Abstract
In 64 patients with Parkinson's disease (PD), the basal level of prolactin (PRL) was normal. Bromocriptine (BCT) caused a significant suppression of PRL in all parkinsonian patients and controls. When given after BCT treatment, thyrotropin-releasing hormone (TRH) induced a significantly lower PRL rise in recent-onset parkinsonian patients than in controls or advanced patients. In advanced parkinsonian patients with daily fluctuations in disability, the corresponding TRH-induced PRL response was significantly higher than in controls. In advanced parkinsonian patients without fluctuations, the PRL response to TRH was almost the same as in controls.
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