1395

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