503 ANTIPYRINE FOR PROPHYLAXIS OF NEONATAL JAUNDICE
HUNTER AND VENEREAL DISEASE a celebrated experiand syphilis gonorrhoea, has lately been challenged. Qvist’ and Dempsterpoint out that the passage in the first edition of Hunter’s A Treatise on the Venereal Disease where this experiment is described is given in the third person, and they argue that there are also other reasons for believing that the experiment was done on a patient. Livesley and Pentelow3 suggest that the patient was Everard Home and that Home destroyed Hunter’s manuscripts to remove all evidence relating to the identity of the patient.
SIR,-The notion that John Hunter, in
SIR,-Dr Lewis and Mr Friedman (Feb. 10, p. 300) found that antipyrine (phenazone) given two weeks before delivery reduced the incidence of neonatal hyperbilirubinasmia, but is it seriously suggested that all pregnant women should take antipyrine or ’Welldorm’ (dichloralphenazone) before the delivery date (always somewhat uncertain) for the sake of the 4% of babies who have significant and perhaps serious hyperbilirubinxmia? Obstetricians have, for over a decade, seen not only increasing diagnosis and recognition of physiological jaundice but also considerable maternal anxiety because jaundice is now the commonest condition which prevents early discharge of mother and baby from maternity units. Prolonged observation-and that is often the only treatment-is not associated with any difference in the outcome for the baby. Surely what is required is for the neonatal specialist, in conjunction with his obstetric colleague, to use his clinical acumen rather than rely on the total bilirubin level before deciding which few babies require intensive investigation, treatment, and prolonged hospital stay. The obstetrician, when consulted, can not only often alert the pxdiatrician about those babies that are likely to have neonatal jaundice but also warn him of the recently delivered mother’s particular fears
ment, infected himself with both
Dempster traces the source of the traditional belief about the subject of this experiment to a note by G. G. Babington in his edition of The Surgical Works of John Hunter (1835, vol. 11, p. 146) but says there is no evidence to support this
and anxieties. New Cross
Hospital,
Wolverhampton
ALAN M. SMITH
NO MATERNAL EFFECT IN CHILDHOOD LEUKÆMIA WITH NEUROFIBROMATOSIS
SIR,-Miller and Hall’ have reported that neurofibromatosis in children was more severe when the mother transmitted the autosomal dominant gene than when the father did or when the condition developed as a spontaneous mutation. Kantor and Eldridge2 confirmed a similar adverse maternal effect in patients with central neurofibromatosis (acoustic neuroma). Maternal effects of the gene on the intrauterine environment were thought to mediate these findings. To test this concept further we examined lineal transmission of neurofibromatosis in children who had the non-lymphoblastic form of leukxmia, which is unusually prevalent in this disorder.3 Family histories in 22 patients revealed maternal transmission in 13, paternal in 5, and spontaneous mutation in 4. Clearly maternal transmission was more frequent than paternal. The excess was, however, not significantly greater than the expected 182:1 maternal: paternal transmission ratio, derived from the observed higher fertility-rate among affected females than males’·4 (P=0.34, one-sided exact binomial test). Thus, although maternal (?intrauterine) factors apparently exacerbate non-htmatological manifestations of neurofibromatosis, different factors probably enhance the induction of non-lymphoblastic leukemia. Rhabdomyosarcoma5 and, perhaps, Wilms’ tumour6.7 are also unusually prevalent with neurofibromatosis, but too few family histories are yet available to test for a maternal effect on their genesis. Curiously, these three tumours, unlike neurofibromatosis itself, are not known to be derived from the neural crest. Clinical Epidemiology Branch, National Cancer Institute, Bethesda,Maryland 20014, U.S.A 1.
JUDITH L. BADER ROBERT W. MILLER
Part of Brooks’ manuscript copy of Hunter’s lectures.
claim. Recently the Edward G. Miner Library of the University of Rochester School of Medicine and Dentistry acquired a volume of manuscript notes on Hunter’s lectures on venereal disease which does lend support to this claim. On p. 5 of this manuscript Hunter is quoted as saying: "It has often been disputed whether the matter of a chancre and or whether they are the same. But as gonorrhoea essentially differ I have produced in myself a chancre by matter from a gonorrhoea that point is now settled. I am led to conclude that there is no difference -
This manuscript was acquired at an auction in together with a volume of notes in the same hand
New York the lectures of Lowder on midwifery. The notes were made by I. (or J.) Brooks sometime after 1800. The watermark in the paper contains the names "Portal" and "Bridges," and the partnership of these two papermakers seems to have been formed shortly after 1800.4,5 Since Hunter died in 1793 this manuscript must have been copied from an earlier exemplar. on
The notes, which seem to be a verbatim transcript of Hunter’s lectures, follow roughly the order of presentation of Hunter A Treatise on the Venereal Disease, but they are not merely an abridgement of that work. The passage quoted above occurs fairly early on in the Miner Library manuscript, in a place corresponding to the section to which Babington appended his note. Hunter’s description of the experiment itself occurs much later in the Treatise, and there is no corresponding section in the Miner Library manuscript.
Miller, M., Hall, J. G. Lancet, 1978, ii, 1071.
2. Kantor, W. R., Eldridge, R. ibid 1978, ii, 903. 3. Bader, J. L., Miller, R. W J. Pediat 1978, 93, 992. 4. Crowe, F. W., Schull, W J., Neel, J. V. Multiple Neurofibromatosis; p. 162. Springfield, Illinois, 1956. 5. McKeen, E A, Bodurtha, J., Meadows, A. T., Douglass, E. C., Mulvihill,
J. J. J. Pediat. 1978, 93, 992 6 Stay, E. J., Vawter, G Cancer, 1977, 39, 2550. 7. W alden, P. A. M., Johnson, A. G , Bagshawe, K. D. Br. med.
J. 1977, i,
813.
1. Qvist, G. Ann. R Coll. Surg. Eng. 1977, 59, 205. 2. Dempster, W. J. Lancet, 1978, i, 316. 3. Livesley, B., Pentelow, G. M. Ann. R Coll. Surg Engl. 1978, 60, 79. 4. Coleman, D. C. The British Paper Industry 1495-1860; p. 159. Oxford, 1958. 5. Shorter, A. H. Paper Mills and Paper Makers in England 1495-1800; p. 169.
Hilversum, 1957.
504
Very likely the examination of other volumes of lecture (there must have been some in the library of the Lock Hospital which closed in 1952) would shed additional light on this subject. notes
Edward G. Miner Library, University of Rochester Medical Center Rochester, N.Y. 14642, U. S. A.
PHILIP J.
Department of Pathology, University of Rochester Medical Center
GOETZ W. RICHTER
WEIMERSKIRCH
COMPUTERISED TOMOGRAPHY AND SUBDURAL HÆMATOMAS
SIR,-Acute and chronic subdural hxmatomas have different clinical features, require different operations and have a very different prognosis. Their computerised tomographic (c.T.) scan appearances are also very different, and this is another reason why they should not be confused. Unfortunately, Dr Garcia-Bunuel (Jan. 13, p. 110) fails to make this distinction when he refers to the possibility of a subdural hsematoma being present in a patient with a negative c.T. scan. This certainly may happen in a patient with a chronic subdural hxmatoma, and the papers he cites as illustrating this problem either refer to chronic subdural haematomas or give no information about the stage after injury at which the patients were studied.’-3 In acute traumatic intracranial hxmatoma, weand others4·6 have found that c.T. scanning is very reliable and, provided that ventricular shift is taken into account, there are no false negatives. If a recently head-injured patient has a normal c.T. scan, exploratory burr holes or angiography are therefore unnecessary. If, however, the patient’s condition subsequently changes, the scan should be repeated because occasionally a new lesion will appear.’7 Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF
SAMUEL GALBRAITH SAMUEL GALBRAIT GRAHAM TEASDALE
FAMILIAL BRAIN TUMOUR
SIR, The significance of genetic factors in the pathogenesis of gliomatous brain tumours remains controversial. Several writers have urged that all cases of brain tumours of this type showing familial incidence should be analysed closely and published to provide a clearer picture of the genetic, environmental, demographic, and clinical features and so help identify risk groups. While
Swedish coastal island we found six confirmed cases of primary cerebral tumour (three men and three women) and one suspected case of a similar tumour (a man). The figure shows the familial relationships. It was possible to demonstrate consanguinity between the parents in only one of the brain-tumour patients, but in every case the families of both parents can be traced back at least to the 18th century in the same very isolated country district. The six confirmed brain-tumour cases were diagnosed when the patients were 26, 35, 36, 39, 42, and 57 years of age. In the youngest patient the tumour was discovered at necropsy after her death from eclampsia at the time of delivery. We do not know whether the tumour had caused any symptoms before this. In four cases the tumour was situated in the left
studying
a
family
Partial family tree. Full-shaded symbols=brain tumour; half-shaded symbol=suspected brain tumour. Only brain-tumour cases and healthy intermediate forebears are shown.
frontal lobe, in one case it was in the right frontal lobe and in the remaining case (the above-mentioned woman) in the left temporal lobe. In the three cases examined histologically the diagnosis was astrocytoma. The man with suspected brain tumour was not operated upon and there was no post-mortem examination of the central nervous system. He became ill at the age of 42 and carotid angiography then showed evidence of a left-sided temporal space-occupying lesion with scanty vascularisation. Because a second angiogram two months later showed considerable regression, no surgical exploration was undertaken. He subsequently had occasional epileptic seizures and attacks with obscure neurological symptoms. He was found dead in his home 12 years after the onset of symptoms; the cause of death was given as myocardial infarction. We found a high proportion of the other members of the family who have had epilepsy and other attacks of obscure nature, and several members of the family with pathological electroencephalograms, in some cases with focal signs. Sometimes brain tumour was suspected and neuroradiological investigation was undertaken but there were no positive findings. Some members of the family areunder hospital care for mental disorder, among other things cyclid psychosis and temporal-lobe psychosis. One of the brain-tumour patients had been admitted to hospital on a couple of occasions for depression and it was through this case that our interest in the family was aroused. A
more
on a
detailed report is in
Research Centre University of Göteborg,
Psychiatric
St. Jörgen’s Hospital, S-422 03 Hisings Backa, Sweden
preparation. INGA THUWE BENGT LUNDSTRÖM
JAN WÅLINDER
SMOKING IN DIABETICS
SIR,-Cigarette smoking in diabetics may contribute to the development of proliferative retinopathyl and nephropathy.2
Smoking3 and diabetes mellitus4 are also risk factors for cardiovascular disease. However, information on the smoking habits of diabetics is limited and conflicting.s-’ We have exam1.
Paetkau, M. E., Boyd, T. A. S., Winship, B., Grace, M. Diabetes, 1977, 26, 46.
1 Kim, K. S., Hemmati, M., Weinberg, P. E. Radiology, 1978, 128, 71. 2 Dublin, A B , French, B M., Rennick, J. M ibid. 1977, 122, 365. 3 Forbes, G. S., Sheedy, P. F., Piepgrass, D G., Houser, O. W. ibid.
2.
1978,
126, 143. 4. Galbraith, S., Teasdale, G., Blaiklock, C. Br. med. J. 1976, ii, 1371. 5. Ambrose, J., Gooding, M. R., Uttley, D. Lancet, 1976, i, 847 6 Svendson, P. Br J. Radiol. 1976, 49, 1004. 7 Snoek, J., Jennett, B., Adams, H., Graham, D. I., Doyle, D. J. Neurol. Neurosurg. Psychiat. (in the press).
Christiansen, J. S., Nerup, J. Lancet, 1978, i, 605. 3. Royal College of Physicians of London. Smoking and Health Now. London, Pitman, 1971 4. Jarrett, R. J., Keen, H. in Complications of Diabetes (edited by H. Keen and J. Jarrett); chap. 5. London, 1975. 5. Nilsén, R., Persson, G. Lancet, 1972, i, 1283. 6. Reid, D. D., Brett, G. Z., Hamilton, P. J. S., Jarrett, R. J., Keen, H, Rose, G. A. ibid. 1974, i, 469. 7. Czyzyk, A., Królewski, A. S. Diabetes, 1976, 25, 717.
HUNTER AND VENEREAL DISEASE a celebrated experiand syphilis gonorrhoea, has lately been challenged. Qvist’ and Dempsterpoint out that the passage in the first edition of Hunter’s A Treatise on the Venereal Disease where this experiment is described is given in the third person, and they argue that there are also other reasons for believing that the experiment was done on a patient. Livesley and Pentelow3 suggest that the patient was Everard Home and that Home destroyed Hunter’s manuscripts to remove all evidence relating to the identity of the patient.
SIR,-The notion that John Hunter, in
SIR,-Dr Lewis and Mr Friedman (Feb. 10, p. 300) found that antipyrine (phenazone) given two weeks before delivery reduced the incidence of neonatal hyperbilirubinasmia, but is it seriously suggested that all pregnant women should take antipyrine or ’Welldorm’ (dichloralphenazone) before the delivery date (always somewhat uncertain) for the sake of the 4% of babies who have significant and perhaps serious hyperbilirubinxmia? Obstetricians have, for over a decade, seen not only increasing diagnosis and recognition of physiological jaundice but also considerable maternal anxiety because jaundice is now the commonest condition which prevents early discharge of mother and baby from maternity units. Prolonged observation-and that is often the only treatment-is not associated with any difference in the outcome for the baby. Surely what is required is for the neonatal specialist, in conjunction with his obstetric colleague, to use his clinical acumen rather than rely on the total bilirubin level before deciding which few babies require intensive investigation, treatment, and prolonged hospital stay. The obstetrician, when consulted, can not only often alert the pxdiatrician about those babies that are likely to have neonatal jaundice but also warn him of the recently delivered mother’s particular fears
ment, infected himself with both
Dempster traces the source of the traditional belief about the subject of this experiment to a note by G. G. Babington in his edition of The Surgical Works of John Hunter (1835, vol. 11, p. 146) but says there is no evidence to support this
and anxieties. New Cross
Hospital,
Wolverhampton
ALAN M. SMITH
NO MATERNAL EFFECT IN CHILDHOOD LEUKÆMIA WITH NEUROFIBROMATOSIS
SIR,-Miller and Hall’ have reported that neurofibromatosis in children was more severe when the mother transmitted the autosomal dominant gene than when the father did or when the condition developed as a spontaneous mutation. Kantor and Eldridge2 confirmed a similar adverse maternal effect in patients with central neurofibromatosis (acoustic neuroma). Maternal effects of the gene on the intrauterine environment were thought to mediate these findings. To test this concept further we examined lineal transmission of neurofibromatosis in children who had the non-lymphoblastic form of leukxmia, which is unusually prevalent in this disorder.3 Family histories in 22 patients revealed maternal transmission in 13, paternal in 5, and spontaneous mutation in 4. Clearly maternal transmission was more frequent than paternal. The excess was, however, not significantly greater than the expected 182:1 maternal: paternal transmission ratio, derived from the observed higher fertility-rate among affected females than males’·4 (P=0.34, one-sided exact binomial test). Thus, although maternal (?intrauterine) factors apparently exacerbate non-htmatological manifestations of neurofibromatosis, different factors probably enhance the induction of non-lymphoblastic leukemia. Rhabdomyosarcoma5 and, perhaps, Wilms’ tumour6.7 are also unusually prevalent with neurofibromatosis, but too few family histories are yet available to test for a maternal effect on their genesis. Curiously, these three tumours, unlike neurofibromatosis itself, are not known to be derived from the neural crest. Clinical Epidemiology Branch, National Cancer Institute, Bethesda,Maryland 20014, U.S.A 1.
JUDITH L. BADER ROBERT W. MILLER
Part of Brooks’ manuscript copy of Hunter’s lectures.
claim. Recently the Edward G. Miner Library of the University of Rochester School of Medicine and Dentistry acquired a volume of manuscript notes on Hunter’s lectures on venereal disease which does lend support to this claim. On p. 5 of this manuscript Hunter is quoted as saying: "It has often been disputed whether the matter of a chancre and or whether they are the same. But as gonorrhoea essentially differ I have produced in myself a chancre by matter from a gonorrhoea that point is now settled. I am led to conclude that there is no difference -
This manuscript was acquired at an auction in together with a volume of notes in the same hand
New York the lectures of Lowder on midwifery. The notes were made by I. (or J.) Brooks sometime after 1800. The watermark in the paper contains the names "Portal" and "Bridges," and the partnership of these two papermakers seems to have been formed shortly after 1800.4,5 Since Hunter died in 1793 this manuscript must have been copied from an earlier exemplar. on
The notes, which seem to be a verbatim transcript of Hunter’s lectures, follow roughly the order of presentation of Hunter A Treatise on the Venereal Disease, but they are not merely an abridgement of that work. The passage quoted above occurs fairly early on in the Miner Library manuscript, in a place corresponding to the section to which Babington appended his note. Hunter’s description of the experiment itself occurs much later in the Treatise, and there is no corresponding section in the Miner Library manuscript.
Miller, M., Hall, J. G. Lancet, 1978, ii, 1071.
2. Kantor, W. R., Eldridge, R. ibid 1978, ii, 903. 3. Bader, J. L., Miller, R. W J. Pediat 1978, 93, 992. 4. Crowe, F. W., Schull, W J., Neel, J. V. Multiple Neurofibromatosis; p. 162. Springfield, Illinois, 1956. 5. McKeen, E A, Bodurtha, J., Meadows, A. T., Douglass, E. C., Mulvihill,
J. J. J. Pediat. 1978, 93, 992 6 Stay, E. J., Vawter, G Cancer, 1977, 39, 2550. 7. W alden, P. A. M., Johnson, A. G , Bagshawe, K. D. Br. med.
J. 1977, i,
813.
1. Qvist, G. Ann. R Coll. Surg. Eng. 1977, 59, 205. 2. Dempster, W. J. Lancet, 1978, i, 316. 3. Livesley, B., Pentelow, G. M. Ann. R Coll. Surg Engl. 1978, 60, 79. 4. Coleman, D. C. The British Paper Industry 1495-1860; p. 159. Oxford, 1958. 5. Shorter, A. H. Paper Mills and Paper Makers in England 1495-1800; p. 169.
Hilversum, 1957.
504
Very likely the examination of other volumes of lecture (there must have been some in the library of the Lock Hospital which closed in 1952) would shed additional light on this subject. notes
Edward G. Miner Library, University of Rochester Medical Center Rochester, N.Y. 14642, U. S. A.
PHILIP J.
Department of Pathology, University of Rochester Medical Center
GOETZ W. RICHTER
WEIMERSKIRCH
COMPUTERISED TOMOGRAPHY AND SUBDURAL HÆMATOMAS
SIR,-Acute and chronic subdural hxmatomas have different clinical features, require different operations and have a very different prognosis. Their computerised tomographic (c.T.) scan appearances are also very different, and this is another reason why they should not be confused. Unfortunately, Dr Garcia-Bunuel (Jan. 13, p. 110) fails to make this distinction when he refers to the possibility of a subdural hsematoma being present in a patient with a negative c.T. scan. This certainly may happen in a patient with a chronic subdural hxmatoma, and the papers he cites as illustrating this problem either refer to chronic subdural haematomas or give no information about the stage after injury at which the patients were studied.’-3 In acute traumatic intracranial hxmatoma, weand others4·6 have found that c.T. scanning is very reliable and, provided that ventricular shift is taken into account, there are no false negatives. If a recently head-injured patient has a normal c.T. scan, exploratory burr holes or angiography are therefore unnecessary. If, however, the patient’s condition subsequently changes, the scan should be repeated because occasionally a new lesion will appear.’7 Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4TF
SAMUEL GALBRAITH SAMUEL GALBRAIT GRAHAM TEASDALE
FAMILIAL BRAIN TUMOUR
SIR, The significance of genetic factors in the pathogenesis of gliomatous brain tumours remains controversial. Several writers have urged that all cases of brain tumours of this type showing familial incidence should be analysed closely and published to provide a clearer picture of the genetic, environmental, demographic, and clinical features and so help identify risk groups. While
Swedish coastal island we found six confirmed cases of primary cerebral tumour (three men and three women) and one suspected case of a similar tumour (a man). The figure shows the familial relationships. It was possible to demonstrate consanguinity between the parents in only one of the brain-tumour patients, but in every case the families of both parents can be traced back at least to the 18th century in the same very isolated country district. The six confirmed brain-tumour cases were diagnosed when the patients were 26, 35, 36, 39, 42, and 57 years of age. In the youngest patient the tumour was discovered at necropsy after her death from eclampsia at the time of delivery. We do not know whether the tumour had caused any symptoms before this. In four cases the tumour was situated in the left
studying
a
family
Partial family tree. Full-shaded symbols=brain tumour; half-shaded symbol=suspected brain tumour. Only brain-tumour cases and healthy intermediate forebears are shown.
frontal lobe, in one case it was in the right frontal lobe and in the remaining case (the above-mentioned woman) in the left temporal lobe. In the three cases examined histologically the diagnosis was astrocytoma. The man with suspected brain tumour was not operated upon and there was no post-mortem examination of the central nervous system. He became ill at the age of 42 and carotid angiography then showed evidence of a left-sided temporal space-occupying lesion with scanty vascularisation. Because a second angiogram two months later showed considerable regression, no surgical exploration was undertaken. He subsequently had occasional epileptic seizures and attacks with obscure neurological symptoms. He was found dead in his home 12 years after the onset of symptoms; the cause of death was given as myocardial infarction. We found a high proportion of the other members of the family who have had epilepsy and other attacks of obscure nature, and several members of the family with pathological electroencephalograms, in some cases with focal signs. Sometimes brain tumour was suspected and neuroradiological investigation was undertaken but there were no positive findings. Some members of the family areunder hospital care for mental disorder, among other things cyclid psychosis and temporal-lobe psychosis. One of the brain-tumour patients had been admitted to hospital on a couple of occasions for depression and it was through this case that our interest in the family was aroused. A
more
on a
detailed report is in
Research Centre University of Göteborg,
Psychiatric
St. Jörgen’s Hospital, S-422 03 Hisings Backa, Sweden
preparation. INGA THUWE BENGT LUNDSTRÖM
JAN WÅLINDER
SMOKING IN DIABETICS
SIR,-Cigarette smoking in diabetics may contribute to the development of proliferative retinopathyl and nephropathy.2
Smoking3 and diabetes mellitus4 are also risk factors for cardiovascular disease. However, information on the smoking habits of diabetics is limited and conflicting.s-’ We have exam1.
Paetkau, M. E., Boyd, T. A. S., Winship, B., Grace, M. Diabetes, 1977, 26, 46.
1 Kim, K. S., Hemmati, M., Weinberg, P. E. Radiology, 1978, 128, 71. 2 Dublin, A B , French, B M., Rennick, J. M ibid. 1977, 122, 365. 3 Forbes, G. S., Sheedy, P. F., Piepgrass, D G., Houser, O. W. ibid.
2.
1978,
126, 143. 4. Galbraith, S., Teasdale, G., Blaiklock, C. Br. med. J. 1976, ii, 1371. 5. Ambrose, J., Gooding, M. R., Uttley, D. Lancet, 1976, i, 847 6 Svendson, P. Br J. Radiol. 1976, 49, 1004. 7 Snoek, J., Jennett, B., Adams, H., Graham, D. I., Doyle, D. J. Neurol. Neurosurg. Psychiat. (in the press).
Christiansen, J. S., Nerup, J. Lancet, 1978, i, 605. 3. Royal College of Physicians of London. Smoking and Health Now. London, Pitman, 1971 4. Jarrett, R. J., Keen, H. in Complications of Diabetes (edited by H. Keen and J. Jarrett); chap. 5. London, 1975. 5. Nilsén, R., Persson, G. Lancet, 1972, i, 1283. 6. Reid, D. D., Brett, G. Z., Hamilton, P. J. S., Jarrett, R. J., Keen, H, Rose, G. A. ibid. 1974, i, 469. 7. Czyzyk, A., Królewski, A. S. Diabetes, 1976, 25, 717.
