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thiazine derivatives such as promethazine,9 10 the pooranalgesic properties of low concentrations of halothane,lldilution of the gas mixture owing tojeaks in the apparatus, 112and the difficulty of recognising a lightening of ansesthesiain the paralysed patient. Movements, sweating, and

bronchospasm may indicate that the level of ansesthesia istoo light; but patients may afterwards complain eventhough no sign of returning consciousness has beenobserved.5 Amnesia may imply that a painful episode hasbeen repressed 13; on the other hand, some patients recallincidents without any apparent distress. Recent work hasshown that the effect on consciousness of a given tensionof nitrous oxide or carbon dioxide in the blood varies fromone individual to another. 1-4 1.5 Careful electroence-

phalographic studies are needed.16Nitrous oxide with adequate oxygen is a very safe but

very weak anaesthetic agent; and Hutchinson’s paper isa timely reminder that muscular relaxation and hyper-ventilation, insufficiently supplemented by more powerfuldrugs, will, not invariably ensure unconsciousness. Theanaesthetist’s first concern is to relieve pain and apprehen-sion, and the patient should be assured of oblivion as wellas of safety.

9. Moore, J. Dundee, J. W. Brit. J. Anœsth. 1961, 33, 3.10. Moore, J., Dundee, J. W. ibid. p. 422. See Lancet, 1961, i, 268.11. Dundee, J. W. Brit. J. Anœsth. 1960, 32, 450.12. Cole, W. H. J. Anœsthesia, 1955, 10, 46.13. Cobb, S. Anesthesiology, 1961, 22, 314.14. Henrie, J. R., Parkhouse, J., Bickford, R. C. ibid. p. 247.15. McAleavy, J. C., Way, W. L., Alstatt, A. H., Gualagni, N. P.,

Severinghaus, J. W. ibid. p. 260.16. Clutton-Brock, J. Brit. J. Anœsth. 1961, 33, 214.17. Page, I. H. Amer. J. med. Sci. 1935, 190, 9.18. Bennett, I. L., Jr., Heyman, A. Amer. J. Med. 1948, 5, 729.19. Penfield, W. Arch. Neurol. Psychiat. 1929, 22, 358.20. Montgomery, B. M. Arch. intern. Med. 1961, 108, 559.

PAROXYSMAL HYPERTENSION OFCEREBRAL ORIGIN

PHaeOCHROMOCYTOMA is the most widely recognisedcause of paroxysmal hypertension; and it is probably themost important cause to recognise, because timely removalof the tumour effects cure. Of the many other causes of

paroxysmal hypertension most are neurological disorders.A common benign type is that found in young or middle-aged people with an unusually labile autonomic nervoussystem. Unfamiliar experiences, such as a medical exami-nation, and particularly the recording of the blood-

pressure, evoke signs of overactivity of the sympatheticnervous system such as palpitation, sweating, and erythemaover the upper chest and root of the neck; and this isaccompanied by an abrupt rise in blood-pressure. Thesepatients, with what Pagel7 has designated " the hyper-tensive diencephalic syndrome ", have no organic diseaseand need no treatment. Indeed, hypertension associatedwith tachycardia and " necklace erythema " can usuallybe disregarded.Paroxysmal hypertension may also betoken organic

brain disease. It has been described in tabes dorsalis,18usually in association with other evidence of sympathetic-nervous-system discharge. There is a classical account byPenfield19 of paroxysmal hypertension associated with aball-valve tumour intermittently blocking egress of

cerebrospinal fluid from the lateral ventricles. Mont-

gomery20 has lately drawn attention to paroxysmal hyper-tension in basilar-arterial insufficiency. He describes threepatients over the age of 60 with blood-pressures at or alittle above the upper limit of normal in whom the systolicpressure rose abruptly by 90 mm. Hg and the diastolicpressure by 60 mm. Hg; the hypertension lasted for

periods varying from seven minutes to four hours and then

fell to the previous level. These attacks were repeated overa period of weeks or months, later becoming associatedwith signs of periodic medullary dysfunction such asdysphagia, dysarthria, and weakness and sensory disordersof the limbs. All three patients ultimately developed signsof medullary infarction; and in one this was seen at

necropsy, which also showed a grossly sclerotic basilarartery and abnormally small posterior communicatingbranches of the circle of Willis. The absence of a chromaffintumour was confirmed in this patient. In these three cases,when the paroxysms of hypertension were associated withneurological crises, the diagnosis of basilar arterial in-

sufficiency was not difficult; but in two the earlier

paroxysms were not accompanied by any neurologicalsigns. The fact that all three patients died under observa-tion suggests that this syndrome carries a grave prognosis.Millikan and Sickert2l gave a good description of thesyndrome of intermittent insufficiency of the basilararterial system. They treated six of their ten patients withanticoagulants, and their experience suggested that thistreatment was beneficial.

21. Millikan, C. H., Sickert, R. G. Proc. Mayo Clin. 1955, 30, 61.22. Lord Roseberry. Napoleon: The Last Phase. London, 1900.23. Keith, A. Hunterian lecture, 1913.

NAPOLEON’S DEATH

Napoleon Buonaparte was the first man about whoseadult private life we know almost everything: everything,that is, except the cause of his death. In his lifetime he wasrecognised universally as a nonesuch: his privacy was notprotected by the sacred aura of an ancient crown; hishabits were not such as to win the loyalty of all the mem-bers of his entourage. In health and sickness his actionsand reactions were recorded again and again. We knowleast about the last three years of his life, because by thenmost of his memorialists had, willy nilly, left St. Helenaand the one who remained was, although a physician, anabandoned liar.22 Since his surrender Buonaparte’s healthhad fluctuated; sometimes he rode and gardened and talkedwith vigour and enthusiasm, at other times he sank intoquerulous torpor. Medical attendants came and went, andtheir accounts of his symptoms are so diverse as to justifyany or all of the diagnoses which have been made retro-spectively.23 After some bouts of violent abdominal painhe died slowly and apparently in peace. He himself hadasked that a necropsy should be made, and for once SirHudson Lowe was only too glad to comply with hisrequest. The examination was made in the presence ofsix British doctors by Francesco Antommarchi, hisCorsican physician, who had studied anatomy under thegreat Mascagni. It was probably performed as well asmight be expected at that time, but the findings were indispute. There was general agreement that the stomachcontained altered blood and that the pyloric part wasulcerated. No secondary deposits were detected. Dr.

Shortt, the principal medical officer of the island, thoughtthat the liver was abnormally large and hard, but on theorders of the Governor this sentence was struck out of the

report. This gave " cancer of the stomach " as the causeof death and was signed by the P.M.o. and four otherdoctors-one of whom had not seen the necropsy.Antommarchi refused to sign. On his return to Europe heproduced his own report (together with some pathologicalspecimens) and four years later a second (and contra-dictory) version.

Taking into account the clinical history of his later

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years and the arguments at the postmortem table, it is areasonable guess that for some time Buonaparte hadsuffered from an affliction of the liver. No organ is morefruitful of suppositious diagnoses, and all the obvious

possibilities have been advanced at one time or another.One of these is arsenical poisoning-a useful stick withwhich to beat perfidious Albion-and this gained somesupport when the body was found in good preservationwhen it was returned to France in 1840. Quite recently thedepartment of forensic medicine at Glasgow had theopportunity of analysing by a new activation technique atuft of hair believed to have been removed from the bodysoon after death.24 The test showed that the Napoleoniclock had an arsenic content of 10-38 p.p.m., compared witha normal value of about 0-8 p.p.m. Unfortunately therewas not enough hair to discover whether the arsenic wasdistributed evenly along its length.

Assuming that the hair came from Buonaparte’s head-and the substitution of relics, both holy and medicolegal, isnot unknown-chronic arsenical poisoning with acute

exacerbations must be considered seriously as a cause ofdeath. The symptoms are suggestive-and equallysuggestive of beriberi. If Buonaparte died of arsenicalpoisoning it might have been accidental or homicidal. Itseems that St. Helena had a bad name for inducing hepaticdisorders. Did some of the springs-including that whichsupplied Longwood-give water with a high content ofarsenic ? Rats were the curse of the island. What rat

poison-if any-was used in 1821 ? We can think of

cooking-pots made of metal containing arsenic and all theother examples in the books on forensic medicine, but noother inmate of Longwood seems to have had a similardisease. This was the heroic age of therapeutics, and itmay be that for years his doctors had been overgenerouswith their arsenical tonics. As to deliberate poisoning,there were so many inhabitants of St. Helena whowould have welcomed his death that it is hard to knowwhere to start the guessing-game. There were two brigsand two frigates on guard duty and three battalions ofinfantry on shore. Everyone from colonels to campfollowers would have liked to leave this gloomy rock wherethey were imprisoned as securely as their one prisoner.Sir Hudson Lowe was a stupid man and rather an un-pleasant one, but his whole history suggests the bureaucratwho would do nothing without the backing of " higherauthority ". Higher authority was Lord Bathurst. He wasno genius; but poisoning for political ends is not, as far aswe know, a common habit among English noblemen. Themost damning evidence against the Governor was hisanxiety to suppress the postmortem evidence of an enlargedliver. His task was twofold: to keep Buonaparte alive, andto prevent his escape. Neither he nor Lord Bathurst northe Cabinet were anxious to face the accusation that theyhad gaoled the most valuable prisoner in the world in aplace where he was likely to die of the endemic hepatitis-whatever this may have been. It is far more difficult to

suspect any of the French attendants. They had sacrificedeverything to serve the man whom they adored. Theywere, as might be expected, an odd lot and they quarrelledamong themselves like children. Who knows to what

lengths venom or misguided loyalty might have persuadeda mind already unsettled by long confinement in closecompany ? (Antommarchi, an obvious suspect, is excusedbecause the symptoms had begun before he arrived.) Orwas it a self-inflicted injury ? On St. Helena the Emperor24. Forshufvud, S., Smith, H., Wassen, A. Nature, Lond. 1961, 192, 103.

had only one wish-to get away. His courage soared andlapsed. In the times of depression the thought must havecome to him that if he .could not return to power and gloryhe could at least ruin his oppressor, Sir Hudson Lowe-and in this he was entirely successful. Writers of detectivefiction can begin at this point.

1. See Lancet, 1960, ii, 1397.2. Jones, C. M. Digestive Tract Pain. New York, 1938.3. Tuttle, S. G., Rufin, F., Bettarello, A. Ann. intern. Med. 1961, 55, 292.4. Siegel, C. I., Hendrix, T. R. Clin. Res. 1960, 8, 369.5. Palmer, E. D. New Engl. Med. J. 1960, 262, 927.

MECHANISMS OF HEARTBURN

HEARTBURN is a burning sensation, felt behind thesternum and rising to the throat, often associated withregurgitation of acid or bitter fluid into the back of themouthy The cause of this familiar symptom is undecided.We do know that heartburn can be reproduced in normalpeople by distension of a balloon in the lower oesophagus .2such a mechanism may explain the pain as beer is gulpedtoo fast, but it must be rare outside the pub.A careful study of the mechanism of heartburn has been

reported by Tuttle et awl. in Los Angeles. Simultaneousrecords of oesophageal and gastric pressures, and of pHin the lower oesophagus, were made in patients withoesophagitis during spontaneous and induced heartburn.Perfusion of the lower oesophagus with N110 hydrochloricacid (HCI) produced heartburn, together with a distinctfall in oesophageal pH. Equal volumes of physiologicalsaline solution, sucrose solution, and more dilute HC1 didnot produce heartburn. The oesophageal pressure roseslightly and equally with all solutions, indicating thatHCI produced heartburn by changing acidity withoutincreasing muscular activity. These patients were studiedin the sitting position. Other workers 4 have reportedsignificant increases in oesophageal pressure during acidperfusion in recumbency; and in this position, when heart-burn usually develops, fluid accumulation with distensionmay well cause increased muscular activity. HCI isknown to cause heartburn only in the presence of ceso-phagitis,2 and heartburn can occur in association withachlorhydria 5; so oesophageal acidity is not alone respon-sible.More transient heartburn was observed by Tuttle et al.

in association with belching; the oesophageal pressure rosesharply, but there were no consistent pH changes.Belching was found to be a stronger stimulus in provokingheartburn; as oesophagitis improved, pain developed withbelching, but not with HCI, and finally neither inducedheartburn. Disordered oesophageal mobility was rarelyassociated with gastro-cesophageal reflux; of 209 patientswith reflux, only 9 had notably increased oesophagealpressures and increased peristalsis of the lower half of theoesophagus.

Increased acidity, therefore, and distension duringbelching will produce heartburn in an inflamed reso-

phagus. In the erect position increased muscular activityis rarely responsible, but it may be more important, inassociation with acid reflux, when the patient is recumbent.

Mr. E. C. BEVERS, consulting surgeon to the RadcliffeInfirmary, Oxford, and a former chairman of the UnitedOxford Hospitals, died on Dec. 13.

Sir HENRY DALE has resigned from the chairmanship of thegoverning body of the Lister Institute of Preventive Medicine,which he has held for twenty years. He is now succeeded bySir CHARLES DODDS.