Different mechanisms have been suggested to explain hypersexuality in response to antiparkinsonian therapy. The dopaminergic system, which is widely distributed in the central nervous system (CNS) and pelvic organs, is necessary for male sexual arousal and ejaculation, as documented in animal experiments and human studies.65 The serotonergic system, which is also widely distributed in the CNS, has an inhibitory role in the sexual response cycle. Dopaminergic agents such as levodopa, bromocrip-tine, and pergolide may promote sexual behavior by activating the dopaminergic system and lowering serotonin concentrations at postsynaptic sites.25
Prolactin decreases libido. It has been hypothesized that dopaminergic therapy precipitates hypersexual behavior by decreasing serum prolactin levels.11 Dopam-ine inhibits prolactin secretion from the anterior pituitary. Patients with hyperprolactinemia, treated with bromocrip-tine, demonstrate improved libido and decreased prolactin levels. Less than 1% of PD patients exhibit hypersexuality as a response to therapeutic interventions.25 It has been postulated that hypersexuality is a symptom of dopamin-ergic overstimulation in susceptible individuals.21
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