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DIABETIC HEPATOMEGALY
248 adds that an anti-E. coli conjugate which has now been prepared is more specific than that prepared with E. histolytica. Other amœbæ that may be found in faeces, such as Dierttarnccba fragilis and Endolirriax oana, do not react with the anti-E. histolytica conjugate ; but other protozoa, including the small race of E. histolytica, have not been investigated with this technique. Although still in the experimental stage, Coldman’s method gives promise of an entirely new method of Since the detecting and identifying E. histolytica. criterion is the presence or absence of fluorescence, the test could be done by relatively untrained staff. Even where amœbæ or cysts are very scanty, the fluorescence from these should make identification certain, provided that the fæces contain no other fluorescent material. THE
TEMPORAL-LOBE
EPILEPSIES
IN the past few years a group of epileptic disturbances has been recognised in which the site of abnormality is the temporal lobe or a closely related area. This group has been rather loosely termed " the temporal-lobe epilepsies." The clinical attacks, although varying in detail, have enough in common to suggest the diagnosis ; and this may be confirmed by electro-encephalography (E.E.G.), which shows a local or focal abnormality in temporal leads. The clinical picture includes attacks with a pronounced visceral or vasomotor aura or content ; and the group embraces many of the cases with automatism (apart from the postictal ones), and those with Jackson’s " dreamy " or intellectual aura, the déjà vu phenomenon, and psychomotor disturbances. It includes also a large proportion of the difficult so-called " epileptic " personalities and probably some of the strikingly episodic behaviour abnormalities of childhood. In addition to these "local signs" of the site of discharge, there may be frank grand-mal attacks. Despite these pleomorphic symptoms however, automatism, visceral or vasomotor features, and clouding (rather than complete loss) of consciousness are often distinguishing features of the group. The E.E.G. may show a focal spike discharge from one or other temporal lobe. However, a localised abnormality, especially if paroxysmal, or even a bilateral abnormality confined to the temporal areas, is of some value as a clue to a focus. This may be defined by placing electrodes as near as possible to the temporal lobes. They may be introduced into the nasopharynx, or needle electrodes may be inserted, as for a trigeminal-root injection, against the base of the temporal fossa. The focus may also be sought by enhancing or provoking a local Of these " provocation techelectrical abnormality. niques " one of the most useful is recording during sleep induced by quinalbarbitone (’ Seconal’) ; at this time a local discharge or even a clear-cut spike focus, which was hidden in the general activity of the wakeful cortex, may emerge. The discovery of a focal abnormality is valuable not but in planning treatment. These only in epilepsies often respond poorly to the usual anticonsometimes associated vulsants ; and the with them may make management difficult. They are therefore especially open to consideration for surgical excision if some clearly defined focus can be found in an area whose function can be sacrificed with impunity. With operation, of course, such a focus can be defined more precisely by recording directly from the dura or the surface of the cortex itself. In treatment, excision of the anterior parts of the temporal lobes has been practised in America,1in this country,3 and in France.4 In assessing this treatment it is necessary to "
"
diagnosis
personality general
1. 2. 3. 4.
Penfield, W., Flanigin, H. Arch. Neurol. Psychiat. 1950, 64, 491. Bailey, P., Gibbs, F. A. J. Amer. med. Ass. 1951, 145, 365. Hill. D., Falconer, M. A. Proc. R. Soc. Med. 1953, 46, 965. Petit-Dutaillis, D., et al. Sem. Hóp. Paris, 1953, 29, 3838.
consider both change in frequency of actual attacks and any alterations in the associated mental and personality traits. Of the 20 French cases recently reported, 16 had been followed for ½-2½ years ; of these 16, 9 had their attacks abolished, 2 had only minor attacks postoperatively, and 5 still had attacks and were classed as therapeutic failures even if the frequency of attacks was reduced. Mental changes are only briefly mentioned, but some general improvement is claimed. Judging by other series, it seems that reduction in epileptic attacks is more satisfactory and consistent than is any improvement in personality or conduct : but here opinion is still divided. In this field enthusiasm should be tempered with caution until prolonged follow-up studies have been published. Before the recording of cerebral electrical activity was possible, elevation of depressed bone, freeing of dural adhesions, and excision of brain scars were all used-and with effect-in abolishing epileptic attacks, for a time. After three or four years, however, relapses A similar trend is already were increasingly frequent. apparent where cortical excision has been based on abnormal electrical discharge. Possibly in temporal-lobe epilepsy, which is notoriously unresponsive to medical treatment, the reasonable chance of controlling fits even for a few years would, in a severely disabled person, justify a major cerebral operation, especially if improvement in conduct and behaviour was also to be expected. No adverse consequences have been reported, and the procedure undoubtedly calls for further trial ; but for its final assessment, especially if it is to be applied to the young, the follow-up should be considered in terms of a decade rather than of six months or a year. DIABETIC HEPATOMEGALY The incidence of hepatomegaly in diabetics has received scant attention except in children, in whom the liver edge is much more easily felt. In adult as well as child diabetics, enlargement of the liver is commonest where the diabetes is poorly controlled, and of course patients reporting regularly at clinics are less likely to be poorly controlled than those not attending any clinic. Probably the most important reason, however, for failure to find hepatomegaly, even in unbalanced cases, is the difficulty of assessing liver size by palpation. It is notoriously difficult to feel a liver edge in obese or heavily muscled patients, and even if the edge is felt this may only mean that a normal-size liver is situated low, perhaps because of a flat diaphragm and emphysema. Goodman1 emphasises that hepatomegaly is much more easily and more reliably assessed by measuring, with percussion, the distance between the upper and lower borders of the liver in the midclavicular line. The upper limit of normality for this distance he finds to be 7 cm. in women and 7-5 cm. in men ; and he claims almost equal facility in measuring it in the obese and in the thin. In a series of 459 unselected diabetics, liver enlargement, judged in this way, was noted in 9% of those with well-controlled diabetes, in 60% of those with uncontrolled diabetes, and in each of the 10 patients with ketosis. Early studies 2-5 of liver function in diabetes yielded no striking evidence of abnormality, but the tests were not particularly sensitive. Since then Gray et al. have investigated the more sensitive serum colloidal-gold reaction in 247 diabetics. Their results parallel closely those of Goodman. Thus a positive colloidal-gold reaction was regarded as evidence of hepatic dysfunction Goodman, J. I. Ann. intern. Med. 1953, 39, 1077. Diamond, J. S. Amer. J. med. Sci. 1928, 176, 321. Meyer, E. L. Arch. intern. med. 1931, 47, 182. Rabinowitch, J. M. Brit. J. exp. Path. 1936, 17, 249. Marble, A., White, P., Bogan, I. K., Smith, R. M. Arch. intern. Med. 1938, 62, 740. 6. Gray, S. J., Hook, W., Batty, J. L. Ann. intern. Med. 1946, 24, 72.
1. 2. 3. 4. 5.
249 in 36-8% of the 247 diabetics. As with hepatomegaly, the colloidal-gold test was positive in a higher proportion of obese than of non-obese patients, but there was a more striking association between this reaction and the control Just over 43% of diabetics receiving of the diabetes. irregular care had a positive reaction, compared with 27% of those who were well supervised. Before diabetes can be held responsible for the hepatomegaly in diabetes, other causes of liver enlargement must be excluded. Goodman7 himself recognised two other causes. One was obesity, which he considered was seldom associated with more than moderate enlargement of the liver ; and the other was deficiency of lipotropic agents, such as choline and methionine, as determined by the dietary history. He ascribed hepatomegaly to this hypothetical deficiency in Iof 101unselected diabetics ; It was based but this assumption is questionable. presumably on the known incidence of fatty liver in depancreatised dogs maintained on insulin ; but such dogs lack the exocrine secretion of the pancreas, which must be rare in human diabetes, and moreover the fatty liver can be restored to normal by feeding raw pancreas or lipotropic agents. Raw pancreas has in fact proved ineffective in reducing the hepatomegaly of 2 child diabetics ; and betaine hydrochloride, a potent lipotropic agent, was definitely less effective (in 12 such cases) than was protamine zinc insulin (in 19).8 White and her co-workers concluded from this study that hepatomegaly in diabetic children is usually.due chiefly to poor control of the diabetes and not to a lack of choline or of some other agent derived from raw pancreas. In 60 diabetic children the association of hepatomegaly with other evidence of poor diabetic control was striking, and the attacks of abdominal pain to which they were prone were thought possibly to be due to stretching of the liver 8
capsule.
It has
long
been
thought, mainly
on
circumstantial
evidence, that in diabetics enlarged livers may have
are
fatty,
normal glycogen content ; and this view has received more direct confirmation. Reinberg -and Lipson 9 reported that of 102 diabetics who before death were in coma or ketosis, 51% were found at necropsy to have fatty livers. Fatty changes in diabetic livers have also been shown by aspiration biopsv.1o but only in patients whose livers were proved to be insensitive to the effect of insulin in decreasing the hepatic glucose output. Such patients are typically middle-aged obese diabetics who rarely experience ketosis or hypoglycemia. Young thin diabetics, who readily become ketotic or hypoglycaemic, show a good hepatic response to insulin except when ketotic, but even at this time the microscopic appearance of the liver is remarkably normal. When diabetes coexists with a functionally deranged liver, there may be a significant interplay between the two conditions.il Not only will poor control of the diabetes tend to impair further the function of the liver, but reduced glycogenetic and glycogenolytic function of the liver will accentuate postprandial hyperglycsemia and tend to reduce the fasting blood-sugar level. But hepatomegaly in diabetes is perhaps chiefly important as an indication that the diabetes is being inadequately controlled 12; and in diabetic clinics it would certainly be more valuable to record by percussion the distance between the upper and lower borders of liver dullness than to note only whether the liver is palpable.
although they
a
7. Goodman, J. I. Amer. J. dig. Dis. 1951, 18, 181. 8. White, P., Marble, A., Bogan, I. K., Smith, R. M. Arch. intern. Med. 1938, 62, 751. 9. Reinberg, M. H., Lipson, M. Ann. intern. Med. 1950, 33, 1195. 10. Bearn, A. G., Billing, B. H., Sherlock, S. Lancet, 1951, ii, 698. 11. Conn, J. W., Newburgh, L. H., Johnston, M. W., Sheldon, J. M. Arch. intern. Med. 1938, 62, 765. 12. Leevy, C. M., Ryan, C. M., Fineberg, J. C. Amer. J. Med. 1950,
8, 290.
SURGICAL TREATMENT OF ANGINA PECTORIS SURGICAL endeavour in the treatment of angina pectoris has been of three types : (1) an attempt to improve cardiac blood-supply by anastomosis to the ventricle of
alien tissue, such as pectoral muscle or omentum ; (2) reduction of the demands on the heart by depressing the basal metabolic rate by means of thyroidectomy and thiouracil ; and (3) interruption of the sympathetic cardiac nerves carrying pain sensation. Hitherto the most usual, and probably the most effective, of these three approaches has been section of the pain pathways by cervicothoracic ganglionectomy. The stellate and cervical sympathetic ganglia were first removed for this disorder by Jonnesco1 in 1921. The extent of the sympathectomy was later extended to include the stellate and the upper thoracic sympathetic ganglia on one or both sides, after it had been shown, both clinically and anatomically, that the afferent fibres from the heart run not only in the cervical cardiac nerves but also through the first four or five thoracic ganglia. This operation removes fairly successfully the oppressive rest or exercise pain of angina Lindgren and Olivecrona2 reported 71 cases of severe angina in which they had done a cervicothoracic ganglionectomy by the anterior approach. 6 patients died within a month of operation, but most of the remainder were freed from severe pain for months or years. Evans and Poppen3 have obtained a satisfactory result in 13 out of 16 cases in which they did sympathetic resection by a transthoracic approach. They suggest that the operation should be confined to patients with severe angina associated with hypertension and normotensive patients with an over-alarm syndrome. After sympathectomy, which is usually staged for the right and left sides, the patient still recognises the " warning-signal when he has gone beyond his exercise tolerance, but instead of the intense and frightening pain he has a sense of fullness or constriction or a mild ache. Occasionally the severe anginal pain migrates to the jaw or neck, which suggests that the pain afferent fibres run, not only in the sympathetic but also in the vagal and phrenic nerves.4 Although cervicothoracic sympathectomy usually results in bradycardia, it has been criticised because it may destroy the dilator fibres supplying the coronary vessels. Arnulf5 has devised an operation which involves resection of the left second rib and removal by an extrapleural route of the superficial aortic plexus, which usually consists of five recognisable fibres. This, he claims, destroys all the autonomic fibres, including the parasympathetic vagal branches, which supply the base of the aorta, the left coronary artery, and probably the right coronary artery. Arnulf states that the operation is followed by tachycardia and a fall in blood-pressure, but that the main sequel is dilatation of the coronary vessels. The mechanisms of the vasomotor control of the coronary arteries are, however, confusing, and Lindgren and Olivecrona remark that clinical, experience suggests that most of the ’vasoconstrictor fibres run in the sympathetic and not in the parasympathetic supply. Nor, if evidence from blood-flow in calf muscle is translated to the heart, would we expect a significant long-term increase in the blood-flow through atherosclerotic vessels from any denervating operation. Whether the Arnulf operation, which is an incomplete attack on the main cardiac plexus, should supersede the better-established cervicothoracic sympathectomy can only be judged by a careful follow-up of cases. Experimentally Beck and Hahn 6 have adapted to the coronary circulation the technique of reversing blood-
pectoris.
"
"
"
Jonnesco, T. Pr. m d. 1921, 29, 193. Lindgren, I., Olivecrona, H. J. Neurosurg. 1947, 4, 19. Evans, J. A., Poppen, J. L. New Engl. J. Med. 1953, 249, 791. Mitchell, G. A. G. Brit. Heart J. 1953, 15, 159. 5. Arnulf, G. J. Chir., Paris, 1950, 66, 97. 6. Beck, C. S., Hahn, R. S. Circulation, 1952, 5, 801.
1. 2. 3. 4.
TEMPORAL-LOBE
EPILEPSIES
IN the past few years a group of epileptic disturbances has been recognised in which the site of abnormality is the temporal lobe or a closely related area. This group has been rather loosely termed " the temporal-lobe epilepsies." The clinical attacks, although varying in detail, have enough in common to suggest the diagnosis ; and this may be confirmed by electro-encephalography (E.E.G.), which shows a local or focal abnormality in temporal leads. The clinical picture includes attacks with a pronounced visceral or vasomotor aura or content ; and the group embraces many of the cases with automatism (apart from the postictal ones), and those with Jackson’s " dreamy " or intellectual aura, the déjà vu phenomenon, and psychomotor disturbances. It includes also a large proportion of the difficult so-called " epileptic " personalities and probably some of the strikingly episodic behaviour abnormalities of childhood. In addition to these "local signs" of the site of discharge, there may be frank grand-mal attacks. Despite these pleomorphic symptoms however, automatism, visceral or vasomotor features, and clouding (rather than complete loss) of consciousness are often distinguishing features of the group. The E.E.G. may show a focal spike discharge from one or other temporal lobe. However, a localised abnormality, especially if paroxysmal, or even a bilateral abnormality confined to the temporal areas, is of some value as a clue to a focus. This may be defined by placing electrodes as near as possible to the temporal lobes. They may be introduced into the nasopharynx, or needle electrodes may be inserted, as for a trigeminal-root injection, against the base of the temporal fossa. The focus may also be sought by enhancing or provoking a local Of these " provocation techelectrical abnormality. niques " one of the most useful is recording during sleep induced by quinalbarbitone (’ Seconal’) ; at this time a local discharge or even a clear-cut spike focus, which was hidden in the general activity of the wakeful cortex, may emerge. The discovery of a focal abnormality is valuable not but in planning treatment. These only in epilepsies often respond poorly to the usual anticonsometimes associated vulsants ; and the with them may make management difficult. They are therefore especially open to consideration for surgical excision if some clearly defined focus can be found in an area whose function can be sacrificed with impunity. With operation, of course, such a focus can be defined more precisely by recording directly from the dura or the surface of the cortex itself. In treatment, excision of the anterior parts of the temporal lobes has been practised in America,1in this country,3 and in France.4 In assessing this treatment it is necessary to "
"
diagnosis
personality general
1. 2. 3. 4.
Penfield, W., Flanigin, H. Arch. Neurol. Psychiat. 1950, 64, 491. Bailey, P., Gibbs, F. A. J. Amer. med. Ass. 1951, 145, 365. Hill. D., Falconer, M. A. Proc. R. Soc. Med. 1953, 46, 965. Petit-Dutaillis, D., et al. Sem. Hóp. Paris, 1953, 29, 3838.
consider both change in frequency of actual attacks and any alterations in the associated mental and personality traits. Of the 20 French cases recently reported, 16 had been followed for ½-2½ years ; of these 16, 9 had their attacks abolished, 2 had only minor attacks postoperatively, and 5 still had attacks and were classed as therapeutic failures even if the frequency of attacks was reduced. Mental changes are only briefly mentioned, but some general improvement is claimed. Judging by other series, it seems that reduction in epileptic attacks is more satisfactory and consistent than is any improvement in personality or conduct : but here opinion is still divided. In this field enthusiasm should be tempered with caution until prolonged follow-up studies have been published. Before the recording of cerebral electrical activity was possible, elevation of depressed bone, freeing of dural adhesions, and excision of brain scars were all used-and with effect-in abolishing epileptic attacks, for a time. After three or four years, however, relapses A similar trend is already were increasingly frequent. apparent where cortical excision has been based on abnormal electrical discharge. Possibly in temporal-lobe epilepsy, which is notoriously unresponsive to medical treatment, the reasonable chance of controlling fits even for a few years would, in a severely disabled person, justify a major cerebral operation, especially if improvement in conduct and behaviour was also to be expected. No adverse consequences have been reported, and the procedure undoubtedly calls for further trial ; but for its final assessment, especially if it is to be applied to the young, the follow-up should be considered in terms of a decade rather than of six months or a year. DIABETIC HEPATOMEGALY The incidence of hepatomegaly in diabetics has received scant attention except in children, in whom the liver edge is much more easily felt. In adult as well as child diabetics, enlargement of the liver is commonest where the diabetes is poorly controlled, and of course patients reporting regularly at clinics are less likely to be poorly controlled than those not attending any clinic. Probably the most important reason, however, for failure to find hepatomegaly, even in unbalanced cases, is the difficulty of assessing liver size by palpation. It is notoriously difficult to feel a liver edge in obese or heavily muscled patients, and even if the edge is felt this may only mean that a normal-size liver is situated low, perhaps because of a flat diaphragm and emphysema. Goodman1 emphasises that hepatomegaly is much more easily and more reliably assessed by measuring, with percussion, the distance between the upper and lower borders of the liver in the midclavicular line. The upper limit of normality for this distance he finds to be 7 cm. in women and 7-5 cm. in men ; and he claims almost equal facility in measuring it in the obese and in the thin. In a series of 459 unselected diabetics, liver enlargement, judged in this way, was noted in 9% of those with well-controlled diabetes, in 60% of those with uncontrolled diabetes, and in each of the 10 patients with ketosis. Early studies 2-5 of liver function in diabetes yielded no striking evidence of abnormality, but the tests were not particularly sensitive. Since then Gray et al. have investigated the more sensitive serum colloidal-gold reaction in 247 diabetics. Their results parallel closely those of Goodman. Thus a positive colloidal-gold reaction was regarded as evidence of hepatic dysfunction Goodman, J. I. Ann. intern. Med. 1953, 39, 1077. Diamond, J. S. Amer. J. med. Sci. 1928, 176, 321. Meyer, E. L. Arch. intern. med. 1931, 47, 182. Rabinowitch, J. M. Brit. J. exp. Path. 1936, 17, 249. Marble, A., White, P., Bogan, I. K., Smith, R. M. Arch. intern. Med. 1938, 62, 740. 6. Gray, S. J., Hook, W., Batty, J. L. Ann. intern. Med. 1946, 24, 72.
1. 2. 3. 4. 5.
249 in 36-8% of the 247 diabetics. As with hepatomegaly, the colloidal-gold test was positive in a higher proportion of obese than of non-obese patients, but there was a more striking association between this reaction and the control Just over 43% of diabetics receiving of the diabetes. irregular care had a positive reaction, compared with 27% of those who were well supervised. Before diabetes can be held responsible for the hepatomegaly in diabetes, other causes of liver enlargement must be excluded. Goodman7 himself recognised two other causes. One was obesity, which he considered was seldom associated with more than moderate enlargement of the liver ; and the other was deficiency of lipotropic agents, such as choline and methionine, as determined by the dietary history. He ascribed hepatomegaly to this hypothetical deficiency in Iof 101unselected diabetics ; It was based but this assumption is questionable. presumably on the known incidence of fatty liver in depancreatised dogs maintained on insulin ; but such dogs lack the exocrine secretion of the pancreas, which must be rare in human diabetes, and moreover the fatty liver can be restored to normal by feeding raw pancreas or lipotropic agents. Raw pancreas has in fact proved ineffective in reducing the hepatomegaly of 2 child diabetics ; and betaine hydrochloride, a potent lipotropic agent, was definitely less effective (in 12 such cases) than was protamine zinc insulin (in 19).8 White and her co-workers concluded from this study that hepatomegaly in diabetic children is usually.due chiefly to poor control of the diabetes and not to a lack of choline or of some other agent derived from raw pancreas. In 60 diabetic children the association of hepatomegaly with other evidence of poor diabetic control was striking, and the attacks of abdominal pain to which they were prone were thought possibly to be due to stretching of the liver 8
capsule.
It has
long
been
thought, mainly
on
circumstantial
evidence, that in diabetics enlarged livers may have
are
fatty,
normal glycogen content ; and this view has received more direct confirmation. Reinberg -and Lipson 9 reported that of 102 diabetics who before death were in coma or ketosis, 51% were found at necropsy to have fatty livers. Fatty changes in diabetic livers have also been shown by aspiration biopsv.1o but only in patients whose livers were proved to be insensitive to the effect of insulin in decreasing the hepatic glucose output. Such patients are typically middle-aged obese diabetics who rarely experience ketosis or hypoglycemia. Young thin diabetics, who readily become ketotic or hypoglycaemic, show a good hepatic response to insulin except when ketotic, but even at this time the microscopic appearance of the liver is remarkably normal. When diabetes coexists with a functionally deranged liver, there may be a significant interplay between the two conditions.il Not only will poor control of the diabetes tend to impair further the function of the liver, but reduced glycogenetic and glycogenolytic function of the liver will accentuate postprandial hyperglycsemia and tend to reduce the fasting blood-sugar level. But hepatomegaly in diabetes is perhaps chiefly important as an indication that the diabetes is being inadequately controlled 12; and in diabetic clinics it would certainly be more valuable to record by percussion the distance between the upper and lower borders of liver dullness than to note only whether the liver is palpable.
although they
a
7. Goodman, J. I. Amer. J. dig. Dis. 1951, 18, 181. 8. White, P., Marble, A., Bogan, I. K., Smith, R. M. Arch. intern. Med. 1938, 62, 751. 9. Reinberg, M. H., Lipson, M. Ann. intern. Med. 1950, 33, 1195. 10. Bearn, A. G., Billing, B. H., Sherlock, S. Lancet, 1951, ii, 698. 11. Conn, J. W., Newburgh, L. H., Johnston, M. W., Sheldon, J. M. Arch. intern. Med. 1938, 62, 765. 12. Leevy, C. M., Ryan, C. M., Fineberg, J. C. Amer. J. Med. 1950,
8, 290.
SURGICAL TREATMENT OF ANGINA PECTORIS SURGICAL endeavour in the treatment of angina pectoris has been of three types : (1) an attempt to improve cardiac blood-supply by anastomosis to the ventricle of
alien tissue, such as pectoral muscle or omentum ; (2) reduction of the demands on the heart by depressing the basal metabolic rate by means of thyroidectomy and thiouracil ; and (3) interruption of the sympathetic cardiac nerves carrying pain sensation. Hitherto the most usual, and probably the most effective, of these three approaches has been section of the pain pathways by cervicothoracic ganglionectomy. The stellate and cervical sympathetic ganglia were first removed for this disorder by Jonnesco1 in 1921. The extent of the sympathectomy was later extended to include the stellate and the upper thoracic sympathetic ganglia on one or both sides, after it had been shown, both clinically and anatomically, that the afferent fibres from the heart run not only in the cervical cardiac nerves but also through the first four or five thoracic ganglia. This operation removes fairly successfully the oppressive rest or exercise pain of angina Lindgren and Olivecrona2 reported 71 cases of severe angina in which they had done a cervicothoracic ganglionectomy by the anterior approach. 6 patients died within a month of operation, but most of the remainder were freed from severe pain for months or years. Evans and Poppen3 have obtained a satisfactory result in 13 out of 16 cases in which they did sympathetic resection by a transthoracic approach. They suggest that the operation should be confined to patients with severe angina associated with hypertension and normotensive patients with an over-alarm syndrome. After sympathectomy, which is usually staged for the right and left sides, the patient still recognises the " warning-signal when he has gone beyond his exercise tolerance, but instead of the intense and frightening pain he has a sense of fullness or constriction or a mild ache. Occasionally the severe anginal pain migrates to the jaw or neck, which suggests that the pain afferent fibres run, not only in the sympathetic but also in the vagal and phrenic nerves.4 Although cervicothoracic sympathectomy usually results in bradycardia, it has been criticised because it may destroy the dilator fibres supplying the coronary vessels. Arnulf5 has devised an operation which involves resection of the left second rib and removal by an extrapleural route of the superficial aortic plexus, which usually consists of five recognisable fibres. This, he claims, destroys all the autonomic fibres, including the parasympathetic vagal branches, which supply the base of the aorta, the left coronary artery, and probably the right coronary artery. Arnulf states that the operation is followed by tachycardia and a fall in blood-pressure, but that the main sequel is dilatation of the coronary vessels. The mechanisms of the vasomotor control of the coronary arteries are, however, confusing, and Lindgren and Olivecrona remark that clinical, experience suggests that most of the ’vasoconstrictor fibres run in the sympathetic and not in the parasympathetic supply. Nor, if evidence from blood-flow in calf muscle is translated to the heart, would we expect a significant long-term increase in the blood-flow through atherosclerotic vessels from any denervating operation. Whether the Arnulf operation, which is an incomplete attack on the main cardiac plexus, should supersede the better-established cervicothoracic sympathectomy can only be judged by a careful follow-up of cases. Experimentally Beck and Hahn 6 have adapted to the coronary circulation the technique of reversing blood-
pectoris.
"
"
"
Jonnesco, T. Pr. m d. 1921, 29, 193. Lindgren, I., Olivecrona, H. J. Neurosurg. 1947, 4, 19. Evans, J. A., Poppen, J. L. New Engl. J. Med. 1953, 249, 791. Mitchell, G. A. G. Brit. Heart J. 1953, 15, 159. 5. Arnulf, G. J. Chir., Paris, 1950, 66, 97. 6. Beck, C. S., Hahn, R. S. Circulation, 1952, 5, 801.
1. 2. 3. 4.