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causing the hemianopia to a point higher in the visualprocess than the calcarine cortex-i.e., the parastriatecortex of the left hemisphere. Angiography and surgeryconfirmed this. A superficial arteriovenous malformation(2 x 2 cm.) with a small (10 ml.) haematoma was removedfrom the convexity of the left inferior parietal lobe. Visionreturned and alexia cleared promptly. The late waves ofthe flash-evoked potential recorded from the involvedside were now present.From recordings of flash-evoked potentials it is possible,

for the first time, to differentiate between suprastriate andinfrastriate types of hemianopia.

Neuro-ophthalmology Unit,Department of Neurosurgery,

University of CaliforniaMedical Center,

San Francisco, California 94143, U.S.A.

MOSHE FEINSODWILLIAM F. HOYTW. BRUCE WILSON.

EFFECT OF PROSTAGLANDIN E2 THERAPY ONTHE CEREBRAL CORTEX

SIR,-Lyneham et al. reported epileptic seizures andatypical electroencephalograms (E.E.G.S) in patients abortedby intra-amniotic instillation of prostaglandin (P.G.) F2a.lWe (Feb. 9, p. 218) and other workers 2,3 have since com-mented upon the absence of convulsions among patientshaving termination of pregnancy or induction of labourwith prostaglandins. Since p.G.E2 is also being used fortherapeutic purposes, we investigated the effect of thisdrug on the E.E.G. So far, nine subjects have been studied.

Five women undergoing termination of pregnancy withP.G.E2 had an E.E.G. taken 20 hours before and 4 hoursafter the start of therapy (additional E.E.G.S were taken incase 4). Gestational age, indication for the interruption ofpregnancy, route of administration, and dosage are listedin the accompanying table. None of the patients was aknown epileptic and none took anticonvulsants. Sedatives,anti-inflammatory agents, and analgesics were withhelduntil after the second E.E.G. had been recorded. Informedconsent had been obtained in all cases.

All E.E.G.S were recorded on the same 16-channel ElemaSchonander apparatus, under the usual conditions, includ-ing hyperventilation and stroboscopy. The tracings werenormal, both before and after administration of p.G.E2, inall patients except patient 4.

Case 4.-This 29-year-old woman (gravida 3, para 2) wasadmitted at 23 weeks’ gestation with fetal death of unknowncause. Her medical history was not relevant and there had beenneither hypertension nor proteinuria during this pregnancy. Acontrol B.B.G., taken before instillation of P.G., showed slowactivity with diffusely located sharp waves, which were morepronounced during overbreathing. The slow waves were

slightly more pronounced in the right temporal area. These

changes were accentuated on the second tracing, tecorded 4 hours

1. Lyneham, R. C., Law, P. A., McLeod, J. G., Shearman, R. P.,Smith, I. D., Korda, A. R. Lancet, 1973, ii, 1003.

2. MacKenzie, I. Z., Hillier, K., Embrey, M. P. ibid. p. 1323.3. Craft, I. ibid. p. 1389.

EFFECT OF P.G.E, ON THE E.E.G. PATTERN

N.S. = not significant.

after intra-amniotic injection of 3-5 mg. p.G.E2. A third E.E.G.was taken 24 hours later, when the patient had not yet abortedand was receiving p.G.E. intravenously (4 !Jog. per minute).There was further slowing of activity, with more frequent sharpwaves, especially during hyperventilation. Pregnancy was

eventually terminated by a second intra-amniotic instillation of5 mg. P.G.E,. A fourth B.E.G. taken 23 hours afterwards (12 hoursafter expulsion of fetus and placenta) showed a trend towards thereturn of the pretreatment pattern. A fifth E.E.G., 1 week afterP.G. therapy, was comparable with the control B.B.G. Duringtermination the patient’s temperature never exceeded 38°C.

Four healthy adult male volunteers had E.E.G.s recordedbefore and during intravenous administration of P.G.E2(5 jjLg. per minute). The infusion was started 30-35 minutesbefore-and was continued throughout the recording ofthe second E.E.G. All tracings were normal.

p.G.E2 does not seem to be epileptogenic when givento subjects with normal cortical activity. However,patients with a pre-existing anomaly may have to betreated cautiously.The P.G. E2 was kindly supplied by Dr J. M. Decoster (Upjohn).Departments of Neurology

and Obstetrics,State University,De Pintelaan 135,B-9000 Gent,

Belgium.

L. VAN DER PLAETSENM. THIERYJ. J. AMYD. DE HEMPTINNE.

PROSTAGLANDINS AND INDUCTIONOF LABOUR

SIR,-Professor Brosens and others (April 27, p. 808)suggested that the use of prostaglandins for induction oflabour in pregnancies complicated by hypertensive statesmight result in a high incidence of fetal distress.Our programme of prostaglandin clinical investigation

has, over the past three years, generated case-records of1044 women whose labour was induced with either p.G.E2or p.G.F2a. Among these records are reports of 283 casesin which the reason for inducing labour was either pre-eclamptic toxaemia or hypertension. The mean Apgarscores, at 1 and 5 minutes, respectively, for the infants inthis group were 8-15 and 9-42. The respective modes were9 and 10. Of the four infants with Apgars of under 5 at5 minutes, 2 had mid-cavity forceps deliveries for fetaldistress in the second stage. All infants were followed upfor at least one week after delivery and, at that time, allwere normal. It is submitted that these figures do notsuggest an abnormal incidence of fetal distress.With regard to the animal studies which Professor

Brosens and his colleagues suggested, the article byClark et al.1 is of interest. These workers infused p.G.F2ainto uterine arteries of pregnant dogs in doses between 1and 100 flog. per minute, and were unable to demonstrate anyalteration in vascular tone. It should be remembered thatthe usual recommended infusion rate of P.G.F2a for mduc-

1. Clark, K. E., Ryan, M. J., Brody, M. J. Adv. Biosci. 1972, 9, 779.