fluoride

697

part energy absorbed in overcoming viscosity, and in partenergy absorption by the syrinx. This may be the most

elegant method of proving any hypothesis to explain thesource of the energy that both Dr. Gardner and myselfagree comes through the communication and damagesthe cord.

I cannot agree with all Dr. Gardner’s observations made

during screening in the course of myodil examinations ofthe C.N.S. I agree that commonly the first movementafter straining or coughing is cephalad. This is probablydue to the distension of epidural veins. But the greaterpart of the movement is nevertheless usually caudad. Also,in a particularly violent Valsalva’s manoeuvre, for example invomiting, myodil in the cervical region and the bottompart of the fourth ventricle may be displaced violentlyand immediately caudad. Myodil in the aqueduct mayinitially move upwards and then a split second later reversecaudally through the fourth ventricle to shoot into theneck with great speed. I interpret such observations asmeaning that a wave of ballistic intensity hits the jugularbulb in the posterior fossa displacing fluid initially bothupwards and downwards. As the wave passes supraten-torially the fluid is forced downwards once again carryingthe myodil with it. These observations are difficult tomake and are past in a fraction of a second. We do nothave a videotape recording of any such thing, and I may beguilty of observer error due to prejudice. Readers will beable to make their own observations and draw their ownconclusions.

I should like to mention another piece of evidence infavour of the venous hypothesis, and that is that occa-

sionally the onset of symptoms in communicating syringo-myelia is precipitated by an acute venous distension. EricTurner and I are at present preparing a report on onesuch case. Lastly I should like to stress that I intend nodisrespect to Dr. Gardner in the views I express. I do so

only because I find as Luther said, " Ich kann nichtanders ".

BERNARD WILLIAMS.

Department of Neurosurgery,Oueen Elizabeth Hospital,

Birmingham.

FLUORIDE

MEG DOUGAL.

SiR,ŅThe last paragraph in Professor Jenkins’ letter

(Sept. 6, p. 542) points to the tottering and inadequatebackground to the water-fluoridation proposals. It is truethe Ministry of Health advanced studies to refute possiblereported hazards from increased fluoride intake 1; but whydid the Ministry do that rather than carry out the normalprocedure that guides those permitting additions to food ?The Law, of course, does not include water in its foodregulations, but these regulations are a means by which thepublic has protection. Surely the Ministry of Healthofficials were showing a fine disregard for proper conduct inlaunching water-fluoridation proposals without the assess-ments which precede additions of toxic agents to food.Further, the Ministry of Health failed to state whether theminimum chronic toxic level of fluoride has been deter-mined, and if so what it is; nor has it shown any seriousinquiry into fluoride intake from food. The study support-ing the calculations of fluoride intake from food 1 wasconducted on the dry diet of 22 old folks in eventide homes.

It is of little consequence that the Ministry of Healthfound no excessive osteochondritis in a group of boysbetween the ages of 11 and 14 in high-fluoride areas.2 It is,however, of considerable consequence that the Ministry ofHealth failed to demonstrate that there is the margin of1. Rep. publ. Hlth med. Subj. 1962, no. 105.2. Eley, A. J., Kemp, F. H., Kerby, P. J., Berry, W. T. Lancet, 1957,

ii, 712.

safety with water fluoridation that the Ministry of Agri-culture has laid down for any additive to food.The pressures being exerted in the cause of water ’r

fluoridation would be better directed towards initiatingpractical dental-health programmes in schools, using theSwedish fluoride-mouthrinsing scheme which shows resultson a par with those claimed for water fluoridation in this

country.Linlithgow,Scotland.

GENETICS OF ANENCEPHALY ANDSPINA BIFIDA

STELLA YENBRIAN MACMAHON.

Department of Epidemiology,Harvard School of Public Health,

Boston, Massachusetts.

SIR,-We must apologise for an oversight in the sectionof our article 1 last year which dealt with the frequency ofanencephaly and spina bifida in twins. In assembling thepublished series we overlooked the data reported byGittelson and Milham as part of a general survey of con-genital malformations in New York State.2The oversight is particularly unfortunate in that the

New York State data are at variance with those from the8 series we did locate. The 8 series yielded 108 sets oftwins with one affected member and none with bothaffected. The New York series includes 86 affected setsin 10 of which both members were affected. It is difficultto reconcile these 2 sets of observations-certainly thedifference seems unlikely to be due to chance (p < 0-001)-but our conclusion as to the rarity of concordance in affectedtwin sets must obviously be treated with caution in thelight of the New York series. The New York series alsosuggests a somewhat higher concordance-rate in like-sexed (8 in 55) than in unlike-sexed (2 in 31) pairs,although the difference could readily be due to chance(P.0-3). The discrepancy between the New York seriesand the series we assembled emphasises the need formore large representative series of affected twins to

elucidate the role of genetic and environmental factors inthese anomalies.

In apologising for overlooking Dr. Gittelson’s article,we can only note that, being published as part of theproceedings of a conference, it was not indexed by IndexMedicus.

CATECHOLAMINE HYPERPN&OElig;A

SIR,-May I reply briefly to the letter by Professor Peartand his colleagues (Sept. 13, p. 595) ? My remarks were inno way intended to question the numerous accounts ofhyperpnoea induced by intravenous catecholamines in man.Indeed, the similarity between catecholamine hyperpnoeain man and animals is emphasised in the paper to whichI referred in my original letter. I was merely interested toestablish whether Professor Peart and his colleagues hadfailed to observe adrenaline hyperpnoea in their mostrecent investigations, in view of the fact that they onlyspecifically mentioned that they noted noradrenalinehyperpnoea. Their prime interest was, of course, a studyof flushing rather than hyperpnoea.The conditions under which catecholamine hyperpncea is

obtained are of great interest in view of the confusingevidence we have about the mechanism of the responseboth in the human subject and in animals. It was this that

prompted me to express a note of caution in accepting that1. Yen, S., MacMahon, B. Lancet, 1968, ii, 623.2. Gittelson, A. M., Milham, S. Publ. Hlth Serv. Pubis, Wash. 1965,

no. 1163.3. Joels, N., White, H. J. Physiol., Lond. 1968, 197, 1.