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immersed in water, it will swell to an amazing extent.Charnley’6 pointed out that a disc immersed in four-times physiological saline solution increases in weightalmost as much as does one immersed in physiologicalsaline; this suggests that the mechanism of hydration isnot simple osmosis.Hendry found that the annulus takes up water by

osmosis but that the degree of hydration of the nucleus doesnot vary with the osmotic pressure of the surroundingfluid. Gels can imbibe fluid against pressure. He com-

pared the imbibition characteristics of disc material

(assumed to be normal) removed at necropsy with that ofdisc material removed at operation. The latter materialshowed less affinity for fluid than the necropsy material-i.e., the discs were less hydrated and had less ability tohold fluid when subjected to pressure. Hendry suggestedthat lack of nuclear turgor predisposed to disc prolapse-a suggestion which accords with the experimental findingsof Roaf," who found that compression of a disc and

adjacent vertebra usually produced a fracture of thevertebral end-plate and intracorporeal nuclear prolapse.Only if the nucleus had lost its turgor could he produceannular tears and a characteristic intraspinal disc prolapse.Hendry’s results might be criticised on two grounds:

first, usually the material removed at a " disc operation "is mainly annulus, and if any nuclear material is removedit is so entirely different from a normal nucleus pulposusthat it can hardly give any useful information about themechanical and chemical properties of the nuclear pulpo-sus when the disc first became mechanically incompetent.Anyone with experience of the appearance of a normalnucleus pulposus in the living body will confirm this.Secondly, while it is comparatively easy to isolate thenucleus pulposus from the annulus in the cadaver, thereare very considerable differences in the degree of hydra-tion of the normal nucleus pulposus seen in the livingbody from that seen in the cadaver. The chemical andmechanical properties of a cadaveric disc are not neces-sarily normal.Without attempting to decide whether the dehydration

" or hyperhydration " theory of disc degeneration iscorrect we can form two conclusions. First, furtherstudies of the chemical and biomechanical properties ofnormal and abnormal nuclei pulposi are urgently required.Secondly, if the nucleus is hypohydrated (i.e., lacks turgor)the disc resembles an underinflated tyre whose walls (i.e.,the annulus fibrosus) are likely to split when subjected topressure. If the nucleus is hyperhydrated (i.e., has a highturgor), it resembles an overinflated tyre whose wall is

likely to burst. The normal shock-absorbing mechanismof the intervertebral disc depends on the nucleus pulposushaving the right amount of hydration and the annulus andvertebral end-plate being intact. When compressed, bothannulus and end-plate bulge, and, in addition, blood issqueezed out of the venous sinuses of the vertebral bodyinto the paravertebral vein. If the intra-disc pressure istoo high or too low this shock-absorbing mechanism doesnot work properly and excessive strain is thrown on theannulus fibrosus, which may then tear.Nachemson 11 found that the normal intra-disc pressure

is quite low but that when the spine is loaded the intra-.

disc pressure is 50% higher than the applied load per uniti of area. For instance, if the load is 10 kg. per sq. cm. theE stia-disc pressure is 13-15 kg. per sq. cm. Pressures in

76. Charnley, J. Lancet, 1952, i, 124.77. Roaf, R. J. Bone Jt Surg. 1960, 42B, 810.78. Nachemson, A. Acta orthopœd. scand. 1960, suppl. 43.

young people tend to be lower than in older people.Nachemson also estimated that the tangential stresses inthe peripheral part of the annulus fibrosus may be threeto five times the applied external load per unit of area. Ifthe disc is degenerate the annulus is subject to a relativelyhigher stress than in a healthy disc.The efficient mechanical functioning of our nuclei

pulposi is clearly of great importance. Much more workis needed. As Naylor observes, " we are still only on thethreshold of this problem ".

MEDICARE 1963

President Kennedy has sent a message to Congressoutlining his plans for the welfare of old people.1 Last

year his " Medicare " Bill, dealing largely with hospitalinsurance through social security, was rejected by theSenate and never got beyond the Ways and Means Com-mittee of the House of Representatives. The new pro-posals are broadly similar to last year’s 2 except that peoplewould be allowed to choose at 65 whether they wouldprefer to have 45 days’ hospital care free, or 90 days’ carewith deductions up to 90 dollars, or 180 days’ care with adeduction equal to 21/2 days’ hospital costs. A more

important change, which meets some of the objections tolast year’s Bill, would extend the benefits to the largeminority of people not covered by social security-thoughmost of the financing of the new measures would bethrough an increase in the social-security tax. Some liberalRepublicans have introduced a Bill which is broadlysimilar but would allow beneficiaries to accept care

financed through private rather than Government plans,and would allow private organisations and States to helpadminister the programme. The President’s new pro-posals deal, besides hospital insurance, with plans forincreased aid through the States to old people who are ill,and for housing, recreation centres, and employment forold people.

Last November’s election changed the complexion ofCongress but slightly. Political observers give theAdministration’s proposals little better chance of passingthe new Congress than last year’s.

ÆTIOLOGY OF TRIGEMINAL NEURALGIA

TiC DOULOUREUX in a patient under forty years of ageis often a manifestation of disseminated sclerosis. In the

elderly it has no recognisable cause. The disorder issimilar in these two settings. If it is accepted that thesame mechanism operates in each group, then the site ofthe lesion is likelier to be central than peripheral, since theevidence points to a brain-stem location in disseminatedsclerosis. Yet operations on the gasserian ganglion willoften cure the idiopathic variety of tic, and complete pre-ganglionic root section hardly ever fails to do so. The con-flict is to some extent resolved by the repeated observationthat tic is essentially a reflex pain: trigger zones have to bestimulated to produce a bout. If this is so, then cuttingthe afferent pathways would be expected to cure the con-dition, and this would not necessarily indicate that thecausal lesion was peripheral to the section.Kerr 3 now suggests that pressure on the gasserian

ganglion by the carotid artery as it comes up to form thesyphon is the cause of idiopathic tic. Several features

1. Christian Science Monitor, Feb. 21.2. Lancet, 1962, i, 1231.3. Kerr, F. W. L. Arch. Neurol. 1963, 8, 15.

542

accord with this suggestion-for instance, the higherincidence in elderly women and in those with arterio-sclerosis. But Kerr’s anatomical reason for the rarity offirst-division tics-that, although the artery is in intimatecontact with the first-division portion of the ganglion, it ishere cushioned by the blood in the cavernous sinus-seems a little forced, and the intermittence of the com-plaint is not accounted for. Nevertheless) the generalexplanation is ingenious and well argued. It remains at

present an exercise in logic. Like other supposed causalmechanisms, this one may act as a precipitating factor inthe presence of a more central causal lesion.

ISONIAZID IN PROPHYLAXIS

ISONIAZID is a cheap, safe, convenient, and effectivekiller of tubercle bacilli. That it should be used to preventas well as to treat tuberculosis is not surprising.Some have applied the word " chemoprophylaxis " to

both the prevention of infection and the prevention ofrelapse, particularly in those with a positive tuberculintest but no other abnormality. The former has beencalled " primary " and the latter " secondary " prophy-laxis. This seems unnecessary. Skin sensitivity to

tuberculin does not necessarily indicate that there areliving tubercle bacilli in the body; but it is a reasonableassumption that in young people tuberculin sensitivityusually indicates tuberculous lesions. To give isoniazid tosuch persons is to treat them, for the disease already exists:terming this prophylaxis obscures the truth by suggestingthat these patients are not tuberculous and can be treateddifferently from those who are.The experimental basis for isoniazid prophylaxis-the

prevention of tuberculosis-has been reviewed byMitchison and Lambert. Schmidt 3 kept non-infectedmonkeys in cages with others known to have pulmonarytuberculosis and gave all the animals isoniazid in the dietin daily doses up to 20 mg. per kg. body-weight. Fromprevious experience it was known that the survival ofuntreated monkeys kept under similar conditions of

exposure to infection was short, and in one such experi-ment all previously uninfected animals had become hyper-sensitive to tuberculin, developed tuberculosis, and diedwithin a year. Of those given isoniazid, on the other hand,none became hypersensitive and none died during theyear that they received the drug. After both the isoniazidand exposure to diseased animals had been simultaneouslystopped, almost half the healthy animals became hyper-sensitive and had manifest pulmonary tuberculosis.Unless all these animals are assumed to have been infectedon the day that the last dose of isoniazid was given-whichis unlikely-the findings suggest that isoniazid in the doseused and under the prevailing conditions of exposuredoes not entirely prevent multiplication of tubercle bacilli.While the drug is being taken, growth is suppressedsufficiently to prevent hypersensitivity developing, but notsufficiently to kill all the bacilli in the tissues; after thedrug is stopped, the bacilli can grow and eventually pro-duce lesions. In other experiments under different

conditions, Schmidt 4 was able to prevent infection

entirely by even small doses of isoniazid for sixteen totwenty-four weeks, and the animals showed no signs oftuberculosis for at least a year after the drug was stopped.The monkey is a highly susceptible animal, and this

1. Mitchison, D. A. Advanc. Tuberc. Res. 1957, 8, 304.2. Lambert, H. P. Amer. Rev. resp. Dis. 1959, 80, 648.3. Schmidt, L. H. Amer. Rev. Tuberc. 1956, 74, 138.4. Schmidt, L. H. ibid. 1956, suppl. p. 5.

prevention by isoniazid is impressive. But the apparentsuppression of disease only for as long as isonizaid wasbeing taken suggests a need for caution in applying theprocedure to whole human populations. Isoniazid

prophylaxis and treatment has been extensively investi-gated by the United States Public Health Service.Comstock 5 reported a study in an area of Alaska wheretuberculosis is highly prevalent, the infection-rate beingestimated as more than 10 times that for the rest of theUnited States.

7333 persons were included in the population studied, morethan 95 % being Eskimos. Almost 45 % of them had previouslybeen diagnosed as tuberculous, including 10% who were

receiving treatment, and 14% who had had treatment. Of theremaining 4077 individuals, 2576 were known to have had noX-ray evidence of pulmonary tuberculosis within the year

preceding the investigation, and in 1501 it was not knownwhether or not they were tuberculous. This whole populationwas divided by random allocation into households which wereto receive isoniazid tablets (300 mg. daily for. adults) and thosewho were to receive inert tablets. 14% did not, in fact, begin totake the tablets for various reasons, almost half of them becausethey were already being treated for tuberculosis. 211 took bothtypes of tablets through moving from one household to another.A total of 3017 took the inert tablets only and 3049 isoniazid, but14% stopped taking tablets before the end of the year, half ofthem because of symptoms attributed to the tablets or the fear ofsuch symptoms. It was estimated that about a third of bothgroups took 90% or more of the year’s dosage and a third lessthan 60%. Tuberculosis in the population during the year wasestimated, not by routine examinations of the whole population(a highly difficult task in such an environment) but by routinenotifications arranged by the Alaska Department of Health andWelfare. There was apparently no important differencebetween the groups in degree of exposure to known cases oftuberculosis.

Among the group receiving inert tablets, 41 new casesof tuberculosis were notified (1-4% of the populationstudied) ; among the isoniazid group there were 13 (0’4%).In the following two years there were 37 additional newcases in the group who had had inert tablets and 25 inthe isoniazid group. It was calculated that, for the wholeobservation period of three years, 85 new cases were

prevented-a reduction of almost 50% in the tuber-culosis incidence. There does not seem to have been

any obvious recrudescence of suppressed infections, suchas was observed in Schmidt’s monkeys.

This study of a whole population does not answer thequestion whether isoniazid can prevent infection in man,as it does in monkeys; for it was not known whichmembers of the population were uninfected-only whichmembers probably had no radiographically visible lesions.It is an important study of mass chemotherapy andchemoprophylaxis combined.A further study by the United States Public Health

Service was reported by Ferebee and Mount. Thisconcerned contacts of patients with pulmonary tuber-culosis and was designed like the Alaska investigation.It was estimated that two-thirds of the whole populationof 25,000 people took all the tablets prescribed; but abouta sixth stopped taking them before the year ended.Isoniazid was given on the basis of 5 mg. per kg. body-weight daily (100 mg. three times a day). The groupswere similar in the proportions of tuberculin sensitiveand insensitive before the start of treatment and in totalnumbers. Among those taking inert tablets there were16 cases of manifest primary tuberculosis in individuals

5. Comstock, G. W. Amer. Rev. resp. Dis. 1962, 86, 810.6. Ferebee, S. H., Mount, F. W. ibid. 1962, 85, 490.