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

doi:10.1055/s-2007-973711

Neuropediatrics, Inhaltsverzeichnis

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

Original articles

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

Abstract

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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

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