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to ten minutes. There was almost dysenteric diarrhoeaand some collapse. The temperature was 984° 1’., thepulse-rate 110. The tongue was clean. The whole abdomenwas at first so rigid as to suggest an abdominal emergency.There was tenderness in the right iliac fossa. In two daysthe man was well again, except for lassitude, which con-tinued for several days. The second case was a boy of 19,who, after an initial rigor, collapsed one morning withdiarrhoea and vomiting. This lasted a few hours only, andwas followed by pain in the right side of the chest, with asmall area of pleural friction. I saw him at this stage, whenhe looked thoroughly

" toxic " ; temperature, 100-1° F. ;pulse-rate, 110 ; respirations, 20. No further signs developedexcept severe headaches on the second and third day. Heinformed me later that he had coughed up blood-stainedsputum three times at the onset of his illness. He wasin bed for five days, picked up again very slowly, andretained signs in the upper lobe of his right lung, which,together with his initial haemoptysis, made me doubt thecause of his pleurisy. A month later, however, no addedsounds could be detected in the lungs ; slight impairmentof percussion note alone remained. During the remainingweek of the voyage acute catarrhal conditions of the upperrespiratory tract were rife among the passengers, officers.and crew. Some were mere " colds " without fever. Insome mild tonsillitis with a spasmodic feverish cold occurred.In two cases marked laryngitis was the chief feature. Inseveral there was some huskiness. Sporadic cases ofdiarrhoea occurred here and there, but this is, of course, acommon condition in ships traversing tropical waters.The influenza cold ran its course through the ship,

cases occurring at intervals during the 24 days ofthe outward voyage and during a subsequent fort-night in dock in Buenos Aires, and ended with oneor two sore-throats, and one moderately severe

laryngitis during the first few days of the homewardvoyage. No one was affected twice, except a sailorwith large ragged tonsils, who had two attacks ofacute tonsillitis, with three weeks’ interval between.

A CASE OF

SUBACUTE COMBINED SCLEROSIS OF THECORD OF SUDDEN ONSET.

BY S. C. H. WORSELDINE, M.R.C.S.ENG.,CAPTAIN, INDIAN MEDICAL SERVICE.

THE following case seems worthy of record :-A native driver in a mule corps, aged 25, was admitted to

the Indian Military Hospital, Maymyo, suffering from lossof use of both legs, due, in his opinion, to witchcraft in hisvillage in the Northern Punjab. He stated that he hadnever been in hospital before, and denied venereal disease.Seven days previously he had noticed weakness in his legsafter the day’s work ; this weakness had steadily progresseduntil on the seventh morning he had been unable to standup. No history of any pain or peripheral sensations could beelicited, nor any history of trauma.

Condition on Examination.-Patient appears to be a

muscular, fit man. There is complete inability to moveeither leg from the hip downwards. Both legs are veryspastic, and considerable force is required to flex the knees.Knee-jerks equal but exaggerated. Ankle-clonus presenton both sides. Plantar reflex : Marked extensor bilaterally.Both eyes react to light and accommodation. Pupils equaland normal size. No nystagmus.

MsaMoMs.—Pain : : diminished over both legs, and anarea extending from the pubes to 2 inches above theumbilicus. An area of hypersesthesia from this to thexiphisternum. Sensations of touch, deep pressure, heatand cold lost to legs and area below umbilicus. Diminishedsensation on rectal examination. No abnormality in urine,heart, and lungs, optic discs or retine. Spleen not palpable.Wassermann reaction negative. Cerebro-spinal fluid : notunder pressure, clear, with normal cell count.Blood examination : Total red cells, 2,340,000 per c.mm. ;

haemoglobin, 80 per cent. ; colour-index, 1-7. Poikilocytosisand anisocytosis present. Normoblasts and megaloblastspresent; no myelocytes seen ; 5 per cent. eosinophilia.

Diagnosis and Progress.-A diagnosis of subacutecombined degeneration of the cord was made, althoughmegaloblasts are rarely seen except in perniciousanaemia.Two days after admission retention of urine

developed. Fseces passed voluntarily. After a weekin hospital the spasticity increased and there wasloss of sensation to pain over the areas where it was

previously diminished. A painless effusion of fluidappeared in the left knee-joint.The case could not be followed up, as he was

invalided to his home.

A NOTE ON THE

FALLACY OF THE COLOUR-INDEX.

BY B. DERHAM, M.D., M.CH. R.U.I.,LATE MEDICAL OFFICER OF HEALTH FOR GARSTANG.

THE technique employed to ascertain the colour-index may be divided into two stages. The first partof the test identifies by means of a comparison oftints a standard aqueous heamoglobin, the informa-tion being furnished in the form of percentages. Thestandard, of course, is fixed by the perpetuation ofthe tint which determines the identification ; andwhen that standard is attained the blood is said tocontain 100 per cent. haemoglobin. The second partof the test is derived from an enumeration of thecorpuscles actually present in 1 cubic millimetre ofblood. Its utility depends upon the fact that thisinformation can also be stated in the form of per-centages, as follows.

It has been ascertained by careful observation that acubic millimetre of healthy blood contains 5,000,000 redcorpuscles, within fairly narrow limits of variation, whichevidently must exist in a case of this kind, whatever standardbe adopted. These 5,000,000 corpuscles will thus alsorepresent 100 per cent. haemoglobin ; and it is evident thatsmaller numbers than 5,000,000 can also be correctly repre-sented as percentages on that basis. But the percentageobtained in this manner can perform a different functionand be treated as percentages of abstract number merely,without any special reference to haemoglobin. Hence ifthe percentages of the standard haemoglobin obtained bythe colour test be divided by the percentages derived fromthe enumeration of the corpuscles, it is claimed that thequotient represents the haemoglobin content of the individualcell.

The reasoning is plausible and seemingly con-

vincing, yet there is an underlying fallacy which robsthe colour-index of the greater part of its scientificvalue. The fallacy lies in the tacit assumption thatin the course of the attenuation of the haemoglobinof a corpuscle in anaemia the weight and volume ofwater introduced into the cell are precisely equal tothe weight and volume of the haemoglobin removedfrom the cell. This criticism is established by thefact that (taking an extreme case) the colour-indexof 0-5 is interpreted to mean that one-half of theattenuated cell is normal haemoglobin and the otherhalf water. Now since we begin the process ofattenuation with a normal haemoglobin of colour-index unity, and end with an attenuated haemoglobinof colour-index 0-5, and since no other factor thanthe addition of water intervenes, it is evidentthat the underlying assumption is that the waterexactly replaces the haemoglobin in the constitutionof the cell, weight for weight and volume for volume-in other words, that the specific gravity of the wateris identical with that of the haemoglobin which itreplaces in the cell.

This is the fundamental fallacy of the currenttheory of the colour-index, because the specific gravityof normal haemoglobin is much greater than that ofwater. Therefore if we attentively follow the processof attenuation we will perceive that, weight forweight. the volume of water introduced into the cellwould be much greater than the volume of haemo-globin withdrawn from the cell, with the necessaryconsequence that there would be a very great andconstantly accelerating augmentation of the totalvolume of the attenuating haemoglobin far in excess.of what is attributed to it by the current procedure.

An 7KM.s<ra’’iM.I will now select a concrete case to illustrate some

of the consequences of the fallacy which I haveindicated.To begin with, a definition of hemoglobin is required. A

healthy blood corpuscle is an almost chemically pure colloidaL