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The Irritable Bowel
1112
It is the basis of treatment of rhesus-negative mothers with anti-D antiserum to prevent their becoming sensitised against rhesus-positive cells of their offspring. BILLINGHAM et al.17 referred to the" inhibition of active immunisation by antibody as an afferent " block of the immune response. Presumably the administered antibody combines with antigen, partially or wholly abolishing its power to immunise. It is of course necessary in the context of graft enhancement that the injected antibody does not cause an irreversible state of damage to the graft, and it is interesting that the longest enhancement observed by FRENCH and BATCHELOR was when heterozygous rat donors were used. Such donors would be expected to have quantitatively less antigen on their cells than would homozygotes, and therefore their organs would be less vulnerable to immune damage. The second mechanism believed to be important in enhancement is the competition for antigen sites that is postulated to exist between humoral antibody and immunologically committed lymphocytes which mediate cellular immunity.18-2o Since immunological enhancement can follow active immunisation, inhibition of immunisation (the first mechanism) cannot be a complete explanation. There is considerable evidence in support of the idea that antibody and immune cells compete for the same antigenic recep" tors-i.e., an efferent " block in the immune response. 17 It has been shown that anti-graft antibody can prevent immune lymphocytes from destroying target graft cells both in vivo 18,19 and in vitro.21,22 In the experiments of FRENCH and BATCHELOR the antibody-treated rats did develop an active antibody response; therefore the prolonged survival of the kidney grafts cannot be attributed solely to an inhibition of immunisation. FRENCH and BATCHELOR believe that the injected antibody covered a sufficient number of antigen sites on the transplanted kidney to protect it from irreversible damage by immune lymphocytes, but, on the other hand, sufficient antigen remained uncombined with antibody to permit some active immunisation of the recipient. Subsethe quently antibody actively synthesised by recipient continued to protect the graft-that is, a state of autoenhancement had been reached. These findings and those of STUART et al. 23 and HILDEMANN et al. 24 show that there is a good prospect of immunological enhancement being put to clinical use. 17. 18.
Billingham, R. E., Brent, L., Medawar, P. B. Transplant. Bull. 1956, 3, 84. Batchelor, J. R., Silverman, M. S. in Transplantation (edited by G. E. W. Wolstenholme and M. Cameron); p. 216. London,
1962. 19. Moller, G. J. natn. Cancer Inst. 1963, 30, 1205. 20. Batchelor, J. R. Cancer Res. 1968, 28, 1410. 21. Brunner, K. T., Mauel, J., Cerottini, J. C., Chapuis, B. 22.
Immunology, 1968, 14, 181. Hellström, I., Hellström, K. E., Evans, C. A., Heppner, G. H., Pierce, G. E., Yang, J. P. S. Proc. natn. Acad. Sci. 1969, 62, 362.
23.
Stuart, F. P., Saitoh, T., Fitch, F. W. Science, N. Y. 1968, 160,
1463. 24. Hildemann, W. H.
Transplant. Revs (in the press).
The Irritable Bowel ONE of the commonest causes of abdominal pain is what has been called the " irritable colon" or " spastic colon " syndrome; but, despite excellent descriptions of the characteristic symptoms, many
patients undergo biochemical and radiological investigations1 of all accessible abdominal viscera before the diagnosis is reluctantly accepted. This situation arises partly because insufficient attention is paid to the details of the symptoms and signs, and partly because the mechanism of symptom production is ill understood and visible or tangible evidence of pathological change is lacking. One consequence of the lack of objective " evidence is the doctor’s continuing anxiety about the diagnosis, and another is the purposive use of synonyms such as " colon neurosis " functional colon ", and " psychogenic "
diarrhoea ". CONNELL et al.demonstrated, in a selected group subjects, that after a meal the sigmoid colon responded with recurring peaks of high pressure in tubes placed within it. They recorded this manifestation of gut activity in the colon of three groups: (1) those with a duodenal ulcer in remission and no bowel symptoms; (2) those with " spastic colon"" whose abdominal pain was not brought on by eating during the investigation; and (3) those with " spastic colon " whose symptoms were brought on or aggravated by a meal eaten during the study. Those who had pain after eating produced waves of higher pressure and for a greater proportion of the recording time, both before and after a meal, than did the other groups. Hypermotility usually began some minutes before discomfort was noticed, but the conclusion was that the hypermotility was in some way related to the development of abdominal pain. The pain was not felt in the region of the sigmoid, and it did not correspond in its time-intensity pattern with the change in pressure within. the recording system. Indeed, each of three recording tubes, spaced 5 cm. apart, registered independent changes of pressure so that, if the high peak of pressure was responsible for pain, then a very large number of sites of production of "pain" impulses must exist. In one subject a similar pattern of hypermotility was recorded by telemetering capsule in the terminal ileum after a meal. of
HOLDSTOCK et al. have extended the investigations to another group of patients with severe abdominal pain for which no cause was found after a variety of investigations, but in whom unusually high peaks of pressure were recorded from the colon or small intestine. As in the previous inquiry, the patients included were those with an abnormal pattern in the pressure record. What is particularly interesting in 1. 2. 3.
Waller, S. L., Misiewicz, J. J. Lancet, Oct. 11, 1969, p. 753. Connell, A. M., Jones, F. A., Rowlands, E. N. Gut, 1965, 6, 105. Holdstock, D. J., Misiewicz, J. J., Waller, S. L. ibid. 1969, 10,
1113
this further report is that unusually high pressures were recorded by radiotelemetering from both small and large intestine as well as from the sigmoid colon. The only reasonable interpretation is that parts or the whole of the small and large intestine are involved in this abnormal response, which is either a discrete disturbance or simply one facet, recorded in a particular way, of what might be better called the irritable-gut syndrome, rather than limiting attention to the colon. 5, and probably at least 7, of the 9 patients had the irritable-colon syndrome. One man had had a partial gastrectomy followed by dumping, diarrhoea, steatorrhoea, and abdominal pain after eating. His pain was found to coincide with bursts of small-intestine activity either after eating or induced by intravenous injections of 5-hydroxytryptamine. Both pain and pressure-inducing activity were abolished by intravenous propantheline. In another patient with a partial gastrectomy upper abdominal
pain developed the same time as bursts of pressureinducing activity in the small intestine after eating; and 0-75 mg. neostigmine induced upper and lower abdominal pain and hyperactivity of the jejunum, sigmoid, and rectum. This activity, and the pains, were abolished by intravenous propantheline. In a patient with constipation and pain, sigmoid activity did not change, but activity in the small intestine increased at the same time as the pain; and again both were abolished by intravenous propantheline. 5 other patients showed a similar coincidence of pain and colon activity after a meal or an injection of neostigmine. 2 patients showed similar changes in colonic pressure in response to eating, but they did not have coincident pain, although pain was an important feature of their illness. Indeed, in these 2 patients the pressures recorded by the transducer approached the level of the arterial bloodpressure, suggesting that ischxmia of the bowel wall is unlikely to be important in the production of this type of abdominal discomfort. The simultaneous relief of pain and cessation of pressure-inducing activity after intravenous propantheline in the other patients suggest either that pain and motility are sometimes directly linked or that propantheline blocks the action of a common causal agent. Clearly, hypermotility does not always cause pain, but pain might result from a particular hypermotility in a at
particular place. These observations provide interesting material for speculation. It is not uncommon for patients with symptoms suggestive of irritable colon to have a very noisy abdomen-noise which because of its high
pitch and duration seems likely to be produced by movement of gas-liquid interfaces in the small intestine, providing evidence for small-intestine hyperactivity, although it might result from colon hypermotility. A barium follow-through examination often shows rapid transit through the small intes-
tine.4 If the irritable colon is really an irritable gut, at least from pylorus to rectum, then where is the lesion? Orthodox histological examination reveals no cause, and such evidence as there is suggests that the disturbance is an excess of phasic contractility of smooth muscle which might arise in muscle or in nerve. The role of the neural elements in the gut wall is probably to modify but not to initiate the contractile activity of the smooth muscle. The effects of propantheline and neostigmine in abolishing and exaggerating respectively the motility response to food might suggest that the lesion is in the neural control of motility, but this is not necessarily so: the irritability might be a primary disturbance of myogenic conduction and initiation of contraction, potentiated by a normal neural control mechanism; and the search for treatment might be better directed towards the muscle cell rather than the neural
pathway. The second question raised by these observations the mechanism of pain production and the site of the sensitive endings. Because the recording device happened to be there at the time, the abnormal activity was recorded in the sigmoid colon and in various parts of the small intestine and proximal colon. It would be a remarkable coincidence if the pain was produced only at the sites of the pressurerecording devices, unless the pain and hypermotility But were a reaction of the gut to their presence. hypermotility is not always accompanied by pain. It is reasonable to suppose that hypermotility is widespread and that pain production may be widespread or localised or absent. Pain in this syndrome is often steady, but sometimes colicky, and when it varies in intensity the time-intensity curve has a scale 5-50 times slower than that of the recorded changes in pressure. In some of the tracings a wave of pressure rises from and falls to its basal level in about 3-5 seconds in both small and large intestine, sometimes superimposed on a slower and considerable upward shift of the baseline over 20-30 seconds. The sensation of pain seems likely to be a summation of impulses from many parts of the gut produced by many local contractions of the wall. concerns
Two common features of the irritable-gut syndrome tenderness of part or the whole of the colon and small intestine to local pressure; and a sensation of pain deep to the surface marking of the transverse or descending colon and provoked by pressure on the caecum or ascending colon. These signs suggest that the colon may be tender to pressure not only from without but also from within-a situation not dissimilar to the aseptic bladder and urethral irritation which afflict many women and which is not uncommonly associated with the irritable-bowel syndrome. Moreover, this tenderness of the colon is
are
4.
Kaiser, M. H., Zion, 31, 69.
D.
E., Bockus, H. L. Gastroenterology, 1956,
1114
commonly present when pain is absent. HOLDSTOCK et awl. suggest that some of the activity which they recorded might be excessive segmentation activity which produces a functional obstruction and distension of the bowel proximal to the hypersegmenting segment. They postulate that this distension may be the cause of pain, by analogy with the pain produced by distending the small intestine with a balloon; but they cannot reconcile pain due to functional obstruction with simultaneous diarrhoea due to increased propulsive activity in some patients. They have produced convincing evidence that hypersegmentation of an intense degree, the nearest activity to the popular but nebulous concept of
Annotations MEDICAL ASPECTS OF BOXING
THE investigations by the Royal College of Physicians that led to the publication of their report on boxing1 began after a debate in the House of Lords in 1962 on Baroness Summerskill’s controversial Bill to ban boxing, in which the late Lord Brain suggested that an independent and scientific inquiry should be made. An interim report issued in 1964 stated that conclusions about the medical hazards of boxing could not be reached on the evidence examined. A controlled study was planned and this has been carried out by Dr. A. H. Roberts, an honorary research fellow of the College. His survey2 was designed to establish the prevalence of boxing injuries. A random-sampling technique was used to select 250 boxers from a population of 16,781 men registered with the British Boxing Board of Control between 1929 and 1955. Only professional boxers were studied, since the records for amateurs did not contain the required information. The number of registered boxers has fallen steadily since the late 1930s, and since those chosen to take part in the study formed a fixed proportion of the number registered each year, the majority were boxing in the earlier part of the period under study. But the evidence does not apply solely to this time, for it illustrates clearly how injuries develop. This is pertinent to boxing at any stage in its history. 224 men from the sample were given a physical examination, a brief psychiatric interview, and a number of memory tests. Apart from an electroencephalogram, no technical neurological tests were done. 1 in 6 boxers (17%) showed evidence of brain damage, and a third of these had severe chronic traumatic encephalopathy. The neurological damage was multifocal, with symptoms predominantly referable to the cerebellar, pyramidal, or extrapyramidal systems. This corresponds with findings of previous investigations. In general terms, there are estimated to be 200 severely " punch drunk" ex-boxers in Royal College of Physicians of London. Committee on Boxing: Report on The Medical Aspects of Boxing. 1969. 2. Brain Damage in Boxers. By A. H. ROBERTS. London: Pitman Medical Scientific Publishing Co.: 1969. 40s. (hardback), 30s. 1.
(paperback). 3. See Lancet, 1969,
i,
746.
"
spasm " so far demonstrated, may appear without pain-a finding perhaps as worthy of note as the coincidence of pain and hypersegmentation, and one which deepens the mystery. Many writers on " irritable colon " believe it to be a manifestation of neurosis; others have been kinder and termed it psychosomatic. Either HOLDSTOCK et al. have discovered a way of separating a genuine disease from a man-made rag-bag syndrome, or they have demonstrated that in this syndrome the small and large intestine are capable of violent,
non-propulsive, uncoordinated, presumably useless, and sometimes excruciatingly painful motor activity. Britain, and a further 400-500 men with damage recognisable only on physical examination. Very few chronic eye or ear injuries were reported. Roberts demonstrated conclusively that the length of a boxer’s career and the total number of bouts fought were closely linked to the severity of the ultimate neurological damage. In other words, the prevalence of clinical signs of brain damage of the kind that are
found in ex-boxers increases with exposure
to
boxing. Unexpectedly, psychometric testing showed no relation between impaired memory and length of boxing career. But boxers complained of forgetfulness, and those who found it most troublesome were older men and those who had had long careers in boxing. Only 2 men were indisputably demented, and both had severe chronic traumatic encephalopathy. Paranoid states and personality change with increased aggressiveness were seldom encountered. Better supervision, reduction in the number of bouts a boxer fights each year, and other safeguards introduced by boxing authorities have considerably reduced the frequency and severity of injuries. But further studies, using information from both professional and amateur bodies, are essential if public confidence in the management of boxers is to be increased.
EPIDEMIOLOGY OF DRUG ABUSE
THE study of the spread of drug misuse is beset with difficulties, largely because much of our information is clinic-based and therefore related to a rather artificial situation in which an individual has identified himself as a drug user in a very overt way. He has acknowledged-even proclaimed-his position. But we need to learn more about the spread of drug misuse in order to understand its natural history. For this reason other models are necessary, and of these the study of the spread of drug use in a community is likely to be especially profitable. The study by Kosviner et al. of the spread of heroin use in a provincial town is a good example. 1.
Willis, J. H. in Scientific Basis of Drug Dependence. London,
1969. 2. Kosviner, A., Mitcheson, M. C., Myers, K., Ogborne, A., Stimson, G. V., Zacune, J., Edwards, G. Lancet, 1968, i, 1189.
It is the basis of treatment of rhesus-negative mothers with anti-D antiserum to prevent their becoming sensitised against rhesus-positive cells of their offspring. BILLINGHAM et al.17 referred to the" inhibition of active immunisation by antibody as an afferent " block of the immune response. Presumably the administered antibody combines with antigen, partially or wholly abolishing its power to immunise. It is of course necessary in the context of graft enhancement that the injected antibody does not cause an irreversible state of damage to the graft, and it is interesting that the longest enhancement observed by FRENCH and BATCHELOR was when heterozygous rat donors were used. Such donors would be expected to have quantitatively less antigen on their cells than would homozygotes, and therefore their organs would be less vulnerable to immune damage. The second mechanism believed to be important in enhancement is the competition for antigen sites that is postulated to exist between humoral antibody and immunologically committed lymphocytes which mediate cellular immunity.18-2o Since immunological enhancement can follow active immunisation, inhibition of immunisation (the first mechanism) cannot be a complete explanation. There is considerable evidence in support of the idea that antibody and immune cells compete for the same antigenic recep" tors-i.e., an efferent " block in the immune response. 17 It has been shown that anti-graft antibody can prevent immune lymphocytes from destroying target graft cells both in vivo 18,19 and in vitro.21,22 In the experiments of FRENCH and BATCHELOR the antibody-treated rats did develop an active antibody response; therefore the prolonged survival of the kidney grafts cannot be attributed solely to an inhibition of immunisation. FRENCH and BATCHELOR believe that the injected antibody covered a sufficient number of antigen sites on the transplanted kidney to protect it from irreversible damage by immune lymphocytes, but, on the other hand, sufficient antigen remained uncombined with antibody to permit some active immunisation of the recipient. Subsethe quently antibody actively synthesised by recipient continued to protect the graft-that is, a state of autoenhancement had been reached. These findings and those of STUART et al. 23 and HILDEMANN et al. 24 show that there is a good prospect of immunological enhancement being put to clinical use. 17. 18.
Billingham, R. E., Brent, L., Medawar, P. B. Transplant. Bull. 1956, 3, 84. Batchelor, J. R., Silverman, M. S. in Transplantation (edited by G. E. W. Wolstenholme and M. Cameron); p. 216. London,
1962. 19. Moller, G. J. natn. Cancer Inst. 1963, 30, 1205. 20. Batchelor, J. R. Cancer Res. 1968, 28, 1410. 21. Brunner, K. T., Mauel, J., Cerottini, J. C., Chapuis, B. 22.
Immunology, 1968, 14, 181. Hellström, I., Hellström, K. E., Evans, C. A., Heppner, G. H., Pierce, G. E., Yang, J. P. S. Proc. natn. Acad. Sci. 1969, 62, 362.
23.
Stuart, F. P., Saitoh, T., Fitch, F. W. Science, N. Y. 1968, 160,
1463. 24. Hildemann, W. H.
Transplant. Revs (in the press).
The Irritable Bowel ONE of the commonest causes of abdominal pain is what has been called the " irritable colon" or " spastic colon " syndrome; but, despite excellent descriptions of the characteristic symptoms, many
patients undergo biochemical and radiological investigations1 of all accessible abdominal viscera before the diagnosis is reluctantly accepted. This situation arises partly because insufficient attention is paid to the details of the symptoms and signs, and partly because the mechanism of symptom production is ill understood and visible or tangible evidence of pathological change is lacking. One consequence of the lack of objective " evidence is the doctor’s continuing anxiety about the diagnosis, and another is the purposive use of synonyms such as " colon neurosis " functional colon ", and " psychogenic "
diarrhoea ". CONNELL et al.demonstrated, in a selected group subjects, that after a meal the sigmoid colon responded with recurring peaks of high pressure in tubes placed within it. They recorded this manifestation of gut activity in the colon of three groups: (1) those with a duodenal ulcer in remission and no bowel symptoms; (2) those with " spastic colon"" whose abdominal pain was not brought on by eating during the investigation; and (3) those with " spastic colon " whose symptoms were brought on or aggravated by a meal eaten during the study. Those who had pain after eating produced waves of higher pressure and for a greater proportion of the recording time, both before and after a meal, than did the other groups. Hypermotility usually began some minutes before discomfort was noticed, but the conclusion was that the hypermotility was in some way related to the development of abdominal pain. The pain was not felt in the region of the sigmoid, and it did not correspond in its time-intensity pattern with the change in pressure within. the recording system. Indeed, each of three recording tubes, spaced 5 cm. apart, registered independent changes of pressure so that, if the high peak of pressure was responsible for pain, then a very large number of sites of production of "pain" impulses must exist. In one subject a similar pattern of hypermotility was recorded by telemetering capsule in the terminal ileum after a meal. of
HOLDSTOCK et al. have extended the investigations to another group of patients with severe abdominal pain for which no cause was found after a variety of investigations, but in whom unusually high peaks of pressure were recorded from the colon or small intestine. As in the previous inquiry, the patients included were those with an abnormal pattern in the pressure record. What is particularly interesting in 1. 2. 3.
Waller, S. L., Misiewicz, J. J. Lancet, Oct. 11, 1969, p. 753. Connell, A. M., Jones, F. A., Rowlands, E. N. Gut, 1965, 6, 105. Holdstock, D. J., Misiewicz, J. J., Waller, S. L. ibid. 1969, 10,
1113
this further report is that unusually high pressures were recorded by radiotelemetering from both small and large intestine as well as from the sigmoid colon. The only reasonable interpretation is that parts or the whole of the small and large intestine are involved in this abnormal response, which is either a discrete disturbance or simply one facet, recorded in a particular way, of what might be better called the irritable-gut syndrome, rather than limiting attention to the colon. 5, and probably at least 7, of the 9 patients had the irritable-colon syndrome. One man had had a partial gastrectomy followed by dumping, diarrhoea, steatorrhoea, and abdominal pain after eating. His pain was found to coincide with bursts of small-intestine activity either after eating or induced by intravenous injections of 5-hydroxytryptamine. Both pain and pressure-inducing activity were abolished by intravenous propantheline. In another patient with a partial gastrectomy upper abdominal
pain developed the same time as bursts of pressureinducing activity in the small intestine after eating; and 0-75 mg. neostigmine induced upper and lower abdominal pain and hyperactivity of the jejunum, sigmoid, and rectum. This activity, and the pains, were abolished by intravenous propantheline. In a patient with constipation and pain, sigmoid activity did not change, but activity in the small intestine increased at the same time as the pain; and again both were abolished by intravenous propantheline. 5 other patients showed a similar coincidence of pain and colon activity after a meal or an injection of neostigmine. 2 patients showed similar changes in colonic pressure in response to eating, but they did not have coincident pain, although pain was an important feature of their illness. Indeed, in these 2 patients the pressures recorded by the transducer approached the level of the arterial bloodpressure, suggesting that ischxmia of the bowel wall is unlikely to be important in the production of this type of abdominal discomfort. The simultaneous relief of pain and cessation of pressure-inducing activity after intravenous propantheline in the other patients suggest either that pain and motility are sometimes directly linked or that propantheline blocks the action of a common causal agent. Clearly, hypermotility does not always cause pain, but pain might result from a particular hypermotility in a at
particular place. These observations provide interesting material for speculation. It is not uncommon for patients with symptoms suggestive of irritable colon to have a very noisy abdomen-noise which because of its high
pitch and duration seems likely to be produced by movement of gas-liquid interfaces in the small intestine, providing evidence for small-intestine hyperactivity, although it might result from colon hypermotility. A barium follow-through examination often shows rapid transit through the small intes-
tine.4 If the irritable colon is really an irritable gut, at least from pylorus to rectum, then where is the lesion? Orthodox histological examination reveals no cause, and such evidence as there is suggests that the disturbance is an excess of phasic contractility of smooth muscle which might arise in muscle or in nerve. The role of the neural elements in the gut wall is probably to modify but not to initiate the contractile activity of the smooth muscle. The effects of propantheline and neostigmine in abolishing and exaggerating respectively the motility response to food might suggest that the lesion is in the neural control of motility, but this is not necessarily so: the irritability might be a primary disturbance of myogenic conduction and initiation of contraction, potentiated by a normal neural control mechanism; and the search for treatment might be better directed towards the muscle cell rather than the neural
pathway. The second question raised by these observations the mechanism of pain production and the site of the sensitive endings. Because the recording device happened to be there at the time, the abnormal activity was recorded in the sigmoid colon and in various parts of the small intestine and proximal colon. It would be a remarkable coincidence if the pain was produced only at the sites of the pressurerecording devices, unless the pain and hypermotility But were a reaction of the gut to their presence. hypermotility is not always accompanied by pain. It is reasonable to suppose that hypermotility is widespread and that pain production may be widespread or localised or absent. Pain in this syndrome is often steady, but sometimes colicky, and when it varies in intensity the time-intensity curve has a scale 5-50 times slower than that of the recorded changes in pressure. In some of the tracings a wave of pressure rises from and falls to its basal level in about 3-5 seconds in both small and large intestine, sometimes superimposed on a slower and considerable upward shift of the baseline over 20-30 seconds. The sensation of pain seems likely to be a summation of impulses from many parts of the gut produced by many local contractions of the wall. concerns
Two common features of the irritable-gut syndrome tenderness of part or the whole of the colon and small intestine to local pressure; and a sensation of pain deep to the surface marking of the transverse or descending colon and provoked by pressure on the caecum or ascending colon. These signs suggest that the colon may be tender to pressure not only from without but also from within-a situation not dissimilar to the aseptic bladder and urethral irritation which afflict many women and which is not uncommonly associated with the irritable-bowel syndrome. Moreover, this tenderness of the colon is
are
4.
Kaiser, M. H., Zion, 31, 69.
D.
E., Bockus, H. L. Gastroenterology, 1956,
1114
commonly present when pain is absent. HOLDSTOCK et awl. suggest that some of the activity which they recorded might be excessive segmentation activity which produces a functional obstruction and distension of the bowel proximal to the hypersegmenting segment. They postulate that this distension may be the cause of pain, by analogy with the pain produced by distending the small intestine with a balloon; but they cannot reconcile pain due to functional obstruction with simultaneous diarrhoea due to increased propulsive activity in some patients. They have produced convincing evidence that hypersegmentation of an intense degree, the nearest activity to the popular but nebulous concept of
Annotations MEDICAL ASPECTS OF BOXING
THE investigations by the Royal College of Physicians that led to the publication of their report on boxing1 began after a debate in the House of Lords in 1962 on Baroness Summerskill’s controversial Bill to ban boxing, in which the late Lord Brain suggested that an independent and scientific inquiry should be made. An interim report issued in 1964 stated that conclusions about the medical hazards of boxing could not be reached on the evidence examined. A controlled study was planned and this has been carried out by Dr. A. H. Roberts, an honorary research fellow of the College. His survey2 was designed to establish the prevalence of boxing injuries. A random-sampling technique was used to select 250 boxers from a population of 16,781 men registered with the British Boxing Board of Control between 1929 and 1955. Only professional boxers were studied, since the records for amateurs did not contain the required information. The number of registered boxers has fallen steadily since the late 1930s, and since those chosen to take part in the study formed a fixed proportion of the number registered each year, the majority were boxing in the earlier part of the period under study. But the evidence does not apply solely to this time, for it illustrates clearly how injuries develop. This is pertinent to boxing at any stage in its history. 224 men from the sample were given a physical examination, a brief psychiatric interview, and a number of memory tests. Apart from an electroencephalogram, no technical neurological tests were done. 1 in 6 boxers (17%) showed evidence of brain damage, and a third of these had severe chronic traumatic encephalopathy. The neurological damage was multifocal, with symptoms predominantly referable to the cerebellar, pyramidal, or extrapyramidal systems. This corresponds with findings of previous investigations. In general terms, there are estimated to be 200 severely " punch drunk" ex-boxers in Royal College of Physicians of London. Committee on Boxing: Report on The Medical Aspects of Boxing. 1969. 2. Brain Damage in Boxers. By A. H. ROBERTS. London: Pitman Medical Scientific Publishing Co.: 1969. 40s. (hardback), 30s. 1.
(paperback). 3. See Lancet, 1969,
i,
746.
"
spasm " so far demonstrated, may appear without pain-a finding perhaps as worthy of note as the coincidence of pain and hypersegmentation, and one which deepens the mystery. Many writers on " irritable colon " believe it to be a manifestation of neurosis; others have been kinder and termed it psychosomatic. Either HOLDSTOCK et al. have discovered a way of separating a genuine disease from a man-made rag-bag syndrome, or they have demonstrated that in this syndrome the small and large intestine are capable of violent,
non-propulsive, uncoordinated, presumably useless, and sometimes excruciatingly painful motor activity. Britain, and a further 400-500 men with damage recognisable only on physical examination. Very few chronic eye or ear injuries were reported. Roberts demonstrated conclusively that the length of a boxer’s career and the total number of bouts fought were closely linked to the severity of the ultimate neurological damage. In other words, the prevalence of clinical signs of brain damage of the kind that are
found in ex-boxers increases with exposure
to
boxing. Unexpectedly, psychometric testing showed no relation between impaired memory and length of boxing career. But boxers complained of forgetfulness, and those who found it most troublesome were older men and those who had had long careers in boxing. Only 2 men were indisputably demented, and both had severe chronic traumatic encephalopathy. Paranoid states and personality change with increased aggressiveness were seldom encountered. Better supervision, reduction in the number of bouts a boxer fights each year, and other safeguards introduced by boxing authorities have considerably reduced the frequency and severity of injuries. But further studies, using information from both professional and amateur bodies, are essential if public confidence in the management of boxers is to be increased.
EPIDEMIOLOGY OF DRUG ABUSE
THE study of the spread of drug misuse is beset with difficulties, largely because much of our information is clinic-based and therefore related to a rather artificial situation in which an individual has identified himself as a drug user in a very overt way. He has acknowledged-even proclaimed-his position. But we need to learn more about the spread of drug misuse in order to understand its natural history. For this reason other models are necessary, and of these the study of the spread of drug use in a community is likely to be especially profitable. The study by Kosviner et al. of the spread of heroin use in a provincial town is a good example. 1.
Willis, J. H. in Scientific Basis of Drug Dependence. London,
1969. 2. Kosviner, A., Mitcheson, M. C., Myers, K., Ogborne, A., Stimson, G. V., Zacune, J., Edwards, G. Lancet, 1968, i, 1189.