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
Further Information

Publication History

Publication Date:
13 March 2007 (online)

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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