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

H Maeda1, S Furune, K Nomura

  • 1Department of Radiological Technology, College of Medical Technology, Nagoya University.

Neuropediatrics
|December 31, 1997
PubMed
Summary
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Adrenocorticotropic hormone (ACTH) therapy for infantile spasms may cause brain shrinkage by affecting N-acetylaspartate (NAA) levels. This study suggests ACTH has catabolic effects on brain tissue, impacting neuronal integrity.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pediatric Neurology

Background:

  • Adrenocorticotropic hormone (ACTH) therapy is used for infantile spasms.
  • Brain atrophy is frequently observed after ACTH therapy.
  • Hypotheses include catabolic effects, mineralocorticoid effects, and increased CSF pressure.

Purpose of the Study:

  • To investigate the biochemical changes in the brain following ACTH therapy in infantile spasms patients.
  • To determine if ACTH therapy affects brain water content and specific metabolites.

Main Methods:

  • Nine patients with infantile spasms received ACTH therapy (0.21 mg/kg/day for 14-17 days).
  • In-vivo 1H magnetic resonance spectroscopy (MRS) was used to measure brain water content, N-acetylaspartate (NAA), creatine/phosphocreatine (Cr+PCr), and choline (Cho).

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  • Measurements were taken before, immediately after, and several months after ACTH therapy.

    • Main Results:

    • NAA concentration significantly decreased during and after ACTH therapy (p=0.017).
    • No significant changes were observed in Cr+PCr, Cho, or water content.
    • The findings suggest a catabolic effect of ACTH on brain tissue.

    Conclusions:

    • ACTH therapy may induce brain shrinkage through catabolic mechanisms.
    • Decreased NAA levels indicate potential cell loss or impaired synthesis/release.
    • These effects highlight the need for careful monitoring during ACTH treatment.