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Decrease of N-acetylaspartate after ACTH therapy in patients with infantile spasms.

H Maeda·S Furune·K Nomura·O Kitou·Y Ando·T Negoro·K Watanabe
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Abstract

Apparent brain atrophy has been frequently observed at CT and MRI after ACTH therapy in patients with infantile spasms. There are several hypotheses to explain ACTH-induced brain shrinkage: 1) a catabolic effect of ACTH on brain tissue, 2) a mineralocorticoid effect resulting in a loss of water and 3) an increase in cerebrospinal fluid (CSF) pressure compressing the brain. An average of 0.21 +/- 0.03 mg/kg of ACTH was administered to nine patients over a period of 14 to 17 days. Water content and concentrations of N-acetylaspartate (NAA), creatine and phosphocreatine (Cr + PCr), and choline (Cho) were measured before, immediately after, and several months after the ACTH therapy by using in-vivo 1H magnetic resonance spectroscopy (MRS). Only NAA concentration exhibited a significant change during the study (6.6 +/- 1.5 mmol/kg, 5.4 +/- 1.1, and 7.0 +/- 1.5, p = 0.017). There was no significant change in Cr + PCr, in Cho, or in water content. These data suggest catabolic effects of ACTH on brain tissue, such as cell loss, decrease in NAA synthesis in mitochondria, and leakage of NAA from cell membrane.

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Adrenocorticotropic HormoneAnalysis of VarianceAnticonvulsantsAspartic AcidAtrophyBrainChild, PreschoolCholineCreatineFemaleHumansInfantLongitudinal StudiesMagnetic Resonance SpectroscopyMaleProduct Surveillance, PostmarketingSpasms, InfantileTime FactorsWaterJournal Article

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H Maeda, S Furune, K Nomura, O Kitou, Y Ando, T Negoro, K Watanabe. 1997. Decrease of N-acetylaspartate after ACTH therapy in patients with infantile spasms.. https://doi.org/10.1055/s-2007-973711

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