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Structural and functional changes in skeletal muscle in anorexia nervosa
D M McLoughlin1, E Spargo, W S Wassif
1Department of Psychiatry, Institute of Psychiatry, London, UK.
Acta Neuropathologica
|July 3, 1998
Summary
Severe malnutrition in anorexia nervosa causes significant muscle dysfunction, a metabolic myopathy. Refeeding is recommended to treat this under-recognized skeletal myopathy in patients.
Area of Science:
- Neurology
- Metabolic Disorders
- Muscle Physiology
Background:
- Protein-energy malnutrition is a key factor in anorexia nervosa.
- Muscle dysfunction is an under-recognized complication of severe anorexia nervosa.
Purpose of the Study:
- To comprehensively examine skeletal muscle function and structure in patients with severe anorexia nervosa.
- To characterize the metabolic myopathy associated with severe malnutrition in anorexia nervosa.
Main Methods:
- Evaluated muscle function through strength and exercise testing in eight female patients with severe weight loss.
- Utilized electromyography and muscle biopsy for structural and electro-physiological analysis.
- Assessed muscle fiber atrophy and myofibril integrity via ultrastructural examination.
Main Results:
- All patients exhibited impaired muscle function, with significantly reduced maximum voluntary contraction force.
- Electromyography indicated myopathy in five patients, with four showing concurrent neuropathy.
- Muscle biopsies revealed myopathic changes, specifically severe type 2 fiber atrophy, without neuropathic evidence. Ultrastructural analysis showed myofibril damage and abundant glycogen granules.
Conclusions:
- Severe protein-energy malnutrition in anorexia nervosa results in a metabolic myopathy affecting skeletal muscles.
- No direct association was found between specific abnormal dieting behaviors and histological muscle changes.
- Appropriate refeeding programs are recommended for treating myopathy in anorexia nervosa patients.