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GENETICS OF ANENCEPHALY AND SPINA BIFIDA
697
part energy absorbed in overcoming viscosity, and in part energy absorption by the syrinx. This may be the most elegant method of proving any hypothesis to explain the source of the energy that both Dr. Gardner and myself agree comes through the communication and damages the cord. I cannot agree with all Dr. Gardner’s observations made during screening in the course of myodil examinations of the C.N.S. I agree that commonly the first movement after straining or coughing is cephalad. This is probably due to the distension of epidural veins. But the greater part of the movement is nevertheless usually caudad. Also, in a particularly violent Valsalva’s manoeuvre, for example in vomiting, myodil in the cervical region and the bottom part of the fourth ventricle may be displaced violently and immediately caudad. Myodil in the aqueduct may initially move upwards and then a split second later reverse caudally through the fourth ventricle to shoot into the neck with great speed. I interpret such observations as meaning that a wave of ballistic intensity hits the jugular bulb in the posterior fossa displacing fluid initially both upwards and downwards. As the wave passes supratentorially the fluid is forced downwards once again carrying the myodil with it. These observations are difficult to make and are past in a fraction of a second. We do not have a videotape recording of any such thing, and I may be guilty of observer error due to prejudice. Readers will be able to make their own observations and draw their own conclusions. I should like to mention another piece of evidence in favour of the venous hypothesis, and that is that occasionally the onset of symptoms in communicating syringomyelia is precipitated by an acute venous distension. Eric Turner and I are at present preparing a report on one such case. Lastly I should like to stress that I intend no disrespect to Dr. Gardner in the views I express. I do so only because I find as Luther said, " Ich kann nicht anders ". Department of Neurosurgery, Oueen Elizabeth Hospital, Birmingham.
BERNARD WILLIAMS.
FLUORIDE SiR,ŅThe paragraph in Professor Jenkins’ letter (Sept. 6, p. 542) points to the tottering and inadequate background to the water-fluoridation proposals. It is true the Ministry of Health advanced studies to refute possible reported hazards from increased fluoride intake 1; but why did the Ministry do that rather than carry out the normal procedure that guides those permitting additions to food ? The Law, of course, does not include water in its food regulations, but these regulations are a means by which the public has protection. Surely the Ministry of Health officials were showing a fine disregard for proper conduct in launching water-fluoridation proposals without the assessments which precede additions of toxic agents to food. Further, the Ministry of Health failed to state whether the minimum chronic toxic level of fluoride has been determined, and if so what it is; nor has it shown any serious inquiry into fluoride intake from food. The study supporting the calculations of fluoride intake from food1 was conducted on the dry diet of 22 old folks in eventide homes. It is of little consequence that the Ministry of Health found no excessive osteochondritis in a group of boys between the ages of 11 and 14 in high-fluoride areas.2It is, however, of considerable consequence that the Ministry of Health failed to demonstrate that there is the margin of last
1. 2.
Rep. publ. Hlth med. Subj. 1962, no. 105. Eley, A. J., Kemp, F. H., Kerby, P. J., Berry, W. T. Lancet, 1957, ii, 712.
water fluoridation that the Ministry of Agriculture has laid down for any additive to food. The pressures being exerted in the cause of water’r fluoridation would be better directed towards initiating practical dental-health programmes in schools, using the Swedish fluoride-mouthrinsing scheme which shows results on a par with those claimed for water fluoridation in this country. Linlithgow, MEG DOUGAL. Scotland.
safety with
GENETICS OF ANENCEPHALY AND SPINA BIFIDA SIR,-We must apologise for an oversight in the section of our article1 last year which dealt with the frequency of anencephaly and spina bifida in twins. In assembling the published series we overlooked the data reported by Gittelson and Milham as part of a general survey of congenital malformations in New York State.2 The oversight is particularly unfortunate in that the New York State data are at variance with those from the 8 series we did locate. The 8 series yielded 108 sets of twins with one affected member and none with both affected. The New York series includes 86 affected sets in 10 of which both members were affected. It is difficult to reconcile these 2 sets of observations-certainly the difference seems unlikely to be due to chance (p < 0-001)but our conclusion as to the rarity of concordance in affected twin sets must obviously be treated with caution in the light of the New York series. The New York series also suggests a somewhat higher concordance-rate in likesexed (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 series and the series we assembled emphasises the need for more large representative series of affected twins to elucidate the role of genetic and environmental factors in these anomalies. In apologising for overlooking Dr. Gittelson’s article, we can only note that, being published as part of the proceedings of a conference, it was not indexed by Index Medicus. Department of Epidemiology, STELLA YEN Harvard School of Public Health, BRIAN MACMAHON. Boston, Massachusetts.
CATECHOLAMINE HYPERPNŒA
SIR,-May I reply briefly to the letter by Professor Peart and his colleagues (Sept. 13, p. 595) ? My remarks were in no way intended to question the numerous accounts of hyperpnoea induced by intravenous catecholamines in man. Indeed, the similarity between catecholamine hyperpnoea in man and animals is emphasised in the paperto which I referred in my original letter. I was merely interested to establish whether Professor Peart and his colleagues had failed to observe adrenaline hyperpnoea in their most recent investigations, in view of the fact that they only specifically mentioned that they noted noradrenaline hyperpnoea. Their prime interest was, of course, a study of flushing rather than hyperpnoea. The conditions under which catecholamine hyperpncea is obtained are of great interest in view of the confusing evidence we have about the mechanism of the response both in the human subject and in animals. It was this that prompted me to express a note of caution in accepting that 1. 2.
Yen, S., MacMahon, B. Lancet, 1968, ii, 623. Gittelson, A. M., Milham, S. Publ. Hlth Serv. Pubis, Wash. 1965, no.
3. Joels,
1163.
N., White, H. J. Physiol., Lond. 1968, 197,
1.
part energy absorbed in overcoming viscosity, and in part energy absorption by the syrinx. This may be the most elegant method of proving any hypothesis to explain the source of the energy that both Dr. Gardner and myself agree comes through the communication and damages the cord. I cannot agree with all Dr. Gardner’s observations made during screening in the course of myodil examinations of the C.N.S. I agree that commonly the first movement after straining or coughing is cephalad. This is probably due to the distension of epidural veins. But the greater part of the movement is nevertheless usually caudad. Also, in a particularly violent Valsalva’s manoeuvre, for example in vomiting, myodil in the cervical region and the bottom part of the fourth ventricle may be displaced violently and immediately caudad. Myodil in the aqueduct may initially move upwards and then a split second later reverse caudally through the fourth ventricle to shoot into the neck with great speed. I interpret such observations as meaning that a wave of ballistic intensity hits the jugular bulb in the posterior fossa displacing fluid initially both upwards and downwards. As the wave passes supratentorially the fluid is forced downwards once again carrying the myodil with it. These observations are difficult to make and are past in a fraction of a second. We do not have a videotape recording of any such thing, and I may be guilty of observer error due to prejudice. Readers will be able to make their own observations and draw their own conclusions. I should like to mention another piece of evidence in favour of the venous hypothesis, and that is that occasionally the onset of symptoms in communicating syringomyelia is precipitated by an acute venous distension. Eric Turner and I are at present preparing a report on one such case. Lastly I should like to stress that I intend no disrespect to Dr. Gardner in the views I express. I do so only because I find as Luther said, " Ich kann nicht anders ". Department of Neurosurgery, Oueen Elizabeth Hospital, Birmingham.
BERNARD WILLIAMS.
FLUORIDE SiR,ŅThe paragraph in Professor Jenkins’ letter (Sept. 6, p. 542) points to the tottering and inadequate background to the water-fluoridation proposals. It is true the Ministry of Health advanced studies to refute possible reported hazards from increased fluoride intake 1; but why did the Ministry do that rather than carry out the normal procedure that guides those permitting additions to food ? The Law, of course, does not include water in its food regulations, but these regulations are a means by which the public has protection. Surely the Ministry of Health officials were showing a fine disregard for proper conduct in launching water-fluoridation proposals without the assessments which precede additions of toxic agents to food. Further, the Ministry of Health failed to state whether the minimum chronic toxic level of fluoride has been determined, and if so what it is; nor has it shown any serious inquiry into fluoride intake from food. The study supporting the calculations of fluoride intake from food1 was conducted on the dry diet of 22 old folks in eventide homes. It is of little consequence that the Ministry of Health found no excessive osteochondritis in a group of boys between the ages of 11 and 14 in high-fluoride areas.2It is, however, of considerable consequence that the Ministry of Health failed to demonstrate that there is the margin of last
1. 2.
Rep. publ. Hlth med. Subj. 1962, no. 105. Eley, A. J., Kemp, F. H., Kerby, P. J., Berry, W. T. Lancet, 1957, ii, 712.
water fluoridation that the Ministry of Agriculture has laid down for any additive to food. The pressures being exerted in the cause of water’r fluoridation would be better directed towards initiating practical dental-health programmes in schools, using the Swedish fluoride-mouthrinsing scheme which shows results on a par with those claimed for water fluoridation in this country. Linlithgow, MEG DOUGAL. Scotland.
safety with
GENETICS OF ANENCEPHALY AND SPINA BIFIDA SIR,-We must apologise for an oversight in the section of our article1 last year which dealt with the frequency of anencephaly and spina bifida in twins. In assembling the published series we overlooked the data reported by Gittelson and Milham as part of a general survey of congenital malformations in New York State.2 The oversight is particularly unfortunate in that the New York State data are at variance with those from the 8 series we did locate. The 8 series yielded 108 sets of twins with one affected member and none with both affected. The New York series includes 86 affected sets in 10 of which both members were affected. It is difficult to reconcile these 2 sets of observations-certainly the difference seems unlikely to be due to chance (p < 0-001)but our conclusion as to the rarity of concordance in affected twin sets must obviously be treated with caution in the light of the New York series. The New York series also suggests a somewhat higher concordance-rate in likesexed (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 series and the series we assembled emphasises the need for more large representative series of affected twins to elucidate the role of genetic and environmental factors in these anomalies. In apologising for overlooking Dr. Gittelson’s article, we can only note that, being published as part of the proceedings of a conference, it was not indexed by Index Medicus. Department of Epidemiology, STELLA YEN Harvard School of Public Health, BRIAN MACMAHON. Boston, Massachusetts.
CATECHOLAMINE HYPERPNŒA
SIR,-May I reply briefly to the letter by Professor Peart and his colleagues (Sept. 13, p. 595) ? My remarks were in no way intended to question the numerous accounts of hyperpnoea induced by intravenous catecholamines in man. Indeed, the similarity between catecholamine hyperpnoea in man and animals is emphasised in the paperto which I referred in my original letter. I was merely interested to establish whether Professor Peart and his colleagues had failed to observe adrenaline hyperpnoea in their most recent investigations, in view of the fact that they only specifically mentioned that they noted noradrenaline hyperpnoea. Their prime interest was, of course, a study of flushing rather than hyperpnoea. The conditions under which catecholamine hyperpncea is obtained are of great interest in view of the confusing evidence we have about the mechanism of the response both in the human subject and in animals. It was this that prompted me to express a note of caution in accepting that 1. 2.
Yen, S., MacMahon, B. Lancet, 1968, ii, 623. Gittelson, A. M., Milham, S. Publ. Hlth Serv. Pubis, Wash. 1965, no.
3. Joels,
1163.
N., White, H. J. Physiol., Lond. 1968, 197,
1.