DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY. 1974, 16

3. Dent, C. E., Richens, A., Rowe, D. J. F., Stamp, T. C. B. (1970) ‘Osteomalacia with long-term anti-

4. Dennis, N. R. (1972) ‘Rickets following anticonvulsant therapy.’ Proceedings of the Royal Society of

5. Borgstedt, A. D., Bryson, M. F., Young, L. W., Forbes, G. B. (1972) ‘Long-term administration of

6. Varkey, K., Raman, P. T., Bhaktaviziam, A., Taori, G. M. (1973) ’Osteomalacia due to phenytoin

7. Schutze, I., Salomon, B., Thal, W. (1973) ‘Ausgepragte Rachitis unter antiepileptische Dauermedikation.’

8. Kichens. A,. Rowe. D. J. F. (1970) ‘Disturbance of calcium metabolism by anticonvulsant drugs.’

convulsant therapy.’ British Medical Joiirnril, 4, 69.

Medicine, 65, 730.

antiepileptic drugs and the development of rickets.’ Journal of Pediatrics, 81, 9.

sodium.’ Joirrnal of the Neiirological Sciences, 19, 287.

Kinderarztliche Pralis. 41, 76. .. . .~.~ ~.~ . ~

British Medical Jorrrnnl, 4, 13. 9. Hunter, J., Maxwell, J . D.. Stewart, D. A., Parsons, V., Williams, R. (1971) ‘Altered calcium metabolism

in epileptic children on anticonvulsants.’ British Medico1 Journal, 4, 202. 10. Hahn. T. J., Hendin, B. A., Scharp, C . R.. Haddad, J. G . (1972) ’Effect of chronic anticonvukant

therapy on serum 25-hydroxycholecalciferol levels in adults.’ New England Joirrnal of Medicine, 287,

’

9 0 . 11 . I le Luca. K . , Masotti, R. E., Partington, M. W. (1972) ‘Altered calcium metabolism due to anticon-

vulsant drugs.’ Developnientcrl Medicine and Child Neurologj,, 14, 3 18. 12. Christiansen, C., Kristensen, M., Rodbro, P. (1972) ‘Latent osteomalacia in epileptic patients on anti-

convulsants.’ British Medico1 Joirrnnl, 3, 738. 11. Viukari, N. M. A., TammistG. P., Kauko, K. (1972) ‘Low serum calcium levels in forty mentally sub-

normal epileptics.’ Joiirriol of Mental Deficiencj Research. 16, 192. 14. Reynolds, E. H., Hallpike, J. F.. Phillips, B. M., Matthews, D. M. (1965) ‘Reversible absorptive defects

in anticonvulsant megaloblastic anaemia.’ Joirrrial ,?f’ Clinicd Pathology, 18, 593. 15. Kraft. O., Schaefer, K.. Bochentin, W., von Herrath, D., Opitz. A., Koeppe, P. (1973) ‘Untersuchungen

zum Calcium-Stcffwechsel bei antiepileptischer Therapi:.’ Nervenarzt, 44, 150. 16. Koch, H. U., Kraft, D., von HeTath, D., Schaefer, K., (1972) ‘Influence of diphenylhydantoin and

phenobarbital on intestinal calcium transport in the rat.’ Epilepsia, 13, 829. 17. Schaefer, K. , Kraft, D., von Herrath, D., Opitz. J. A. (1972) ‘Intestinal absorption of vitamin D, in

epileptic patients and phenobarbital treated rats.’ Epilepsia, 13, 509. 18. Stamp, R. C. B. , Round, J . M.. Rowe, D. J . F., Haddad, J. G. (1972) ‘Plasma levels and therapeutic

effect of 25-hydroxycholecalciferol in epileptic patients taking anticonvulsant drugs.’ British Medical Joirrriol, 3, 9.

19. Silver, J., Neale, G., Davies, D., Breckenridge. A,, Thompson, G. R. (1972) ‘The effect of phenobarbi- tone-induction on vitamin D metabolism.’ Clinical Science. 42, 12P.

20. Hahn, T. J., Birge, S . J.. Scharp, C. R., Avioli, L. V. (1972) ‘Phenobarbital-induced alterations in vitamin D metabolism.’ Joirrnal of Clinical Znveytigatiori, 51, 741.

21. Kuntzman, R . (1969) ‘Drugs and enzyme induction.’ Anniial Reviews of Plimrnncologj, 9, 21.

SPECULATIONS ON NON-ACCIDENTAL INJURY AS A CAUSE OF CHRONIC BRAIN DISORDER

I F some children die from non-accidental head injury, i t seems likely that others will survive with chronic neurological disorders.

At necropsy, children dead of child abuse are found to have subdural haemorrhage, nearly always with contusion of the cerebral cortex’. The associated cerebral contusion is more likely to give fatal or lasting cerebral deficit than is the subdural haematoma. It is easier to establish the presence of subdural haematoma than of ccrebral contusion, but the late sequelae of ‘subdural haematoma’ will in fact probably depend on the associated cerebral contusion. TILL’ and AICARDI and GOu71kRE3 have reported follow-up studies on children with subdural haematoma. Making an approximate average of their figures, we find that about 8 per cent were dead, and 30 per cent were moderately or severely in- capacitated. For every child dead with subdural haematoma, there were at least four incapacitated.

In 1970. the UK DEPARTMENT OF HEALTH^ calculated that 2 per cent of deaths of children between the ages of four weeks and one year were caused by wilful violence. There were 679 deaths in this age-group, which suggests 13 deaths a year from non-accidental injury (IAI) and, on the calculation of four handicapped for every death, about 50 children surviving each year with chronic incapacity due to NAI.

216

ANNOTATIONS

The incidence of NAI is believed by KEMPE‘ to be six per 1,000 live births. For the USA, this makes 40,000 cases a year. In 1967, the number of reported cases was 6,0006. For the UK, The Lancet suggested 3,000 cases a year7.

The mortality rates reported for NAI vary from 1.3 to 13 per cent.*-14 Suppose we allow that the higher figures are for cases seen in hospital, we may conclude that mortality is perhaps 3.5 per cent. From a NAI case incidence for the UK of 3,000 a year and a mortality of 3 .5 per cent, we arrive at an annual death-rate of 105. If we once again use our factor of four handicapped survivors for each death, this implies an incidence of about 400 new cases a year with lasting incapacitation, i.e. physical or mental handicap.

Follow-up studies of NAI are scanty and the data given inexact. In 1962, K E M P E et al.R estimated that 15 per cent were left with ‘permanent brain-damage’, a term that does not differentiate between cerebral palsy and mental deficiency. MARTIN15 reported that of 42 children re-examined three years after child abuse, 43 per cent were impaired neuro- logically: ‘They were a pathetic lot and had little capacity for enjoyment and spent time mothering adults around them, and a minority had given up relating normally to other people.’

Perhaps we may estimate from these observations that 15 per cent of NAI children show lasting damage. On The Lancet estimate of 3,000 cases a year7 in the UK, we can expect 450 new cases a year of chronic physical or mental handicap. This figure is similar to the figure of 400 arrived at above, and is to be contrasted with the other estimate of 50 new cases a year. Perhaps 400 is as good a guess as is possible at the moment.

the incidence varying from 3 to 33 per cent. We may recall also that after subdural haematoma, 30 per cent are more or less incapacitated. Speculating again, we may conclude that after NAI at least 5 pzr cent are left severely subnormal and another 5 per cent less severely mentally handicapped. On The Lancet estimate of 3,000 cases a year’, we have 150 new cases of mental deficiency a year, a figure to be compared with the known incidence in the UK of 600 new cases a year of mental deficiency.

In the UK there are 1,600 new cases a year of cerebral palsy and 600 of severe mental handicap, and in half of these new cases we find no adequate cause of the condition. When the handicapped children are seen for assessment, the parents will have matured, the phase of most frequent NAI may be some years in the past, and the possibility of earlier abuse may never be considered.

It seems that there may be 400 new cases a year of chronic brain-damage due to child abuse. In such cases, cerebral palsy could only arise from brain injury (by contusion); mental handicap could arise from brain injury or from deprivation.

These figures are based on speculations drawn from reports which often give no exact data, but they may be of some significance.

2C22 Mortimer Street, London W 1 N 7RD.

Educational difficulties as late sequelae of NAI are r ep~r t ed ,~ . 11$ 159

RONALD MAC KEITH

REFERENCES 1. Weston, J. T. (1968) In Helfer, R. E., Kempe, C. H. (Eds.) The Batreved Child. Chicago: University of

2. Till, K. (1968) ‘Subdural haematoma and effusion in infancy.’ British Medical Journal, 3,400. 3. Aicardi, J., Goutikre, S. F. (1971) ‘Les epanchements sous-duraux du nourisson.’ Archives Frangaises

4. Department of Health and Social Security (1970) The Battered Baby. London: H.M.S.O.

Chicago Press.

de PPdiatrie, 28, 233.

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9.

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Kempe. c‘. H. ( 1971) ‘Paediatric implications of the battered baby.’ Archives of Discme iti Childhood,

Gil. D. G . (1969) ‘Physical abuse of children: findings and implications of a nationwide survey.’

Ltincet (1971 ) ’Violent parents.’ (annotation), 2, 1017. Kempe, C. H . , Silverman. F. N., Steele, B. F., Droegemuller, W., Silver, H. K. (1962) ‘The battered

Gil, D. G . (1968) Irr Heifer, R. E., Kempe, C. H. (Eds.) Tlw Britrcwd Child. Chicago: University of

Skinner, A. E., Castle. R. L. (1969) ‘78 battered children: a retrospective survey.’ London: N.S.P.C.C. Gregg, G . S., Elmer. E. (1969) ‘Infant injuries: accident or abuse?’ Pedinfrics, 44, 434. Moszer. M., Bach. Ch. (1969) ‘Le syndrome des enfants maltraites.’ ProgrPs Midical, 97, 303. Swedish Department of Health ( I 969) ‘Barnniishandel. Socialstyrekens redovisar.’ Stockholm: Swedish

Cooper, C . (1973) Personal communication. Martin, H. P. (1974) I/r Schulman, I . (Ed.) Adi.ntrcc,s iir Pediatrics (in the press). Morse. C. W. , Sahler, 0. K. Z., Friedman, S. B. (1970) ‘A three year follow-up study of abused and

46, 28.

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child syndrome.’ Joririrnl of tlie Atnericcin Mediccil Associntiorr. 181, 17.

Chicago Press.

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neglected children.’ rltirerictin Joiirtiril of Diseases n / ChiMrvn, 120, 439.

THE SIGNIFICANCE OF LIFE EVENTS JOHN RYLE‘S advice to ‘measure the measurable and make measurable the immeasurable’ is irreproachable, but in practice it may be dificult to know what to measure and heart- breakingly so to know what to measure it with anyway. ‘Life events’ (LES) occurring in the external environment prior to the onset of illness have been used as a gauge, though ‘death events‘ might sometimes be more accurate and no clumsier. Perhaps the terms ‘socio- psychological events‘ or ‘psycho-social stresses’ have an inbuilt bias, though they sound less bom bastic.

I have a suspicion that LES can be-like teething or the menopause-traditionally blamed for everything within their time-span: and I have a feeling that with teething, menopause or I.ES the peculiarities of the individual’s reactions are in danger of being played down.

All the same, LES can be assessed in the following sort of way. You conscientiously make out a list of them, probably based on what the patients themselves consider to be relevant. You may then ask involved professionals how they rate them, and to decide which are major LES and which are minor. You then rate the patient according to the degree of exposure to them. In spite of this admittedly over-simplified account, I should agree with claims that i t would not be dificult to draw up a short list of LES that would be acceptable, with perhaps minor caveats, not only to academic psychologists but also to practising doctors.

Before LES can be relied on as a yardstick, we should require a standard; and if the standard is true to form we should expect i t to vary with age. As a standard or base-line with children, the birth of a sibling has been used’. At different ages, various LES such as loss of the father‘s job, parental divorce or mother going out to work were related to the child’s age in terms of the degree of adjustment required. When a population of 3,500 healthy children were investigated on this basis’, rather surprisingly the effects of sex, race and social class were not significant. Age itself proved to be the significant variable. This is an important conclusion and a thought-provoking claim to establishing measuring standards that clearly merits further study.

In the study by HEISEI- P t L ~ I . ~ , groups of i l l children were compared with previously established ‘normals’. In children with psychiatric disorders, rheumatoid arthritis or appendicitis. for example, an increase in frequency and/or severity of LES prior to the illness was found. The results are interpreted as evidence that one factor in the pathogenesis of illnesc is socio-psychological. The conclusion is consistent with other work, sparse though

218