Parameters of catecholamine and acetylcholine metabolism were investigated in 55 patients with Huntington's chorea. Heterogeneous nature of the results obtained by examining excretion of catecholamines, their precursors, and metabolites appears to reflect varying degrees of the damage to the cerebral neurotransmitter systems and their imbalance in different patients. It is suggested that the level of catecholamine metabolism in the body is genetically determined. A decrease in the homovanillic acid in the ventricular fluid is attributed to a low pool of dopamine in atrophied basal ganglia and/or hydrocephalus concomitant with Huntington's chorea. The activity of the blood cholinergic system was shown to be decreased, which suggests a generalized nature of acetylcholine metabolism disorder. The data obtained indicate that the biochemical mechanisms of the pathogenesis of Huntington's chorea are intricate in their nature and involve different neurotransmitter systems, which explains insufficient efficacy of the current conclusive methods used for controlling this disease. The development of multiple modality treatment affecting various sides of impaired metabolism of neurotransmitters seems to be promising.
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