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1347 THE KING’S ILLNESS. THE LANCET. LONDON: SATURDAY, DECEMBER 29, 1928. WE are happy to believe that His MAJESTY THE KING is now making slow but steady progress towards recovery. A week ago an official statement issued by his doctors through our columns spoke of dangerous phases in the illness having been surmounted and of increasingly solid grounds for hope of recovery. On the following afternoon the Regius professors con- firmed this opinion with the statement that the KiNG’s progress is now established on a firmer basis. Day by day since then the local and general condition have improved, natural sleep has been restored, and the desire for food is returning. A significant sign of relaxed anxiety was the issue of a single daily bulletin on Sunday last. It may yet be too soon to speak of I convalescence in view of the exhaustion which still remains as the sequel of broncho-pneumonia, empyema, and septicaemia, an evil triad which would have taxed any constitution however young or sound. No one but a medical man or a nurse knows the tediousness of recovery in these cases-the daily ups and downs among which it is hard to distinguish the slow gradual improvement. But convalescence is now in sight, and the relief has been enough to make the Christmas season more solidly and quietly happy, within and without the Palace, than would have been deemed possible earlier in the month. THE CAUSATION OF MYOPIA. SHORT-SIGHTEDNESS in young children is an elusive problem. Many have been the theories to account for the fact that whereas in the majority of individuals the growth of the sclerotic coat of the eyeball is approximately adapted to the purpose of focusing distant objects on to the retina, among the minority where this is not the case there are some in whom the sclerotic is unduly stretched during the early years of life so that accurate focusing can only be obtained by the use of concave lenses. Sir ARTHUR KEITH was altogether right when, a few years ago,l he termed myopia a disorder of growth and attri- buted it to a faulty reaction of the fibroblasts of the sclerotic to the stresses to which they are subject from intraocular pressure during the period of growth. This, no doubt, is a true way of putting it, and the factor of heredity, which in certain families I is very prominent, obviously has to do with a defect 1 See THE LANCET, 1925, i., 32. in the process of growth. But though this primary cause exists in all myopes, and in some of them- especially cases of high myopia beginning in pre- school years-may be of such importance as to put all secondary causes into the shade, it by no means follows that all other causes may be ignored, or that we should take up a fatalistic attitude with regard to the mitigation of myopia by hygienic measures. That the constant wearing of accurately prescribed glasses itself has a favourable influence in retarding or stopping the myopic process is a belief held by many ophthalmic surgeons of very wide experience in this matter, though we know of no statistics actually proving that such is the case. Of the various secondary causes to which the phenomenon of increasing myopia has been attributed the one which has received most attention is prolonged convergence of the eyes on any near work, which is supposed to involve an increase of pressure by the external muscles of the eye and especially the superior oblique. Unfortunately for this theory it has never been proved that the pres- sure of the external muscles actually does increase intraocular pressure. More probable is the theory that the chief secondary cause of myopia is venous engorgement, and since this would naturally result from prolonged stooping of the head and neck, such as most forms of work at short range entail, and since it is often especially noticeable in school- children, the hypothesis seems to be a reasonable one. Twenty years ago Prof. GEORG LEvINSOHN, of Berlin, laid stress on this factor in the causation of myopia, and since that time he has attempted to reinforce his view by experiments on young apes by keeping them in the horizontal position, the result of which was not only to make them decidedly myopic, but also to produce the fundus changes typical of myopia in man. In a recent paper 2 he states that these experiments have lately been repeated and confirmed in Java by W. F. R EssED and M. SOEWARNO. Of seven apes experimented on, five became myopic, while the refraction of three control animals remained unchanged. In two of the animals experimented on a myopic crescent was produced, while in a third there was venous hypersemia. The eyes were excised and sent to Prof. LEVINSOHN, who confirmed the findings by pathological examination. The proportion of animals in whom myopia was produced artificially (70 per cent.) contrasts with the 16 per cent. in which myopia is said to be normally present. By these experiments Prof. LEVINSOHN claims to have provided an irrefutable proof of his theory. To some this claim, based on such compara- tively small evidence, may seem to be rather bold; nevertheless the truth of the theory is highly pro- bable. So far as the experimental evidence goes, the most striking point is the artificial production of an myopic crescent in two monkeys. It has been objected that the myopic crescent is no proof of myopia, as it is occasionally seen in eyes that are not myopic. The answer to this is that the typical myopic crescent is not congenital, but is the result of the stretching of the eyeball during the period of growth. If the process is started in an eye originally hypermetropic it may never proceed so far as to render it myopic, but may only lessen the degree of hypermetropia. This point is well explained in a recent article 3 by A. SouRASKY on the development of myopia. 2 Schweizerische Medicinische Wochenschrift, November, 1928 ; also see Klin. Monatsbl. f. Augenh., 1928, lxxx., 56. 3 British Jour. of Ophthalmology, December, 1928, p. 641. CC 3

THE CAUSATION OF MYOPIA

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1347

THE KING’S ILLNESS.

THE LANCET.

LONDON: SATURDAY, DECEMBER 29, 1928.

WE are happy to believe that His MAJESTY THEKING is now making slow but steady progress towardsrecovery. A week ago an official statement issued byhis doctors through our columns spoke of dangerousphases in the illness having been surmounted and ofincreasingly solid grounds for hope of recovery. Onthe following afternoon the Regius professors con-firmed this opinion with the statement that theKiNG’s progress is now established on a firmer basis.

Day by day since then the local and general conditionhave improved, natural sleep has been restored, andthe desire for food is returning. A significant sign ofrelaxed anxiety was the issue of a single daily bulletinon Sunday last. It may yet be too soon to speak of Iconvalescence in view of the exhaustion which stillremains as the sequel of broncho-pneumonia, empyema,and septicaemia, an evil triad which would havetaxed any constitution however young or sound.

No one but a medical man or a nurse knows thetediousness of recovery in these cases-the daily upsand downs among which it is hard to distinguish theslow gradual improvement. But convalescence is

now in sight, and the relief has been enough to makethe Christmas season more solidly and quietly happy,within and without the Palace, than would have beendeemed possible earlier in the month.

THE CAUSATION OF MYOPIA.SHORT-SIGHTEDNESS in young children is an elusive

problem. Many have been the theories to accountfor the fact that whereas in the majority of individualsthe growth of the sclerotic coat of the eyeball is

approximately adapted to the purpose of focusingdistant objects on to the retina, among the minoritywhere this is not the case there are some in whomthe sclerotic is unduly stretched during the earlyyears of life so that accurate focusing can only beobtained by the use of concave lenses. Sir ARTHURKEITH was altogether right when, a few years ago,lhe termed myopia a disorder of growth and attri-buted it to a faulty reaction of the fibroblasts of thesclerotic to the stresses to which they are subjectfrom intraocular pressure during the period of

growth. This, no doubt, is a true way of putting it,and the factor of heredity, which in certain families Iis very prominent, obviously has to do with a defect

1 See THE LANCET, 1925, i., 32.

in the process of growth. But though this primarycause exists in all myopes, and in some of them-

especially cases of high myopia beginning in pre-school years-may be of such importance as to putall secondary causes into the shade, it by no meansfollows that all other causes may be ignored, or thatwe should take up a fatalistic attitude with regardto the mitigation of myopia by hygienic measures.That the constant wearing of accurately prescribedglasses itself has a favourable influence in retardingor stopping the myopic process is a belief held by manyophthalmic surgeons of very wide experience in thismatter, though we know of no statistics actuallyproving that such is the case. Of the various secondarycauses to which the phenomenon of increasing myopiahas been attributed the one which has received mostattention is prolonged convergence of the eyes on

any near work, which is supposed to involve an increaseof pressure by the external muscles of the eye andespecially the superior oblique. Unfortunately forthis theory it has never been proved that the pres-sure of the external muscles actually does increaseintraocular pressure. More probable is the theorythat the chief secondary cause of myopia is venousengorgement, and since this would naturally resultfrom prolonged stooping of the head and neck, suchas most forms of work at short range entail, andsince it is often especially noticeable in school-children, the hypothesis seems to be a reasonableone. Twenty years ago Prof. GEORG LEvINSOHN, ofBerlin, laid stress on this factor in the causation ofmyopia, and since that time he has attempted toreinforce his view by experiments on young apes bykeeping them in the horizontal position, the resultof which was not only to make them decidedlymyopic, but also to produce the fundus changestypical of myopia in man. In a recent paper 2 hestates that these experiments have lately been

repeated and confirmed in Java by W. F. R EssED andM. SOEWARNO. Of seven apes experimented on, fivebecame myopic, while the refraction of three controlanimals remained unchanged. In two of the animals

experimented on a myopic crescent was produced,while in a third there was venous hypersemia. The

eyes were excised and sent to Prof. LEVINSOHN, whoconfirmed the findings by pathological examination.The proportion of animals in whom myopia wasproduced artificially (70 per cent.) contrasts with the16 per cent. in which myopia is said to be normallypresent. By these experiments Prof. LEVINSOHNclaims to have provided an irrefutable proof of histheory. To some this claim, based on such compara-tively small evidence, may seem to be rather bold;nevertheless the truth of the theory is highly pro-bable. So far as the experimental evidence goes, themost striking point is the artificial production of anmyopic crescent in two monkeys. It has been objectedthat the myopic crescent is no proof of myopia, asit is occasionally seen in eyes that are not myopic.The answer to this is that the typical myopic crescentis not congenital, but is the result of the stretchingof the eyeball during the period of growth. If the

process is started in an eye originally hypermetropicit may never proceed so far as to render it myopic,but may only lessen the degree of hypermetropia.This point is well explained in a recent article 3 by

A. SouRASKY on the development of myopia.2 Schweizerische Medicinische Wochenschrift, November,

1928 ; also see Klin. Monatsbl. f. Augenh., 1928, lxxx., 56.3 British Jour. of Ophthalmology, December, 1928, p. 641.

CC 3