Employing a triple-column ionexchange fluorometric procedure, 29 amino compounds, including amino acid neurotransmitters, were measured in lumbar cerebrospinal fluid (CSF) from two groups of patients with idiopathic Parkinson‧s disease de novo (n = 6) and those who were treated with carbidopa levodopa (n = 6), and from neurologically normal controls (n = 10). Consideration was given to in vivo and in vitro factors known to influence levels of various CSF constituents. Results showed statistically significant decreases in the levels of γ-aminobutyric acid, homocarnosine, phosphoethanolamine, and threonine, and elevation of ornithine levels, in the CSF of de novo patients with Parkinson‧s disease compared with controls. These changes “normalized” following treatment with carbidopa/levodopa. This study suggests that Parkinson‧s disease may be characterized by defects in specific amino compound metabolic pathways, resulting in central nervous system amino compound imbalances that may contribute to the pathophysiology of this disorder. Carbidopa /levodopa therapy tends to “normalize” these amino compound imbalances.
|Original language||English (US)|
|Number of pages||3|
|Journal||Archives of Neurology|
|State||Published - Jan 1 1988|
All Science Journal Classification (ASJC) codes
- Arts and Humanities (miscellaneous)
- Clinical Neurology