DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY. 1967, 9

organic brain injury, but this is a small omission in comparison with the wealth of informa- tion included. Some previous findings are substantiated-e.g. those of the NEW SONS,^ who found 30 encopretics among their 7c)o-odd 4-year-olds when the only positive correlations they could find were a lack of fathers’ participation and the parents’ punitive attitudes towards the children. BELLMAN has been unable to differentiate between cases with a purely physical causation and those with multiple causes, but she shows that encopresis does not exist as an isolated factor. Few, if any, would contradict her view that ‘encopresis does not have a uniform aetiology . . . the aetiology seems to involve a complex interaction between several factors, with excessive demands occupying a prominent place.’ Intelligence is again shown to have no significant effect on the encopresis. What is still not answered and may be unanswerable is whether encopresis causes the neurotic manifestations, or whether the accompanying neuroses are part and parcel of the disorder. As BELLMAN points out, the reasonable comparison again appears to be with the immature enuretic who gives up his neurotic symptoms when his enuresis clears up.

The follow-up after two years showed that, without any treatment, 56 per cent of the boys had been free from symptoms for at least six months, whereas cases treated by routine paediatric methods, with enemas, suppositories and laxatives, showed a recovery-rate of 61 per cent (SELANDER and TOR OLD^) while with oral laxatives and ‘simple psychological treatment’ BERG and JONES~ obtained remissions in 87 per cent, BELLMAN’S statistical analysis shows four factors strongly positively correlated to the criterion variable ‘still encopretic’--i.e., anxiety in the child, nervous symptoms, disturbed contact with the mother (from the Machover Personality Test), and common interest with the mother. The method of obtaining the follow-up information-by telephone interview-is perhaps the weakest point in the study. If the original interviews and tests had been repeated a great deal more information might have been gained.

There are some delightfully unexpected gems in BELLMAN’S monograph, such as the lucid explanation of Machover’s figure-drawing tests, and it can be strongly recommended to paediatricians, child psychiatrists and the ancillary staff of child guidance clinics for the light it throws on children suffering from this distressing but intriguing symptom.

Child Guidance Clinic, The Shirehall, Abbey Foregate, Shrewsbury, Salop.

1. Bellrnan, M. (1966) ‘Studies on encopresis.’ Acta paediat. scand., suppl. 170. 2. Berg, I., Jones, K. V. (1964) ‘Functional faecal incontinence in children.’ Arch. Dis. Childh., 39, 465. 3 . Newson, J., Newson, E. (1965) Patterns of Infant Care in an Urban Community, 2nd ed. London:

4. Selander, P., Torold, A. (1964) ‘Enkopresis.’ Nord. Med., 72, 1110. 5 . Vaughan, G. F., Cashmore, A. A. (1954) ‘Encopresis in childhood.’ Guy’s Hosp. Rep., 103, 360.

D. R. BENADY

REFERENCES

Penguin Books.

HEART FAILURE FROM BRAlN DAMAGE THERE are a number of causes of heart failure in the newborn which lie outside the heart. These include abnormal arteriovenous communications in the liver, lungs and brain, where failure results from a high cardiac output and the abnormality is structural outside the heart. Recently GRAY and PROSSER~ have drawn attention to an association between brain damage and heart failure. They describe three full-term newborn infants who developed

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unequivocal signs of heart failure some hours after birth, and in whom cerebral signs, such as hypotonia, irritability, convulsions, raised intracranial tension and absence of sucking, Moro and grasp reflexes, preceded and accompanied the cardiac signs. In one of the infants who died at 36 hours, autopsy showed severe cerebral oedema, subarachnoid haemorrhage and coning; the heart was large with a big right atrium, but no anatomical abnormality was detected. In the two survivors the heart failure receded, and at follow-up 8 months and 3 months later the heart was normal: in one infant there was evidence of brain damage at 8 months.

The cause of the suggested association is unknown, but the hypothesis most favoured by GRAY and PROSSER is that cerebral damage is responsible. The evidence for this arises from the experimental work of CAMERON and D E , ~ who showed that pulmonary oedema occurred following a rise in intracranial tension and from clinical observations in adults by PAINE eE a].,? HARRISON and GlBB,’ SRIVASTAVA and ROBSON* and MEN ON.^ An alter- native sequence of events, that asphyxia causes the heart failure, has been fully discussed by BURNARD and J A M E S . ~ ,

The importance of these observations is to remind us that heart failure in the newborn is not always due to anatomical defects of the heart or blood vessels. Department of Paediatrics, Guy’s and Brompton Hospitals, London.

MICHAEL JOSEPH

REFERENCES 1. Burnard, E. D., James, L. S. (196 I ) ‘Failure of the heart after undue asphyxia at birth.’ Pediuirics, 28,545. -. - - (1963) ‘Atrial pressures and cardiac size in the newborn infant. Relationships with degree of

3. Cameron, G. R., De, S. N . (1949) ‘Experimental pulmonary oedema of nervous origin.’ J. Path. Bart.,

4. Gray, 0. P., Prosser, R. (1967) ‘Heart failure with brain damage in the newborn.’ Brit. Heart J., 29, 30. 5. Harrison, M. T., Gibb, B. H. (1964) ’Electrocardiographic changes associated with a cerebrovascular

6. Menon, I. S. (1964) ‘Electrocardiographic changes simulating myocardial infarction in cerebrovascular

7. Paine, R., Smith, J. R., Howard, F. A. (1952) ‘Pulmonary oedema in patients dying with disease of

8. Srivastava, S. C., Robson, A. 0. (1964) ‘Electrocardiographic abnormalities associated with subarachnoid

birth asphyxia and size of placental transfusion.’ J. Pediut., 62, 815.

61, 375.

accident.’ Lancet, ii, 429.

accidents.’ Lancet, ii, 433.

the central nervous system.’ J. Amer. med. Ass., 149, 643.

haemorrhage.’ Lancet, ii, 431.

HEMISPHERECTOMY FOR INFANTILE HEMIPLEGIA THE treatment of infantile hemiplegia by hemispherectomy was developed enthusiastically by KRYNAUW~, who reported his first twelve cases in 1950. In the next five years the operation was carried out by many neurosurgeons who applied the treatment to selected groups of patients for whom little help seemed otherwise available. The ‘ideal’ patient seemed to be one whose good hemisphere was not affected by disease, who had developed serious behaviour disorders (usually temper tantrums), whose seizures were insufficiently affected by drugs or who required enough drugs to severely impair his daily activities. It was thought also that the intelligence should not be too greatly impaired; an arbitrary lower limit such as an IQ of 60 was sometimes selected. (The difficulties and hazards of attempting to assess intelligence in some of these patients are obviously great, yet the improvement in IQ of many severely retarded patients cannot be doubted. The exclusion from operation of low-IQ patients is no longer permissible; some institutionalised patients have been enabled to lead an indepen- dent wage-earning existence. More importantly, the operation arresfs an otherwise inevitable deterioration of intelligence.)

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