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stenedione, cortisol, and progesterone; 10 neurotensinand adrenaline;l2 and luteinising-hormone releasing factor. 11 lThe most consistent change (though disputedl2) is theincrease in blood luteinising hormone but, unfortunately,this and many other changes do not precede but follow theonset of the hot flush.1O The latest theory of hot flushespostulates an involvement of endogenous opioids, sincenaloxone reduced the number of hot flushes.13 This theoryhas serious flaws. Firstly, it is based on a wrong analogy-comparison of alcohol-precipitated flushing in chlorpro-pamide users (which is said to be alleviated by naloxone14)with menopausal hot flushes. Chlorpropamide flush is notaccompanied by sweating, and people who have experiencedboth types regard them as different.15 Alcohol-

chlorpropamide flushing is a disulfiram-like reactionassociated with raised blood acetaldehydel6 and may have agenetic basis.15 Secondly, without objective detection of hotflushes-for example, by plethysmography I 7 and bymeasurement of skin temperature and conductance5, 18—evaluation of any therapy is inconclusive. Moreover, theplacebo effect in hot flushes is pronounced6,8 and in one studymore than 75% of women with severe hot flushes were"cured" by the laboratory environment only.l’ Thirdly, theeffect of naloxone has been inconsistent and is based on obser-vation in six women only; one of these became worse afternaloxone, one became better on placebo, and one or two hadno change. 13,19Menopausal women are commonly oversensitive to heat,

feeling warm when other members of their family do not,dressing more lightly than before the menopause, and

becoming uncomfortable or exhausted in hot weather. 3,17They may complain of hot waves passing over the whole bodyand some are plagued by profuse sweating at night,necessitating several changes of night clothes. Tataryn et al.17observed that, during hot flushes, the finger temperature rosewhile the core temperature actually fell, presumably owing toa sudden downward setting of the central thermostat in thehypothalamus. Since heat sensitivity arises even in

menopausal women who do not have hot flushes,17 perhapsmore attention should be paid to dysfunction of

thermoregulation in the menopause.

EPILEPSY AND VIOLENCE

EXPERTS on epilepsy from four countries have reported astudy in which 5400 epileptic patients were screened to findcases with aggressive phenomena during seizures. 1

12. Kronenberg F, Carraway R, Côté LJ, Linkie DM, Crawshaw LI, Downey JA. Changesin thermoregulation, immunreactive neurotensin, catecholamines and LH duringmenopausal hot flashes. Proceedings of the 62nd Annual Meeting of the AmericanEndocrine Society, 1981: 141 (abstr. no. 236)

13. Lightman SL, Jacobs HS, Maguire AK, McGarrick G, Jeffcoate SL. Climactericflushing: Clinical and endocrine response to infusion of naloxone. Br J ObstetGynaecol 1981; 88: 919-24.

14. Leslie RDG, Pyke DA, Stubbs WA. Sensitivity to enkephalin as a cause of non-insulindependent diabetes. Lancet 1979; i: 341-43.

15. Leslie RDG, Pyke DA. Chlorpropamide-alcohol flushing: a dominantly inherited traitassociated with diabetes. Br Med J 1978; ii: 1519-21.

16. Jerntorp P, Almér L-O, Melander A. Is the blood chlorpropamide concentrationcritical in chlorpropamide alcohol flush? Lancet 1981; i: 165-66.

17. Ginsburg J, Swinhoe J, O’Reilly B. Cardiovascular responses during the menopausalhot flush. Br J Obstet Gynaecol 1981; 88: 925-30.

18. Tataryn IV, Lomax P, Meldrum DR, Bajorek JG, Chesarek W, Judd HL. Objectivetechniques for the assessment of postmenopausal hot flashes. Obstet Gynecol 1980;57: 340-44.

19. Lightman SL, Jacobs HS. Naloxone: non-steroidal treatment for postmenopausalflushing? Lancet 1979; ii· 1071.

1. Delgado-Escueta AV, Mattson RH, King L et al. The nature of aggression duringepileptic seizures. N Engl J Med 1981, 305: 711-16.

Eventually 19 were found, but even this small number wasreduced to 13 because of diagnostic disagreements. Video-tapes were then made of the patients’ seizures and the tapeswere rated by the panel of epileptologists. Good agreementwas obtained among the panel and they rated 7 patients asexhibiting significant aggression during their seizures. Theaggression varied from shouting of insults and spitting tokarate chops and smashing of property, 5 of the 7 patientsbeing rated as showing an angry mood during the seizure. Inother words, this study has neatly confirmed the clinical viewthat aggressive phenomena, including quite destructive acts,can arise during epileptic seizures but that such aggression israre. An interesting aspect of this study is that it included 2cases in which the patient became aggressive when restrained3 or 4 minutes after the seizure was over-a phase whenpatients are known to be irritable and during which tragediescan happen.2 Unfortunately it is not clear whether patientswere routinely provoked by touching or moving during thepost-ictal phase and whether aggression beginning later (sayan hour after the seizure) was included. The research seems tohave been stimulated by an increasing number of cases in theUnited States in which "epilepsy" is used as a defence againsta murder charge. As the international group points out, thereare in fact very few published reports of homicidal behaviourduring the phases of altered consciousness of epilepticseizures. In the United Kingdom Gunn and Fenton3described 2 cases, and Gunn2 another.Part of the American medicolegal problem seems to be that

the bogey of the "epileptic equivalent" lives on. That is to saythere is still a readiness to attribute impulsive violence, in anindividual with a minor or non-specific electroencephalo-graphic abnormality, to epilepsy, with the speculation thatthe only manifestation of epilepsy in the individual concernedis an occasional outburst of impulsive violence. This is ofcourse a circular argument. The only tenable clinical positionin the present state of knowledge is to insist that epilepsyshould be diagnosed only when there is definite evidence ofaltered consciousness or stereotyped motor or sensoryphenomena-preferably coinciding with laboratory evidenceof electrical dysrhythmia in the brain. If other behaviour,such as a criminal assault, is to be attributed to epilepsy thenthe assault itself should meet established criteria for epilepsyand, best of all, arise in an individual in whom epilepsy can bediagnosed confidently from phenomena other than theincident in question. Post-ictal irritability, confusion, andoccasionally psychosis may also lead to assaultative

behaviour, but again the evidence for the epilepsy and the,alleged ictus preceding the assault should be rigorous.Some workers are impatient with this conservative

approach to the relation between epilepsy and violence. Markand Ervin4 talk of episodic dyscontrol; Pincus,5 in a signededitorial commenting on the paper from the internationalgroup, is worried by the small number of cases amassed afterso extensive a search, wonders if the entry criteria to the studywere too strict, and raises the possibility that epileptics have atendency to violence between seizures. What motivates theenthusiasm for associating violence and epilepsy? Theanswer is complex but important factors are the legalconsequences of successfully pleading epilepsy as a deter-minant of violence, and therapeutics. In the U.S.A. someStates still have capital punishment and a successful plea of

2. Gunn J. Epileptic homicide: a case report. Br J Psychiatry 1978; 132: 510-13.3. Gunn J, Fenton G. Epilepsy, automatism, and crime. Lancet 1971, i: 1173-764. Mark VH, Ervin FR. Violence and the brain. New York: Harper and Row, 19705. Pincus J. Violence and epilepsy. N Engl J Med 1981; 305: 696-98

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illness, or automatism, will prevent the death sentence beingpronounced. There is less pressure of this kind in Britain,which has abolished the death penalty; in England a defenceof epileptic automatism to a violent crime, if successful, leadsto hospital confinement at the pleasure of the HomeSecretary.6 As for treatment, Mark and Erwin4 haveadvocated surgery for the dyscontrol syndrome, but fewsurgeons would operate without unequivocal evidence of adiscrete unilateral lesion well away from the speech centreand other vital areas. There are a few uncontrolled reports7,8of anticonvulsants improving violent patients but it has to beremembered that most anticonvulsants are sedative to some

degree and that controlled trials against other sedatives haveyet to be done.The non-specific relation between epilepsy and violence

referred to by Pincus5 was examined by Gunn9 in his surveyof epileptic prisoners. He found no statistical relationbetween violence and epilepsy but suggested indirect ways inwhich the two phenomena may be linked in individual cases.Some epileptics are brain-damaged and disinhibited. Manyepileptics are resentful about their condition and its socialconsequences, and a few of these cope with their resentment

aggressively. Some individuals were taught a violent

approach to life from violent uncaring parents; lack of

parental care led also to head injuries, ear infections, and thelike which are associated with an increased prevalence ofconvulsive disorders. Finally violent, reckless behaviour

brings an increased risk of head injury and seizures.

THE HYPERKINETIC HEART

LONGITUDINAL studies are not easy in medicine. The needfor quick returns in such an uncertain and insecure field asmedical reseach ensures that knowledge of the natural historyof disease tends to be assumed from cross-sectional studies.The dangers are obvious and any attempt to follow the courseof an illness in a particular group of patients is therefore to bewelcomed. This is particularly so when the identity of thedisease is questionable. "Primary hyperkinetic heart

syndrome" is a case in point.’,’Most physicians are familiar with the patient who presents

with a disturbing awareness of his heart beat, perhaps associ-ated with palpitations, atypical chest discomfort, and anxiety:there may also be an unconvincing history of fatigue,dyspnoea, or tachypnoea. Over the years various diagnoseshave been attached to such patients including Da Costa’ssyndrome, neurasthenia, effort syndrome, soldier’s heart,irritable heart, neurocirculatory and vasoregulatory asthenia,and anxiety neurosis.2 The wide range and rather uncon-vincing nature of the symptoms suggest that the last-nameddiagnosis is close to the truth. However, as the opportunitiesfor physiological investigation grew it became clear that someof these patients had well defined features which indicated thatthe circulation was "hyperkinetic". Thus, cardiac output ishigh3 and although peripheral resistance is relatively low therelationship between the two may be slightly altered so that

6 Bratty v Attorney General for N. Ireland. All E.R. 523, 1961.7. Turner WJ Anticonvulsant agents in the treatment of aggression. In: Garattini S, Sigg

EB, eds. Aggressive behaviour. Amsterdam: Excerpta Medica, 19698 Monroe RR. Anticonvulsants in the treatment of aggression. J Nerv Ment Dis 1975;

160: 119-26.9 Gunn J. Epileptics in prison London: Academic Press, 1977.1 Gorlin R. The hyperkinetic heart syndrome. JAMA 1962; 182: 823-29.2. Fioreatini C, Olivarai MT, Moruzzi P, Guazzi MD. Long-term follow-up of the

primary hyperkinetic heart. Am J Med 1981; 71: 221-27.

systolic blood pressure is often modestly raised. The highcardiac output is associated with an increased heart rate andleft ventricular ejection rate.3 Clinically, the pulse usually hasa large volume and there is a systolic ejection murmur. Thefindings in this condition strongly suggest increased sym-pathetic nervous system activity and beta adrenoceptor res-ponsiveness. Thus these patients show an enhanced

circulatory response to the beta-agonist drug isoprenaline,4and beta-adrenoceptor blockade with propranolol restoresthe circulation to normal.s To judge by the scanty publishedwork, this condition is neither homogeneous nor well-defined. Those patients who have been studied intensivelyhave presumably been selected from a much larger group inwhom the clinical features were less conspicuous. It is

possible therefore that the hyperkinetic circulation is one endof a spectrum of circulatory variation. There is clearly a goodprecedent here with current views of the distribution of bloodpressure. The hyperkinetic heart syndrome will not neces-sarily therefore lose clinical status even if it is not a discreteentity.Before the full significance of the "syndrome" can be

assessed some important questions require to be answered.Firstly, what is the relation between the symptoms and thecirculatory changes? Is an anxious personality influencing thecirculation through changes in the autonomic nervous

system, or are these patients individuals with a particularcardiovascular abnormality whose subjective complaints area result of visceral feedback? There is a second clinically moreimportant question. What are the long term consequences ofa hyperkinetic circulation? There is no evidence that thesepatients proceed to fixed "essential" hypertension. However,there is growing awareness of the possibility that activity ofcardiac sympathetic nerves acts as a trigger to hypertrophythrough noradrenaline release.6 Theoretically, therefore,cardiac hypertrophy could develop in hyperadrenergic statessuch as this even in the absence of hypertension.The resolution of these questions clearly requires a long-

term study involving both clinical observation and prolongedpharmacological intervention. A praiseworthy attempt hasbeen made by a Milanese group.2 14 patients with

"hyperkinetic heart syndrome" were observed for five years.Half the patients were treated with propranolol, the other halfwith placebo. The treated group lost their predominantcomplaint of cardiac awareness and palpitations as the

hyperkinetic circulation was restored to normal. But as soonas treatment was stopped these symptoms returned. Clearly avicious circle of anxiety and visceral feedback was not brokeneven by long-term pharmacological correction. More

important, perhaps, is the observation that there was no

echocardiographic evidence of left-ventricular hypertrophyat any stage in either the treated or the control group.We still do not know therefore which came first-a neurotic

personality or the hyperadrenergic state-although thelikelihood is that these patients represent a subset of thegeneral population with a somewhat overactive autonomicnervous system. Physicians can reassure them that on

existing evidence there is nothing to fear from the conditionother than the unhappiness it causes.

3 Gorlin R, Brachfeld N, Turner JD, Messer JV, Salazar E. The idiopathic high cardiacoutput state. J Clin Invest 1959; 38: 2144-53.

4. Frohlich ED, Tarazi RC, Dustan HP. Hyperdynamic beta-adrenergic circulatory state.Arch Intern Med 1969; 123: 1-7.

5. Guazzi M, Polese A, Magrini F, et al. Long-term treatment of the hyperkinetic heartsyndrome with propranolol. Am J Med Sci 1975; 270: 465-74.

6 Ostman-Smith I. Cardiac sympathetic nerves as the final common pathway in theinduction of adaptive cardiac hypertrophy. Clin Sci 1981; 61: 265-72.