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development into IQ type differences, even in infancy and earlychildhood.s Lately, a study of separated identical twins has fullysubstantiated traditional claims that IQ differences are of mainlygenetic origin,6 the genetic influences presumably being mediatedby lasting differences in nervous system functioning.

Biological and environmental differences probably set up mentalspeed differences that lead to variations in general ability, tested IQ,and life chances. Even tested IQ differences, which develop towardsthe end of a complex causal chain, are demonstrably reliable,heritable, and predictive. How, then, can intelligence be so easilyconsidered an illusion?

Department of Psychology,University of Edinburgh,7 George Square,Edinburgh EH8 9JZ, UK

C. R. BRANDP. G. CARYLI. J. DEARYV. EGANH. C. PAGLIARI

1. Schwartzman AE, Gold D, Andres D, Arbuckle TY, Chaikelson J. Stability ofintelligence: a 40-year follow-up. Can J Psychol 1987; 41: 244-56.

2. Hunter JE, Hunter RF. Validity and utility of alternative predictors of jobperformance. Psychol Bull 1984; 96: 72-98.

3. Blaha J, Wallbrown FH. Hierarchical factor structure of the WAIS-Revised. J ConsulClin Psychol 1982; 50: 652-60.

4. Kranzler JH, Jensen AR. Inspection time and intelligence: a meta-analysis. Intelligence1989; 13: 329-47.

5. Bornstein MH, Sigman MD. Continuity in mental development from infancy. ChildDev 1986; 57: 251-74.

6. Bouchard TJ Jr, Lykken DT, McGue M, Segal NL, Tellegen A. Sources of humanpsychological differences: the Minnesota Study of twins reared apart. Science 1990;250: 223-28.

So longSIR,-In your editorial of Feb 23 (p 460), you comment that

"nobody dies of old age-that is to say, simply through the passageof time". Is this so? Many doctors will have had experience ofelderly patients-frail, no doubt, but basically healthy and alert andquite active-who simply "died in their sleep". I have known threesuch patients, all women, two in their mid-80s and one in her early90s. To me, people like that, rather than dying, simply stop living.

So, the cause of death? To invoke a symptomless myocardialinfarction in the absence of any evidence for it is clearly wrong.Admittedly, serial 5 fim sections of the whole of the brain and heartmight reveal a cluster of cells that had undergone dissolution fromthe collapse, for some reason at some time, of some organelle. Then,after international agreement on the nature of the syndrome, theindividual could be said to have died from this novel "disintegrationxyz" rather than "old age". A search on this scale is impracticableso, in these circumstances, what explanation remains but old age?Your editorial refers later to a "fundamental interference with the

species ’clock’, which determines potential lifespan". I submit thatit is precisely this fundamental interference, nature as yet unknown,that allows some fortunate people to die just of old age-and what adignified entry that makes on a death certificate.

Gowranes,Kinnaitd PH14 9QY, UK WALLACE PARK

What do doctors know of statistics?

SIR,-Dr Dodwell (Feb 16, p 432) raises an issue of concernwhen he asserts that "it is easier for a doctor to build up his personalstatistical toolkit than for a statistician to attain sufficientlyilluminating medical knowledge". Statisticians and doctors alikewill recognise his satirical caricature of a consultation beween them.The question, however, is whether psychiatrists have devised moreilluminating answers than those of the apocryphal statistician: ifthey have, they ought to let someone know, for statisticians havelong sought the elixir that apparently resides in Dodwell’s toolkit.The ideal he recommends, exemplified by junior pyschiatric

doctors receiving an education in research methodology, isworrying in the light of the research of Wulff et al.1 Medicalparticipants in a course on postgraduate research methods scored amedian of 4-0 correct answers out of 9 multiple choice questionsrelating to the understanding of elementary statistical expression(SD, SE, p < 0-05, p > 0 05, and r). These doctors would have found

less comfort from a senior colleague than from a hospital statisticianfor statistical advice-the median score dropped to 2-4 in a randomsample of doctors, and the median was 2-1 among those who hadqualified more than 15 years ago. The conclusion was that "thestatistical knowledge of most doctors is so limited that they cannotbe expected to draw the right conclusions from those statisticalanalyses which are found in papers in medical journals".

Collaboration between doctors and statisticians has provided thescientific basis of contemporary medicine, and an increased

knowledge of statistics among doctors can only improve the chancesof fruitful communication. Before Dodwell advocates the scornfuldismissal of expert advice in favour of the sparse contents of a

personal toolkit he should consider something that Oscar Wildeactually did say: "The truth is seldom pure and never simple".Social Paediatricand Obstetric Research Unit,

University of Glasgow,Glasgow G12 8RZ, UK

A. H. LEYLANDC. W. PRITCHARD

1. Wulff HR, Anderson B, Brandenhoff P, Guttler F. What do doctors know aboutstatistics? Stat Med 1987; 6: 3-10.

Assessment of risks and control inoccupational infection

SIR,-Professor Scully and Dr Porter (Jan 19, p 178) refer to mygeneral practice decontamination study’ as showing "poor"infection control in general practice. Rather, we reported asurprisingly large increase in autoclave ownership by UK generalpractitioners (49% of practices), compared with 8%2 and 25%3 ofpractices reported a year earlier. Many of our respondents indicatedthat they were planning to purchase an autoclave, and if our findingsreflected a true increase in ownership over time then it is likely thatmore than three-quarters of general practices are now equippedwith effective steriliser systems, as recommended by the BritishMedical Association (BA4A).’A follow-up study will be undertakento reassess autoclave ownership and compliance with other infectioncontrol measures, such as glove use.

Scully and Porter also raise the very important issue of hepatitis Bvaccination for medical students. They report that as a matter ofcourse dental students are vaccinated before qualification. There areabout 8000 clinical medical students in the UK for whomvaccination should also be standard policy, as recommended by theBMA. S,6 However, not all medical schools and hospital authoritiesaccept this recommendation and educational programmes continueto be needed to raise awareness among clinical students, doctors,nurses, and other health care professionals. Risk assessment inclinical practice is an underestimated and vitally important matter.The risk of infection after needlestick injury with a sharp itemcontaminated with HIV-positive blood is substantial (1 in 200) andmay relate to the amount of blood (and infectious virions)transferred during injury.’ Hepatitis B infection, however, is a farmore likely risk (6-20%) after needlestick exposure, and hepatitis Crisk has yet to be estimated but might be similar.

I have piloted a simple interview test, based on an Americanhealth care worker risk assessment scale project (HCWRAS)(Jackson MM, Lynch P, personal communication), which can beused to assess individual perceptions about potential risk of

occupational infection. Participants were asked to select the fivefactors, from a list of fourteen, that they regarded as most importantin potential bloodborne infection. The five factors were then placedin order of risk, indicating particularly the factors of highest and oflowest risk. Three nurses, one doctor, one psychologist, and onescience researcher took part. There was no consensus as to a majorrisk factor (identified in the US project as prevalence of bloodbomepathogens in the population). Medium to low risk factors included,again without apparent consensus, condition of skin, frequency ofperformance of procedures with sharp items, emergency versusroutine activity, amount of operator experience, or degree of bloodexposure. This test is imprecise but as in the US HCWRAS study itseems that such an exercise involves considerable subjectiveassessment and the degree of risk posed by each factor is difficult forthe individual to quantify; in the UK a "sharps" national code of

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practice is now available to help health care managers to formulatepolicy, comply with legal requirements, and train staff.6 Furtherwork, however, is urgently needed in this important area of clinicalsafety, and new risk reduction strategies to prevent sharps injury areessential.

Professional and Scientific Division,British Medical Association,London WC1 H 9JP, UK DAVID R. MORGAN

1. Morgan DR, Lamont TJ, Dawson JD, Booth C. Decontamination of instruments andcontrol of cross infection in general practice. Br Med J 1990; 300: 1379-80.

2. Farrow SC, Kaul S, Littlepage BC. Disinfection methods in general practice andhealth authority clinics: a telephone survey. J R Coll Gen Pract 1988; 38: 447-49.

3. Hoffman PN, Cooke EM, Larkin DP, et al. Control of infection m general practice: asurvey and recommendation. Br Med J 1988; 297: 34-36.

4. British Medical Association. A code of practice for the sterilisation of instruments andcontrol of cross infection. London: BMA Board of Science and Education, 1989.

5. British Medical Association. Immunisation against hepatitis B. London: BMA Boardof Science and Education, 1987.

6. British Medical Association. A code of practice for the safe use and disposal of sharps.London: BMA Board of Science and Education, 1990.

7. Morgan DR. HIV and needlestick injuries. Lancet 1990; 335: 1280.

Response to cytarabine in progressivemultifocal leucoencephalopathy in AIDSSIR,-A progressive multifocal leucoencephalopathy (PML), an

opportunistic papovavirus (usually polyomavirus JC) infection,develops in up to 4% of patients with AIDS.’ Hemiparesis is themost common presenting symptom. Headaches and seizures arerare and intracranial pressure is not raised. The disease is usuallyfatal. The cerebrospinal fluid (CSF) shows no specificabnormalities but magnetic resonance imaging (MRI) reveals areasof high signal intensity, predominantly in the white-matter andusually non-enhancing after contrast.2,3 The MRI lesions are notconfined to a vascular territory and are less diffuse than theabnormalities seen in AIDS dementia complex.4 Histologicalconfirmation remains the gold standard but the risks of brainbiopsyS justify a presumptive diagnosis of PML on the basis of thefollowing criteria: relentlessly progressive focal brain disease, lack ofspecific CSF abnormalities, and non-enhancing asymmetricalwhite-matter lesions on MRI without a mass effect.

Although prolonged survival and spontaneous partial recovery inAIDS-associated PML have been described average life

expectancy from disease onset is less than a year,’ and no effectivetreatment has been identified. Some non-AIDS patients with PMLhave improved with cytarabine. We describe here three consecutiveAIDS patients with PML who, during treatment with cytarabine,showed clinical improvement and resolution of lesions on MRI.

Patient 1 (35, M)&mdash;He presented in November, 1989, withhemiparesis. He was taking zidovudine for severe HIV-1 relatedsymptoms. On admission he had a right-sided atactic hemiparesiswith hyperreflexia and extensor plantar response. Sensoryfunctions were normal. The CSF showed three mononuclear

cellsjlll, protein 0-49 g/1, and glucose 3-2 mmot/1. MRI revealed alarge area of hyperintensity in the white-matter of the left

parieto-occipital region, non-enhancing with gadolinium andwithout mass effect. The presumptive diagnosis was PML andcytarabine was started at 2 mg/kg intravenously per day for 5 days.This was repeated with intervals increasing from 1 week to 4 weeks.In the first 2 weeks he deteriorated with a slight mixed aphasia, butafter three courses he showed slight clinical improvement, thoughthe MRI picture was worse (figure). After another three coursesclinical improvement continued, resulting in normal speech andincreasing strength of his right arm and leg, and the MRI lesion wasmuch improved (figure). Zidovudine had been continued withouttoxicity.

Patient 2 (44, M)-He presented in November, 1989, withnumbness and paresis of the left arm. Computed tomography (CT)of the brain showed a small hypodense white-matter lesion,non-enhancing and without mass-effect. Empirical treatment fortoxoplasmosis was unsuccessful. Motor and sensory abnormalitiesof the left leg developed and the patient was referred to our hospitalwith left facial weakness and hemiparesis plus diminished vibratorysensation, joint position, temperature, and pinprick perception onthe left, hyperactive deep tendon reflexes on the left side, and a left

MRI scans in patient 1.

Upper: second scan, 6 weeks after first showing increase in lesion in lefthemisphere and new lesion in nght parieto-occipital lobe Lower: after 6months of therapy scan shows almost complete resolution.

Babinski sign. He was anti-HIV-1 seropositive. The CSFcontained 3 mononuclear cells/1, protein 05 g/1, and glucose 2-9mmol/1. MRI of the brain showed a right-sided parietal white-matter lesion of high signal intensity, without mass-effect. Thepresumptive diagnosis was PML and zidovudine 1000 mg per daywas started. However, the patient’s neurological conditiondeteriorated and cytarabine, 2 mg/kg body weight intravenously for5 days, was started. Because of bone-marrow toxicity zidovudinewas discontinued and cytarabine was interrupted for 3&frac12; weeks,after which the patient could tolerate the antiviral treatment. Afterthree consecutive courses his left leg was stronger though parietalMRI lesion had enlarged and high-intensity areas in the lefthemisphere were present. Even so, clinical improvement continuedand after 6 months MRI lesions were much improved and while oncytarabine the patient can now walk with a stick.

Patient 3 (57, M)- This HIV-1 seropositive man had been onzidovudine but discontinued in April, 1990, because of myalgia and