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but occasionally nausea, precordial distress, and

dyspnoea occur, and much more rarely there maybe a rise of temperature. Clinical and haematologicalimprovement are said to occur consistently aboutfive days after treatment is instituted, irrespectiveof the previous duration of the illness. The preparationappears to be of no value in leukaemia, aleukaemicleukaemia, or aplastic anemia. This is important inso far as the differential diagnosis between agranulo-cytic angina and aleukaemio leukaemia is not easywithout examination of the bone-marrow. Toxic

symptoms following arsenobenzol therapy are now

happily rare, but as we pointed out two years agolagranulocytosis is probably far commoner than thenumber of cases recorded would suggest. It hashitherto proved fatal in a large proportion of thecases diagnosed, and the results recorded by theHarvard workers with nucleotide are therefore most

encouraging. ____

AGE OF DENTISTS.

IN the course of his twenty-second address fromthe chair at the Dental Board of the United Kingdom,Sir Francis Acland gave some interesting figureswhich had been got out in his office as to the agesof dentists registered under the Act of 1921. Their

average age is 47!- and the average expectation oflife of persons of this age is 22 years.

" I am afraid,"said Sir Francis, " to dogmatise about averages, forI do not visualise them in a concrete form like the

boy who said they were things hens laid eggs on,’and therefore I cannot say whether this means thatthis is the average expectation of life of persons ofthis average age, nor whether the figures mean thatin 22 years half the total number, which is 6748,will probably still be alive." It may be of interest,he added, to give the numbers in different age-groups. There are 5 between 80 and 84 years, 103between 70 and 80, 687 between 60 and 70, 1683between 50 and 60, 2676 between 40 and 50, and1594 between 32 and 40 years.

THE CAROTID BODY.

IN an annotation last week we quoted the statementthat Czermak was the first to note that compressionof the vasculo-nervous bundle in the neck produces ’,slowing of the heart beat. But, as Sir Thomas Lewis z’

points out in a lecture on vasovagal syncope and thecarotid sinus mechanism,2 this observation was

really made by Caleb H. Parry, who described itin his Inquiry into the Symptoms and Causes ofthe Syncope Anginosa, commonly called AnginaPectoris (1799). In his lecture Lewis brings forwardthe interesting hypothesis that the central andefferent parts of the carotid sinus reflex mechanism aredisturbed in the syndrome of common fainting attacks- nor, as he calls them, vasovagal syncope-in whichstrong vagal effects are combined with depressorvasomotor effects. In support of this he suggeststhat the alimentary symptoms associated withvasovagal syncope may be the result of alterationin the alimentary tract movements previously notedby Danielopolu to take place when pressure wasmade on the carotid sinus-namely, an initial inhibi-tion followed by increased activity of the stomach.The form of syncope to which he refers shouldbe distinguished from the " vasovagal"

" attacksdescribed by Gowers in which consciousness is seldomor never lost. Dr. J. A. Ryle,3 however, defends the i

1 THE LANCET, 1930, ii., 1405. 2 Brit. Med Jour., May 14th, p.873. 3 Ibid., May 21st, p. 956.

latter use of the term, since his experience suggeststhat both vagal and vasomotor phenomena form partof Gowers’s syndrome. ____

ÆTIOLOGY OF ALOPECIA AREATA.

OF all dermatological problems none is more

provocative than alopecia areata. The currenttheories of its causation are generally familiar. Thereis focal sepsis in teeth, tonsils, and alimentarytract ; Jacquet’s dental reflex hypothesis ; the oldertheory of exogenous infection ; trophic nervous

disturbance ; and finally an endocrine vago-sympa-thetic syndrome. But none of these suffices to

explain the symptoms in a scientific sense. Armas

Cederberg,l of Helsingfors, holds that of all concurrentor associated manifestations oral sepsis appears tobe the commonest, and this is perhaps true. Butthe association does not imply that the sepsis isto blame for the alopecia, and Sabouraud in hislatest monograph on the subject 2 cites more than oneunhappy case of total dental clearance without aparticle of benefit to the hair loss. H. W. Barber,on the other hand, has seen recovery after tonsillec-tomy and the use of a streptococal vaccine, and ithas certainly become the custom in English clinicsto examine the mouth and throat in every case ofalopecia areata and usually in vitiligo too. Cederberg,however, is not content with the streptococcal asthe specific element in causation. According tohis researches, oral and dental spirillse are the truecause, and reach the lymph channels and the generalcirculation either through microscopic abrasions ofthe mucous membrane, or in symbiosis with otherorganisms. A further stage in the thesis asserts thatspirillar infections are characterised by a character-istic affinity for the pigment and pigment-formingapparatus of the skin, whether manifested by hyper-chromia or a deficiency in that respect, as in vitiligo.The most obvious example of such cause and effectis the case of syphilis, in which modified types ofalopecia and vitiligo are both observed, while aspirillar (not spirochaetal) balanoposthitis is not

infrequently followed by more or less permanentlocal leucoderma and marked disturbances of the

genital pigment distribution. For direct proof of thesetiological role of spirillae in alopecia, their demon-stration in situ is necessary, and Cederberg claimsto have succeeded in several cases after prolongedsearch. He submits two microphotographs in

support of his claim, taken from sections of a recentcase of alopecia areata. Single organisms are observed,stained by the Levaditi process in the intersticesbetween epithelial cells, and in the lymph channelsboth in the epidermis and the derma. Groups orcolonies are also evident, and the polymorphismsuggests treponemata and leptospirillae. In thebasal cell layer the place of the normal pigment appearsto have been taken by the stained organisms. Of

greatest interest is their presence and apparent growthalong the walls and in the sheaths of hair follicles,where a toxic pilopapillitis explains the resultinghair loss and occasional destruction of the hairfollicle. It cannot be definitely ascertained at

present whether the cell itself can be penetrated, butit is clear that the pigment-forming cells are highlysusceptible, a fact which sustains Sabouraud’soriginal observation that in alopecia areata the

ordinary tissue reactions and proliferations are of theslightest. " Toutes aussi concordent a temoignerd’une intoxication locale profonde."

1 Derm. Woch., 1932, No. 16, p. 539.’ Pelades et alopécies en aires, Paris, 1929.