Management of craniopharyngiomas is still controversial. 28 children with this tumor were studied. GH deficiency was present in 22 patients following surgery, 10 of these GH-lacking patients had normal or accelerated growth (usually associated with rapid weight gain) postoperatively. Somatomedin levels were normal in three of six normally growing patients. After craniotomy their basal and TRH-stimulated prolactin levels were in the normal range, but their insulin secretion was markedly increased. Postoperatively there was a significant correlation between peak insulin levels following arginine infusion and growth velocity in all patients. Complete tumor removal could be performed in 28% of our patients. Altogether 36% of all patients had at least one tumor recurrence. Recent literature with the addition of our series showed tumor recurrence in 22% of patients with "total" tumor excision and in 72% of patients with partial tumor removal. Radiotherapy seems to be capable of destroying craniopharyngioma tissue. The recurrence rate was only 26% in patients with subtotal excision plus radiotherapy. Unless radical tumor removal can be attempted with safety, subtotal tumor removal plus radiotherapy appears to be the treatment of choice for craniopharyngioma.
8 children with different petit mal epilepsies were systematically treated with ACTH and dexamethasone. CCT examinations were performed before, during and after treatment. In all children severe cerebral changes. enlargement of ventricles and subarachnoid space developed during the initial phase of treatment with Depot-ACTH. Similar changes, but to a less severe degree, could be demonstrated during the phase of dexamethasone therapy thereafter. In all patients cerebral changes disappeared after hormonal treatment had ended. At this point many children had a developmental spurt, developmental relapses could not be observed. It is suggested that these reversible changes seen on CCT scans represent a form of morphological plasticity of brain structures. These results bear certain consequences as to the therapy of cerebral edema.
Referring to the article of Pente/la et al in this issue of Neuropediatrics we report on experiences with ACTH therapy in infantile spasms. In addition we want to point out the reasons which led us to use ACTH fragments for therapeutic trials in children with infantile spasms.Adrenocorticotropic hormone (ACTH) has been a useful drug in the treatment of petit mal since 1950 (Klein and Livingstone 1950). The compound was successfully used in its natural form with 39 amino acids (ACTHI-39) and in its fragmented form with 24 amino acids (ACTHI-24), the latter being the most common and most frequently applied form of ACTH. We recently completed a prospective study on infan.. tile spasms and Lennox syndrome (Lagenstein et al 1978a, b) in which we administered an ACTH-fragment consisting of 23 amino acids (ACTHI-23). All the ACTH molecules mentioned caused marked hypercortisolaemia which was not sig.. nificantly different when induced by ACTHI-23 (Willig et al 1978). As a result maximal stimulated adrenals led to severe side efTects -these are familiar from Cushing's disease.Conventional ACTHI-24 was very efTective upon infantile spasms (Singer et al 1980). Particularly in infantile spasms beginning within the first year of life, and in centrencephalic myoclonic-astatic petit mal cases of older children ACTH seems to be a suitable drug and also seems to be most effective if it is applied within the first month of the spasm onset as far as infantile spasms are concemed.In spite of good seizure control with ACTH, physicians he.. sitate to administer corticotropins because the side effects may appear even more impressive than the seizures them.. selves when treatment is carried out for aperiod of 3 to 6 months at an ACTH dose of80 IV per day.After one of our patients on ACTH therapy had died from pneumonia, we strongly considered how the side effects could be reduced withoutjeopardizing the positive effects ofACTH. Our own observations during the hormonal seizure treatment led us to the conclusion that the therapeutical aministration ofACTH has a direct effect on the central nervous system and not via the adrenocortical hormones: a) Dose-dependency in relation to the effect of ACTH From the tenth treatment day on ACTH led to a maximal cortisol level of 100 J.1g/dl on average with large individual fluctuations. The moment of therapy success was not con.. nected to the level of cortisol. One patient who showed the highest cortisol plasma level (440 Jlg/dl) did not react to the ACTH therapy. This was an indication that ACTH has a direct effect upon the brain and possibly does not have an effect via the adrenal cortex. The fact that only 15 IU ACTH is required in order to achieve a maximal adrenocortical effect also supports this theory. In addition, the results which have been reported in the literature clearly indicate that therapy success is dependent on the ACTH dose level. In our opinion these facts indicate that ACTH acts directly on the brain. b) Investigations of adrenocortical insufficiencyWe had the opportunity of...
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