Seizures and steroids.

Annotations Seizures and steroids For over 40 years we have known that some children with otherwise intractable fits improve with steroids, ' and for over 30 years that a similar response may be obtained with adrenocortico-trophic hormone.2 Since that time a considerable amount of work has centred on infantile spasms, particularly on the relative efficacies of prednisone and adrenocorticotrophic hormone. For each report asserting the superiority of one, it is possible to find another giving the opposite view. Close comparison is confounded by the fact that drugs, dosage, and duration of treatment have varied between the trials. One recent paper3 was unable to find any convincing difference of effect between the two. Despite this, certain facts have emerged; more patients respond to adrenocorticotrophic hormone than to prednisone;4 there are a few, however, who will respond to the latter but not the former.5 The relation between the spasms and hypsarrhythmia is not a close one as the electroencephalographic changes may appear considerably later than the onset of spasms. Recurrence of spasms after hormone treatment is rarely attended by reappearance of hypsarrhythmia and neither the spasms nor the hypsarrhythmia by themselves are likely to affect long term development. What conclusions can be drawn from all this work? The first and most obvious conclusion is that adrenocorticotrophic hormone acts independently of its effect on the adrenal glands. It is just conceivable that adrenocorticotrophic hormone acts via steroid metabolites intermediate on the biosyn-thetic pathway; it is difficult otherwise to see how some patients do better on adrenocorticotrophic hormone and a few on prednisone. This also makes the clinical observation that pharmacological doses of adrenocorticotrophic hormone (80 IU) may be more effective than lower doses (20 IU), more plausible. Perhaps, most convincingly, adrenocorti-cotrophic hormone can control fits in adrenal suppressed patients, including those concurrently on prednisone, even in the presence of documented low serum cortisol concentrations. The most simple alternative is that adrenocorticotrophic hormone has a direct effect on neurons or glial cells, or both. A second conclusion must be that infantile spasms are associated with almost every condition affecting infants known to the paediatric neurologists. It is unlikely that conditions as disparate as phenylketo-94 nuria, subdural haematomas, and tuberose sclerosis elicit this stereotypic response by precisely the same mechanisms. Once this heterogeneity of the condition is accepted, it is easier to see that more appropriate questions might be why some patients respond to one …