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FRANCIS E. STOCK.Department of Surgery,University of Liverpool.

schools. Attached to the newer universities and withteachers determined to meet the country’s need, the newschools might well within a short time eclipse the presentschools.

HYPERTENSION IN IDENTICAL TWINS

C. G. HAMES.Claxton, Georgia.Department of Epidemiology,

School of Public Health,Chapel Hill, North Carolina. J. R. MCDQNOUGH.

JOHN L. ELLIOTTPresident, Georgia Heart Association.

SIR,-During 1960-62, a survey of cardiovasculardisease was made in Evans County, Georgia. It includeda census of the county population, and also identifiedthe twins in the population. 56 twin pairs were studied forconcordance of serum-cholesterol 2; and in the summer of1960 blood-pressure was also recorded. But, because nohypertension was found, the blood-pressure data were notreported.During March, 1964, hypertension (B.P. 200/110) was

discovered by one of us (C. G. H.) in routine clinicalexamination of a man of 54; and the patient (A. B.)afterwards mentioned that he was one of the twins whohad been studied four years previously. The recordsshowed that he had been classified as an identical twin,and that his brother had been living in Savannah, about60 miles away.The next step was to obtain blood-pressure readings on

the brother (C. D.). His physician in Savannah (J. L. E.)was notified, and a record of blood-pressure determinationsdating back to 1946 was obtained. Except one in 1951,all pressures taken before 1962 appeared normal. In 1962four pressures were taken, and the diastolic pressure wasfound to be 100. The patient was given antihypertensivemedication, and in 1963 his pressure was recorded at140/80. When again recorded in 1964 (after a periodwithout-any antihypertensive drug), it was 190/105. Thetable shows these readings, together with the twin-

survey blood-pressure readings (a mean of ten readingstaken on each arm).

Both twins were normotensive until 1960 (with thepossible exception of the 1951 reading on C. D.), and bothbecame hypertensive by 1964. The level of blood-

pressure was then remarkably similar (200/110 for A. B.,and 190/105 for C. D.). The twins had lived apart sincebefore 1946-A. B. in the rural area of Claxton, and C. D.in the urban area of Savannah.

Platt has reported three sets of identical twins in whichthe co-twins are all hypertensive.3 The present case addsanother to the literature. Although concordance for hyper-tension was unexpected in this twin pair, it could be care-1. McDonough, J. R., Hames, C. G., Stulb, S. C., Garrison, G. E. Publ.

Hlth Rep., Wash. 1963, 78, 1051.2. McDonough, J. R., Hames, C. G., Greenberg, B. G., Griffin, L. H., Jr.,

Edwards, A. J., Jr. Observations on Serum Cholesterol Levels in theTwin Population of Evans County, Georgia. Circulation, 1962, 25, 962.

3. Platt, R. Heredity in Hypertension. Lancet, 1963, i, 899.

BLOOD-PRESSURE DETERMINATIONS OF A PAIR OF IDENTICAL CO-TWINS

* Twin survey data. These are means of ten determinations on each arm.t On antihypertensive drug.

fully documented both in terms of the blood-pressurelevel and in the time of expression. The twin methodcannot show the mechanism of inheritance (whetherthrough a single gene or polygenic) but it can sometimesbe useful in assessing the " strength " of genetic versusenvironmental processes. The appearance of hyper-tension in two 54-year-old identical twins living underdifferent circumstances is striking, especially since the timeof onset of hypertension was similar; and this suggeststhat genetic factors have a powerful role in the expressionof hypertension.The survey was made with support from U.S. Public Grant

no. H3341. -

Savannah, Georgia.

The twins.

POST-MEASLES ENCEPHALITIS

SiR,ňYour readers may be interested in the followingcase, which seems to illustrate rather succinctly thedilemma of using steroids in postviral encephalitis.A girl of 5 years was admitted to my care on May 10, 1964,

on account of diminishing awareness developing that day, aftertypical measles where the rash had been fully out three daysbefore, on May 7. On admission, the girl was abnormallydrowsy, but her central nervous system showed no objectivephysical signs and her general condition was satisfactory. Thenext day she become stuporose, her temperature rose to

100-6°F, and her stupor became deeper. She responded onlyto painful stimuli; and recourse was had to nasal feeding.During the next seven days her condition remained the same,but the tendon reflexes remained absent. There was retentionof urine, afid the left plantar reflex was anomalous, the rightremaining definitely flexor. She finally became apyrexial onMay 22, 12 days after admission.During the period of deterioration the question of giving

steroids arose; but I was not convinced of their efficacy inpostviral encephalitis, and believed that they should never beadministered except when there was the clearest possible posi-tive indication-for instance, in a patient with the Stevens-

Johnson syndrome under my care at the sametime.Between May 25 and May 28 the child’s

mother was warned that, although the patientwould probably live, there was little hope ofmore than a vegetable existence. At this timethe girl remained almost comatose, with com-plete flaccid paralysis of the lower limbs, reten-tion of urine, and no spontaneous movements ofthe upper limbs.On May 28 spontaneous movements of the

upper limbs were observed, and on May 30 thechild was able to speak and moved all her limbsactively. By June 9 she was sitting up, talkingclearly and normally, and eating normally, butshe still needed catheterisation. By June 30 shecould walk without help and was passing urine