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TEMPOROMANDIBULAR-JOINT SYNDROME
859 EXPERTS AND AMATEURS IN STROKE THERAPY MosT doctors concerned with the management of strokes make full use of whatever paramedical rehabiliare to hand—occupational therapy, speech therapy, physiotherapy. With this intervention an improvement is expected and is usually seen. If a skilled therapist has substantial impact on stroke recovery, one would wish to see this personal service available to every patient. Anthony Hopkins, in Health Trends’ shows that at present it would be impossible to provide qualified speech therapy for all the strokes expected to benefit. He calculates that, if all the working speech therapists in the country were absorbed into the treatment of dysphasic strokes alone, they would still not meet the demand. Before investing in a great expansion of speechtherapy training, it is right to ask whether personal attention from these highly trained people is the only
tative skills
whereby the dysphasic stroke patient may be improved. Hopkins notes that speech therapy is largely empirical in the absence of a complete understanding of dysphasia, and after reviewing published work he concludes that there is hardly any controlled evidence of significant benefit from speech therapy, as such. He suggests, and quotes speech therapists as saying, that any improvement hinges mainly on the personal relationship established and on the encouragement given-the implication being that less highly trained persons might, with some guidance, achieve as good a result. This view finds sup-
means
port in Valerie Griffith’s2 account of the recruitment of untrained volunteers, in Oxford and the Chilterns, to encourage and support dysphasic stroke victims. The volunteers were given some simple rules to follow, but were required mainly to form a relationship with the patient and help him in his own efforts. Two hundred persons, mostly housewives, were recruited by one organiser to treat thirty-one patients in their homes. After nine months, twenty-one of these patients were believed by their general practitioners to have made a definite improvement as regards speech and understanding. All but one of the rest were thought to have improved in confidence and attitude to life. This experience makes a case for prompt exploration of the value of unskilled support to the speech therapist in meeting the needs of the hundred thousand people in Britain with stroke. Might not the same be said of stroke rehabilitation in general? There is no doubt about the relation between rehabilitative effort and improved patient performance; but controlled investigations34 suggest that the personal intervention of trained workers does not significantly improve recovery-rates compared with less intensive regimens. Marquardsen, reviewing published work and his own cases, concluded that "few stroke patients would benefit from long continued and extensive treatment ir rehabilitation institutions". Dr Monica Stewart6 latel) called for much greater use of the home, rather than tht hospital, for rehabilitation. Any attempt to do this ona 1. Hopkins, A. Health Trends, 1975, 7, 58. 2 Griffith, V. E. Br. med. J. 1975, iii, 633. 3 Stern, P. H., McDowell, F., Miller, J. M., Robinson, M. Archs phys. Med. Rehab. 1970, 51, 526. 4 Peacock, P. B., Riley, C. P., Lampton, T. D., Raffel, S. S., Walker, J. S. in Trends in Epidemiology (edited by G. T. Stewart); p. 231. Springfield, Illinois, 1972. 5 Marquardsen, J. The Natural History of Acute Cerebrovascular Disease.
Copenhagen, 1969. Paper read at Annual Conference, Royal College of Physicians, Oct. 9, 1975.
6. Stewart, M.
British Geriatric
Society,
scale using trained workers would be foredoomed in the present state of recruitment. Hopkins1 would prefer "a band of ’rehabilitation workers’ who would possess some of the skills of the physiotherapist, the occupational therapist and the speech therapist". Family participation is also important. The most important role of the therapist might therefore be as initiator and trainer. Depending on the circumstances, she might guide the family, or volunteers, or rehabilitation aides in developing a regimen of activities and encouragement appropriate to each stroke patient, without intervening personally except as a monitor. This could be the best, and indeed the only, way of effectively reaching the majority of those who need help, without exhausting resources of trained personnel. Most of the demands made on paramedical workers’ time originate from doctors’ requests. It may now be up to doctors to help them meet these commitments.
large
TEMPOROMANDIBULAR-JOINT SYNDROME
temporomandibular-joint (T.M.J.) syndrome is by pain in the ear, the face, and the temple. Symptoms are usually unilateral and intermittent and young women are predominantly affected, many of them being compulsive bruxists (teeth grinders) or chewing-gum devotees. Trauma may be another cause of the syndrome, and dysfunction of the T.M.J. has followed cervical whiplash injuries.8 One useful sign of the syndrome is a reduction of mobility on opening the mouth, THE
characterised
with deviation of the chin to the affected side when the condition is unilateral.9 Treatment includes reassurance, analgesics, tranquillisers, heat treatment, local anxsthesia to the painful muscles, correction of malocclusion, and exercises to stretch spastic muscles and restore coordinated motion. 10 Costen described a syndrome that may be associated with T.M.J. dysfunction including impaired hearing, a feeling of fullness in the ears, tinnitus, facial pain, earache, vertigo, nystagmus, occipital headache, burning sensations in the throat, tongue, and side of the nose, dry mouth, and a snapping noise while chewing.l 12 He suggested that the condition was due to loss of molar support, resulting in damage to the T.M.]. and associated structures. Schwartz and Chayes’O do not agree that such a large collection of symptoms should be included in the T.M.J. syndrome. They regard the condition as a paindysfunction syndrome with two phases-an incoordination phase characterised by clicking, subluxation, or dislocation of the T.M.J., and a limitation phase with painful muscle spasm, which, if of long enough duration, may lead to contracture. They see malocclusion as a contributing factor only, and emotional tension as one of the most important causes of the syndrome. Schwartz and Chayes’ hypothesis is that stress leading to tension may result in muscle spasm, occlusal wear, loosening of teeth, pulp death, or no reaction at all. A monograph 13 from the University of Sydney deals Pathy, J. Geront. clin. 1975, 17, 61. Roydhouse, R. H. Lancet, 1973, i, 1394. 9. Foged, J. ibid. 1949, ii, 1209. 10. Schwartz, L., Chayes, C. M. Facial Pain and Mandibular Dysfunction. Philadelphia 1968. 11. Costen, J. B. Ann. Otol. 1934, 43, 1. 12. Costen, J. B. J. Am. med. Ass. 1936, 107, 252. 13. The Temporomandibular Joint Syndrome: the masticatory apparatus of man in normal and abnormal function (Monographs in Oral Science, vol. iv). Edited by C. J. GRIFFIN and R. HARRIS. Basle: Karger, 1975. Pp. 205. 7. 8.
Sw Fr 93.
860 with the anatomy, histology, and physiology of the T.M.J. in normal and abnormal function. Chapters on neuromuscular mechanisms and electro-myography (E.M.G.) of the muscles of mastication are followed by a study of E.M.G. analysis of treatment results in 22 patients. In 13 patients symptoms were localised to areas innervated by the trigeminal nerves, but in 9 patients symptoms were also present in the neck, shoulders, thorax, and arms. All patients had malocclusion (in some due to loss of molar support), and treatment with dental prostheses restored E.M.G. activity to almost normal in the
temporalis and masseter muscles during an open-close-clench cycle. R. Harris and C. J. Griffin show that pain in the T.M.J. syndrome may be relieved by injecting local anaesthetic solution into the hypertonic mandibular elevator muscles. Anaesthetising the right medial pterygoid muscle in one patient with the T.M.J. syndrome not only removed the local symptoms but also relieved pain and restored full movement in the right arm, which had previously been weak and restricted in movement. This exemplifies the complex nature of the syndrome: other motor nuclei may be affected by hypertonicity of the motorneurones of the medial pterygoid muscle. Discussing treatment, Griffin reports details of 586 patients, some of whom have been under observation for 15 years. Of those with their own teeth, 91% had centric slides, and all the patients wearing full upper and lower dentures were found to slide into centric occlusion. Treatment was by occlusal splints initially, with relief of symptoms after a few days in most cases. On follow-up after treatment, which often involved further prosthetic work, great improvement or complete relief of symptoms was recorded in 503 patients, 3 of whom were diagnosed as having trigeminal neuralgia, and there was no improvement in 83 patients, 2 of whom had trigeminal neuralgia. Malocclusion and muscle spasm seem equally important factors. In the T.M.]. syndrome the standard radiographs of the T.M.j. are normal, but on simultaneous cineradiography of the two joints one mandibular head is sometimes seen to move out of the articular fossa before the other. 14 In contrast, temporomandibular osteoarthrosis, which affects an older age group, has definite radiographic changes with erosion of the articular surface of the condyle (best detected by a transpharyngeal projection1S). Radiographic abnormalities of the T.M.]. may also be found in rheumatoid arthritis and Still’s disease, and have lately been described in ankylosing spondylitis.16 These conditions should therefore be excluded before T.M.J. syndrome is diagnosed.
BUMETANIDE BUMETANIDE (3-n-butylamino-4-phenoxy-5-sulfamylbenzoic acid) represents a new group of potent diuretics whose action closely resembles that of frusemide." Clearance studies in dogs and man have confirmed that it is equipotent with frusemide at a fortieth the molar dosage and suggest that it inhibits sodium reabsorption in the ascending limb of Henle’s loop and probably in the proximal tubule as well. IS 19 Until the appropriate 14.
Ward, J. R., Dolowitz, D. A., Baukol, J. L., Smith, C., Fingerle, C. O. Archs intern. Med. 1963, 112, 693. 15. Toller, P. A. Proc. R. Soc. Med. 1974, 67, 153. 16. Davidson, C., Wojtulewski, J. A., Bacon, P. A., Winstock, D. Ann. rheum. Dis. 1975, 34, 87. 17. Feit, P. W. J. med. Chem. 1971, 14, 432.
single-nephron work, using micropuncture and microperfusion techniques, has been done, the precise sites of action must remain speculative. In common with other potent diuretics which increase the delivery of sodium to the distal tubule, potassium is inevitably lost in exchange for sodium at this site. There is some evidence that bumetanide may have an initial uricosuric effect but this is offset by the contraction in extracellular fluid resulting in retention of urate. 20 There is not enough evidence to assess the effect of bumetanide on carbohydrate metabolism. Bumetanide can be measured in serum and urine by labelling it with a radioactive isotope—an important point for a drug today if pharmacokinetic and pharmacodynamic studies are to be conducted in parallel. It is rapidly and well absorbed from the gut, achieves peak plasma-levels within one hour, is limited to an apparently small volume of distribution, and is rapidly excreted by the kidney. A carboxylic-acid group confers a high degree of protein-binding which is readily reversible but it does prevent much of the drug from entering the tissues. The pharmacological effect of bumetanide in man correlates well with its concentration in serum and urine. There is no evidence that bumetanide is metabolised by the liver in man but in renal failure the drug probably is excreted in bile. Several clinical trials have confirmed the value of bumetanide in cardiac,22 23 renal ’24 21 and hepatic failure.26 27 It usually induces a peak diuresis 1-2 hours after an oral dose and its action is complete within 4-6 hours. If diuresis becomes inadequate, responsiveness may be restored by increasing the dose-that is, it has a steep dose-response curve and the maximum or ceiling dose produces a peak sodium excretion of more than 25% of the filtered load (hence the term high-ceiling diuretic). Like frusemide and ethacrynic acid, bumetanide continues to act in the presence of acidosis or alkalosis, and in high doses it is effective even in advanced renal failure. Adverse reactions are few, but myalgia has been troublesome in patients with chronic renal failure, in whom the drug should be avoided. Old habits die hard, and clinicians who have depended on frusemide during the past decade will hesitate to drop a trusted friend. At the moment, bumetanide is slightly cheaper than frusemide and it may prove an effective alternative on the rare occasion when frusemide fails. Diuretics inhibit sodium reabsorption in the tubule by a direct action on the transporting cells themselves but the receptor is still unknown, so biological activity cannot yet be related to chemical structure. Research associated with the discovery of bumetanide has shed more light on these structure/activity relationships. If the receptors can be identified, it may be possible to separate the clinically desirable diuretic effect from the unwanted effects such as hyperuricaemia, hypokalxmia, and impaired glucose tolerance. Ostergaard, E. H., Magnussen, M. P., Kaegaard Nielsen, C., Eilertsen, E, Frey, H. -H. Arzneimittel-Forsch. 1972, 22, 66. 19. Bourke, E. Postgrad. med. J. 1975, 51, suppl. 6, p. 23. 18.
20. Lant, A. F. ibid. p. 35. 21. Davies, D. L., Lant, A F., Millard, N. R., Smith, A. J., Ward, J W., Wilson. G. M. Clin. Pharm. Ther. 1974, 15, 141. 22. Olesen, K. H., Sigurd, B., Hesse, B., Steiness, E., Leth, A. Postgrad. medJ
1975, 51, suppl. 6, p. 54. 23. Seth, H. C., Coulshed, N., Epstein, E. J. Br. J. clin. Pract. 1975, 29,7. 24. Barclay, J. E., Lee, H. A. Postgrad. med. J. 1975, 51, suppl. 6, p. 43. 25. Allison, M. E. M., Lindsay, M. K., Kennedy, A. C. ibid. p. 47. 26. Ring-Larsen, H. ibid. p. 77. 27. Moult, P. J. A., Lunzer, M. R., Trash, D. B., Sherlock, S. ibid. p. 81.
tative skills
whereby the dysphasic stroke patient may be improved. Hopkins notes that speech therapy is largely empirical in the absence of a complete understanding of dysphasia, and after reviewing published work he concludes that there is hardly any controlled evidence of significant benefit from speech therapy, as such. He suggests, and quotes speech therapists as saying, that any improvement hinges mainly on the personal relationship established and on the encouragement given-the implication being that less highly trained persons might, with some guidance, achieve as good a result. This view finds sup-
means
port in Valerie Griffith’s2 account of the recruitment of untrained volunteers, in Oxford and the Chilterns, to encourage and support dysphasic stroke victims. The volunteers were given some simple rules to follow, but were required mainly to form a relationship with the patient and help him in his own efforts. Two hundred persons, mostly housewives, were recruited by one organiser to treat thirty-one patients in their homes. After nine months, twenty-one of these patients were believed by their general practitioners to have made a definite improvement as regards speech and understanding. All but one of the rest were thought to have improved in confidence and attitude to life. This experience makes a case for prompt exploration of the value of unskilled support to the speech therapist in meeting the needs of the hundred thousand people in Britain with stroke. Might not the same be said of stroke rehabilitation in general? There is no doubt about the relation between rehabilitative effort and improved patient performance; but controlled investigations34 suggest that the personal intervention of trained workers does not significantly improve recovery-rates compared with less intensive regimens. Marquardsen, reviewing published work and his own cases, concluded that "few stroke patients would benefit from long continued and extensive treatment ir rehabilitation institutions". Dr Monica Stewart6 latel) called for much greater use of the home, rather than tht hospital, for rehabilitation. Any attempt to do this ona 1. Hopkins, A. Health Trends, 1975, 7, 58. 2 Griffith, V. E. Br. med. J. 1975, iii, 633. 3 Stern, P. H., McDowell, F., Miller, J. M., Robinson, M. Archs phys. Med. Rehab. 1970, 51, 526. 4 Peacock, P. B., Riley, C. P., Lampton, T. D., Raffel, S. S., Walker, J. S. in Trends in Epidemiology (edited by G. T. Stewart); p. 231. Springfield, Illinois, 1972. 5 Marquardsen, J. The Natural History of Acute Cerebrovascular Disease.
Copenhagen, 1969. Paper read at Annual Conference, Royal College of Physicians, Oct. 9, 1975.
6. Stewart, M.
British Geriatric
Society,
scale using trained workers would be foredoomed in the present state of recruitment. Hopkins1 would prefer "a band of ’rehabilitation workers’ who would possess some of the skills of the physiotherapist, the occupational therapist and the speech therapist". Family participation is also important. The most important role of the therapist might therefore be as initiator and trainer. Depending on the circumstances, she might guide the family, or volunteers, or rehabilitation aides in developing a regimen of activities and encouragement appropriate to each stroke patient, without intervening personally except as a monitor. This could be the best, and indeed the only, way of effectively reaching the majority of those who need help, without exhausting resources of trained personnel. Most of the demands made on paramedical workers’ time originate from doctors’ requests. It may now be up to doctors to help them meet these commitments.
large
TEMPOROMANDIBULAR-JOINT SYNDROME
temporomandibular-joint (T.M.J.) syndrome is by pain in the ear, the face, and the temple. Symptoms are usually unilateral and intermittent and young women are predominantly affected, many of them being compulsive bruxists (teeth grinders) or chewing-gum devotees. Trauma may be another cause of the syndrome, and dysfunction of the T.M.J. has followed cervical whiplash injuries.8 One useful sign of the syndrome is a reduction of mobility on opening the mouth, THE
characterised
with deviation of the chin to the affected side when the condition is unilateral.9 Treatment includes reassurance, analgesics, tranquillisers, heat treatment, local anxsthesia to the painful muscles, correction of malocclusion, and exercises to stretch spastic muscles and restore coordinated motion. 10 Costen described a syndrome that may be associated with T.M.J. dysfunction including impaired hearing, a feeling of fullness in the ears, tinnitus, facial pain, earache, vertigo, nystagmus, occipital headache, burning sensations in the throat, tongue, and side of the nose, dry mouth, and a snapping noise while chewing.l 12 He suggested that the condition was due to loss of molar support, resulting in damage to the T.M.]. and associated structures. Schwartz and Chayes’O do not agree that such a large collection of symptoms should be included in the T.M.J. syndrome. They regard the condition as a paindysfunction syndrome with two phases-an incoordination phase characterised by clicking, subluxation, or dislocation of the T.M.J., and a limitation phase with painful muscle spasm, which, if of long enough duration, may lead to contracture. They see malocclusion as a contributing factor only, and emotional tension as one of the most important causes of the syndrome. Schwartz and Chayes’ hypothesis is that stress leading to tension may result in muscle spasm, occlusal wear, loosening of teeth, pulp death, or no reaction at all. A monograph 13 from the University of Sydney deals Pathy, J. Geront. clin. 1975, 17, 61. Roydhouse, R. H. Lancet, 1973, i, 1394. 9. Foged, J. ibid. 1949, ii, 1209. 10. Schwartz, L., Chayes, C. M. Facial Pain and Mandibular Dysfunction. Philadelphia 1968. 11. Costen, J. B. Ann. Otol. 1934, 43, 1. 12. Costen, J. B. J. Am. med. Ass. 1936, 107, 252. 13. The Temporomandibular Joint Syndrome: the masticatory apparatus of man in normal and abnormal function (Monographs in Oral Science, vol. iv). Edited by C. J. GRIFFIN and R. HARRIS. Basle: Karger, 1975. Pp. 205. 7. 8.
Sw Fr 93.
860 with the anatomy, histology, and physiology of the T.M.J. in normal and abnormal function. Chapters on neuromuscular mechanisms and electro-myography (E.M.G.) of the muscles of mastication are followed by a study of E.M.G. analysis of treatment results in 22 patients. In 13 patients symptoms were localised to areas innervated by the trigeminal nerves, but in 9 patients symptoms were also present in the neck, shoulders, thorax, and arms. All patients had malocclusion (in some due to loss of molar support), and treatment with dental prostheses restored E.M.G. activity to almost normal in the
temporalis and masseter muscles during an open-close-clench cycle. R. Harris and C. J. Griffin show that pain in the T.M.J. syndrome may be relieved by injecting local anaesthetic solution into the hypertonic mandibular elevator muscles. Anaesthetising the right medial pterygoid muscle in one patient with the T.M.J. syndrome not only removed the local symptoms but also relieved pain and restored full movement in the right arm, which had previously been weak and restricted in movement. This exemplifies the complex nature of the syndrome: other motor nuclei may be affected by hypertonicity of the motorneurones of the medial pterygoid muscle. Discussing treatment, Griffin reports details of 586 patients, some of whom have been under observation for 15 years. Of those with their own teeth, 91% had centric slides, and all the patients wearing full upper and lower dentures were found to slide into centric occlusion. Treatment was by occlusal splints initially, with relief of symptoms after a few days in most cases. On follow-up after treatment, which often involved further prosthetic work, great improvement or complete relief of symptoms was recorded in 503 patients, 3 of whom were diagnosed as having trigeminal neuralgia, and there was no improvement in 83 patients, 2 of whom had trigeminal neuralgia. Malocclusion and muscle spasm seem equally important factors. In the T.M.]. syndrome the standard radiographs of the T.M.j. are normal, but on simultaneous cineradiography of the two joints one mandibular head is sometimes seen to move out of the articular fossa before the other. 14 In contrast, temporomandibular osteoarthrosis, which affects an older age group, has definite radiographic changes with erosion of the articular surface of the condyle (best detected by a transpharyngeal projection1S). Radiographic abnormalities of the T.M.]. may also be found in rheumatoid arthritis and Still’s disease, and have lately been described in ankylosing spondylitis.16 These conditions should therefore be excluded before T.M.J. syndrome is diagnosed.
BUMETANIDE BUMETANIDE (3-n-butylamino-4-phenoxy-5-sulfamylbenzoic acid) represents a new group of potent diuretics whose action closely resembles that of frusemide." Clearance studies in dogs and man have confirmed that it is equipotent with frusemide at a fortieth the molar dosage and suggest that it inhibits sodium reabsorption in the ascending limb of Henle’s loop and probably in the proximal tubule as well. IS 19 Until the appropriate 14.
Ward, J. R., Dolowitz, D. A., Baukol, J. L., Smith, C., Fingerle, C. O. Archs intern. Med. 1963, 112, 693. 15. Toller, P. A. Proc. R. Soc. Med. 1974, 67, 153. 16. Davidson, C., Wojtulewski, J. A., Bacon, P. A., Winstock, D. Ann. rheum. Dis. 1975, 34, 87. 17. Feit, P. W. J. med. Chem. 1971, 14, 432.
single-nephron work, using micropuncture and microperfusion techniques, has been done, the precise sites of action must remain speculative. In common with other potent diuretics which increase the delivery of sodium to the distal tubule, potassium is inevitably lost in exchange for sodium at this site. There is some evidence that bumetanide may have an initial uricosuric effect but this is offset by the contraction in extracellular fluid resulting in retention of urate. 20 There is not enough evidence to assess the effect of bumetanide on carbohydrate metabolism. Bumetanide can be measured in serum and urine by labelling it with a radioactive isotope—an important point for a drug today if pharmacokinetic and pharmacodynamic studies are to be conducted in parallel. It is rapidly and well absorbed from the gut, achieves peak plasma-levels within one hour, is limited to an apparently small volume of distribution, and is rapidly excreted by the kidney. A carboxylic-acid group confers a high degree of protein-binding which is readily reversible but it does prevent much of the drug from entering the tissues. The pharmacological effect of bumetanide in man correlates well with its concentration in serum and urine. There is no evidence that bumetanide is metabolised by the liver in man but in renal failure the drug probably is excreted in bile. Several clinical trials have confirmed the value of bumetanide in cardiac,22 23 renal ’24 21 and hepatic failure.26 27 It usually induces a peak diuresis 1-2 hours after an oral dose and its action is complete within 4-6 hours. If diuresis becomes inadequate, responsiveness may be restored by increasing the dose-that is, it has a steep dose-response curve and the maximum or ceiling dose produces a peak sodium excretion of more than 25% of the filtered load (hence the term high-ceiling diuretic). Like frusemide and ethacrynic acid, bumetanide continues to act in the presence of acidosis or alkalosis, and in high doses it is effective even in advanced renal failure. Adverse reactions are few, but myalgia has been troublesome in patients with chronic renal failure, in whom the drug should be avoided. Old habits die hard, and clinicians who have depended on frusemide during the past decade will hesitate to drop a trusted friend. At the moment, bumetanide is slightly cheaper than frusemide and it may prove an effective alternative on the rare occasion when frusemide fails. Diuretics inhibit sodium reabsorption in the tubule by a direct action on the transporting cells themselves but the receptor is still unknown, so biological activity cannot yet be related to chemical structure. Research associated with the discovery of bumetanide has shed more light on these structure/activity relationships. If the receptors can be identified, it may be possible to separate the clinically desirable diuretic effect from the unwanted effects such as hyperuricaemia, hypokalxmia, and impaired glucose tolerance. Ostergaard, E. H., Magnussen, M. P., Kaegaard Nielsen, C., Eilertsen, E, Frey, H. -H. Arzneimittel-Forsch. 1972, 22, 66. 19. Bourke, E. Postgrad. med. J. 1975, 51, suppl. 6, p. 23. 18.
20. Lant, A. F. ibid. p. 35. 21. Davies, D. L., Lant, A F., Millard, N. R., Smith, A. J., Ward, J W., Wilson. G. M. Clin. Pharm. Ther. 1974, 15, 141. 22. Olesen, K. H., Sigurd, B., Hesse, B., Steiness, E., Leth, A. Postgrad. medJ
1975, 51, suppl. 6, p. 54. 23. Seth, H. C., Coulshed, N., Epstein, E. J. Br. J. clin. Pract. 1975, 29,7. 24. Barclay, J. E., Lee, H. A. Postgrad. med. J. 1975, 51, suppl. 6, p. 43. 25. Allison, M. E. M., Lindsay, M. K., Kennedy, A. C. ibid. p. 47. 26. Ring-Larsen, H. ibid. p. 77. 27. Moult, P. J. A., Lunzer, M. R., Trash, D. B., Sherlock, S. ibid. p. 81.