648

The clinical features of the five patients were identicalwith the exception of the added cerebral manifest tionsin the patient previously described. In four of thepatients an arrest in the progress of the symptoms’andsigns occurred with the removal of the adenoma. Inthe fifth patient, post-mortem examination showed apancreatic adenoma and severe and widespread degenera-tion of the anterior horn cells of the spinal cord. Barris

points out that to conclude that adenomas of the pancreasare usually responsible for the syndrome seen in progres-sive muscular atrophy is not warranted. It did seem

important, however, to show that sufficient hormonalimbalance or altered hormonal function existed to causeultimate damage to the anterior horn cells of the spinalcord.

Blau et al. have reported a case which adds to theconfusion. The symptoms and signs in this patientwere almost entirely of a neuropsychiatric nature andincluded changes in the psyche and in the central, peri-pheral, and vegetative nervous systems. The patientsuffered from convulsions, parkinsonism, pyramidalsigns, ataxia, generalised muscular weakness with myo-tatic irritability, and sensory changes, and from pro-gressive emotional and intellectual deterioration accom-panied by paranoid delusions. During several hypo-glycæmic attacks coarse fibrillations were noted in theright forearm. The outstanding features were a persistentParkinson syndrome and evidence of progressive internalhydrocephalus as shown by several encephalograms.Attention was called to the coexistence of the manifesta-tions of chronic disease of the periventricular nuclei andthe constant hypoglycaemic state. The authors were notable, however, to establish whether the disease of thecentral nervous system or the hypoglycæmia came first.

Also confusing is the fact that spontaneous hypo-glycæmia, without a functioning islet-cell tumour of thepancreas, does not necessarily produce the symptoms ofhypoglycaemic shock. Hypoglycaemia and hypoglycæmicshock are not the same, nor is the latter always producedby the former.Practically all patients with hypoglycæmia will have

neurologic symptoms. The earlier diagnosis and propertreatment of such patients necessitates that the physicianbecome more - conscious of the syndrome due to

hypoglycsemia.Veterans Administration JOSEPH M. MILLER.

Fort Howard, Maryland, U.S.A.JOSEPH M. MILLER.Veterans Administration,

Fort Howard, Maryland, U.S.A.

6. Blau A., Rieder, N., Bender, M. B. Ibid, 1936, 10, 910.

MENTAL ACTIVITY IN INFANCY

EIRENE COLLIS.Cerebral Palsy Unit,

Queen Mary’s Hospital for Children,Carshalton, Surrey.

SIR,—May I comment briefly on the letters last weekabout my article on mental activity in infants ?

It is clearly impossible in a letter to answer allDr. Doniger’s questions ; she may care to know that astatistical paper on the work already done has beenprepared for publication, and that the Medical ResearchCouncil is supporting further research by Dr. WilliamDunham and myself into the problems of early diagnosisof neurological defect.The specific points raised by Dr. and Mrs. Bobath

are dealt with in the original text of my article. Theirstatement that mental development depends on physicaldevelopment as it stands cannot be upheld. If byphysical development they mean neural maturation, therelationship between this and mental development isnot disputed. There can be no doubt that motor retarda-tion occurs in cases of mental deficiency, though, exceptin amentia, motor development is, in due time, attainedby the mentally deficient child. Indeed, many " thera-peutic successes " in such cases are attributable to thisprocess. On the other hand, no useful purpose is servedby disregarding the fact that syndromes occurring in thepresence of neural defect differ. The purpose of mypaper was to show that mental and motor defects both

affect physical activity, though in differing ways. Thedifferences are not effaced by indiscriminate applicationto all abnormalities of the label " release phenomenon."

1. Fetcher, E. S., Hall, J. F., Shaub, H. G. U.S. Air Force Memraudum, March, 1949,

OSTEOPATHY

DONALD TURNER.

SIR,—I should like to correct any false impressioncreated by Dr. Cyriax’s letter last week.

No-one would seek to deny that he has taught " spinalmanipulation " to physiotherapists over a period of tenyears. The point at issue, it seems to me, is that whereasDr. Stoddard and the osteopathically trained apply verygentle forces, very strictly localised and guarded, in orderto obtain a specific result at a joint, Dr. Cyriax and hisadherents indiscriminately mobilise the intervertebral-

joint systems by applying uncontrolled torsional forces.I do not seek to suggest that even this may not at timesrelieve pain ; but it can hardly do so by " reducing adisplaced fragment of annulus," unless by the process ofreductio ad absurdum. The annulus fibrosus is livingtissue, not dry friable matter.

In cases of pain due directly to pressure upon nerve-roots-a process caused by : (1) narrowing of the inter.vertebral distance, from (2) disc-nucleus leakage whichmay sometimes cause (3) actual pressure on the radix bynucleus pulposus or by annulus-bulging (because ofnucleus pressure)-in such cases the radix will sufferfrom localised inflammatory reaction as a direct con-

sequence of pressure.In these cases osteopathic methods, of gentle traction

followed by specific movement, seek to relieve the

pressure by altering the relationship of the affectednerve-root to the compressing factor ; relief of pressurewill at once allow better drainage, and decongestion.Those of us who use the gentle specific methods ofosteopathy would never seek to deny Dr. Cyriax and histrainees their satisfaction in their own manoeuvres;rather do we say that we find the gentler methods we havelearned effective without that element of uncontrolpresent in

"

spinal manipulation."London. W.1. DONALD TURNER.

INVOLVEMENT OF AUTONOMIC NERVE-FIBRESIN DIABETIC NEUROPATHY

SIR,—It is to be expected that autonomic nerve-fibresare involved in diabetic neuropathy, and that thisinvolvement produces changes in the vasomotor reflexes.I think, however, that Dr. Martin (March 21) too readilyassumes that he has demonstrated this.The validity of his investigations depends on the

reliability of skin-temperature measurements as a.

method of estimating skin blood-flow ; and unfortu-

nately Lewis’s statement (referred to by Dr. Martin)that these are most reliable cannot be substantiated.Fetcher et al.1 in a most careful study compared the skin-temperature of the finger with the blood-flow of the samefinger measured by means of a Goetz plethysmograph.They demonstrated that with an ambient room-tempera-ture of 21°C (comparable to that used by Dr. Martin)there is scarcely any correspondence between finger-surface temperature and changes in blood-flow. In theirexperiments an increase in finger blood-flow of 400%over a period of 10 minutes (i.e., from 15 to 60 ml. per100 c.cm. per min.) did not produce any significantchange in skin-temperature. These workers concludedthat to obtain a good correspondence between skin-temperature and skin blood-flow " the part of the bodyunder investigation must lose heat at a rate of at least240 K. Cal/hr/M2." —conditions which can only beobtained in still air at room-temperatures below 0°C.

649

Cooper et al.2 also cast doubt on the reliability of skin-temperature measurements as an estimate of blood-flow,particularly as the skin-temperature approached 32°34°C.My own investigations comparing the temperature ofthe skin over the pulp of the big toe with occlusion-plethysmograph estimations of blood-flow show that

in normal people at room-temperatures of 20°-25°C a

340% increase in foot blood-flow produces an increase inskin-temperature of only 3°C when measured for 60min. after warming.

I think most observers agree that except under theconditions described by Fetcher et al. skin-temperaturemeasurements are of no value as an estimate of the

degree of vasoconstriction occurring in the skin. More-

over, the temperature changes recorded by Dr. Martinafter exposing the patient to room-temperature are in anumber of cases he illustrates so small as to be insignifi-cant. It would perhaps be better in any case if Dr.Martin produced reflex vasoconstriction by means of asudden stimulus-e.g., ice on the forehead or pain.Unless the vasomotor changes in diabetic neuropathy

are investigated by means of a flow method it would seemnecessary to preserve an open mind on Dr. Martin’sconclusions, even though the changes he describes mightbe expected on a-priori grounds.

Physiology Department,St. Mary’s Hospital Medical School,

London, W.2. ANGUS MCPHERSON.ANGUS MCPHERSON.

Physiology Department,St. Mary’s Hospital Medical School,

London, W.2.

2. Cooper, K. E., Cross, K. W., Greenfield, A. D. M., Hamilton,D. McK., Scarborough, H. Clin. Sci. 1949, 8, 217.

3. Cathcart, E. P. Lancet, 1938, ii, 1480.4. Booth, W. G. Ibid, 1952, i, 1258.5. Engle, E. T., Morton, D. J. J. Bone Jt Surg 1931, 13. 311.6. James, C. S. Lancet, 1939, ii, 1390.7. Elmslie, M. Ibid, p. 1260.

HALLUX VALGUS

R. WHEELER HAINES.Department, of Anatomy,University of Sheffield.

A. MCDOUGALL.Department of Orthopædics,Glasgow Royal Infirmary.

SIR,—Cathcart 3 and others asked : If footwear isalone to blame, why is it that the feet of peoples who arein the habit of going barefoot so commonly differ fromwhat is regarded as the ideal ’? This question is still

troubling students of hallux valgus. Your correspondentDr. Booth 4 suggested that W.H.O. should investigatebarefoot peoples, and your leading article of Feb. 14

suggests that such work might throw further light onthis problem. May we refer to two important works onthis subject ?The African expedition by Columbia University and the

American Museum of Natural History 5 made the studyof feet one of their main objectives. The great thicknessof skin is noted : the ’’ negroes sat for some time at asmall outdoor fire with their feet resting on live coals."There is a peculiar wrinkling of the skin about the anklesin natives over 40 years of age. There is no hallux valgus,for " where we suffer from arch strains, they lose a toeor two" from injury, chiggers, or yaws ! They are notablyfree from the ordinary types of static foot trouble withwhich we are familiar in our civilised centres of population.James 6 in ten years’ work in the Solomon Islands

found "neither footgear nor flat foot "-only yaws,ulcers, infections, contractures, and loss of toes. Henoticed a great difference between shod Europeans onthe one hand and unshod. Europeans and natives on theother, involving narrowing of the metatarsal region ofthe foot and lateral displacement of the toe in shodpeople. This change corresponds closely to Elmslie’s 7description of alteration in 80% of children on beginningto wear shoes.One of us in the course of four years’ work in an

Egyptian anatomy school found not a single instance ofhallux valgus. The material came entirely from theFellahin, among whom the men work barefoot, thoughthey may attend the mosque in shoes and leave them atthe entrance, while the women seldom wear shoes at all.In the streets, on the contrary, typical valgus wascommonly observed in the better-off women wearingshoes of European type whose open-work toes allowed

careful observation ; deviation of the great toe, bunionformation, and clawing of the other toes were common.In Egypt the distinction between the classes is sharp,and the distribution of valgus follows the class structure.

It seems, then, that footwear can still be blamed forthe ordinary hallux valgus of the European adolescent.There are of course other causes, for there is certainly a,congenital form, and hallux valgus may also appearrapidly with various forms of arthritis even though thepatient is not wearing shoes. Probably these additionalfactors account for the odd cases of valgus found inunshod Annamites and Transvaal natives mentioned byHardy and Clapham 8 ; and causation by arthritis isconsistent with Booth’s statement (Feb. 21) that

among the barefoot people hallux valgus is found onlyin adults.

8. Hardy, R. H., Clapham, J. C. R. Ibid, 1952, i, 1180.9. Walsh, B. J., Bland, E. J., Jones, T. D. Arch. intern. Med.

1940, 65, 321.10. Gorlin, R., Gorlin, S. G. Amer. Heart J. 1951, 41, 1.

MITRAL STENOSIS

SIR,—We have read with great interest your annotationof Jan. 10 and the subsequent letters from Dr. Wade(Jan. 24) and Dr. Gorlin (Jan. 31). We would like tocomment on Mr. Brock’s view that the mitral-valveorifice at operation is always the same size.Walsh et al.9 have described quite clearly the evolution

of the murmur of pure mitral stenosis following rheumaticfever five or ten years before. The first sign is an earlydiastolic murmur, to which is added in later years a

presystolic murmur. Taking into account Henderson’swork on ventricular filling curves, it is reasonably certainthat in the earliest stages of mitral stenosis adequateleft ventricular filling can be achieved without an increasein left auricular systole. When the stenosis is moresevere, the characteristic presystolic murmur appearsand flow is maintained for a considerable period untildiminished right ventricular competence leads to a fallin cardiac output. This usually occurs when the valvearea is in the range 0-9-1-0 sq. cm. It is at this or a later-

stage that most patients nowadays see the surgeon. In

nearly 100 cases of pure mitral stenosis treated surgically,Mr. F. H. Mills has found quite definite variations inthe size of the valve orifice which agreed very well withthe size predicted from the symptoms and the dataobtained at cardiac catheterisation. Moreover, followinga good valvotomy the presystolic murmur disappears,and only a diastolic murmur following the third heartsound remains.

In answer to your comment that resting pressures inthe pulmonary artery may apparently be nearly normalin the presence of disabling symptoms, it should be

pointed out that in the presence of auricular fibrillation,.a narrow valve orifice, and a lowered cardiac output,the pulmonary-artery pressure is an unreliable index ofthe severity of the disease. For reasons which are not

entirely clear the onset of auricular fibrillation causes aconsiderable fall in cardiac output; and as stenosis is.almost invariably already severe, it follows from the lawsgoverning mitral valve flow 10 that a fall in pulmonary-artery flow will be associated with a considerable fall inpulmonary-artery pressure. Calculation of the elasticityresistance of the pulmonary vessels in such cases willshow that the vasculature is less tense than in the usualcase of mitral stenosis, suggesting that it has previouslybeen more distended. A similar state is occasionallyfound in patients with sinus rhythm, and it is reasonableto attribute it in both cases to diminished right ventri-cular competence, though congestive failure has not

necessarily occurred. Support for this view is found whenthe patients are exercised, for pulmonary vascular