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senses the clarity of underground air leaves nothingto be desired, but the finest particles, those mosteasily dissolved in the tissues of the lung, still persist.It is at least as difficult to explain the incidence ofsilicosis under modern conditions on the assumptionthat the inhaled dust acts only in combination withthe tubercle bacillus. There is no reason to supposethat more tuberculous recruits, either European ornative, enter the service of the mines now than informer years. And although native workers are notexamined radiographically to the same extent as arethe Europeans, it is surely reasonable to suppose thatthe simpler diagnostic methods are as carefully andefficiently employed now as in days gone by. Thedifficulties and the enormous labour involved in thethorough initial and periodic examination of thisenormous industrial population must be obvious, andthere can be no doubt that a high average of successin diagnosis is attained on the Rand. Nevertheless,diagnosis is by no means a perfect science ; finer lesionsmust inevitably be undiscoverable from time to time,and there must be a danger in developing pathologicaltheories on a basis of clinical observations.

Silica and its relation to the tubercle bacillus is thebig problem with which the Miner’s Phthisis Bureauhas to contend, and we have dwelt chiefly on thisaspect of the report. But the publication containsmuch other matter which is equally worthy of seriousattention.

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INHERITANCE OF PERONEAL ATROPHY.A REMARKABLE family afflicted with peroneal

atrophy has recently been described by Dr. MadgeThurlow Macklin and Dr. J. Thornley Bowman.1 Itpresents an excellent opportunity for study of thedisease from the point of view of inheritance, sincefive generations are affected and 21 of the 101 personsin the direct line of descent show peroneal atrophy.These writers conclude that the condition isdominant to the normal and is not sex-linked ; in alarge family with one affected parent half the childrenare likely to develop it whether the signs are apparentat the time of procreation or not. No member of thefamily reported has inherited more than a singlefactor for peroneal atrophy, and it is not known whatwould be the result of inheriting a factor from bothparents. The question arises whether it is safe formembers of an affected family to marry, and here thepresent investigators give a pessimistic verdict. Theysay: " Although it is safe for persons having adominant factor for disease in their family to marryif they themselves are free of it, the same cannot besaid of peroneal atrophy, for one cannot tell until oneis past middle age and so past the reproductive periodwhether one has inherited the disease. The only saferule for all persons who are born of affected parents,or born of parents who died young, but who had comeof affected stock, is either not to marry or to takeabsolutely safe precautionary measures against havingchildren. This applies to unaffected as well as

affected children of affected parents." Males andfemales suffer equally. The disease does not seem tomake any difference to the longevity of the individual,but it produces very serious crippling, and Dr. Macklinand Dr. Bowman consider that strict precautionsagainst having children are necessary because onlythus can it be eradicated from the community;sporadic cases in families which give no previoushistory are explained on the supposition that theparents have the disease latent and would develop itin later life if they lived long enough. They commenton the fact that their conclusions differ from those ofHerringham, who described a somewhat similar familyin which only males were affected, the disease beingtransmitted by unaffected females to their sons exceptin one instance in which an affected father had anaffected son. Apart from this one case the record ofthis family suggests that peroneal atrophy is sex-

linked andrecessive. but Herringham himself remarkedthat this type of inheritance is not typical of the

1 Journal of American Medical Association, Feb. 27th, p. 613.

disease except as it occurs in this particular family.The ’present investigators suggest that possibly thefamily described by Herringham was suffering notfrom peroneal atrophy, but from some form of distalmyopathy, and that the difference of inheritance isexplicable on this basis ; the fact that atrophy of theforearms was an almost constant feature in Herring-ham’s cases, but is absent in those now reported,lends colour to this suggestion. In this respect thepresent cases differ from those described by Charcotand Marie, and Tooth ; peroneal atrophy withoutwasting of the forearms is a rarer type, and patientscorresponding to Herringham’s are more commonlymet with. It is generally considered that as thedisease does not usually come on later than the seconddecade of life it is rather unlikely that parents willdevelop it after their children have been born. It ispossible, however, that the signs may be so slight asto escape notice during several generations, whichwould explain the apparently sporadic cases. A grossexample might be produced by any extra strain, suchas infection, thrown on cells hereditarily weak.Ormerod and Batten report cases following an attackof measles. This work of Dr. Macklin and Dr. Bowman,by comparison with that of Herringham, shows thatthere are, at any rate, two types of peroneal atrophydistinguishable clinically and by their method ofinheritance. It shows the risk that a member of anaffected family may run of giving it to his children.Probably, however, there are other types of thedisease varying in severity and method of transmission,so that in isolated cases in which the family appearshealthy or in which no family history can be obtained,no very definite prognosis can be given either for thepatient or his offspring.

BERNHARD HEINE: A PIONEER IN EXPERI-MENTAL PHYSIOLOGY.

A PATRIOTIC if belated assertion of the claim tosurgical fame of an almost forgotten German worthydeserves acknowledgment. The family of Heine waswell known in South Germany through its medicalmembers, one of whom, Johann Georg, was the founderof a celebrated orthopaedic institute in Wiirzburg, andanother, Jakob, who was ennobled and became vonHeine, gave his name (in Germany at least) to theHeine-Medin disease, also known as anterior polio-myelitis. It appears that Bernhard Heine, the nephewof Johann Georg, whose daughter he married, was apioneer of bone surgery. J. G. Heine’s orthopaedic insti-tute was devoted to the mechanical treatment of defor-mities, and in it the making and fitting of applianceswere carried out with great skill. Probably experiencesin his uncle’s workshops led Bernhard Heine to turnhis attention to the invention of an osteotome.This ingenious but apparently complicated machineachieved a great reputation, and in 1837 Heine visitedRussia on the invitation of the Emperor Nicholas inorder to instruct Russian surgeons in the use of hisinstrument, hundreds of which seem to have been sentto St. Petersburg. With his osteotome Heine claimedto be able to perform all kinds of operations on thebones, and to remove parts of them of any desiredsize at any depth and in any direction. He performeda large number of experiments on dogs in order tostudy the processes of repair and regeneration of bone.Many of the preparations which he made are now inthe Anatomical Institute of the University of Wiirz-burg and have recently been carefully studied withthe help of X rays. They form a great part of thesubject-matter of a volume of essays 1 in which hispioneer work has been recalled. Despite the fact thatHeine relied entirely on naked-eye appearances andthat results were often complicated and processes

1 Bernhard Heine’s Versuche fiber Knochenregeneration, SeinLeben und Seine Zeit. Von der deutschen Gesellschaft fürChirurgie anlässlich ihre 50 Tagung den Fachgenossen unter-breitet. By Drs. K. Vogeler, E. Redeuz, H. Walter, and Prof.B. Martin, with a preface by Prof. A. Bier. With 105 illustrationsin the text and one portrait. Berlin : Julius Springer. 1926.Pp. 224. 7.50 Reichsmarks.

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obscured by suppuration, it appears that he antici-pated by some years the observations of Flourens andOllier on the regeneration of bone and on the partstaken respectively by the periosteum and the bone-marrow in forming new bone. Bernhard Heine receivedhonours from the Emperor of Austria, the Kings ofPrussia and Bavaria, and the ruler of his nativecountry of Wurttemberg. He became professorhonorarius of the University of Wiirzburg, and in1844 he was made extraordinary professor of experi-mental physiology. His communications to theAcademy of Sciences in Paris were favourablyreceived and won a prize for him in 1838. He diedat the early age of 46 in Switzerland, whither he hadgone to seek relief from pulmonary tuberculosis.

It is remarkable that the work of such a man shouldhave been almost completely lost sight of for so manyyears. There is no mention of his famous osteotome or of his work on bone growth in Hoffa’s text-book ofOrthopaedic Surgery, although Hoffa himself was aprofessor at Wiirzburg and gives a good account ofJ. G. Heine’s orthopaedic institute. Any reproachesthat might have been founded on German neglectof a native hero of pathology and physiology are

set aside by the publication of this interesting book,in which Heine’s countrymen have fully vindicatedhis right to be accounted a pioneer in the investigationof the phenomena attending injuries and diseases ofbone. -

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BIRTH INJURIES TO THE EYE.

AT the discussion on this subject at the recentannual congress of the Ophthalmological SocietylDr. Comyns Berkeley, speaking for himself and themajority of his obstetric colleagues, professed profoundignorance on the subject. As a matter of fact, it issafe to say that the majority of ophthalmic surgeonshave never seen a case of retinal haemorrhage in anewly-born infant. But this is simply because anophthalmoscopic examination of an infant withinthe first week of life is hardly ever undertaken.When a series of systematic observations of thissort has been carried out the results have been some-what surprising. Drs. Ernest Thomson and LeslieBuchanan, more than 20 years ago,2 quoted continentalauthorities who had observed retinal haemorrhagesfollowing normal labour respectively in 10 per cent.,32 per cent., and 26-5 per cent. of all cases, andDr. Thomson, in his opening remarks at therecent discussion, so far confirmed these figures thathe found the percentage of Glasgow cases some-

where between 10 and 20. Mr. F. A. Juler, who hadexamined a series of 50 cases at Queen Charlotte’sHospital in London, arrived at a similar conclusion.The great majority of these cases are slight retinalhaemorrhages which clear up, leaving no trace aftera few days. In some cases, however, the haemor-rhages, occurring at the macula, may leave permanentlyserious effects, and it is freely surmised that certaindefects in one eye only, discovered in later life,including cases diagnosed as " congenital amblyopia "may in some instances be due to this cause. It isto be remarked that haemorrhages are by no meansconfined to those cases where instruments have beenused. They apparently occur in many cases ofprolonged labour and non-instrumental delivery,and even in cases where labour has been perfectlynormal or even premature. Obviously rules as toprophylaxis are very difficult to formulate, and wecannot complain that until this can be doneobstetricians take little interest in the matter. Onereason why such ophthalmoscopic examinationsare not more frequently made is doubtless theextreme patience and tact required in the case of anew-born baby; but before any useful conclusionscan be drawn as to their connexion on the one handwith prolonged natural labour, and, on the other,with the use of instruments, this will have to bedone. Other ocular lesions occur. Apart from

1 THE LANCET, May 22nd, p. 994.2 Trans. Ophth. Soc., 1903, p. 296.

sensational cases which have been recorded, such asextrusion of the eyeball on to the cheek as the resultof instrumental pressure, or the gouging out of anorbit by the fingers of a doctor who had mistaken itfor an anus, perhaps the most interesting lesionis the rupture of the posterior elastic membraneof the cornea, described by Dr. Thomson andDr. Buchanan first in 1903 and again at therecent discussion. In these cases there is subsequentformation of cicatricial tissue which may remainas a permanent linear scar. These scars are alwaysvertical, or approximately so, a fact probablyrelated to the direction of pressure by the forceps.They naturally escape notice in most cases untilthe child’s vision is found to be defective in oneeye and the corneal scar is discovered. In some casesa considerable amount of corneal astigmatism results,and it was even suggested by some speakers that someof the cases of high monocular myopia, which arenot very uncommon, may owe their genesis to instru-mental pressure at birth. In these cases, althougha rupture of Descemet’s membrane might accountfor a good deal of astigmatism, one would have tosuppose that in order to produce a high degree ofmyopia in both meridia the sclera had yielded to thepressure of the forceps.

SYMPTOMS OF CORONARY OCCLUSION.

THE literature of the interesting condition ofcoronary occlusion is increasing rapidly. We

published a leading article in our issue of Jan. 9thlast giving a brief resume of some of the chiefclinical manifestations of occlusion of branches ofthe coronary arteries. The case described in THELANCET of May 1st by Dr. E. Bulmer and Dr. F. W.Mason Lamb is specially noteworthy, not only for itsrarity, but also for the care with which it is describedand the suggestive comments on the pathologicalconditions observed. The case was one of coronarythrombosis in a man 27 years of age with a pasthistory of syphilis and of subacute or chronicnephritis with acute exacerbations. The thrombosisoccurred on the site of an atheromatous ulcer inthe left coronary artery. Microscopically, a wide-spread deposition of cholesterin and of a special typeof fat was observed in some of the larger vessels,including the aorta and left coronary artery. Theauthors suggest that the premature death of thepatient may have given an insight into the pathologyof arterio-sclerosis in what may be called the pre-fibrotic stage. A critical study of the clinical featuresof coronary occlusion has recently been publishedby Dr. Louis Hamman.1 He gives an interestingaccount of the anatomy of the coronary vessels,quoted largely from Gross,2 and mentions the observa-tion made by him that anastomoses throughoutthe coronary circulation become more extensiveand more effective with advancing years. He suggeststhat, other things being equal, the heart of a manat 60 years of age is better prepared to withstandthe effects of coronary occlusion than that of a manof 20. He maintains that the results of coronaryocclusion depend upon the size and situation of thebranch obstructed, the rapidity with which it occurs,the condition of the general and coronary circulations,and the age of patient. Dr. Hamman gives a usefulclassification of the main symptoms in tabular formin four groups. The first comprises the immediatesymptoms of the occlusion-viz., anginal pain withshock, prostration, fall in blood pressure, andsuppression of urine. The second group includes thesymptoms associated with the myocardial damage-dyspnoea, Cheyne-Stokes breathing, the results ofpassive visceral congestion, and the disturbances ofcardiac rhythm. The third is devoted to the symptomsresulting from the myocardial infarct, includingfever, leucocytosis, pericarditis, embolic phenomena,

1 Bulletin of the Johns Hopkins Hospital, vol. xxxviii., No. 4,p. 273, April, 1926.

2 The Blood-supply to the Heart, New York, 1921.