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and the fellows of these colleges can do equally valuablework by diffusing the views and attitudes of the collegesin the appointment committees. But we would like tosee these representatives enter the committee room.grasping, not a charter, but a guiding light.

Intracranial Hypertension and SteroidsWHENEVER papilloedema is observed in a patient who

complains of headache and vomiting, hydrocephalus ora space-occupying lesion of the skull is likely. Until

recently, benign intracranial hypertension (referred toin the United States as " pseudotumor cerebri ") wasthe only reasonable alternative diagnosis; but over thepast six years it has become clear that corticosteroidscan produce a similar clinical picture, especially inchildren.At the end of last century QUINCKE 1 2 first recognised

that there could be a rise in cerebrospinal-fluid (c.s.F.)pressure in the absence of a space-occupying lesion or ofhydrocephalus; but, until the radiologist was able todemonstrate a normal ventricular system, such a condi-tion was impossible to prove during life. The chieffeatures of " benign intracranial hypertension " are

moderate to severe headache, obscurations of visionwhich may rapidly proceed to total and permanentblindness, diplopia, and sometimes tinnitus, papillae-dema, and abducens palsies. The c.s.F. is normal and

ventriculography invariably demonstrates ventricles thatare either normal in size or slightly smaller than usual.Prognosis for life is good, but rapid relief of the raisedintracranial pressure is essential if sight is to be preserved." Otitic hydrocephalus," in which otitis and sinusthrombosis are associated, forms one group of such cases.For the rest, like most obscure lesions, they have beengiven various names, of which " toxic hydrocephalus "4-6is misleading, because only rarely is there evidence of atoxic cause, and " pseudotumur "’ 8 should perhaps bereserved for cases in which ventriculography demon-strates a space-occupying lesion; biopsy then givesequivocal results, and recovery finally ensues.3 " Intra-cranial hypertension " can hardly be described as"

benign " if it may result in blindness; but, withoutthis prefix, the title seems to fit the facts. The patientsare nearly always women or young girls, often over-weight, and the onset commonly coincides with somehormonal disturbance, such as the menarche or the

puerperium,4 9 10 suggesting that an endocrine dis-turbance may be responsible. The association ofAddison’s disease with cerebral oedema and papill-oedema 11-13 adds further weight to the endocrine

hypothesis, especially since one patient’s papilloedemasubsided when steroids and deoxycortone acetate were

1. Quincke, H. Samml. klin. Vortr. 1893, no. 67 Inn. Med. n. F. 23, 655.2. Quincke, H. Dtsch. Z. Nervenheilk. 1897, 9, 149.3. Davidoff, L. M., Dyke, C. G. J. nerv. ment. Dis. 1936, 83, 700.4. Foley, J. Brain, 1955, 78, 1.5. McAlpine, D. ibid. 1937, 60, 180.6. McAlpine, D. Arch. Middx Hosp. 1952, 2, 149.7. Bailey, P. Arch. Neurol. Psychiat. Chicago, 1920, 4, 401.8. Warrington N. B. Quart. J. Med. 1914, 7, 93.9. Paterson, R., De Pasquale, N., Mann, S. Medicine, Baltimore, 1961, 40,

85.10. Greer, M. Neurology, 1963, 13, 439.11. Boudin, G., Funck-Brentano, J-L., Gayno, M. Bull. Soc. Méd. Hôp.

Paris, 1950, 66, 1736.12. Walsh, F. B. Arch. Ophthal. 1952, 47, 86.13. Jefferson, A. J. Neurol. Psychiat. 1956, 19, 21.

given.12 Intracranial hypertension, it is therefore

suggested, can be the result of adrenocortical suppression.Moreover, functional hypopituitarism is reported to

arise occasionally in Addison’s ’disease. 14A connection between steroids and raised intracranial

pressure was first suggested by MALKINSOÑ,15 who

presumed that steroids suppressed the hypothalamic-pituitary system. Severe headache and dizziness hadbeen noted as side-effects of triamcinolone,16 and thisdrug was at first thought to be especially liable to causeintracranial hypertension17 1S; but it now seems clearthat all steroids can do so when given for conditionssuch as asthma,1S-20 21 nephrosis,l’-22 polyarthritis,24-11osteitis ’26 and the adrenogenital syndrome,27 andindeed even when steroids are applied to the skin ineczema 19 20 22 and psoriasis.28WALKER and ADAMKIEWICZ 23 found papilloedema in

4 children who had had a long spell of steroid therapy;apart from raised pressure, the c.s.F. was normal, andso were the ventriculograms. 24 similar cases in theliterature were all in children, except for one patientof 19. Steroids of all types had been given for an

average of two and a half years (the minimum wasthree months) and had resulted in headache, vomiting,and diplopia (8 patients) and occasionally in drowsinessor stupor (5 patients). Papillcedema was invariable.Sometimes there was diastasis of the skull sutures

(9 patients); and, although the electroencephalogramwas sometimes abnormal, the changes were non-specific.The c.s.F. always had a normal cellular and chemicalcontent, but the pressure was raised in 13 of the 15

patients in whom it was measured. When pneumo-encephalograms were done, they showed normal or

small ventricles. Usually the syndrome followed a

decrease in the dose of steroid or a change to anothercompound. Although 17-ketosteroids were thought tohave been subnormal in some of the patients in whomthey were measured, the values must have little meaningunder the age of puberty. If there is adrenocortical or

pituitary suppression, it seems far from clear why thebrain should become oedematous; where they have beenmeasured the electrolytes have generally been normal.Until we know the reason for this oedema, it seems wiseto treat these patients by temporarily increasing thedose of steroid until symptoms have subsided and thento withdraw the drug cautiously. If vision is threatened,raised intracranial pressure may have to be relieved byintravenous urea or even by ventricular taps.

There is no doubt about the value of steroids as a

lifesaving drug in some diseases of both adults andchildren; but it seems wiser to avoid their use-whenever14. Taylor, A. B., Albert, A., Sprague, R. G. Endocrinology, 1949, 45, 335.15. Malkinson, F. D. J. Invest. Derm. 1958, 31, 19.16. Freyberg, R. H., Bernstein, C. A., Jr, Hellman, J. Arthr. & Rheum.

1958, 1, 215.17. Valentine, G. H. Lancet, 1959, i, 892.18. Laurance, B. M., Matthews, W. B., Shephard, R. H. ibid. 1960, i, 701.19. Dees, S. C., McKay, H. W. Jr. Pediatrics, 1959, 23, 1143.20. Benson, P. F., Pharoah, P. O. D. Guy’s Hosp. Rep. 1960, 109, 212.21. Warin, R. P., Evans, C. D. Lancet, 1960, ii, 42.22. Calcagno, P. L., Rubin, M. I. J. Pediat. 1961, 58, 686.23. Walker, E. A., Adamkiewicz, J. J. J. Amer. med. Ass. 1964, 188, 779.24. Gaisford, W. J. Pediat. 1960, 56, 259.25. Jolly, H. Lancet, 1960, ii, 42.26. Royer, P., Vermeil, G. Med. Hyg. 1961, no. 492, p. 159.27. Green, O. C., Cleveland, W. W., Wilkins, L. Pediatrics, 1961, 20, 292.28. Sneddon, I. B. Lancet, 1960, ii, 42.

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possible, especially in children. When they are

essential, they should be given for as short a time andin as small a dose as possible and the fundi should beexamined regularly. Retardation of growth is not

uncommon in children treated with steroids; so, howeversuccessful such treatment may be, it is well to rememberthat steroids have peculiar dangers for the growing child.

Age and SleepMAN is singularly ill-informed about three of the most

important facts of his existence. We do not know whyhealthy full-term foetuses should leave the uterus andenter the world; nor why there is an ageing process begin-ning early in life and ending in death. And betweenthese extremes we sleep for about a third of our lives-and again for reasons of which we are largely ignorant.Young infants sleep longer, for some 12-17 hours out ofthe 24, and not much less than this even when they are6 months old. Sleeping time then slowly decreases untilit averages 7-8 hours daily for most adults of young andmiddle years. There is a belief that the old not only takeless sleep but need less, though not everyone agrees withthis.! In any event, where the healthy aged are con-cerned, the idea of less sleep is not founded on carefulobservation.The time taken in sleep is not easily measured at any

age: many elderly people, it is true, may sleep for fewerhours at night, but they may compensate with daytimenaps. Nevertheless, an attempt has now been made todecide whether the older person does actually need lesssleep.2 The subjects were 83 active people over theage of 60 who had no organic disease. Qualitative differ-ences in sleep were not considered (though these cannotbe dismissed as of no account). A chart was constructedrelating hours of sleep to symptoms and complaints,such as dizziness, fatigue, apprehension, headache, andtension. Of those who slept less than 7 hours, more thanhalf complained of the insomnia and described continu-ous symptoms of moderate to severe intensity. Some ofthis group believed that their troubles stemmed fromlack of sleep; others maintained that they slept well, eventhough the time was short. In another group with occa-sional or mild insomnia, a few people also complainedof moderate or severe symptoms. Of those who slept 8 ormore hours, less than a third complained of symptoms.Comparing the two extreme groups, there was a pre-ponderance of tension, fatigue, and apprehension in thosewho slept less. The 34 patients who slept for under 7hours were told to spend at least 9-10 hours in bed atnight and to rest during the day as well. There was norestriction of activities in general. After a month of thistreatment alone, in 20 patients the hours of sleep at nightincreased to 8 or more, and the change was sometimesabrupt. There were a few exceptions in those who hadregularly taken sedatives. What is also interesting is thatall the patients said they felt much better: fatigue andtension disappeared and apprehension was reduced. The5 people whose sleeping time increased gradually ratherthan abruptly also improved, particularly in their ability

1. Cruden, W. V. Lancet, 1957, i, 579.2. Tiller, P. M., Jr. Ann. intern. Med. 1964, 61, 98

to endure extra effort and stress. A curious finding in afew persons whose symptoms had been severe was that,at first, longer rest in bed made them feel worse, despitea reduction in tension; they felt drowsy and tired andhad joint pains and severe headaches. After 10-14 days,however, they too felt better. The speed with which anumber of patients learned to sleep longer hours suggeststhat there was nothing wrong with their ability to sleep,simply that they had allowed too little time for it. Inothers there was possibly some impairment of sleepingability. In all, more rest in bed and more sleep amelior-ated the symptoms, even though they did not whollydisappear.These observations suggest that the old need as much

sleep as younger adults and that reduction of sleepinghours may be nothing but a bad habit. Of course, thereare certain to be individual variations in the optimalsleeping hours, and the quality of the sleep may beimportant. For instance, it was noted, in another seriesof observations, that after 48 hours of sleep deprivationthe subjects were restored to normal after only 12-14hours of sleep. The early hours of sleep are usually thedeepest and may be the most important, giving rise to alogarithmic decline in the " value " of sleep.3 A study ofsevere sleep deprivation can perhaps give a clue to theeffects of small repeated deprivations. Children and

animals, whose reactions are more natural and lessconcealed than those of adults, become irritable andbad-tempered, and animals may become vicious.3 In

sleep-deprived men the electroencephalogram shows nopathological features but repeated episodes of a sleeppattern may appear, unless stimulation and concentra-tion are maintained-in other words, keeping awake isan effort. Certainly, performance is lowered and muscletension increased.4 4

Habit and timing are certainly of significance in per-mitting and encouraging sleep, but these are by nomeans the only factors involved. Thus, when LEWIS andMASTERTON 5 were in the Arctic, they studied the on-demand sleeping habits of their colleagues both in thelong daylight and long night. They found that althoughthe distribution of sleeping time might not be the usual,the total time per month spent in sleep was just aboutthe same as in more normal circumstances. Theyconcluded that the one-third of time spent in sleeprepresented a biological need. Why it is a need is theunanswered question.

In the elderly, interference with sleep may come fromvarious sources, apart from bad habits. Degenerativechanges in the central nervous system may give rise tono recognisable symptoms; but if they lie in regionsaffecting sensory input, then the sleep pattern might bechanged. Sleep seems to depend on coordination in thedual mechanism which handles sensory impulses. Thelong-known direct sensory path to the cerebral cortexpasses information, by means of collaterals, to the morerecently recognised reticular formation. The reticular3. Oswald, I. Sleeping and Waking. New York, 1962.4. Wilkinson, R. T. in The Nature of Sleep (edited by G. E. W. Wolsten-

holme and M. O’Connor); p. 329. London, 1961.5. Lewis, H. W., Masterton, J. P. Lancet, 1957, i, 1262.