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EXTRADURAL HÆMATOMA
369 are
in conflict with well-established facts. In rat-liver nuclei
only one X chromosome is heteropyknotic in the female,12 as cited by Ferguson-Smith et al,1o and in your editorial of July 23; but this is a poor argument for the hypothesis that in the normal human female Barr’s sex chromatin should be composed of only one X chromosome. In mammary and granulosa cells of the mouse both X chromosomes are undoubtedly heteropyknotic and show somatic pairing 14; moreover, the degree of allocycly in rodents is variable and the Barr phenomenon often There is direct evidence that the Barr and man is composed of two separate chromosomes.l3 15 16 This is not a technical artefact, for even in unfixed cells in tissue cultures a division of the Barr corpuscle in two distinct elements can be seen. Histological Laboratory, J. JAMES. University of Amsterdam. not
demonstrable.
corpuscle in the female of higher mammals
CHROMOSOME ANOMALIES IN "BLEB DISEASES" SIR,-Bagg and Little 17 demonstrated that the progeny of mice whose ovaries had been irradiated with X rays were liable to multiple deformities, especially of the extremities. These deformities were produced by blebs of cerebrospinal fluid escaping from the fourth ventricle through an abnormally patent area membranacea, exerting pressure in the limb buds and other points of contact, and leading to inflammatory reactions at these sites in the embryo. The malformations proved to be inheritable through an indefinite number of generations. In a previous article 18 I classified ten syndromes of malforma" as a separate group, under the name of bleb diseases ".
tion
They were: (1) dysostosis multiplex (Pfaundler-Hurler); (2) oxycephaly (Virchow); (3) acrocephalo-syndactyly (Apert); (4) dysostosis craniofacialis (Crouzon); (5) Laurence-MoonBiedl syndrome; (6) Morquio’s disease; (7) pleonosteosis familiaris (Leri); (8) mongoloid idiocy; (9) cranio-carpo-tarsal dystrophy; and (10) Turner’s syndrome. Three other syndromes were later added 19 to these ten-namely Sprengel’s deformity (undescended scapula), the Klippel-Feil syndrome, and symbrachydactylia. The reason for separating these syndromes, under the name of bleb diseases, is that they are considered to have a developmental mechanism similar to that of the deformities described in mice by Bagg and Little.l’ I do not consider the abovementioned 13 syndromes to be necessarily the only ones belonging to this group. As a matter of fact, Sir Arthur Keith,2O independently cf me, added some further malformations to it. It is of great interest now to learn that chromosome abnormalities are associated with two of these thirteen syndromes. The normal number of chromosomes in man is 46, including the sex chromosomes, XX in the female and XY in the male. In Turner’s syndrome, cells are found to have only 45 chromosomes, the Y chromosome being absent. In mongolism, there is an extra small autosome, making a total of 47. In another condition called polydysspondylism, which shows multiple bony abnormalities of the skull and spine with low intelligence and which has so far not been classified as bleb disease, again only 45 chromosomes were found. If the analogy postulated between the malformations of Bagg and Little’s mice and the bleb diseases is correct, then the chromosome defects now known to be present in some members of the bleb-disease group may throw some light on the cause of deformities of Bagg and Little’s mice. It is known that chromosomes are electively radiosensitive. Since Bagg and Little’s deformities were produced by radiation of the ovaries, it is almost certain that they were due to some chromosome damage. It would, therefore, be of great interest to investigate whether some chromosome anomalies could be detected in the progeny of Bagg and Little’s mice. Should 14. 15.
16. 17. 18. 19. 20.
Ohno, S., Kaplan, W. D., Kinosita, R. Exp. cell Res. 1959, 16, 462. Klinger, H. P. Acta anat. 1957, 30, 371. Klinger, H. P. Exp. cell Res. 1958, 14, 207. Bagg, H. J., Little, C. C. Amer. J. Anat. 1924, 33, 119. Engel, D. Amer. J. Dis. Child. 1940, 60, 562. J. Bone Jt Surg. 1943, 25, 613. Engel, D. Keith, A. Brit. J. Surg. 1940, 28, 173.
this be confirmed, the further question arises whether the chromosome damage is directly responsible for the anomalies found at the base of the fourth ventricle, and the consequent leakage of cerebrospinal fluid. It would also be of interest to examine the chromosomes in the other ten syndromes of bleb diseases. If chromosome anomalies were found in them, this would give an added support for the separation of these syndromes into a special group. In the light of such future investigations it might be necessary to omit some syndromes now included in this group (e.g., Moon-Biedl syndrome), or to include others not yet classified. It is naturally possible that chromosome damage of the germ cells may occur without injury to the central nervous system. Whether the bleb mechanism is possible without chromosomal damage, only future studies will show. Should the assumed connection between chromosomal damage and bleb mechanism prove to be correct, it will open new vistas for the study of
D. ENGEL. EXTRADURAL HÆMATOMA
SiR,ňIread with great interest the article (July 23) by Mr. McKissock. Do the clinical signs of extradural hsematoma give any indication of the exact position of the hasmatoma ? Are hasmatomas in the frontal region more insidious in onset than those in the temporal fossa ? I ask this because I saw a boy suddenly die of a frontal extradural hasmatoma 10 hours after falling out of bed. Even in retrospect the only abnormal clinical sign was slight drowsiness. Incidentally this child had no fracture of the skull
on
X-ray
or at
postmortem.
West Suffolk General Hospital, Bury St. Edmunds.
ADRIAN M. BAIN.
SHORTAGE OF RADIOGRAPHERS SIR,-I should very much like to support Dr. Osborne’s remarks of July 9 concerning the shortage of radiographers.
At his suggestion, lectures have been given in the Edmonton district in the past few months at girls’ schools, but it is too soon, yet, to assess the results of these lectures in terms of student recruits, since the age at which students can start their training is 18 years, and the age-groups so far concerned are up to 16 years. Considerable interest has been shown. In our case, the lecturer was the male superintendent-radiographer, but in every case he was accompanied by the " young, warm, and vital " in the shape of one of the young and attractive female radiographers. She talked informally to the interested girls after the lectures. In the North East Metropolitan area, a scheme has just been started where five of the board’s hospitals carry out the practical training of radiographers, the formal lectures being given, by kind permission, at The London Hospital. By this method, girls in the neighbourhood of the five principal hospitals can receive their training without too much travelling, as the lectures are completed on two days of the week. Lectures to the schools are followed in a few weeks’ time by advertisements in local papers about the joint training scheme, and so far this has produced three students who will begin their courses in September, 1961, in the Edmonton district. There are many other acceptances in the four districts. One of the great difficulties is the wait of one year from passing the necessary G.C.E. 0-level subjects, and being old enough to start the training. I am strongly of the opinion that the shortage of radiographers could be easily overcome by these methods of lecturing and local advertisement, together with a reduction in the age of entry from 18 to 17 years, with qualification at 19 instead of 20.
I suggest that some of the teaching issue their own diplomas in radiography,
hospitals might as some
of these
in conflict with well-established facts. In rat-liver nuclei
only one X chromosome is heteropyknotic in the female,12 as cited by Ferguson-Smith et al,1o and in your editorial of July 23; but this is a poor argument for the hypothesis that in the normal human female Barr’s sex chromatin should be composed of only one X chromosome. In mammary and granulosa cells of the mouse both X chromosomes are undoubtedly heteropyknotic and show somatic pairing 14; moreover, the degree of allocycly in rodents is variable and the Barr phenomenon often There is direct evidence that the Barr and man is composed of two separate chromosomes.l3 15 16 This is not a technical artefact, for even in unfixed cells in tissue cultures a division of the Barr corpuscle in two distinct elements can be seen. Histological Laboratory, J. JAMES. University of Amsterdam. not
demonstrable.
corpuscle in the female of higher mammals
CHROMOSOME ANOMALIES IN "BLEB DISEASES" SIR,-Bagg and Little 17 demonstrated that the progeny of mice whose ovaries had been irradiated with X rays were liable to multiple deformities, especially of the extremities. These deformities were produced by blebs of cerebrospinal fluid escaping from the fourth ventricle through an abnormally patent area membranacea, exerting pressure in the limb buds and other points of contact, and leading to inflammatory reactions at these sites in the embryo. The malformations proved to be inheritable through an indefinite number of generations. In a previous article 18 I classified ten syndromes of malforma" as a separate group, under the name of bleb diseases ".
tion
They were: (1) dysostosis multiplex (Pfaundler-Hurler); (2) oxycephaly (Virchow); (3) acrocephalo-syndactyly (Apert); (4) dysostosis craniofacialis (Crouzon); (5) Laurence-MoonBiedl syndrome; (6) Morquio’s disease; (7) pleonosteosis familiaris (Leri); (8) mongoloid idiocy; (9) cranio-carpo-tarsal dystrophy; and (10) Turner’s syndrome. Three other syndromes were later added 19 to these ten-namely Sprengel’s deformity (undescended scapula), the Klippel-Feil syndrome, and symbrachydactylia. The reason for separating these syndromes, under the name of bleb diseases, is that they are considered to have a developmental mechanism similar to that of the deformities described in mice by Bagg and Little.l’ I do not consider the abovementioned 13 syndromes to be necessarily the only ones belonging to this group. As a matter of fact, Sir Arthur Keith,2O independently cf me, added some further malformations to it. It is of great interest now to learn that chromosome abnormalities are associated with two of these thirteen syndromes. The normal number of chromosomes in man is 46, including the sex chromosomes, XX in the female and XY in the male. In Turner’s syndrome, cells are found to have only 45 chromosomes, the Y chromosome being absent. In mongolism, there is an extra small autosome, making a total of 47. In another condition called polydysspondylism, which shows multiple bony abnormalities of the skull and spine with low intelligence and which has so far not been classified as bleb disease, again only 45 chromosomes were found. If the analogy postulated between the malformations of Bagg and Little’s mice and the bleb diseases is correct, then the chromosome defects now known to be present in some members of the bleb-disease group may throw some light on the cause of deformities of Bagg and Little’s mice. It is known that chromosomes are electively radiosensitive. Since Bagg and Little’s deformities were produced by radiation of the ovaries, it is almost certain that they were due to some chromosome damage. It would, therefore, be of great interest to investigate whether some chromosome anomalies could be detected in the progeny of Bagg and Little’s mice. Should 14. 15.
16. 17. 18. 19. 20.
Ohno, S., Kaplan, W. D., Kinosita, R. Exp. cell Res. 1959, 16, 462. Klinger, H. P. Acta anat. 1957, 30, 371. Klinger, H. P. Exp. cell Res. 1958, 14, 207. Bagg, H. J., Little, C. C. Amer. J. Anat. 1924, 33, 119. Engel, D. Amer. J. Dis. Child. 1940, 60, 562. J. Bone Jt Surg. 1943, 25, 613. Engel, D. Keith, A. Brit. J. Surg. 1940, 28, 173.
this be confirmed, the further question arises whether the chromosome damage is directly responsible for the anomalies found at the base of the fourth ventricle, and the consequent leakage of cerebrospinal fluid. It would also be of interest to examine the chromosomes in the other ten syndromes of bleb diseases. If chromosome anomalies were found in them, this would give an added support for the separation of these syndromes into a special group. In the light of such future investigations it might be necessary to omit some syndromes now included in this group (e.g., Moon-Biedl syndrome), or to include others not yet classified. It is naturally possible that chromosome damage of the germ cells may occur without injury to the central nervous system. Whether the bleb mechanism is possible without chromosomal damage, only future studies will show. Should the assumed connection between chromosomal damage and bleb mechanism prove to be correct, it will open new vistas for the study of
D. ENGEL. EXTRADURAL HÆMATOMA
SiR,ňIread with great interest the article (July 23) by Mr. McKissock. Do the clinical signs of extradural hsematoma give any indication of the exact position of the hasmatoma ? Are hasmatomas in the frontal region more insidious in onset than those in the temporal fossa ? I ask this because I saw a boy suddenly die of a frontal extradural hasmatoma 10 hours after falling out of bed. Even in retrospect the only abnormal clinical sign was slight drowsiness. Incidentally this child had no fracture of the skull
on
X-ray
or at
postmortem.
West Suffolk General Hospital, Bury St. Edmunds.
ADRIAN M. BAIN.
SHORTAGE OF RADIOGRAPHERS SIR,-I should very much like to support Dr. Osborne’s remarks of July 9 concerning the shortage of radiographers.
At his suggestion, lectures have been given in the Edmonton district in the past few months at girls’ schools, but it is too soon, yet, to assess the results of these lectures in terms of student recruits, since the age at which students can start their training is 18 years, and the age-groups so far concerned are up to 16 years. Considerable interest has been shown. In our case, the lecturer was the male superintendent-radiographer, but in every case he was accompanied by the " young, warm, and vital " in the shape of one of the young and attractive female radiographers. She talked informally to the interested girls after the lectures. In the North East Metropolitan area, a scheme has just been started where five of the board’s hospitals carry out the practical training of radiographers, the formal lectures being given, by kind permission, at The London Hospital. By this method, girls in the neighbourhood of the five principal hospitals can receive their training without too much travelling, as the lectures are completed on two days of the week. Lectures to the schools are followed in a few weeks’ time by advertisements in local papers about the joint training scheme, and so far this has produced three students who will begin their courses in September, 1961, in the Edmonton district. There are many other acceptances in the four districts. One of the great difficulties is the wait of one year from passing the necessary G.C.E. 0-level subjects, and being old enough to start the training. I am strongly of the opinion that the shortage of radiographers could be easily overcome by these methods of lecturing and local advertisement, together with a reduction in the age of entry from 18 to 17 years, with qualification at 19 instead of 20.
I suggest that some of the teaching issue their own diplomas in radiography,
hospitals might as some
of these