ANNOTATIONS

cases, nor is there any evidence of linkage between the condition and a number of blood antigens. As in the Japanese families with dissociated ridges, the anomaly appears to be transmitted as a dominant autosomal character with incomplete penetrance.

SARAH B. HOLT

REFERENCES 1. Abel, W. (1936) ‘Uber Stroungen der PapiIlarmuster. 1. Gestorte Papillarmuster in Verbindung mit

2. Baird, H. W. I11 (1964) ‘Kindred showing congenital absence of the dermal ridges (fingerprints) and

3. Cooke, T. D. (1962) ‘Ridgeless patterns turn up again.’ Fingerprint and Identification Magazine, 44, 12; 4. Ford Walker, N. (1963) ‘The current status of research on dermatoglyphics in medical constitution.

einigen korperlichen und geistigen Anomalien.’ 2. Morph. Anthrop., 36, I.

associated anomalies.’ J. Pediut., 64, 621.

Proc. XI int. Congr. Genet. In Press.

patterns. Proc. Jup. Acud., 33, 410.

5. Furuya, Y. (1961) ‘Genetics of patternless finger dermatogylyphe.’ Jap., J . hum. Genet.,.6, 102. 6. Furuhata, T., Fumya, Y., Tanaka, T., Nakajima, H. (1957) ‘A family wlth unclassifiable papillary

7. Goddard, C. H. (1950) ‘Hands of mystery.’ Fingerprint and Identification Mugazine, 31, 4. 8. Grebe, H. (1940) ‘Untersuchuneen uber Patdarlinienveranderungen bei Syndaktylie und Polydaktylie.’ - . -

Z. Morph. Anthrop., 39, 62. - J. leg. Med., 8, 443.

minded children.’ (Japanese). Shikoku Actu Med., 10, 181.

tion Muguzine, 39, 15.

55, 4.

9. Matukura, T. (1954) ‘A new case of the “hypoplastic papillary patterns of fingers” ’ (Japanese). Jap.

10. Matsukura, T., Matsuura, M., Kubo, A. (1957) ‘Hypoplastic papillary patterns of finger in feeble-

1 1 . Okamoto, K. (1958) ‘The extraordinary fingerprints of the boy of Nagoya.’ Fingerprint and Ident$ca-

12. - (1959) ‘The extraordinary fingerprints of the boy of Nagoya.’(Japunese). Hanzui to Kunshiki,

13. Schade, H. (1937) ‘Zur endogenen Entstehung von Gliedmassendefekten.’ 2. Morph. Anthrop., 36, 375.

ACUTE HEMIPLEGIA IN CHILDHOOD THE sudden onset of hemiplegia in a child is such a calamitous event that it understandably came to be regarded as a disease entity, and much energy has been expended in attempts to establish its single pathological basis. This unitary concept was rejected at the Clevedon study group in 1961,2 when the opinion was repeatedly expressed that many different mechanisms can and do produce hemiplegia in children and that it should no longer be regarded as a specific syndrome. In the words of ORVILLE BAILEY,~ ‘a survey of the pathology found at autopsy . . . would involve a study of most of the lesions within the field of paedia- tric neuropathology’. It follows that the importance of different causative factors is likely to vary in different series, depending on the pattern of disease in the community. In Great Britain, for example, purulent infection has diminished in frequency as a cause, while arterial occlusion, formerly believed to account for only a small proportion of cases, is assuming an increasingly prominent role. These changing trends have lately been described by INGRAM,5 in a masterly review of the causes of acquired hemiplegia. The multitude of possible causes accounts for the many modes of onset, which sometimes escape notice because no physician has personal experience of a large number of cases. Thus only 10 cases were seen in 15 years at the Royal Hospital for Sick Children in Edinburgh,s 23 cases in 10 years at The Hospital for Sick Children in L ~ n d o n , ~ and 15 cases in 8 years at the Midland Centre for Neurosurgery and Neurology3 in Birmingham.

BICKERSTAFF has described the results of arteriography in the Birmingham cases. The 10 children examined within a few days of onset all had some arterial abnormality, and he concluded that an occlusive lesion in the carotid arterial tree is the commonest lesion in acute hemiplegia in childhood. This finding supports the Clevedon view of the importance

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of arterial occlusion as a cause of childhood hemiplegia, but it does not follow that such a high proportion of arterial lesions will necessarily be present in every series. BICKERSTAFF’S series may have been unusual, possibly because of selection on grounds of suitability for further investigation. This is borne out by his description of the ways in which acute hemi- plegia may present in childhood, for he over-emphasises the stereotyped nature of the clinical features. For example, he remarks on the exact repetition of clinical and radio- graphic pictures seen in childhood hemiplegia, whereas the clinical picture is almost infi- nitely varied; he says that ‘fits do not spread to successive parts of one limb nor to alternate sides’, whereas both modes of spread may and he says that ‘the coma recovers after a few hours’, whereas it often persists for long after the seizures have stopped. In his illustrative case-histories BICKERSTAFF describes clinical manifestations which have been considered characteristic of arterial occlusion-viz., the sudden appearance of abnormal neurological signs without tempestuous convulsions and sometimes even without loss of consciousness. The predominance of this type of presentation in his series may explain the frequency of demonstrable arterial lesions. However, we do not yet know enough to correlate clinical features accurately with pathological processes, and carefully documented case-records with detailed descriptions based on meticulous observations are badly needed. BICKERSTAFF’S report is a useful addition to the slowly accumulating mass of information about sudden hemiplegia in childhood, and it underlines once again the urgent need for early investigation of these unfortunate children if advances are to be made in understanding the pathogenic mechanisms and minimising their consequences.

Ross MITCHELL

REFERENCES 1. Bailey, 0. T. (1960) ‘The pathology of juvenile hemiplegia’. G.P., 21,88-97. 2. Bax, M., Mitchell, R. ed. (1962) Acute Hemiplegia in Childhood. London: Spastics Society/Heinernann. 3. Bickerstaff, E. R. (1964) ‘Aetiology of acute hemiplegia in childhood‘. Brit. med. J. ii, 82-87. 4. Evans, P. R. (1962) In Acute Hemiplegia in Childhood. London: Spastics Society/Heinemann. 5. Ingram, T. T. S. (1964) Paediatric Aspects of Cerebral Palsy. Edinburgh: Livingstone. 6. Mitchell, R. G. (1952) ‘Venous thrombosis in acute infantile hemiplegia’. Arch. Dis. Child., 27,95-104. 7. Mitchell, R. G. (1962) In Acute Hemiplegia in Childhood. London: Spastics Society/Heinemann.

ABDOMINAL EPILEPSY A HISTORY of recurrent attacks of abdominal pain during childhood suggests a variety of possible diagnoses and the order of preference may depend to a certain extent on the interests of the observer. To many, symptoms which run to a definite pattern on several occasions will suggest the possibility of migraine or epilepsy. There is no doubt that both these conditions can take unusual forms during childhood and it is then that difficulties of differentiation will arise. This is the borderland of epilepsy so well described by Gowers and sometimes no definite conclusions can be drawn from the history. This may be one of the reasons for the suggestion that migraine headaches and convulsive disorders are related. Both disorders are relatively common in childhood, and allowing for this there seems to be no conclusive evidence to suggest a closer relationship1* 6. If the attacks of abdominal pain are prolonged and associated with much vomiting and perhaps headache, the child is most likely to be suffering from a condition allied to migraine.

Paroxysmal abdominal disturbances of an epileptic nature are much rarer. The re- current pattern of the symptoms may be suggestive but cannot support a diagnosis of epilepsy on its own. The pain is often sudden and of brief duration. It usually starts in the epigastric region and sometimes nausea is a more prominent symptom than the pain.

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