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Neuropediatrics 1997; 28(5): 262-267
DOI: 10.1055/s-2007-973711
Original articles

© Hippokrates Verlag GmbH Stuttgart

Decrease of N-acetylaspartate After ACTH Therapy in Patients with Infantile Spasms

H. Maeda1 , S. Furune2 , K. Nomura2 , O. Kitou2 , Y. Ando3 , T. Negoro4 , K. Watanabe4
  • 1Department of Radiological Technology, College of Medical Technology, Nagoya University,
  • 2Department of Pediatric Neurology, Japanese Red Cross Nagoya First Hospital,
  • 3Department of Radiology, and
  • 4Department of Pediatrics, School of Medicine, Nagoya University
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Publication History

Publication Date:
13 March 2007 (online)

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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.

Key words

Infantile spasms - ACTH-induced brain atrophy - MRS