The monoamine hypothesis for the pathophysiology of paraphilic disorders: an update.
A monoamine hypothesis for the pathophysiology of paraphilic disorders was first articulated in 1997 by Kafka. This hypothesis was based on four converging lines of empirical evidence. First, the monoamine neurotransmitters, dopamine, norepinephrine, and serotonin serve a modulatory role in human and mammalian sexual motivation, appetitive, and consummatory behavior. Second, the sexual effects of pharmacological agents that affect monoamine neurotransmitters can have both significant facilitative and inhibitory effects on sexual behavior. Third, paraphilic disorders appear to have Axis I comorbid associations with nonsexual psychopathologies that are associated with monoaminergic dysregulation. Last, pharmacological agents that enhance central serotonergic function in particular, have been reported to ameliorate paraphilic sexual arousal and behavior. Contemporary data supporting or refuting a monoaminergic hypothesis as a biological component associated with paraphilic sex offending behaviors will be reviewed. Particular attention will be given to pharmacological-metabolic probe studies, reports of Axis I comorbidity, the proposed role of disinhibited sexual motivation or sexual appetitive behavior, and cumulative pharmacological treatment data sets.[1]References
- The monoamine hypothesis for the pathophysiology of paraphilic disorders: an update. Kafka, M.P. Ann. N. Y. Acad. Sci. (2003) [Pubmed]
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