Biomedical subjects
Publications and source records attributed to J M Studler.
We assayed the content of neurotransmitters (or their synthesizing enzymes) and neuropeptides in the hypothalamus of control and parkinsonian brains post mortem. Only dopamine concentrations were lower than normal in Parkinson's disease, suggesting that deficiency in hypothalamic dopamine transmission may play a role in the autonomic and endocrine abnormalities of this disorder.
The regional distribution of immunoassayable CCK-8 was determined in 12 regions of control and parkinsonian human brain, with specific attention to the possible regional coexistence of CCK-8 with dopamine. In Parkinson's disease, CCK-8-I levels were only decreased in the substantia nigra where dopamine cell bodies lie, and not in striatal and corticolimbic dopamine projecting areas. Our results suggest that the major proportion of dopaminergic neurones degenerated in Parkinson's disease may not contain the CCK-8 peptide.
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The four cases of dyskinesia at the "beginning and end of dose" caused by L-Dopa presented in this series were characterized by four essential features: 1) their onset at the beginning and end of the period of effectiveness of a dose of L-Dopa + IDC (benserazide); 2) their ballic and dystonic appearance associated with a reinforcement of Parkinsonian signs; 3) the possibility of their reduction by an increase and fractionning of the daily dose of L-Dopa; 4) the particular nature of the underlying Parkinsonian problem in which they were seen, i.e. the young age at onset of the disease, the severity of akinesia, and the quality of the clinical response to L-Dopa. Thus on the basis of the circumstances of their development, their appearance, and their treatment, such forms of dyskinesia at the "beginning and end of dose" appear to be different from classical "mid-dose" dyskinesia. In addition, they pose a new physiolopathological problem.
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This study involved twleve parkinsonian patients exposed to abnormal movements provoked by L-DOPA. Including six patients with "mid-dose" dyskinesias and six others with "onset and end of dose" dyskinesias, Correlation between the circumstances of onset of abnormal movements and plasma concentrations of DOPA and O-methyl-DOPA, after administration of a dose of L-DOPA + IDC, gave the following results: 1) mid-dose dyskinesias appeared with the highest plasma concentrations of DOPA, at the maximum therapeutic effect; 2) onset and end of dose occurred during rise and fall in plasma levels of DOPA, coinciding with the relief and the reappearance of parkinsonian symptoms respectively; 3) no correlation could be established between plasma concentrations of O-methyl-DOPA and the duration of the period of clinical remission or of abnormal movements. These biochemical data, completed by the neuropharmacological study of one patient with onset and end of dose abnormal movements suggest the predominant role of a disturbance in central dopaminergic mechanisms in the genesis of abnormal movements, whatever their nature.