- Email: [email protected]
NEW THOUGHTS ON HYPERTENSION
786
be found.1O 12 Even experienced observers cannot always distinguish these few, but a lesion with scaling or a vesicular margin is likelier to be associated with fungus than is maceration. The only way to diagnose tinea pedis certainly is to demonstrate the fungus: microscopic examination of material in caustic potash is more reliable than culture, although the two methods together may reveal a few extra cases.’; It is not well understood how the lesions arise when fungus is not present; but hyperhidrosis, maceration, bacterial infection, and eczematous changes are probably responsible. ENGLISH has pointed out that some scaling is to be expected between the toes, where the normal shedding of the skin’s horny layer is prevented-much as it is under a plaster cast. Where hygiene is poor, this type of lesion is commoner; but, surprisingly, the prevalence of fungal infection is not similarly increased. In Florida SARKANY et al.14 have shown that another organism-the bacterium of erythrasma-may often be recovered from scaly toeclefts. This bacterium has also been found in Britain. It produces a coral-red fluorescence under Wood’s light, can be cultured on special media, and is visible with an oil-immersion lens. The ringworm fungi can live only in the horny layer of the epidermis -and cannot invade living tissue. Their ill effects are probably produced by the inward diffusion of toxic substances, allergic sensitivity of the host, and secondary bacterial infection. MARPLES and BAILEY 15 showed a correlation between the presence of Staphylococcus aureus in the lesions and their severity. Tinea pedis is no longer regarded as a simple infectious disease. Indeed, it has even been suggested that the fungus is a harmless saprophyte which happens to find a suitable environment in an abnormal toe-cleft; but experimental and epidemiological evidence seems to show that this is going a little too far. STRAUSS and KLIGMAN4 found great difficulty in initiating lesions even with large infective doses of fungus. They increased the proportion of " takes " by first producing maceration of the feet-either with occlusive dressings or by making their volunteers wear boots, day and night, for several days. These infections were self-limiting. Whether or not a symptomless carrier state occurs is still undecided: ENGLISH concluded that carriers can be found, but only rarely, and that they usually have an infection which is either almost cured or is in the incubation period. STRAUSS and KLIGMAN, however, have shown that fungus can be present in the skin without causing any reaction; this is seldom so in people with normal feet, but is commonly so in the normal skin of feet which are clinically infected elsewhere. Until the question of carriers is settled, no rational public-health measures can be devised. Nevertheless, effective treatment of cases does lower the infection-rate. proven The importance of both soil and seed is evident in the treatment of the single case. The first prerequisite is accurate diagnosis-to establish not only whether fungus is present but also, if it is, to what extent it is responsible 13. 14. 15.
Strauss, J. S., Kligman, A. M. Arch. Derm., Chicago, 1957, 76, Sarkany, I., Taplin, D., Blank, H. J. Amer. med. Ass. 1961, 177, Marples, M. J., Bailey, M. J. Brit. J. Derm. 1957, 69, 381.
70. 130.
for the pathological changes. Measures specifically directed against the fungus often fail. Griseofulvin has not lived up to expectations, and often does not eliminate fungus from the feet. In acute cases, topical fungicides often do more harm than good, and, if there is any doubt, such cases are treated as infected eczema-with rest and bland applications. For chronic cases, Whitfield’s ointment is still the most usual remedy, and some difficult cases are kept free of symptoms by wearing sandals. (Tinea pedis is almost unknown among races who go barefoot.) Careful foot hygiene is important in both long-term treatment and prophylaxis, but the work of STRAUSS and KLIGMAN clearly shows the futility of ritual boiling of socks and disinfection of shoes.
Annotations NEW THOUGHTS ON HYPERTENSION
ALTHOUGH the most important questions about hypertension are still unanswered, the student need never be idle for the lack of something new to read. In the experimental field the renin-angiotensin system continues to attract attention as a possible cause of renal hypertension. Helmer1 reports that in a very large series of cases renin was demonstrable in the blood in malignant and renal hypertension and, less constantly, in the benign form of the disease. The presence of angiotensin in such cases has been asserted2 and denied 3the sensitivity, specificity, and accuracy of present methods of assaying biological fluids leaves much to be desired. It is interesting to learn, however, that the white weal which follows intradermal injection of angiotensin persists much longer in hypertensives than in healthy controls.4 The excretion of salt and water and its response to infusion of angiotensin5are also abnormal in hyper" tensive patients and animals and in both the " ischaemic and the intact kidney7 8 of patients with unilateral renal hypertension,9 but it is still uncertain what these changes mean or whether, indeed, they would persist if the infusion could be continued, bearing in mind that Goldblatt hypertension takes at least several days to develop fully. Although current methods of recovering and assaying aldosterone are far from perfect, there is some evidence that angiotensin increases the secretion of aldosterone 10; and Laragh 11 suggests that angiotensin may be the trophic hormone controlling the secretion of aldosterone. This is in keeping with the observation that the number of granules in the juxtaglomerular cells, which probably secrete renin,12 varies with the salt intake 13 and with the breadth of the zona glomerulosa of the cortex of the suprarenal, which secretes aldosterone. The granularity of these cells is also reported to be increased in the 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
11. 12. 13.
Helmer, O. M. American Heart Association’s Monograph no. 3. Circulation, 1962, 25, 169. Kahn, J. R., Skeggs, L. T., Shumway, N. P., Wisenbaugh, P. E. J. exp. Med. 1952, 95, 523. Peart, W. S. Brit. med. J. 1959, ii, 1353. Jablons, B. Circulation, 1962, 25, 259. Peart, W. S., Brown, J. J. Lancet, 1961, i, 28; Brown, J. J., Peart, W. S. Clin. Sci. 1962, 22, 1. Bock, K. D., Dengler, H., Krecke, H-J., Reichel, G. Klin. Wschr. 1958, 36, 808. Brown, J. J., Robertson, J. I. S. Lancet, March 24, 1962, p. 645. Jones, N. F., Barraclough, M. A. ibid. p. 646. Jones, N. F., Barraclough, M. A. ibid. March 3, 1962, p. 454. Genest, J., Biron, P., Koiw, E., Nowaczinski, W., Boucher, R., Chrétien, M. Ann. intern. Med. 1961, 55, 12. Laragh, J. H. Circulation, 1962, 25, 203. Cook, W. F., Pickering, G. W. J. Physiol. 1958, 143, 78. Hartroft, P. M., Hartroft, W. S. J. exp. Med. 1953, 97, 415.
787
ischxmic " kidney of Goldblatt hypertension; and, since these cells are located in the media of the afferent glomerular arteries, Tobian 14 has suggested that they may act as stretch receptors. Thus the mosaic of data increases steadily, but the pattern is still not clear. Another moot question is whether benign and malignant hypertension differ in kind or only in degree. The answer hinges largely on the causation of the focal arterial necrosis and endothelial hyperplasia which distinguish malignant hypertension. The fact that these lesions do not, except in special circumstances, appear distal to a clamp constricting the renal artery leaves little room for doubt that they are essentially a result of the physical stress imposed by excessive filling tension on overstimulated arteries.15 Although this simple quantitative conception of malignancy is generally accepted as sufficient in itself, some workers 16 17 suspect that an additional factor unrelated to the hypertension may be necessary. X rays have been shown to facilitate the development of "malignant" lesions in hypertensive rats,18possibly by destroying vasomotor nerve-fibres,19 in the absence of which the reactivity of arteries to certain polypeptideand perhaps other-vasoconstrictors is increased.2° Moreover in rats with experimental hypertension, arterial necrosis is especially liable to develop in vessels affected by certain spontaneous lesions (" periarterial granuloma ") which do not in themselves cause arterial necrosis.21 But what matters is not whether factors other than high filling tension may play a part, principal or subsidiary, in determining malignancy but whether they in fact do so. On this point there is at present no direct evidence, though Perera’s 22 report that in a very small series of patients "
with
malignant hypertension an anti-thyroid drug, methimazole, arrested the progress of the disease without lowering the blood-pressure carries a hint that further study may reveal ways of turning malignant into benign hypertension. Nevertheless the dominant role of the hypertensive process in determining malignancy is indicated by the fact that in man and in animals malignant hypertension can be rapidly and completely cured wherever the
be removed. Turning practical matters, the medical treatment of hypertension continues to be empirical; but reports in these columns 23 and elsewhere ’24 25 and two further articles which appear on earlier pages of this issue, suggest that alpha-methyldopa may prove useful. As for surgical treatment, several recent papers 26-31 deal with the complex problem of detecting and treating the rare cases of unilateral renal hypertension which can be cured by surgery. One of these 26 suggests that the condition may be considerably commoner than is realised. Another 27 cause can
to more
14. Tobian, L. Circulation, 1962, 25, 189. 15. Wilson, C., Pickering, G. W. Clin. Sci. 1938, 3, 343. 16. Kincaid-Smith, P., McMichael, J. R., Murphy, E. A.
Quart. J.
1958, 27, 117. 17. Goldblatt, H. F. Physiol. Rev. 1947, 27, 120. 18. Asscher, A. W., Wilson, C., Anson, S. G. Lancet, 1961, i, 580. 19. Ryzewski, J. Acta physiol. polon. 1960, 11, 197. 20. Lloyd, S., Pickford, M. J. Physiol. 1961, 155, 161. 21. McQueen, E. G., Hodge, J. V. Quart. J. Med. 1961, 30, 213. 22. Perera, G. A. Ann. intern. Med. 1961, 55, 29. 23. Irvine, R. O. H., O’Brien, K. P., North, J. D. K. Lancet, Feb. 10,
Med.
1962,
p. 300. 24. Gillespie,
L., Jr., Oates, J. A., Crout, J. R., Sjoerdsma, 1962, 25, 281.
A.
Circulation,
25. Cannon, P. J., Whitlock, R. T., Morris, R. C., Angers, M., Laragh, J. H J. Amer. med. Ass. 1962, 179, 673. 26. Perloff, D., Sokolow, M., Wylie, E. J., Smith, D. R., Polubinskas, A. J. Circulation, 1961, 24, 1268. 27. Torrance, H. B., Davies, R. P., Clark, P. Lancet, 1961, ii, 633. 28. Spencer, F. C., Stamey, T. A., Bahnson, H. T., Cohen, A. Ann. Surg. 1961, 154, 674. 29. Proc. Mayo Clin. 1962, 36, 678. 30. Stamey, T. A., Nudelman, I. J., Good, P. H., Schwenker, F. N., Hendricks, I. Medicine, 1961, 40, 347. 31. Howard, J. E., Connor, T. B. Arch. intern. Med. 1962, 109, 8.
describes the detection of arterial renal stenosis by directional scintillation counting over the loin after intravenous injection of radioactive rubidium. Yet another 28 describes a new diagnostic test based on comparison of the volume and inulin concentration of urine from the two kidneys during the infusion of a saline solution of urea,’, inulin, p-aminohippuric acid, and vasopressin. This rather complex test is claimed to be more reliable than comparison of the output of sodium and water by the two
kidneys. SPOTTING THE LOSER?
STUDIES of
delinquency tend to be incomplete and to only particular period of time. In Glasgow, the alliance of university and probation departhowever, ment promises to produce a steady flow of information which should throw considerable light on the background and development of certain types of delinquent. Dr. D. H. Stott, in a series of reports, is analysing the records of some 400 boys who were placed on probation during 1957. In his third report1 he compares the delinquent group with a group of boys from like social backgrounds and draws three main conclusions. Firstly, the family background of the offenders is often unstable and their cover
a
parents are unreliable. The emotional tone of the home is apparently more likely to produce psychological disturbance than the mere absence of one or other parent, whether because of death, desertion, or divorce. Secondly, boys living in families with a disorganised hand-to-mouth way of life and inadequate standards of hygiene tend to be more disturbed in their behaviour than those from homes with good or adequate standards. Thirdly, the offenders are much more prone to chronic disease and seem to have more physical defects than the control group-so much so, apparently, that Dr. Stott suggests that a large proportion of probationers are children with " constitutional damage to their temperaments ". This last finding conflicts with observations made elsewhere. Glueck and Glueck2 in the United States found that delinquents tended to be more physically robust and energetic than non-delinquents. It may well be that unknown social and nutritional differences between the American and Glasgow delinquents account for these different findings. But the connection between physical health and psychological maladjustment, if real, is of paramount importance in the prevention and treatment of offenders, and clearly more research should be done in other parts of Britain to test Stott’s claim that " there is an underlying factor of physical-neural damage responsible for the proneness to both disease and maladjustment ". When he applied his Bristol social adjustment guide3 to both Glasgow groups, Stott found that the boys in the delinquent group were substantially more disturbed, and he suggests that the application of his guide to all children at an early age might help to identify those who are delinquency-prone so that a watchful eye could be kept on their development. Prognostic techniques should, however, still be used with caution. They might properly help a probation officer to find out which of the boys in his care needed the most intensive help. But to use them to decide whether to put a boy on probation might deny him his final chance of social rehabilitation before more rigorous methods were invoked. Dr. Stott stresses the 1. 2. 3.
University of Glasgow, 1961. Glueck, S., Glueck, E. Unravelling Juvenile Delinquency. York, 1961. Stott, D. H. Social Adjustment of Children. London, 1959.
New
be found.1O 12 Even experienced observers cannot always distinguish these few, but a lesion with scaling or a vesicular margin is likelier to be associated with fungus than is maceration. The only way to diagnose tinea pedis certainly is to demonstrate the fungus: microscopic examination of material in caustic potash is more reliable than culture, although the two methods together may reveal a few extra cases.’; It is not well understood how the lesions arise when fungus is not present; but hyperhidrosis, maceration, bacterial infection, and eczematous changes are probably responsible. ENGLISH has pointed out that some scaling is to be expected between the toes, where the normal shedding of the skin’s horny layer is prevented-much as it is under a plaster cast. Where hygiene is poor, this type of lesion is commoner; but, surprisingly, the prevalence of fungal infection is not similarly increased. In Florida SARKANY et al.14 have shown that another organism-the bacterium of erythrasma-may often be recovered from scaly toeclefts. This bacterium has also been found in Britain. It produces a coral-red fluorescence under Wood’s light, can be cultured on special media, and is visible with an oil-immersion lens. The ringworm fungi can live only in the horny layer of the epidermis -and cannot invade living tissue. Their ill effects are probably produced by the inward diffusion of toxic substances, allergic sensitivity of the host, and secondary bacterial infection. MARPLES and BAILEY 15 showed a correlation between the presence of Staphylococcus aureus in the lesions and their severity. Tinea pedis is no longer regarded as a simple infectious disease. Indeed, it has even been suggested that the fungus is a harmless saprophyte which happens to find a suitable environment in an abnormal toe-cleft; but experimental and epidemiological evidence seems to show that this is going a little too far. STRAUSS and KLIGMAN4 found great difficulty in initiating lesions even with large infective doses of fungus. They increased the proportion of " takes " by first producing maceration of the feet-either with occlusive dressings or by making their volunteers wear boots, day and night, for several days. These infections were self-limiting. Whether or not a symptomless carrier state occurs is still undecided: ENGLISH concluded that carriers can be found, but only rarely, and that they usually have an infection which is either almost cured or is in the incubation period. STRAUSS and KLIGMAN, however, have shown that fungus can be present in the skin without causing any reaction; this is seldom so in people with normal feet, but is commonly so in the normal skin of feet which are clinically infected elsewhere. Until the question of carriers is settled, no rational public-health measures can be devised. Nevertheless, effective treatment of cases does lower the infection-rate. proven The importance of both soil and seed is evident in the treatment of the single case. The first prerequisite is accurate diagnosis-to establish not only whether fungus is present but also, if it is, to what extent it is responsible 13. 14. 15.
Strauss, J. S., Kligman, A. M. Arch. Derm., Chicago, 1957, 76, Sarkany, I., Taplin, D., Blank, H. J. Amer. med. Ass. 1961, 177, Marples, M. J., Bailey, M. J. Brit. J. Derm. 1957, 69, 381.
70. 130.
for the pathological changes. Measures specifically directed against the fungus often fail. Griseofulvin has not lived up to expectations, and often does not eliminate fungus from the feet. In acute cases, topical fungicides often do more harm than good, and, if there is any doubt, such cases are treated as infected eczema-with rest and bland applications. For chronic cases, Whitfield’s ointment is still the most usual remedy, and some difficult cases are kept free of symptoms by wearing sandals. (Tinea pedis is almost unknown among races who go barefoot.) Careful foot hygiene is important in both long-term treatment and prophylaxis, but the work of STRAUSS and KLIGMAN clearly shows the futility of ritual boiling of socks and disinfection of shoes.
Annotations NEW THOUGHTS ON HYPERTENSION
ALTHOUGH the most important questions about hypertension are still unanswered, the student need never be idle for the lack of something new to read. In the experimental field the renin-angiotensin system continues to attract attention as a possible cause of renal hypertension. Helmer1 reports that in a very large series of cases renin was demonstrable in the blood in malignant and renal hypertension and, less constantly, in the benign form of the disease. The presence of angiotensin in such cases has been asserted2 and denied 3the sensitivity, specificity, and accuracy of present methods of assaying biological fluids leaves much to be desired. It is interesting to learn, however, that the white weal which follows intradermal injection of angiotensin persists much longer in hypertensives than in healthy controls.4 The excretion of salt and water and its response to infusion of angiotensin5are also abnormal in hyper" tensive patients and animals and in both the " ischaemic and the intact kidney7 8 of patients with unilateral renal hypertension,9 but it is still uncertain what these changes mean or whether, indeed, they would persist if the infusion could be continued, bearing in mind that Goldblatt hypertension takes at least several days to develop fully. Although current methods of recovering and assaying aldosterone are far from perfect, there is some evidence that angiotensin increases the secretion of aldosterone 10; and Laragh 11 suggests that angiotensin may be the trophic hormone controlling the secretion of aldosterone. This is in keeping with the observation that the number of granules in the juxtaglomerular cells, which probably secrete renin,12 varies with the salt intake 13 and with the breadth of the zona glomerulosa of the cortex of the suprarenal, which secretes aldosterone. The granularity of these cells is also reported to be increased in the 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
11. 12. 13.
Helmer, O. M. American Heart Association’s Monograph no. 3. Circulation, 1962, 25, 169. Kahn, J. R., Skeggs, L. T., Shumway, N. P., Wisenbaugh, P. E. J. exp. Med. 1952, 95, 523. Peart, W. S. Brit. med. J. 1959, ii, 1353. Jablons, B. Circulation, 1962, 25, 259. Peart, W. S., Brown, J. J. Lancet, 1961, i, 28; Brown, J. J., Peart, W. S. Clin. Sci. 1962, 22, 1. Bock, K. D., Dengler, H., Krecke, H-J., Reichel, G. Klin. Wschr. 1958, 36, 808. Brown, J. J., Robertson, J. I. S. Lancet, March 24, 1962, p. 645. Jones, N. F., Barraclough, M. A. ibid. p. 646. Jones, N. F., Barraclough, M. A. ibid. March 3, 1962, p. 454. Genest, J., Biron, P., Koiw, E., Nowaczinski, W., Boucher, R., Chrétien, M. Ann. intern. Med. 1961, 55, 12. Laragh, J. H. Circulation, 1962, 25, 203. Cook, W. F., Pickering, G. W. J. Physiol. 1958, 143, 78. Hartroft, P. M., Hartroft, W. S. J. exp. Med. 1953, 97, 415.
787
ischxmic " kidney of Goldblatt hypertension; and, since these cells are located in the media of the afferent glomerular arteries, Tobian 14 has suggested that they may act as stretch receptors. Thus the mosaic of data increases steadily, but the pattern is still not clear. Another moot question is whether benign and malignant hypertension differ in kind or only in degree. The answer hinges largely on the causation of the focal arterial necrosis and endothelial hyperplasia which distinguish malignant hypertension. The fact that these lesions do not, except in special circumstances, appear distal to a clamp constricting the renal artery leaves little room for doubt that they are essentially a result of the physical stress imposed by excessive filling tension on overstimulated arteries.15 Although this simple quantitative conception of malignancy is generally accepted as sufficient in itself, some workers 16 17 suspect that an additional factor unrelated to the hypertension may be necessary. X rays have been shown to facilitate the development of "malignant" lesions in hypertensive rats,18possibly by destroying vasomotor nerve-fibres,19 in the absence of which the reactivity of arteries to certain polypeptideand perhaps other-vasoconstrictors is increased.2° Moreover in rats with experimental hypertension, arterial necrosis is especially liable to develop in vessels affected by certain spontaneous lesions (" periarterial granuloma ") which do not in themselves cause arterial necrosis.21 But what matters is not whether factors other than high filling tension may play a part, principal or subsidiary, in determining malignancy but whether they in fact do so. On this point there is at present no direct evidence, though Perera’s 22 report that in a very small series of patients "
with
malignant hypertension an anti-thyroid drug, methimazole, arrested the progress of the disease without lowering the blood-pressure carries a hint that further study may reveal ways of turning malignant into benign hypertension. Nevertheless the dominant role of the hypertensive process in determining malignancy is indicated by the fact that in man and in animals malignant hypertension can be rapidly and completely cured wherever the
be removed. Turning practical matters, the medical treatment of hypertension continues to be empirical; but reports in these columns 23 and elsewhere ’24 25 and two further articles which appear on earlier pages of this issue, suggest that alpha-methyldopa may prove useful. As for surgical treatment, several recent papers 26-31 deal with the complex problem of detecting and treating the rare cases of unilateral renal hypertension which can be cured by surgery. One of these 26 suggests that the condition may be considerably commoner than is realised. Another 27 cause can
to more
14. Tobian, L. Circulation, 1962, 25, 189. 15. Wilson, C., Pickering, G. W. Clin. Sci. 1938, 3, 343. 16. Kincaid-Smith, P., McMichael, J. R., Murphy, E. A.
Quart. J.
1958, 27, 117. 17. Goldblatt, H. F. Physiol. Rev. 1947, 27, 120. 18. Asscher, A. W., Wilson, C., Anson, S. G. Lancet, 1961, i, 580. 19. Ryzewski, J. Acta physiol. polon. 1960, 11, 197. 20. Lloyd, S., Pickford, M. J. Physiol. 1961, 155, 161. 21. McQueen, E. G., Hodge, J. V. Quart. J. Med. 1961, 30, 213. 22. Perera, G. A. Ann. intern. Med. 1961, 55, 29. 23. Irvine, R. O. H., O’Brien, K. P., North, J. D. K. Lancet, Feb. 10,
Med.
1962,
p. 300. 24. Gillespie,
L., Jr., Oates, J. A., Crout, J. R., Sjoerdsma, 1962, 25, 281.
A.
Circulation,
25. Cannon, P. J., Whitlock, R. T., Morris, R. C., Angers, M., Laragh, J. H J. Amer. med. Ass. 1962, 179, 673. 26. Perloff, D., Sokolow, M., Wylie, E. J., Smith, D. R., Polubinskas, A. J. Circulation, 1961, 24, 1268. 27. Torrance, H. B., Davies, R. P., Clark, P. Lancet, 1961, ii, 633. 28. Spencer, F. C., Stamey, T. A., Bahnson, H. T., Cohen, A. Ann. Surg. 1961, 154, 674. 29. Proc. Mayo Clin. 1962, 36, 678. 30. Stamey, T. A., Nudelman, I. J., Good, P. H., Schwenker, F. N., Hendricks, I. Medicine, 1961, 40, 347. 31. Howard, J. E., Connor, T. B. Arch. intern. Med. 1962, 109, 8.
describes the detection of arterial renal stenosis by directional scintillation counting over the loin after intravenous injection of radioactive rubidium. Yet another 28 describes a new diagnostic test based on comparison of the volume and inulin concentration of urine from the two kidneys during the infusion of a saline solution of urea,’, inulin, p-aminohippuric acid, and vasopressin. This rather complex test is claimed to be more reliable than comparison of the output of sodium and water by the two
kidneys. SPOTTING THE LOSER?
STUDIES of
delinquency tend to be incomplete and to only particular period of time. In Glasgow, the alliance of university and probation departhowever, ment promises to produce a steady flow of information which should throw considerable light on the background and development of certain types of delinquent. Dr. D. H. Stott, in a series of reports, is analysing the records of some 400 boys who were placed on probation during 1957. In his third report1 he compares the delinquent group with a group of boys from like social backgrounds and draws three main conclusions. Firstly, the family background of the offenders is often unstable and their cover
a
parents are unreliable. The emotional tone of the home is apparently more likely to produce psychological disturbance than the mere absence of one or other parent, whether because of death, desertion, or divorce. Secondly, boys living in families with a disorganised hand-to-mouth way of life and inadequate standards of hygiene tend to be more disturbed in their behaviour than those from homes with good or adequate standards. Thirdly, the offenders are much more prone to chronic disease and seem to have more physical defects than the control group-so much so, apparently, that Dr. Stott suggests that a large proportion of probationers are children with " constitutional damage to their temperaments ". This last finding conflicts with observations made elsewhere. Glueck and Glueck2 in the United States found that delinquents tended to be more physically robust and energetic than non-delinquents. It may well be that unknown social and nutritional differences between the American and Glasgow delinquents account for these different findings. But the connection between physical health and psychological maladjustment, if real, is of paramount importance in the prevention and treatment of offenders, and clearly more research should be done in other parts of Britain to test Stott’s claim that " there is an underlying factor of physical-neural damage responsible for the proneness to both disease and maladjustment ". When he applied his Bristol social adjustment guide3 to both Glasgow groups, Stott found that the boys in the delinquent group were substantially more disturbed, and he suggests that the application of his guide to all children at an early age might help to identify those who are delinquency-prone so that a watchful eye could be kept on their development. Prognostic techniques should, however, still be used with caution. They might properly help a probation officer to find out which of the boys in his care needed the most intensive help. But to use them to decide whether to put a boy on probation might deny him his final chance of social rehabilitation before more rigorous methods were invoked. Dr. Stott stresses the 1. 2. 3.
University of Glasgow, 1961. Glueck, S., Glueck, E. Unravelling Juvenile Delinquency. York, 1961. Stott, D. H. Social Adjustment of Children. London, 1959.
New