473 playing with his parents, only six subsequent occasions. The coma may last up to ten hours and so may his normal consciousness. He remained afebrile throughout. Monitored continually over several hours, the E.E.G. showed no abnormality while he was conscious, nor while he was unconscious, except that, when he was unconscious, the voltage was appropriately low. There were no focal signs. I have not indicated all the negative results; and viral studies have not yet been completed and may not be helpful. There is one additional positive feature. It was noted by the parents and confirmed by us that at the very beginning of an unconscious episode, and usually preceding it by a few minutes, a papular rash developed over the bridge of his nose, his face, and his neck above the scapula. Invariably this rash faded within half an hour, but almost always recurred at the beginning of the unconscious episode. talking normally, eating normally, to relapse into the deepest coma

.

Biochemical estimations: A.S.T., A.L.T., L.D.H., C.P.K., aldolase, glucose, magnesium, calcium, urea, phosphate, albumen, total protein, sodium, electrophosesis, T3, T4, free thyropac index. Immunoglobulins: IgA 9 i.u./ml, IgG 105 i.u./ml, IgM 28 i.u./ml. Bacteriology.-Nose, throat, and rectal swabs sterile, meconium

and

on

I have never seen a case of encephalitis lethargica (von Economo’s disease). Could this be one? I would be grateful for help from any reader by telephone (Sheffield [0742] 71111), telegram, or any other means. The Children’s Hospital, Western Bank, Sheffield S10 2TH

J. LORBER

sterile. Cord-blood serology.-Toxoplasma antibody 1/10 (postnatally, mother’s serum 1/64); rubella H.A.I. 1/320, C.F.T. 1/10; adenovirus

1/20; cytomegalovirus < 1/10. Urine.-No aminoaciduria, cells, or organisms. X-rays.-No abnormal calcifications or other lesions in skull, heart, or lungs.

In the absence of any clinical abnormality and the presence of normal total and differential white counts, and normal plasma viscosity and immunoglobulins, it was felt that the rubella antibody was almost certainly maternal, but this will be pursued. Cord-blood toxoplasma antibody was 1/10, mother’s antenatally was 1/32 and on the fifth postnatal day 1/64, and the infant’s was less than 1/32. Thus, by all tests we failed to demonstrate that the infant had infection, major congenital anomaly, or toxic damage from the Steptoe-Edwards

technique. We greatly appreciate the help from our laboratory colleagues in many centres and the normality of care provided by the midwifery c;;:tff nncipr thi- c-irciimztnnri-q

SUCCESSFUL PREGNANCY FOLLOWING IN-VITRO FERTILISATION

SIR,-It seems prudent to publish the details of the first infant successfully delivered after A.I.H. in vitro by Steptoe and Edwards.’ The findings should allay fears that their technique is necessarily fraught with dangers to the fetus. The apparent normality of the infant should avert controversy that might have arisen had there been a major anomaly, or should there be subsequent illness that might affect her development. Many investigations were performed on the mother and on the cord blood to seek evidence of congenital abnormalities or of infection transmitted in the laboratory. Investigations on the infant were thus minimised. Relevant antepartum maternal features.-Apart from those in your columns’, the maternal thyroid function factors were normal and the toxoplasma antibody dye test was positive, 1/32. The infant.-A 38-week infant was deiivered by elective lower-segment csesarian section by Mr Steptoe. Her airways were drained and cleared and she cried within 20 seconds, before the cord was clamped. The Apgar at 1 minute was 10. She was a normal female weighing 2608 g (5 Ib 12 oz), crying well and maintaining a good colour. Placenta.-Healthy, 18 cm diameter, 450 g (1 lb). Normal umbilical cord, length 60 cm, three blood-vessels. 40 ml cord blood was taken

reported

for to

laboratory investigation of fetal state. The infant was transferred special-care baby unit for further examination and observation.

the

She was fed 20 ml sterile water and 30 ml 5% dextrose at 3 h and 30 ml of dextrose at 5 h; she sucked vigorously and slept between feeds. At 10 h she was put to the breast and fed 3-hourly thereafter, complementing feeds with Cow and Gate Premium milk as demanded. Retinoscopy with 1% homatropine eye-drops was normal. Progress was satisfactory until discharge on the 12th day, when she weighed 2693 g (6 Ib 1 oz), on breast and complementary feeding. Measurements and Investigations Gestational age: 10 -5=approximately 270 days’ gestation.2 The following reflexes were present and normal: Moro; asymmetric tonic neck; hand and foot grasp; stepping, walking, rooting.

DON HILSON R. L. BRUCE D. G. SIMS

Paediatric Department, Oldham and District General Hospital, Rochdale Road, Oldham OL1 2JH

SEASONAL VARIATION IN SUDDEN-INFANT-DEATH SYNDROME

SIR,-Beal’ and Professor Goldberg and

Dr Stein (July 8, 107) have shown that deaths due to sudden-infant-death syndrome (S.LD.S.) are more frequent in the winter months in South Australia and Chicago, at least for children dying at

p.

four months of age or older. Beal found no seasonal variation for those dying under three months of age. We believe that there is an important factor that they both failed to consider. In the United States, the National Center for Health Statistics2 reports that the occurrence of births is not uniform throughout the year and that the major peak occurs in September, with fewest births occurring in April and

May.

reported the number of s.i.D.s. deaths which is dependent on the seasonal variation in the number of births, a reanalysis of their data using life-table survivorship curves for monthly birth cohorts would be a more appropriate means of determining if there is a seasonality in s.i.D.s. deaths, and if this seasonality is ageSince both authors

occurring per month,

dependent. Epidemiology Program, School of Public Health,

University ofIllinois Medical Center, Chicago, Illinois 60680, U.S.A.

MARILYN D. FARBER VIJAY CHANDRA

MEASUREMENT OF THEOPHYLLINE

SIR,-Dr Kelly and Dr O’Malley (July 8, p. 98) criticise the validity of the Schack and Waxler method3for the measurement of theophylline in plasma. There exists a modification4 of this method which is not influenced by theophylline metabolites, caffeine, or barbiturates. This modification offers a simple and satisfactory means of monitoring theophylline levels in blood or plasma. Umbilical cord blood.-The normal laboratory range:

following

factors

were

all within the

Leucocyte count was 12.6x 109/1 (neutrophils 58%, lymphocytes 40, monocytes 2%), plasma viscosity 1-31. 1. 2.

Steptoe, P. C., Edwards, R. G. Lancet, Aug. 12, 1978, p. 366. Parkin, J. M., et al. Archs Dis. Childh 1976, 51, 259.

Biochemistry Department, Infirmary,

Western

Glasgow

G11 6NT

1. Beal, S. Lancer, 1978, i, 1257. 2. National Center for Health Statistics,

D. B.

1970, Series 21, No. 19,18. 3. Schack, J. A., Waxler, S. H.J. Pharmacol. exp. Ther. 1949, 97, 283 4. Jatlow, P. Clin. Chem. 1975, 21, 1518.

JACK