hyperglycaemia, automatism, and insanity

2
912 SERUM LEVELS OF LIPOPROTEIN A AND TOTAL CHOLESTEROL IN FOURTH (LAST) WEEK OF PLACEBO PHASE AND DURING ADMINISTRATION OF LOVASTATIN Results as Lp(a); total cholesterol (both m mg/dl). Patients A, B, F, and H were female. *On bezafibrate before treatment with lovastatin. month or so during treatment with lovastatin, serum Lp(a) and total cholesterol levels were measured. 6,7 Total cholesterol levels fell in all eight patients. However, serum Lp(a) concentrations rose from medium to high levels in five (A, C, E, F, H) and from low temporarily to medium levels in three (B, D, G), probably due to a drug-induced disturbance in lipid metabolism in the liver (table). Since Lp(a) levels of more than 20-30 mg/ml must be considered as a risk for atherosclerosis we would recommend the measurement of serum Lp(a) before and during lovastatin therapy. Institute of Medical Biochemistry, Karl-Franzens Universtat, A-8010 Graz, Austria GUNTHER JURGENS AHMED ASHY Department of Internal Medicine II, Landeskrankenhaus Graz GERALD ZENKER 1. Widhalm K, Senser D. Increased lipoprotein (a) levels in children with familial hypercholesterolaemia. Lancet 1988; ii: 1262. 2. Grundy SM HMG-CoA reductase inhibitors for the treatment of hypercholesterolemia. N Engl J Med 1988, 319: 24-33. 3. Dahlen GH, Guyton JR, Attar M, Farmer JA, Kautz JA, Gotto AM Association of levels of lipoprotein Lp(a), plasma lipids, and other lipoproteins with coronary artery disease documented by angiography Circulation 1986; 74: 758-65. 4. Rhoads GG, Dahlen G, Berg K, Morton NE, Dannenberg AL. Lp(a) lipoprotein as a risk factor for myocardial infarction. JAMA 1986; 256: 2540-44. 5. Murai A, Miyahara T, Fujimoto N, Matsuda M, Kameyama M. Lp(a) lipoprotein as a risk factor for coronary heart disease and cerebral infarction. Atherosclerosis 1986; 59: 199-204. 6 Zenker G, Költringer P, Bone G, Niederkom K, Pfeiffer KP, Jurgens G. Lipoprotein(a) as a strong indicator for cerebro-vascular disease. Stroke 1986; 17: 942-45. 7. Költringer P, Jurgens G. A dominant role of lipoprotein(a) in the investigation and evaluation of parameters indicating the development of cervical atherosclerosis. Atherosclerosis 1985; 58: 187-98. 8. Hoff HF, Beck GJ, Skibinski CI, et al. Serum Lp(a) level as a predictor of vein graft stenosis after coronary bypass surgery in patients. Circulation 1988, 77: 1238-44 RESTRAINING THE OTHER SHOULDER SiR,—The introduction of seat belts for drivers and passengers of motor vehicles has brought a welcome improvement in the mortality and injury from road accidents in the UK. Over the three years from January, 1983, when seat belt wearing became compulsory, the measure is thought to have saved more than 200 lives and more than 7000 serious injuries every year.2 Much research has been done on the efficacy of seat belts.3,4 Today, most seat belts in cars in Britain are of the same design-namely, a transverse strap across the lower abdomen plus a diagonal belt which on right-hand drive cars, passes from above the right shoulder downwards and to the left for the driver and from left to right for the front seat passenger. Two recent necropsies suggest that this design should be changed. A 19-year-old man, the front seat passenger in a car involved in a head-on collision, suffered head injuries and a fractured right femur and died 24 hours after the accident. Necropsy showed that the head injury comprised lacerations and fractures of the right side of the face, fractures of the right orbit, and of the right frontal bone with severe damage to the right frontal lobe of the brain, which had herniated into the site of multiple comminuted fractures. It seemed that, on sudden deceleration, this man had moved forwards and to the left, the movement being directed by the restraint of the passenger seat belt (left shoulder held); and he had struck the right side of his face and head on the windscreen and other internal parts of the car. A 25-year-old woman driver of a car in a head-on collision with a lorry had severe injuries to her left face, left orbit, and left frontal region of the brain. She remained in coma for 12 days until artificial respiration was discontinued. Necropsy revealed a head injury localised to the left face and orbit, and left frontal region of the brain, which was herniating into frontal comminuted fractures. This driver (right shoulder held) had been thrown forwards and to the right, striking the left side of her head on the windscreen and other internal parts of the car. I support the Oxford Road Accident Groups who have recommended the introduction of symmetrical restraint systems that would prevent forward rotary movement to left or right. Department of Neuropathology, Radcliffe Infirmary, Oxford OX3 6HE J. T. HUGHES 1 Editorial. Seat belts reviewed. Lancet 1986; i: 75-76. 2. Seat belt regulations retained. Br Med J 1986; 292: 286. 3. Gallup BM. The assessment of facial injury to fully restrained drivers through full-scale car crash testing. J Trauma 1987; 27: 711-18. 4. Campbell BJ Safety belt injury reduction related to crash severity and front seated position. J Trauma 1987; 27: 733-39 5. McCoy GF, Johnstone RA, Nelson IW, Duthie RB. Facial injuries to restrained drivers caused by steering wheels Lancet 1988; ii: 456. Medicine and the Law Hyperglycaemia, Automatism, and Insanity DIABETIC patients who commit crimes while hypoglycaemic may be able to plead (non-insane) automatism so that in law they are not responsible for their acts. However, crimes committed during hyperglycaemia are different. If the patient claims that his mental processes were so seriously disturbed by his hyperglycaemic condition that he did not know what he was doing, any defence of automatism will be of the insane variety under the M’Naghten rules. The same holds for crimes committed unknowingly during an epileptic seizure,’ as ruled in a much-criticised House of Lords decision in 1983.’ The case of R v Hennessy ([1989] 1 WLR 287), decided in January of this year, concerned a man with insulin-dependent diabetes who had not taken insulin or eaten for several days. He was anxious and depressed. He was charged with taking a car without authority and with driving while disqualified. He argued that the offence was committed while he had hyperglycaemia caused by or contributed to by the stress, anxiety, and depression brought on by marriage and employment difficulties, and he sought to raise the defence of (non-insane) automatism. At the time of his arrest he had appeared to be in full possession of his faculties and quite cheerful and intelligent. However, after being at the police station for some time, he was taken to hospital. He arrived dazed and confused and told a nurse that he had failed to take his insulin for several days, and his blood sugar was over 22 mmol/l. After an injection of insulin he was discharged. His evidence was that he had been diabetic for 10 years and was dependent on insulin injections morning and afternoon. The dose would depend on factors such as stress and eating habits. He was on a strict carbohydrate diet. His general practitioner testified to his medical condition. The judge ruled that any impairment of the mind, if it existed, could not have been caused by anything other than the diabetes, from which the defendant was a long-term sufferer. (Automatism produced by malfunctioning of the mind and caused by an 1. Brahams D. Epilepsy is mental illness Lancet 1983; ii: 116.

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912

SERUM LEVELS OF LIPOPROTEIN A AND TOTAL CHOLESTEROL

IN FOURTH (LAST) WEEK OF PLACEBO PHASE AND DURING

ADMINISTRATION OF LOVASTATIN

Results as Lp(a); total cholesterol (both m mg/dl). Patients A, B, F, and H were female.*On bezafibrate before treatment with lovastatin.

month or so during treatment with lovastatin, serum Lp(a) and totalcholesterol levels were measured. 6,7

Total cholesterol levels fell in all eight patients. However, serumLp(a) concentrations rose from medium to high levels in five (A, C,E, F, H) and from low temporarily to medium levels in three (B, D,G), probably due to a drug-induced disturbance in lipid metabolismin the liver (table). Since Lp(a) levels of more than 20-30 mg/mlmust be considered as a risk for atherosclerosis we wouldrecommend the measurement of serum Lp(a) before and duringlovastatin therapy.Institute of Medical Biochemistry,Karl-Franzens Universtat,A-8010 Graz, Austria

GUNTHER JURGENSAHMED ASHY

Department of Internal Medicine II,Landeskrankenhaus Graz GERALD ZENKER

1. Widhalm K, Senser D. Increased lipoprotein (a) levels in children with familial

hypercholesterolaemia. Lancet 1988; ii: 1262.2. Grundy SM HMG-CoA reductase inhibitors for the treatment of

hypercholesterolemia. N Engl J Med 1988, 319: 24-33.3. Dahlen GH, Guyton JR, Attar M, Farmer JA, Kautz JA, Gotto AM Association of

levels of lipoprotein Lp(a), plasma lipids, and other lipoproteins with coronaryartery disease documented by angiography Circulation 1986; 74: 758-65.

4. Rhoads GG, Dahlen G, Berg K, Morton NE, Dannenberg AL. Lp(a) lipoprotein as arisk factor for myocardial infarction. JAMA 1986; 256: 2540-44.

5. Murai A, Miyahara T, Fujimoto N, Matsuda M, Kameyama M. Lp(a) lipoprotein as arisk factor for coronary heart disease and cerebral infarction. Atherosclerosis 1986;59: 199-204.

6 Zenker G, Költringer P, Bone G, Niederkom K, Pfeiffer KP, Jurgens G.Lipoprotein(a) as a strong indicator for cerebro-vascular disease. Stroke 1986; 17:942-45.

7. Költringer P, Jurgens G. A dominant role of lipoprotein(a) in the investigation andevaluation of parameters indicating the development of cervical atherosclerosis.Atherosclerosis 1985; 58: 187-98.

8. Hoff HF, Beck GJ, Skibinski CI, et al. Serum Lp(a) level as a predictor of vein graftstenosis after coronary bypass surgery in patients. Circulation 1988, 77: 1238-44

RESTRAINING THE OTHER SHOULDER

SiR,—The introduction of seat belts for drivers and passengers ofmotor vehicles has brought a welcome improvement in the

mortality and injury from road accidents in the UK. Over the threeyears from January, 1983, when seat belt wearing becamecompulsory, the measure is thought to have saved more than 200lives and more than 7000 serious injuries every year.2 Muchresearch has been done on the efficacy of seat belts.3,4Today, most seat belts in cars in Britain are of the same

design-namely, a transverse strap across the lower abdomen plus adiagonal belt which on right-hand drive cars, passes from above theright shoulder downwards and to the left for the driver and from leftto right for the front seat passenger. Two recent necropsies suggestthat this design should be changed.A 19-year-old man, the front seat passenger in a car involved in a

head-on collision, suffered head injuries and a fractured right femurand died 24 hours after the accident. Necropsy showed that the headinjury comprised lacerations and fractures of the right side of theface, fractures of the right orbit, and of the right frontal bone withsevere damage to the right frontal lobe of the brain, which had

herniated into the site of multiple comminuted fractures. It seemedthat, on sudden deceleration, this man had moved forwards and tothe left, the movement being directed by the restraint of thepassenger seat belt (left shoulder held); and he had struck the rightside of his face and head on the windscreen and other internal partsof the car.A 25-year-old woman driver of a car in a head-on collision with a

lorry had severe injuries to her left face, left orbit, and left frontalregion of the brain. She remained in coma for 12 days until artificialrespiration was discontinued. Necropsy revealed a head injurylocalised to the left face and orbit, and left frontal region of the brain,which was herniating into frontal comminuted fractures. Thisdriver (right shoulder held) had been thrown forwards and to theright, striking the left side of her head on the windscreen and otherinternal parts of the car.

I support the Oxford Road Accident Groups who haverecommended the introduction of symmetrical restraint systemsthat would prevent forward rotary movement to left or right.

Department of Neuropathology,Radcliffe Infirmary,Oxford OX3 6HE J. T. HUGHES

1 Editorial. Seat belts reviewed. Lancet 1986; i: 75-76.2. Seat belt regulations retained. Br Med J 1986; 292: 286.3. Gallup BM. The assessment of facial injury to fully restrained drivers through

full-scale car crash testing. J Trauma 1987; 27: 711-18.4. Campbell BJ Safety belt injury reduction related to crash severity and front seated

position. J Trauma 1987; 27: 733-395. McCoy GF, Johnstone RA, Nelson IW, Duthie RB. Facial injuries to restrained

drivers caused by steering wheels Lancet 1988; ii: 456.

Medicine and the Law

Hyperglycaemia, Automatism, and InsanityDIABETIC patients who commit crimes while hypoglycaemic may

be able to plead (non-insane) automatism so that in law they are notresponsible for their acts. However, crimes committed duringhyperglycaemia are different. If the patient claims that his mentalprocesses were so seriously disturbed by his hyperglycaemiccondition that he did not know what he was doing, any defence ofautomatism will be of the insane variety under the M’Naghtenrules. The same holds for crimes committed unknowingly duringan epileptic seizure,’ as ruled in a much-criticised House of Lordsdecision in 1983.’The case of R v Hennessy ([1989] 1 WLR 287), decided in

January of this year, concerned a man with insulin-dependentdiabetes who had not taken insulin or eaten for several days. He wasanxious and depressed. He was charged with taking a car withoutauthority and with driving while disqualified. He argued that theoffence was committed while he had hyperglycaemia caused by orcontributed to by the stress, anxiety, and depression brought on bymarriage and employment difficulties, and he sought to raise thedefence of (non-insane) automatism.At the time of his arrest he had appeared to be in full possession of

his faculties and quite cheerful and intelligent. However, after beingat the police station for some time, he was taken to hospital. Hearrived dazed and confused and told a nurse that he had failed totake his insulin for several days, and his blood sugar was over 22mmol/l. After an injection of insulin he was discharged. Hisevidence was that he had been diabetic for 10 years and was

dependent on insulin injections morning and afternoon. The dosewould depend on factors such as stress and eating habits. He was ona strict carbohydrate diet. His general practitioner testified to hismedical condition.The judge ruled that any impairment of the mind, if it existed,

could not have been caused by anything other than the diabetes,from which the defendant was a long-term sufferer. (Automatismproduced by malfunctioning of the mind and caused by an

1. Brahams D. Epilepsy is mental illness Lancet 1983; ii: 116.

913

underlying disease suffered by the defendant may, however, qualifyfor an insanity plea. However, that opportunity was not seized bythe defendant, who immediately changed his plea to guilty.) He wasgiven two suspended prison sentences and disqualified from drivingfor 2 years.On appeal he claimed that he did not know what he was doing

when the offence was committed because of hyperglycaemia andthat he should have been entitled to raise the defence of (non-insane)automatism.Lord Lane C?’, presiding in the Court of Appeal, said that the trial

judge had been right to take the view that the preliminary questionfor him to decide was whether this was truly a case of (non-insane)automatism or legal insanity within the M’Naghten rules. "If thedefendant did not know the nature and quality of his act because ofsomething which did not amount to defect of reason from disease ofthe mind, then he will probably be entitled to be acquitted on thebasis that the necessary criminal intent which the prosecution has toprove is not proved. But if, on the other hand, his failure to realisethe nature and quality of his act was due to a defect of reason fromdisease of the mind, then in the eyes of the law he is suffering frominsanity." What had to be decided, therefore, was whether thedefendant’s condition was a disease of the mind. That means not

just any disease of the brain but a condition that affects the properfunctioning of the mind.

It is important to differentiate between the Hennessy case(hyperglycaemia) and the claim of hypoglycaemia made in R vQuick ([1973] QB 910). The accused, a nurse at a mental hospital,was charged with assaulting a patient. Quick, who had diabetes,relied on the defence of automatism, claiming that he had takeninsulin on the morning of the assault, had drunk spirits, and eatenlittle food thereafter. He said he had no recollection of the assault.He called medical evidence that his condition was consistent with

hypoglycaemia but the judge ruled that such evidence couldsupport a defence of insanity, not automatism. Quick then pleadedguilty. On appeal the conviction was quashed, and the trial judgewas held to have been wrong in that the alleged mental conditionwas not caused by diabetes but by insulin prescribed by thedefendant’s doctor. He was therefore entitled to have his defence ofautomatism left to the jury. Lord Justice Lawton said that the factthat Quick’s condition may have been due to the injections of insulinmeant that the malfunction was due to an external factor and not tothe disease. It was the drug that caused the hypoglycaemia, not thelow blood sugar. However, hyperglycaemia is caused by an inherentdefect.At appeal in Hennessy it was submitted that the defendant’s

depression and marital troubles were sufficiently potent externalfactors to be capable in law of constituting a state of (non-insane)automatism but this argument was rejected. Lord Lane said: " ...stress, anxiety and depression can no doubt be the result of theoperation of external factors, but they are not... external factors ofthe kind capable in law of causing or contributing to a state ofautomatism. They constitute a state of mind which is prone to recur.They lack the feature of novelty or accident, which is the basis of thedistinction drawn up by Lord Diplock in R v Sullivan."l Thepurpose of the legislation relating to the defence of insanity, since itsorigin in 1800, has been to protect society against recurrence ofdangerous conduct.Lord Lane also cited with approval the reasoning of Mr Justice

Devlin in Hill v Baxter ([ 1958] 1 QB 277): "For the purposes of thecriminal law there are two categories of mental irresponsibility, onewhere the disorder is due to disease and the other where it is not.The distinction is not an arbitrary one. If disease is not the cause, ifthere is some temporary loss of consciousness arising accidentally, itis reasonable to hope that it will not be repeated and that it is safe tolet an acquitted man to go entirely free. But if disease is present, thesame thing may happen again, and therefore, since 1800, the law hasprovided that persons acquitted on this ground should be subject torestraint". A verdict of not guilty by reason of insanity requires thedefendant to be detained for an indefinite period and is such anunpopular option that most defendants faced with it will changetheir not guilty plea to one of guilty.

DIANA BRAHAMS,Barrister-at-law

Obituary

FREDERICK KRAUPL TAYLORMD Prague, FRC Psych

Dr Kraupl Taylor, known to his colleagues as KT and tohis friends as Peter, died last month aged 83.As a consultant at the Maudsley Hospital from 1948 to 1971 he

was an important contributor to its great days during the ’50s and’60s. This was an odd position for a Czech who, after qualifying inPrague in 1929, practised general medicine in Berlin and Viennaand the Sudetenland. Harrassed by the Nazis, he was befriended bythe Quakers, who brought him to England just before the war. Until1941 he had no permit to practise medicine and worked in thelaboratory of the York Retreat. His interest in psychiatry wasquickened there, and when he was allowed, he trained first at theCrichton Royal, taking the DPM in 1942, and then at NetherneHospital. His interest lay in the neuroses. Freudianism attracted butnever seduced him. He offered to Maudsley registrars who sharedhis scepticism the only possibility of practising psychodynamicallyoriented psychotherapy without abandoning their critical faculties.His was the firm that the discerning chose to be on.The new element that he introduced into therapy was that once

the patient’s transference had developed (and never until then) heexploited his or her resistance rather than just trying to overcome it.He aimed, by means of "prokaletic therapy" (his term for thechallenging technique), to change the patient’s life situation. Sincehe accepted, from all over the country, patients with severelydisturbed personalities, who often injured or poisoned themselves,this was necessary. The technique required him sometimes to utterdisturbing prophylactic challenges-"you may very well go on andtake an overdose after this interview"-but the intention was to

bring about the opposite by making use of the resistance; and thishappened. Prokaletic therapy, widely practised first by his studentsand now by their students, worked even when the patient hadtumbled to what was going on. Some would say he promoted thetechnique too exclusively, but he certainly used it to good effect. Hisreputation was based on his eclecticism as well as his scholarship andpowerful intelligence. He wrote an important textbook on

psychopathology. He was the first to study, using mathematicalanalysis, what went on in psychotherapeutic groups, of which hewas a pioneer. He created a long-term social club for patients, manyof whom were seriously incapacitated. During his productiveretirement, in which he went on treating patients, he wrote aprofound treatise on concepts of disease.

His second wife Natalie, who survives him, did a great deal tostimulate his interest in people and ideas.

N. K.

International Diary

1989

A lecture on Autoimmunity and the Thyroid: London, UK, June 6(Dr D. R. J. Singer, European Medical Research Group, c/o Fellowship ofPostgraduate Medicine, 6 St Andrew’s Place, London NWI4LB).

19th meeting of the Federation of European Biochemical Societies:Rome, Italy, July 2-7 (Organising Secretariat, Studio EGA srl, Viale Tiziano19, 00196 Rome).

An international conference on Emergency Health Care

Development: Washington DC, USA, Aug 15-18 (Conference Organiser,Medical Care Development International, 1742 R Street NW, Washington,DC 20009).

14th European symposium on Hormones and Cell Regulation:Ste-Odile (near Strasbourg), France, Sept 25-29 (Organiser, Prof J. E.Dumont, Institute of Interdisciplinary Research, Universite Libre de

Bruxelles, Faculty of Medicine, 808 route de Lennik, 1070 Brussels,Belgium).