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AIDS patients commonly complain of fatigue. However, fatigue is a common complaint and there may be many different causes for fatigue in any individual patient. Among AIDS patients, fatigue may arise from direct effects of the disease on the muscles, or may result from other systemic factors that create the perception of fatigue in the brain. Furthermore, there has been some suggestion that azidothymidine (AZT), a drug commonly used in the treatment of AIDS patients, may impair the function of mitochondria; this impairment of the energy-supplying mechanisms of cells might also contribute to fatigue. A study was conducted of muscle function in nine AIDS patients and 25 control subjects to determine if muscle abnormalities might be identified that could account for fatigue. All nine AIDS patients in the present study complained of muscle pain (myalgia) and fatigue. The researchers measured muscle force and electrophysiological characteristics of muscles during exercise involving the lower leg. Furthermore, the technique of nuclear magnetic resonance spectroscopy was used to monitor specific biochemical changes in the muscles during the exercise. No significant differences were found between the AIDS patients and the control subjects. This was also true for the five of the nine AIDS patients who were receiving AZT treatment. The absence of measurable differences in fatiguability, muscle metabolism, or muscle activation suggests that the source of fatigue among AIDS patients does not lie in any abnormality of the muscles themselves. Furthermore, since no abnormalities were detected in the five patients taking AZT, the results do not support the contention that this drug impairs the function of mitochondria in the muscles. (Consumer Summary produced by Reliance Medical Information, Inc.)

Fatigue is a common complaint in some neurological diseases, including spastic paraparesis and multiple sclerosis. Despite the fact that fatigue is a major clinical problem, little is known about the mechanisms responsible for fatigue. Fatigue has been regarded as a reflection of central nervous system dysfunction in cases of spastic paraparesis. However, evidence is beginning to emerge which suggests that at least a portion of the fatigue may be due to changes in muscle, as well. Using both electrophysiologic measurements and magnetic resonance spectroscopy, researchers have demonstrated abnormalities in the performance of the tibialis anterior muscle in the legs of patients with spastic paraparesis. The muscle was electrically stimulated to contract repeatedly. Measurements of the force exerted during the contractions revealed a significantly greater decline in tension in the patients than in normal control subjects. Magnetic resonance spectroscopy is capable of analyzing the phosphocreatine and inorganic phosphate within the functioning muscle. These measurements revealed that the decline of phosphocreatine, a source of energy, in the muscle of the patients was greater than in the control subjects. A decline in phosphocreatine is also likely to reflect an increase in the acidity within the muscle. These results indicate that there are biochemical changes within the muscles themselves of patients with spastic paraparesis. These changes may be responsible for some of the fatigue which is a common source of complaint among these patients. (Consumer Summary produced by Reliance Medical Information, Inc.)