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COMPUTERISED TOMOGRAPHY AND SUBDURAL HÆMATOMAS
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.
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.