CMAJ • October 26, 2004; 171 (9). doi:10.1503/cmaj.1032006.
© 2004 Canadian Medical Association or its licensors
All editorial matter in CMAJ represents the opinions of the authors and not necessarily those of the Canadian Medical Association.
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Right arrow Other neurology

Adrenomyeloneuropathy as a cause of primary adrenal insufficiency and spastic paraparesis

Monika Spurek, Regina Taylor-Gjevre, Stan Van Uum and Hasnain M. Khandwala

All authors are with the Department of Medicine, University of Saskatchewan, Saskatoon, Sask.


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  		Table 1.

 


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  		Fig. 2: Electron micrograph of adrenocortical cell of a young boy with adrenoleukodystrophy, illustrating cytoplasmic inclusions of VLCFAs (arrow). Magnification 35 000. Photo: Courtesy of Dr. James Powers, University of Rochester, Rochester, NY

 


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  		Fig. 1: The catabolism of very-long-chain fatty acids (VLCFAs) in peroxisomes. People with adrenoleukodystrophy or adrenomyeloneuropathy do not produce acylcoenzyme A (acyl-CoA) synthetase, which breaks down VLCFAs to their CoA esters in the first step in their oxidation.

 

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  		Table 2.