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16. Penal Reform and Research. By R. A. BUTLER. Liverpool: UniversityPress. 1960. Pp. 14. 3s. 6d.

17. Chapman, L. F., Ramos, A. O., Goodell, H., Silverman, J., Wolff, H. G.Arch. Neurol. 1960, 3, 223.

compulsory; but the new Bill includes provisions for itsextension to those coming out of detention centres.

Physical health in prisons remains good, and the trendtowards using outside facilities continues; but the

number found insane on remand jumped to almostdouble despite a decline in the number remanded formental observation and report. It is hard to explainthese trehds; perhaps the new outlook inherent in theMental Health Act of 1959 may have permeated theprison medical services more quickly than it has influencedthe judicial authorities.The prison services, avowedly therapeutic organisations

these days, are under as much obligation as, say, themanufacturers of drugs to assess and to publish theirresults, particularly where new techniques such as groupcounselling are introduced. In a recent lecture theHome Secretary 16 endorsed the views on research we putforward last year.15 It is therefore disappointing to findso little about new methods in the report. In support of

group counselling it includes a few staff impressions anda couple of letters from prisoners; only in an appendixis there some worth-while evidence-from a local prisonwhere, despite a rising population, the Norwich systemled to a drop in disciplinary reports of 131 to 369, and thecontinuing lapses were less serious than before. Otherthan this, the cynic might be led to correlate the trendtowards easier relationships in and out of the prison withthe increase of indiscipline, escapes, and overcrowdingwhich the report mentions. A larger chapter on" Research " is needed in this valuable document. TheHome Office research unit, which is already doing a

great deal, should stop hiding its light under a bushel.Bricks and mortar may still be badly needed, but knowledgemust be given a new priority.

HUMORAL AGENT IN MIGRAINE?

BROADLY speaking, the mechanism by which symptomsare produced in an attack of migraine is agreed; but theexact changes in cranial blood-vessels and nearby struc-tures which cause the characteristic head pains are still indispute.Chapman et a1.l7 working on the hypothesis that besides

local vascular change some inflammatory or pain-producingsubstance was produced locally, examined tissue-fluidfrom regions of the head which were tender during amigraine attack. Specimens were collected by slowlyinjecting 2 ml. of sterile physiological saline solution intothe local subcutaneous tissue and then gently withdrawingsome of it. Controls were provided by taking samplesfrom the scalps of migraine patients both during attacksand at other times, from people not subject to headacheattacks, and from the subcutaneous tissue of the forearmsof each subject. In the headache subjects a substance wasfound which bioassay suggested was a polypeptide. Thissubstance, for which Chapman et al. suggest the name"

neurokinin ", was present in small quantities in all

specimens from all subjects; but very much largerquantities were found in tissue-fluid from the scalp ofpatients with headaches at the time the specimens weretaken. It was also found to be released into the segmentalcutaneous tissue-fluid during dorsal root stimulation andin the axon flare reaction. In one subject the substancewas apparently reduced in amount after administration of

ergotamine tartrate; and Chapman et al. suggest thatinterference by ergotamine with an enzyme systemliberating " neurokinin " from a plasma-globulin may bethe basis of this effect.

These results are extremely interesting. They maypossibly explain some of the longer-lasting features ofmigraine which apparently outlast the aura and headache.But bioassay methods can be unreliable, and these find-ings will need to be confirmed and the substances if

possible defined chemically.

TUBERCULOSIS IN AFRICA

IN the first of the four Heath Clark lectures, deliveredin London on Nov. 2, Dr. Charles Wilcocks traced thedevelopment of investigations into tuberculosis in Africa.This disease, he said is still spreading; and drugtreatment by itself is unlikely to provide the wholeanswer.

Wide variations in incidence and mortality amongdifferent races, noted as long ago as the beginning of thecentury, had led Cummins to formulate his " virgin soil

"

theory. According to this, primitive tribes were highlysusceptible because, in the absence of the bacillus, theyhad never in their own surroundings been obliged toprotect themselves against it; while those living in moreurban communities had elaborated protective substancesthrough contact with the bacillus. The high tuberculosisincidence and mortality among African troops in Europein the 1914-18 war seemed to support this theory, thoughsubsequent workers had suggested that the troops involvedhad been in France for some time and that they brokedown under stress: in other words, that the cause laymore in the environment than in racial susceptibility.

Between the wars extensive work by individuals andcommissions, ably supported by administrators, led toan accurate assessment of the distribution and characterof the disease. It was found to be widely distributed andit progressed rapidly to death, with extensive cavitationand little fibrosis, and usually with involvement of bothlungs. The sputum was heavily infected, and this wasclearly a factor in spread when the patient and the restof his family slept together in small, poorly ventilatedhouses.Some idea of the distribution of the disease could be

gained from the large proportion-41%-of the totalhealth expenditure of the Union of South Africa devotedto tuberculosis. In the mines pneumoconiosis had addedto the problem, although more careful selection ofrecruits and measures to cut down dust had reduced thenumber affected.

Treatment, previously limited to bed rest and anoccasional pneumothorax, had been radically changed bythe advent of effective drugs. But these might fail tocontrol the disease, especially if the patient was nottreated in hospital, because many did not take p-amino-salicylic acid with their isoniazid, and others stopped treat-ment before they should. Thus resistance developed on alarge scale.

B.c.G. vaccination was sometimes the only rapidlyapplicable preventive measure; and its value was probablysmall. But these were short-time measures. For wide-

spread improvement, the attitudes of members of verydifferent cultures had to be modified and research under-taken into the means of persuading whole communitiesto change habits which favoured the development oftuberculosis. The most pressing need was improvement

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1. Aldrich, R. A., Steinberg, A. G., Campbell, D. C. Pediatrics, 1954, 13,133.

2. Krivit, W., Good, R. A. A.M.A.J. Dis. Child. 1959, 97, 137.3. Gordon, R. R. Arch. Dis. Childh. 1960, 35, 259.

in environmental conditions. The emphasis had nowshifted to stress as the main causal factor in tuberculosis.Nutrition, housing, working conditions, and hygiene andsanitation all required attention. The E10 million perannum spent by the South African Government in thepast five years on housing for non-Europeans was a stepin the right direction. It was unfortunate that the WorldHealth Organisation, in its last report on the subject,had barely touched on the environmental factor, presum-ably because it was considered self-evident. But any-thing which was not mentioned tended to be forgotten.

It was the doctor’s duty to stimulate the administratorsto improve conditions, just as had been done in Englanda century ago.

A SEX-LINKED FAMILIAL PURPURA

THE classical sex-linked hereditary bleeding diseasesare hsemophilia and its close relation, Christmas disease.In the past six years there have been reports of a purpurichxmorrhagic disorder with a similar mode of inheritanceby a sex-linked recessive gene-i.e., the condition affectsmales but is transmitted by female carriers who are

unaffected, and each male has an equal chance of beingaffected or free. The condition, first described in 1954by Aldrich et aI.,! presents the odd combination of

thrombocytopenic purpura, eczema, and undue liabilityto infection. In the family, of Dutch extraction, observedby Aldrich et al., the male infants were known to beliable to die in the first few years of life with " drainingears, eczematoid dermatitis, and bloody diarrhoea"; inthe last three generations 16 out of 40 males had diedwith this disease before the age of 31 months. Krivitand Good 2 investigated the same family in 1959 and foundthat there were 2 female carriers who were reproducing,and that these had had 8 children since 1954; 2 werehealthy girls and 6 were boys, of whom 3 had the diseaseand 3 were healthy.

2 cases in an English family have now been reportedby Gordon,3 of Sheffield. He points out that seven familiesaffected by the disease have been described, one of thema Negro family. Details of 16 male patients are known,and all have died; 1 of Gordon’s patients has died, and1 is still alive.

Gordon’s lst patient was admitted to hospital at the age of14 months with infantile eczema affecting the head, neck, arms,and legs. A bleeding tendency had been noted from the ageof 4 months, and this had alarmed the mother because she hadhad a brother who had died of " hxmophilia " at the age of1 year. Investigation showed severe thrombocytopenia, whichpersisted except for short periods when the count rose above100,000 per c.mm. Bone-marrow was found to contain platelet-forming megakaryocytes. With treatment the eczema improved,and the patient was sent home. He was in hospital again onaccount of eczema five months later; and at the age of 4 yearshe was admitted with profuse purpura, bleeding gums, dis-charging ears, and impetigo. The thrombocytopenia beingstill present, it was decided to carry out splenectomy, and thiswas followed by a rise of platelets to normal and disappearanceof the purpura. But in the next twelve months the patient hadto be admitted three times-once because he had meningitisdue to pneumococcal and staphylococcal infections, once fordental extraction which caused no trouble, and finally in afatal coma. Necropsy showed bilateral adrenal hxmorrhages;there was no evidence of septicxmia; the platelet-count wasnot recorded.

1. Rendall, C. M. Anæsthesia, 1954, 9, 281.2. Goldman, W. W., Sanford, J. P. Amer. J. Med. 1960, 29, 94.

Gordon’s 2nd case was the brother of his 1st patient, borneight years later; in between, a healthy girl and a healthy boyhad been born. This 4th child of the family showed eczemaat the age of 3 months, and a month later he was investigatedin hospital; he had thrombocytopenia, and furunculosis,pyuria, and bronchitis developed while he was in hospital.His white-blood-cell count was normal; and he did not havedeficient y-globulin. Treatment with prednisolone and thenwith corticotrophin produced only a temporary rise in the

platelet-count. In view of the experience with the elder boysplenectomy was not performed, and the patient has remainedreasonably well for three years, still having occasional purpuraand occasional attacks of respiratory-tract infection.

This syndrome will be easily recognised, though we haveno doubt that children with eczema and thrombocytopenicpurpura will be seen who do not have the syndrome;the added features of recurrent infection and, above all,a positive family history must also be found. The casesso far reported have not been very fully investigated.Krivet and Good sought platelet agglutinins but did notfind them; marrow punctures have shown the same pictureas that of " idiopathic " thrombocytopenic purpura;y-globulins appear normal. But nothing is known aboutthe other blood-clotting factors. No attempt seems to havebeen made to find out whether the condition is linkedin any way with systemic lupus erythematosus and similardiseases, in which thrombocytopenic purpura is some-times an early sign. We hope that pxdiatricians will lookout for cases of Aldrich’s syndrome and see whether morecan be learnt about its xtiology and possible lines oftreatment.

CHEMICAL MENINGITIS

FOLLOWING SPINAL ANÆSTHESIA

FORMERLY, when measures were not taken to avoidcontamination of the subarachnoid space with phenolicdisinfectants, chemical meningitis was a recognised sequelof spinal anxsthesia.1 Sterilisation by autoclaving of

special packs containing all the equipment, including theampoules of local anaesthetic, required for this form ofanxsthesia is now commonly practised to prevent this

complication. But autoclaving by itself is inadequate ifthe syringes and needles have not been previouslyfreed from all traces of disinfectant by cleansing andwashing.The dangers of inadequate washing of equipment are

well brought out in an account of five patients in whomacute meningitis developed very shortly after spinalanaesthesia for obstetric delivery. 2 The cerebrospinalfluid in each case was purulent, with a polymorph leuco-cytosis. These findings, together with pyrexia, suggestedbacterial infection of the subarachnoid space, but no

organisms could be isolated from the cerebrospinal fluidor from blood samples. A review of the procedures usedfor cleansing spinal anaesthetic equipment in the obstetricdepartment concerned revealed that, whereas the ampoulesof local anxsthetic were taken directly from their cartonbefore autoclaving, the syringes used were soaked in asolution of a phenolic disinfectant, washed and rinsed,and finally put in trays ready for autoclaving. Clearlythis washing was ineffective. Fortunately, all five patientsrecovered without permanent neurological sequelx. Theirillnesses illustrate once again the dangers associated withthis mode of anaesthesia when insufficient precautions aretaken to avoid contamination of the subarachnoid space.