMITH

inappropriate circumstances. The concept of “critical periods” is pertinent; if adverse environmental factors, whatever they may be, operate at the appropriate stage in the child’s development the molecular structural change is likely to be irreversible or virtually so - as one presumes, occurred in Harlow’s monkeys (Harlow and Harlow, 1969). At other stages in development similar events may have little or no effect. Manipulation of the environment whether therapeutically or punitively in later life can hardly be expected to exert any profound influence. Such an argument needs to be stated because Cartesian views, if seldom expressed openly, still influence the thinking of many humanists and sociologists and would seem to underlie the belief that there is something immoral about tampering with brain structure unless this is already disordered by structural disease - and by some, even then. Our own view is that if the aggressive behaviour is disruptive and disabling, irrespective of whether there is brain damage or not, treatment should be offered even if it requires an attack upon the brain. To deny such a person, living in fear of the consequences of behaviour which is beyond his control, requesting, and even begging for help, would seem to be a denial of human rights. Yet some who oppose the use of such operations would deny them on the grounds that the treatment itself is a denial of human rights. There are two groups of aggressive individuals that require special consideration. The first are those detained in psychiatric insitutions and secondly those detained in prisons. These may be willing or unwilling to have the operation and some of those in mental hospitals may be judged incapable of making such a decision. In those agreeable to the procedure, whether in mental hospitals or prisons, the question of their consent being “informed” has to be considered. There are some who believe that in such situations consent is never “informed” even when no promises are made of early release should the procedure prove effective. If this view is accepted none of these patients or prisoners could be offered the operation. Of course those who deny them this opportunity might make an exception in those cases in which a lesion has been demonstrated. But what constitutes a lesion? Would an E.E.G. abnormality be acceptable? And what if it is necessary to insert electrodes to find it? In view of what some have termed the “experimental” nature of the treatment and the disquiet felt in some influential - though not necessarily informed - circles about these operations, it would be wise if only for the protection of the doctors involved, if decisions were placed in the hands of a tribunal with medical, lay and legal representation. For patients in mental hospitals incapable of giving consent, such a mechanism would be obligatory. In the present climate it might be wise to acceRt that those unwilling to have the operation should not have it. One cannot expect - or perhaps permit - any neurosurgeon to undertake such operations. By concentrating these procedures in a few designated units staffed by surgeons, neurologists and psychiatrists interested in such procedures and prepared to evaluate their results, we would eliminate one variable at least - that of varied technique. And it would permit meaningful data to be gathered.

REFERENCES Balasubramaniam, V. and Kanaka, T. S. (1975). Amygdaloidotomy and hypothalamotomy in a comparative study. Confinia Neurolugica, 37: 195.

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Barnett, S . A. (1 967 1. Instinct and Intelligence. MacGibbon and Kee, London. (p. 171.) Bingley, T. (1958). Mental symptoms in temporal lobe epilepsy and temporal lobe gliomas. Acta Psychiatrica Scandinavica, (Suppl. 120) 33: 1. Brady, J. V. and Nauta, W. J. H. (1953). Subcortical mechanisms in emotional behaviour: affective changes following septal forebrain lesions in the albino rat. Journal of Comparative and Physiological Psychology, 41: 102. Delgado, J. M. R. (1963). Free behaviour and brain stimulation. International Review of Neurobiology, 6: 349. Delgado, J. M . R. (1968). Aggression and defence under cerebral radio control, .in Brain Function. Vol. 5 Aggression and Defence: Neural Mechanisms and Social Patterns. (eds. Clemente, C. D. and Lindsley, D. B.) University of California Press. Durbin, E. F. M. & Bowlby, J. (1939). Personal Aggressiveness and War. Columbia University Press, New York. Eccles, J . C. (1973). Facing Reality. Springer-Verlag, New York. Egger, M. D. and Flynn, J. P. (1963). Effects of electrical stimulation of the amygdala on hypothalamically elicited attack behaviour in cats. Journal of Neurophysiology, 26: 705. Egger, M. D. and Flynn, J. P. (1967). Further studies on the effect of amygdaloid stimulation and ablation on hypothalamically elicited attack behaviour in cats. Progress in Brain Research, 27: 165. Goddard, G. V. (1964). Functions of the amygdala. Psychological Bulletin, 62: 89. Harlow, H. F. and Harlow, M. K. (1969). Effects of various mother-infant relationships on rhesus monkey behaviours, in Determinants of Infant Behaviour. (ed. Foss, B. M.) Vol. 4, p. 15. Methuen, London. Kaada, B. R., Andersen, P. and Jansen, J. Jr. (1954). Stimulation of the amygdaloid nuclear complex in unanesthetised cats. Neurology, 4: 48. Kiloh, L. G . (1974). The treatment of anger and aggression, in Symposium on Psychosurgery and Society. (eds. Smith, J. S., and Kiloh, L. G.) NSW Health Services Commission (to be published by Pergamon Press, London, 1977). Kiloh, L. G., Gye, R. S., Rushworth, R. G., Bell, D. S. and White, R. T. (1974). Stereotactic amygdaloidotomy for aggressive behaviour. Journal of Neurology, Neurosurgery and Psychiatry, 37: 437. King, F. A. (1958). Effects of septal and amygdaloid lesions on emotional behaviour and conditioned avoidance responses in the rat. Journal of Nervous and Mental Diseases, 126: 57. Kluver, H. and Bucy, P. (1937). “Psychic blindness” and other symptoms following bilateral temporal lobectomy in rhesus monkeys. American Journal oj Physiology, 119: 352. Kluver, H. and Bucy, P. (1938). An analysis of certain effects of bilateral temporal lobectomy in the rhesus monkey, with special reference to “Psychic Blindness”. Journal of Psychology, 5: 33.

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Kluver, H. and. Bucy, P. C. (1939). Preliminary analysis of functions of the temporal lobes in monkeys. Archives of Neurology and Psychiatry, 42: 979. Kluver, H. (1958). The temporal lobe syndrome, in Temporal Lobe Epilepsy. (eds. Baldwin, M . and Bailey, P.) Thomas, Springfield. Maclean, P. D. (1958). The limbic system with respect to self-preservation and the preservation of the species. Journal of Nervous and Mental' Disease, 127: 1. Mark, V. H. and Ervin, F. R. (1970). Violence and The Brain. Harper and Row, New York. Narabayashi, H., Nagao, T., Saito, Y . , Yoshida, M. and Nagahata, M. (1963). Stereotaxic amygdalotomy for behaviour disorders. Archives of Neurology, 9: 1 . Romaniuk, A. (1963). Emotional responses evoked by hypothalamic stimulation in cats. Bulletin de I'dcademie Polonaise des Sciences, 11: 437. Romaniuk, A. (1965). Representation of aggression and flight reactions in the hypothalamus of the cat. Acta Biologiae Experimentalis, 25: 177. Rosvold, H. E., Mirsky, A. F. and Pribram, K. H. (1954). Influence of amygdalectomy on social

Reprint requests to: Professor L.G. Kiloh Prince Henry Hospital Little Bay, NSW 2036

behaviour in monkeys. Journal of Comparative and Physiological Psychology, 47: 173. Sano, K. (1 962). Sedative neurosurgery, with special reference to postero-medial hypothalamotomy. Neurologia Medico-Chirurgica, 4: 1 12. Sano, K. (1 966). Sedative stereoencephalotomy: fornicotomy, upper mesencephalic reticulotomy and postero-medial hypothalamotomy. Progress in Brain Research, 21: 350. Schwartzbaum, J. S., Thompson, J. B. and Kellicutt, M. H. (1 964). Auditory frequency discrimination and generalization following lesions of the amygdaloid area. Journal of Compurative and Physiological Psychology, 57: 257. Smythies, J . R. (1 966). The Neurological Foundations of Psychiatry. Blackwell, Oxford. Smythies, J. R. (1967). Brain mechanisms and behaviour. Brain, 40: 697. Ursin, H. (1960). The temporal lobe substrate of fear and anger. Acta Psychiatrica et Neurologica Scandinavica, 35: 378. Wootten, B. (1959). Social Science and Social Pathology. Allen and Unwin, London.

The neural basis of aggression and its treatment by psychosurgery.

Australian and New Zealand Journal of Psychiatry (1978) 12: 21 THE NEURAL BASIS OF AGGRESSION AND ITS TREATMENT BY PSYCHOSURGERY* Aust NZ J Psychiat...
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