The spinal cord is a major site for the regulation of pro- and anti-erectile outflows as well as the coordination of autonomic and somatic pathways. In patients with spinal cord injuries above the sacral segments, erections are triggered via the spinal reflex arc. The patients have poor-quality erections with premature detumescence because of the lack of supraspinal control (8). However, lesions involving the sacral spinal cord, the sacral roots, or the pelvic or pudendal nerves abolish reflexic erections. Psychogenic erections occur in men with complete lesions of the cord as high as T12, suggesting that the sympathetic pathways in these men mediate them.
Additionally, bilateral anterolateral cordotomies in humans result in the complete loss of erectile function and block orgasm-associated sensations. Because touch and two-point discrimination are not altered by this procedure, it appears likely that the erotic quality of genital stimulation depends on the ascending fibers running with the spinothalamic pathways for pain and temperature. In monkeys, electrical stimulation along the course of the spinothalamic pathways at the level of the brain stem elicits erection and ejaculation (219). The relevant fibers could be traced to the caudal thalamic intralaminar nuclei, which may be the receiving area for erotic genital sensation. Stimulation of these nuclei in humans has been reported to cause erotic feelings and orgasm. Under normal conditions, it seems likely that psychogenic and reflexic stimuli act in a synergistic manner to produce erections. Psychogenic erections in paraplegic men are usually short-lived, only partial, and lack the rigidity needed for coitus (220). Further evidence from animal experiments has also shown the presence of an efferent hypothalamospinal pathway running in the dorsal funiculus of the cord (221).
Penile erections remaining after sacral spinal cord lesions or lesions of the pelvic nerve are attributed to sympathetic outflow, suggesting that erections may be elicited by peripheral information integrated at suprasacral levels that activates sympathetic pathways (222, 223). A report of erectile dysfunction caused by lesions of the paravertebral sympathetic chain in humans provides evidence for this hypothesis (224). Furthermore, stimulation of the hypogastric nerve elicits penile erection in patients with spinal cord injury.
PENILE ERECTION AND FLACCIDITY: CENTRAL NEUROPHYSIOLOGY
Table 8 outlines the central neurophysiology of penile erection and flaccidity.
Five dopamine receptor families have been identified (D1-D5). The family of D1 and D2 receptors and their role in the central regulation of penile erection, copulatory behavior, and genital reflexes (with the D2 receptors playing a major role) are particularly interesting (226). Selective D2 agonists cause penile erections that are accompanied by stretch yawning and sedation, which are typical of central dopaminergic stimuli. Moreover, during copulation, studies have shown an increase in the concentration of dopamine within the cerebrospinal fluid. When injected into the cerebral ventricles, the dopamine precursor L-dopa or the mixed D1-D2 receptor agonist apomorphine increased sexual responses in male rats (227,228). Interestingly, low doses of apomorphine facilitate erec-
Effects of Central Neurotransmitters on Penile Erection and Sexual Behavior
Pharmacological effect on sexual/erectile behavior
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