DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY. 1972, 14

LEARNING DISABILITIES AND HYPERKINESIS THE term ‘learning disability’ is applied as an educational diagnosis and has been defined in various ways. BARSCH, quoted by PAIhE’, probably gives a consensus viewpoint in stating that a child with learning disabilities is one with adequate mental ability, sensory processes and emotional stability who has specific defects in perceptual, integrative or expressive processes which severely impair learning efficiency. It must be emphasised, however, that the degree of specificity is variable; appropriate psychological testing is needed to demon- strate the precise intellectual processes that are imperfect and can reveal large differences in sub-test scores between children with ostensibly similar disorders, such as language or reading retardation. It needs to be added, too, that children with neuro-developmental disorders such as cerebral palsy may also have superimposed learning disorders.

The use of educationally based criteria for the diagnosis of learning disabilities leads to the inclusion of some children whom physicians and psychologists might designate as having ‘minimal cerebral dysfunction’ (the most complete and acceptable definition of which was probably given by CLEMENTS in 1966?). Included also, however, are other children who have specific maturational lags as well as those who are non-motivated or lazy, although children with primary emotional disturbances and secondary educational problems are, by definition, excluded. It has to be explicitly stated, therefore, that learning disabilities are not a synonym for minimal cerebral dysfunction; rather they may be seen as one facet of this heterogeneous collection of clinical features.

In those learning disorders which do have an organic neurological basis, there is a well- recognised association with motor overactivity3, 4. The nature of this relationship varies, as may well be expected given the different degrees and types of hyperactivity5, and its clarifica- tion is important. Firstly, both the learning disorder and the hyperkinesis may both be secondary to the underlying cerebral disorder and not causally related to one another. In this case one would expect to find other abnormal neurological features, given an appropriate history and physical and psychological examination. Secondly, hyperkinesis itself, especially when it is associated with poor ability to concentrate and a limited attention span, may be sufficient to interfere with learning. This is the so-called hyperkinetic impulse disorder of BRADLEY but is probably an uncommon occurrence in children of potentially normal intellectual ability’. Thirdly, learning disabilities themselves, including those in which specific functions such as reading are absent or lagging, may result in behaviour disturbances, one feature of which is disinhibited motor behaviour. A careful history, including the family history, may reveal this sequence of events.

It follows that in the investigations and treatment of learning disorders associated with motor overactivity, a detailed and interdisciplinary evaluation of the problem is mandatory prior to whatever environmental manipulations are decided upon. That the management of these children needs to be educationally based should pass without saying, but two further points do need to be made in this context. Firstly there is the desirability for earlier and better diagnosis of learning disabilities, even in children of pre-school ageR, as this must be the best time to institute treatment. And secondly, the very small place for drug therapy in the management of learning disorders has to be stressed, particularly in view of recent controversial statements on this point by both professional9 and laylo authorities. My own view is that with the exception of amphetamines or methylphenidate-which are sometimes helpful in hyperkinetic impulse disorders-it is difficult to justify the use of these drugs, psychotropic agents, or anticonvulsants in any but the most unusual circumstances; indecd,

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ANNOTATIONS

phenobarbitone is probably the commonest factor with cerebral dysfunction.

Alder Hey Children’s Hospital, West Derby, Liverpool, L12 2AP.

precipitating hyperkinesis in children

LEWIS ROSENBLOOM

I . 2.

3.

4.

5 .

6. 7.

8. 9.

10.

REFERENCES Paine, R. S. (1968) ‘Syndromes of minimal cerebral damage.’Pediutric Clinics of North America, 15, 779. Clements, S . D. (1966) Minimal Brain Dysfunction in Children. NTNDS Monograph No. 3. Washington:

Laufer, M. W., Denhoff, E. (1957) ‘Hyperkinetic behavior syndrome in children.’ Journal of Pediatrics,

Stewart, M. A., Pitts, F. N., Craig, A. G., Dieruf, W. (1966) ‘The hyperactive child syndrome.’ American

Bax, M. C . 0. (1972) ‘The active and over-active school child.’ Developmental Medicine and Child

Bradley, C. ( I 937) ‘Behavior of children receiving benzedrine.’ American Journal ofPsychiatry, 94, 577. Rutter, M., Graham, P., Yule, W. (1970) A Neuropsychiutric Study in Childhood. Clinics in Develop-

Reynell, J. K. (1970) ‘Specific learning disorders in preschool children.’ Forward Trends, (August), 52. Comly, H. H. (1971) ‘Cerebral stimulants for children with learning disabilities.’ Journal of Learning

Wushinpton Post (1970) 29th June.

U.S. Govt. Printing Ofice.

50, 463.

Journal of Orthopsychiatry, 36, 861.

Neurology, 14, 83.

mental Medicine, No. 35/36. London: S.I.M.P. with Heinemann.

Disabilities, 4, 484.

BILIRUBIN NEUROTOXICITY IN recent years there has been a renewed interest in cerebral lesions resulting from uncon- jugated hyperbilirubinemia. Our earlier concepts of age of occurrence and its correlation with the degree of unconjugated hyperbilirubinemia have required modification. The initial impressions that cerebral lesions secondary to hyperbilirubinemia occurred only in the first eight days of the neonatal period1, and only with unconjugated hyperbilirubinemia over 20 mg per cent, have not held true.

In an analysis of 37 patients aged 4 to 7 years who had been jaundiced in the neonatal period, ODELL~ was unable to correlate the level of hyperbilirubinen-ia with cerebral palsy or IYS of less than 80. On the other hand, the degree to which serum albumin was saturated with unconjugated bilirubin, as measured by the salicytate displacement test, correlated well with subsequent brain damage. The many case reports of bilirubin encephalopathy occurring in infants at levels less than 20 mg per cent, of whom the few cases reported by STERN and DENTON3 are an example, serve to emphasize that factors other than the absolute level of unconjugated bilirubin are critical. Studies such as the original one by SILVERMAN et a/.* demonstrate that agents (such as sulfa, salicytate and some antibiotics) which compete with unconjugated bilirubin for albumin-binding sites lead to bilirubin encephalopathy at lower levels of unconjugated hyperbilirubinemia. More recent information, such 2.s that reported by SILBERBERG et Q L . ~ , demonstrates thsrt cerebellar tissue cultures are more sensitive to bilirubin-induced toxicity at low pH values of the media. On the other hand, at pN levels of 7.62, tissue cultures containing up to 50 mg per cent of bilirubin, with a bilirubin-to-albumin ratio of 2:9, werz spared evidence of cytotoxicity. There is no doubt that factors such as acidosis, hypoxia and hypoglycemia, which alter the brain’s susceptibility to bilirubin, as well as agents which compete with bilirubin for albumin-binding sites, are critical factors in the production of bilirubin encephalopathy in the newborn period.

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