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THE MUSICIAN'S MOUTH
1084 when given intramuscularly compared with the potency by the intravenous route. The preparations produced by hydrolysis, and also the crude corticotrophin with which we are mainly familiar, undergo fairly rapid destruction when given intramuscularly and the rate of destruction varies in different batches and in different individuals. Indeed, patients may acquire the ability to inactivate intramuscular corticotrophin while they remain sensitive to that given intravenously. Since the hormone is assayed by an intravenous test and is usually given intramuscularly, it is not surprising that the clinical potency of some batches has appeared to disagree with their label. It is likely that, for intramuscular treatment, purified made up in gelatin so that it is will out to be the most efficient, though turn liberated, Wolfson has noted an unusual complication of peripheral vasodilatation which produced unpleasant symptoms. The ordinary complications of corticotrophin therapy -the result of excessive adrenal stimulation-are of course no more easily avoided than with other prepara-
corticotrophin,
slowly
tions. THE MUSICIAN’S MOUTH
SOME of the physical signs peculiar to the professional musician have already been described in a fascinating monograph by Francesco Ronchese.1 Examination of the musician’s fingers, hands, and mouth may show changes that are characteristic of the instrument he plays. In fact, according to Ronchese, it is possible to distinguish between a musician who plays a ’cello or double-bass in a symphony orchestra, and one who performs in a theatre orchestra or dance band. The symphony player has a hardening of the skin on the thumb from the so-called " thumb-position which is used only in the execution of serious " music. None of these callosities on the fingers or hand seems to hamper his playing. But the acneiform dermatosis which is occasionally seen under the chins of professional violinists may prove a definite handicap, and so may certain .abrasions of the buccal mucous membrane in players of wind instruments-a subject lately discussed by Porter.2 Players of reed instruments often have a characteristic mark on the inner surface of the lower lip, where the lip is compressed between the mouthpiece of the instrument and the lower incisor teeth. This condition can be sufficiently painful to interfere with playing and is aggravated by irregularities of the teeth. Those who play the flute or piccolo are seldom troubled in this way because of the different embouchure they adopt.3 A different embouchure sometimes used by reed instrumentalists may spare the labial mucosa, but only at the expense of the lower incisors, which The saxoare often affected by a pressure osteoclasia. phone is responsible for more oral lesions than any other reed instrument because of its weight (which may be as much as 16 lb.)-a good deal of which is supported by the lower lip. Brass instruments, with their extra-oral mouthpieces, can produce lesions on the cutaneous surface of the lips,l which may actually perforate.44 Although these mucosal injuries are common, there is little evidence to suggest that there is any tendency "
"
towards leukoplakia or malignant change. Porter discusses the various ways in which the dental surgeon can help the musician to enjoy greater comfort in playing-methods that are rather more effective than the time-honoured one of covering the lower teeth with a cigarette paper. These methods include smooth acrylic caps for the lower incisors and cast-metal splints for incisors loosened by bone absorption. Full-denture prostheses present special problems of their own, and 1. Ronchese, F. 2. Porter, M. M. 3. Porter, M. M.
Occupational Marks. New York, 1948. Brit. dent. J. 1953, 95, 152. Ibid, 1952, 93, 66. 4. Reichenbach, E., Brückl, H. Dtsch. zahnärztl. Wschr. 213. 39,
1936,
Porter describes the " embouchure denture" intended to be worn only when playing-an appliance first devised by Reichenbach and Bruckl.4 C.S.F. CHANGES IN POLIOMYELITIS IN poliomyelitis the changes in the cerebrospinal fluid (c.s.F.) usually follow a well-defined pattern similar to that in other neurotropic-virus infections. Early in the disease, in the meningeal and early paralytic stage, there is pleocytosis with both polymorph and lymphocytic cells and some rise in the protein content. If the examination is repeated after a week or so, the cells will be fewer and of lymphocytic type, but the protein may still be increasing ; indeed, the picture may later be that of dissociation cyto-albuminologique, which at one time was thought to be diagnostic of infective polyneuritis. Within this broad framework, however, the cellular response may vary widely from case to case: and many of those who see much of poliomyelitis will recall an occasional case where the patient almost certainly had poliomyelitis and yet the c.s.F. was normal. Bentzon and Hilden1 have reported their findings in 97 paralytic and 627 non-paralytic cases from the 1950 Copenhagen epidemic. Their figures show that the higher the total cell count, the greater the per. centage of polymorphs is likely to be. In children the number of cells is significantly higher than in adults; in neither is there any significant difference in pleocytosis between paralytic and non-paralytic cases, but increase in protein is more distinct in the paralytic cases. They also remark that, allowing for the point in the course of the disease at which the c.s.F. was examined, a strikingly large number of cases in their series had a high total cell count-over 1200 per c.mm. in 19% and over 2400 " per c.mm. in 6%. This may be due to the " antigenic" state of the population at risk, but could also conceiv. ably indicate that a variant form of the virus was responsible for the epidemic-a suggestion that has already been made on other, equally tenuous, grounds. AIR IN THE HEART
THE
entry
of air into the left side of the heart is
a
complication of operations involving a left cardiotomy. The increasing scope of such operations 2 3 dreaded
has stimulated research into the cause of death when air enters the left ventricle. Geoghegan and Lam4 have made a series of observations on dogs. Air in amounts varying from 0’2S to 2-0 c.cm. per kg. body-weight was injected rapidly into the common carotid arteries after thoracotomy, and the aortic blood-pressure was recorded by an impedance manometer. No impairment of cardiac function or fall in aortic pressure occurred ; but signs of neurological damage developed. It was concluded that cerebral air-embolism was probably not the cause of sudden death in similar clinical circumstances. A further series of experiments was done to determine whether a compressible mass of air in the left ventricle would embarrass the heart in the absence of air in the coronary arterial system. In a number of dogs the heart was and a balloon exposed placed in the left ventricle and inflated with air. Records of aortic pressure showed little or no change ;the left ventricle apparently compensated for the reduction in volume produced by the balloon. After removal of the air from the balloon, the same amount of air was injected into the ventricular cavity. In a few moments the heart became cyanotic. the aortic pressure fell sharply, and in animals receiving 1-5 c.cm. of air per kg. ventricular fibrillation or asystole. and death, rapidly followed : rapid aspiration of air Bentzon, J. W., Hilden, T. Acta med. scand. 1953, 146, 93. Bailey, C. P., Bolton, H. E., Redondo-Ramirez, H. P. Surg. Clin. N. Amer. 1952, 32, 1807. 3. Bailey, C. P.. Redondo-Ramirez, H. P., Larzerle, H. B. J. Amer. med. Ass. 1952, 150, 1647. Ann. Surg. 1953, 138, 351. 4. Geoghegan, T., Lam, C. R.
1. 2.
corticotrophin,
slowly
tions. THE MUSICIAN’S MOUTH
SOME of the physical signs peculiar to the professional musician have already been described in a fascinating monograph by Francesco Ronchese.1 Examination of the musician’s fingers, hands, and mouth may show changes that are characteristic of the instrument he plays. In fact, according to Ronchese, it is possible to distinguish between a musician who plays a ’cello or double-bass in a symphony orchestra, and one who performs in a theatre orchestra or dance band. The symphony player has a hardening of the skin on the thumb from the so-called " thumb-position which is used only in the execution of serious " music. None of these callosities on the fingers or hand seems to hamper his playing. But the acneiform dermatosis which is occasionally seen under the chins of professional violinists may prove a definite handicap, and so may certain .abrasions of the buccal mucous membrane in players of wind instruments-a subject lately discussed by Porter.2 Players of reed instruments often have a characteristic mark on the inner surface of the lower lip, where the lip is compressed between the mouthpiece of the instrument and the lower incisor teeth. This condition can be sufficiently painful to interfere with playing and is aggravated by irregularities of the teeth. Those who play the flute or piccolo are seldom troubled in this way because of the different embouchure they adopt.3 A different embouchure sometimes used by reed instrumentalists may spare the labial mucosa, but only at the expense of the lower incisors, which The saxoare often affected by a pressure osteoclasia. phone is responsible for more oral lesions than any other reed instrument because of its weight (which may be as much as 16 lb.)-a good deal of which is supported by the lower lip. Brass instruments, with their extra-oral mouthpieces, can produce lesions on the cutaneous surface of the lips,l which may actually perforate.44 Although these mucosal injuries are common, there is little evidence to suggest that there is any tendency "
"
towards leukoplakia or malignant change. Porter discusses the various ways in which the dental surgeon can help the musician to enjoy greater comfort in playing-methods that are rather more effective than the time-honoured one of covering the lower teeth with a cigarette paper. These methods include smooth acrylic caps for the lower incisors and cast-metal splints for incisors loosened by bone absorption. Full-denture prostheses present special problems of their own, and 1. Ronchese, F. 2. Porter, M. M. 3. Porter, M. M.
Occupational Marks. New York, 1948. Brit. dent. J. 1953, 95, 152. Ibid, 1952, 93, 66. 4. Reichenbach, E., Brückl, H. Dtsch. zahnärztl. Wschr. 213. 39,
1936,
Porter describes the " embouchure denture" intended to be worn only when playing-an appliance first devised by Reichenbach and Bruckl.4 C.S.F. CHANGES IN POLIOMYELITIS IN poliomyelitis the changes in the cerebrospinal fluid (c.s.F.) usually follow a well-defined pattern similar to that in other neurotropic-virus infections. Early in the disease, in the meningeal and early paralytic stage, there is pleocytosis with both polymorph and lymphocytic cells and some rise in the protein content. If the examination is repeated after a week or so, the cells will be fewer and of lymphocytic type, but the protein may still be increasing ; indeed, the picture may later be that of dissociation cyto-albuminologique, which at one time was thought to be diagnostic of infective polyneuritis. Within this broad framework, however, the cellular response may vary widely from case to case: and many of those who see much of poliomyelitis will recall an occasional case where the patient almost certainly had poliomyelitis and yet the c.s.F. was normal. Bentzon and Hilden1 have reported their findings in 97 paralytic and 627 non-paralytic cases from the 1950 Copenhagen epidemic. Their figures show that the higher the total cell count, the greater the per. centage of polymorphs is likely to be. In children the number of cells is significantly higher than in adults; in neither is there any significant difference in pleocytosis between paralytic and non-paralytic cases, but increase in protein is more distinct in the paralytic cases. They also remark that, allowing for the point in the course of the disease at which the c.s.F. was examined, a strikingly large number of cases in their series had a high total cell count-over 1200 per c.mm. in 19% and over 2400 " per c.mm. in 6%. This may be due to the " antigenic" state of the population at risk, but could also conceiv. ably indicate that a variant form of the virus was responsible for the epidemic-a suggestion that has already been made on other, equally tenuous, grounds. AIR IN THE HEART
THE
entry
of air into the left side of the heart is
a
complication of operations involving a left cardiotomy. The increasing scope of such operations 2 3 dreaded
has stimulated research into the cause of death when air enters the left ventricle. Geoghegan and Lam4 have made a series of observations on dogs. Air in amounts varying from 0’2S to 2-0 c.cm. per kg. body-weight was injected rapidly into the common carotid arteries after thoracotomy, and the aortic blood-pressure was recorded by an impedance manometer. No impairment of cardiac function or fall in aortic pressure occurred ; but signs of neurological damage developed. It was concluded that cerebral air-embolism was probably not the cause of sudden death in similar clinical circumstances. A further series of experiments was done to determine whether a compressible mass of air in the left ventricle would embarrass the heart in the absence of air in the coronary arterial system. In a number of dogs the heart was and a balloon exposed placed in the left ventricle and inflated with air. Records of aortic pressure showed little or no change ;the left ventricle apparently compensated for the reduction in volume produced by the balloon. After removal of the air from the balloon, the same amount of air was injected into the ventricular cavity. In a few moments the heart became cyanotic. the aortic pressure fell sharply, and in animals receiving 1-5 c.cm. of air per kg. ventricular fibrillation or asystole. and death, rapidly followed : rapid aspiration of air Bentzon, J. W., Hilden, T. Acta med. scand. 1953, 146, 93. Bailey, C. P., Bolton, H. E., Redondo-Ramirez, H. P. Surg. Clin. N. Amer. 1952, 32, 1807. 3. Bailey, C. P.. Redondo-Ramirez, H. P., Larzerle, H. B. J. Amer. med. Ass. 1952, 150, 1647. Ann. Surg. 1953, 138, 351. 4. Geoghegan, T., Lam, C. R.
1. 2.