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Amantadine, fatigue, and multiple sclerosis.

G A Rosenberg¹, O Appenzeller

¹Department of Neurology, University of New Mexico School of Medicine, Albuquerque 87131.

Archives of Neurology

|October 1, 1988

Summary

Amantadine hydrochloride effectively improved fatigue in multiple sclerosis patients. This treatment correlated with increased beta-endorphin-beta-lipotropin and altered lactate/pyruvate levels, indicating measurable metabolic changes.

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

Fatigue is a common and debilitating symptom in multiple sclerosis (MS).
Current treatments for MS fatigue have limited efficacy.
Understanding the underlying mechanisms of MS fatigue is crucial for developing better therapies.

Purpose of the Study:

To investigate the efficacy of amantadine hydrochloride in treating fatigue in patients with multiple sclerosis.
To explore the potential biochemical and metabolic changes associated with amantadine therapy for MS fatigue.

Main Methods:

A double-blind, placebo-controlled, crossover study was conducted.
Ten patients diagnosed with multiple sclerosis participated in the study.
Measurements included subjective fatigue levels and circulating levels of beta-endorphin-beta-lipotropin, lactate, and pyruvate.

Main Results:

Amantadine hydrochloride therapy was effective in improving fatigability in six out of ten patients.
Responders to amantadine showed significantly higher levels of beta-endorphin-beta-lipotropin compared to non-responders.
Non-responders exhibited significantly higher lactate and lower pyruvate levels.

Conclusions:

Amantadine hydrochloride represents a potential therapeutic option for managing fatigue in multiple sclerosis.
The observed changes in beta-endorphin-beta-lipotropin, lactate, and pyruvate suggest a link between amantadine's efficacy and specific metabolic pathways.
Further research is warranted to elucidate the precise mechanisms by which amantadine influences fatigue and metabolism in MS patients.

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