26th Annual Meeting of the International Academy of Sex Research

Lorraine Dennerstein, AO, MBBS, PhD, FRANZCP, DPM

Disclosures

July 10, 2000

In This Article

Male Sexual Dysfunction

With regard to mechanisms involved in male sexual behavior, an interesting doctoral study was presented by Risa Weisberg, of the Sexuality and Research Program of the Center for Anxiety and Related Disorders, Boston University, Boston, Massachusetts. This study explored the effects of causal attributions for an erectile difficulty on subsequent sexual function.

There is evidence from community-based studies that most men will experience an occasion in their lives when they are unable to maintain or achieve an erection.[8] It is not clear why some men can take this in their stride and others develop erectile dysfunction. Attribution research has shown that attributing a negative event to an internal and/or temporally stable cause relates to negative affect and perceptions of uncontrollability and future expectations of failure (Weisberg et al, unpublished data, 2000).

This intervention study involved 52 young sexually functional male college students who were given false information about their erectile response to erotic movies. Regardless of their actual penile circumferential change, all the men were told that their response did not look like one from someone who is feeling very aroused. They were shown a printed graph suggesting an incomplete erectile response. Half the group were told it must be due to an external fluctuating cause (poor films), and the other half were told it must be due to an internal cause (their own thoughts). All the young men were then shown another erotic movie. Those who were given internal constant causes had a poorer response to the movie than did those who were told that poor response earlier was due to an external cause.

Sexual failure was also predicted by the degree of arousal before the experimental manipulation, negative affect, and perceived erectile control. This study indicates that the cause to which a sexual performance difficulty is ascribed plays an important role in future sexual functioning. An occasion of seeming erectile difficulty may not lead to persistent problems. The impact of such an occurrence depends on the individual's cognitive reaction to it, which can set up permanent negative expectations. These findings have important implications for clinicians. Thus, sex counseling should explore the meaning placed on sexual problems by the patient rather than providing only behaviorally focused or pharmacologic management.

Dr. Eric Janssen and John Bancroft of the Kinsey Institute for Research in Sex, Gender and Reproduction, Indiana University, Bloomington, provided further information on psychologic factors involved in erectile dysfunction. The authors presented a theoretical model of dual control of male sexual response, based on the balance of central excitation and inhibition.[9] The model proposes that central inhibition is adaptive and that individuals vary in their propensity for inhibition and excitation. For the majority of men, the level of inhibition is adaptive, keeping that person out of trouble. When too high, there may be increased vulnerability to erectile dysfunction. If the level of inhibition is too low, the individual may be more likely to engage in high-risk sexual behavior.

A questionnaire was developed and administered to nearly 3000 men (the SIS/SES questionnaire). Data were presented on the relation between inhibition and excitation proneness and self-reported problems with erection, ejaculation, orgasm, sexual arousal, and sexual desire. This study has identified a first inhibition factor associated with fear of performance failure and a second inhibition factor related to external threats (from within the relationship, for example), as well as an excitation factor.[10] The first inhibition factor seems to reflect a trait inhibition, which may render the individual vulnerable to erectile dysfunction. The authors hypothesize a tonic state of inhibition, which has to be reduced or exceeded by excitation for sexual response to occur. The tonic state of inhibition may have been indicated by Weisberg's finding above of the importance of the degree of arousal present before the experimental manipulation. It was unfortunate that Weisberg had not had access to the SIS/SES questionnaire to include in her study.

An anatomic basis for excitation and inhibitory tone is provided by the work of Dr. Kevin McKenna, Departments of Physiology and Urology, Northwestern University School of Medicine. He noted that male sexual response of erection and ejaculation are generated by spinal reflexive mechanisms, which are under descending excitatory and inhibitory control. The source of some of the supraspinal centers has only recently been elucidated.

The nucleus paragigantocellularis in the rostral medulla projects directly to the inhibitory tracts of the spinal cord and uses serotonin. Lesions of this nucleus disinhibit the spinal cord in a similar manner to transection of the cord. An excitatory site is the paraventricular nucleus of the hypothalamus. This can be activated by genital stimulation. Stimulation of these neurons can elicit erection and ejaculation. These neurons use the neurotransmitter oxytocin. Dopamine, nitrous oxide, and oxytocin are involved in a sequence of neurotransmitters activating sexual behavior. The clinical relevance is that substances that block excitation by acting to reduce dopamine (such as antipsychotic drugs) will reduce sexual function, as will substances that increase inhibitory tone by facilitating serotonin (such as the selective serotonin reuptake inhibitors [SSRIs]). These central mechanisms are likely to be analogous for the female.

Professor Elaine Hull, Department of Psychology, State University of New York at Buffalo, highlighted the role of dopamine in the central nervous system in sexual motivation and response. Although dopamine is facilitative to sexual function, serotonin is generally inhibitive. Increasing serotonin in the anterior lateral hypothalamus of the rat by microinjection of an SSRI increased the latency to beginning copulation and to ejaculation.[11] Serotonin may have effects on sexual motivation by decreasing the release of dopamine in the nucleus accumbens septi. Effects on sexuality in the female are analogous. These mechanisms may explain the adverse effects seen on sexuality in men and women taking SSRIs, which increase the amount of serotonin, and antipsychotic drugs, which decrease the amount of available dopamine.

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