Sexual Function After Surgery for Prostate or Bladder Cancer

Alejandro J. Miranda-Sousa, MD; Hugo H. Davila, MD; Jorge L. Lockhart, MD; Raul C. Ordorica, MD; Rafael E. Carrion, MD


Cancer Control. 2006;13(3):179-187. 

In This Article

Sexual Dysfunction Classification and Pathophysiology


The penis is composed of three cylindrical structures, the paired corpus cavernosum (CC) and the corpus spongiosum. A cross-section of the mid-penis depicts the relationship between the various anatomic elements (Fig 1). The penis is innervated by both the autonomic and somatic nervous systems. Somatic innervation is derived from the S2-S4 sacral nerve roots via the pudendal nerve. These paired nerves supply the pelvis, perineum, and penis. They terminate as the dorsal nerve of the penis. Sexual stimulus releases nitric oxide from the terminal ends of the cavernosal nerves. This increases the level of guanosine 3′,5′-cyclic monophosphate (cGMP) with subsequent smooth-muscle relaxation of the arteries and CC, thus allowing significant blood inflow. To maintain an erection, this blood needs to be trapped within the CC. This is achieved by the passive mechanical compression of the CC against the tunica albuginea, thus occluding the venous drainage and maintaining the erection.[12,13,14,15] Physiologically, phosphodiesterase (PDE) enzymes modulate this pathway by inactivating cGMP, which results in elevated cytosolic calcium concentrations and smooth-muscle contraction. Hence, the interactions of the autonomic nervous system, coupled with the mediating transmitters, are integral in the contraction and relaxation physiology of the cavernous smooth-muscle cell (Fig 2).[16,17,18]

Figure 1.

Cross-section of the penis demonstrating relationships between penile layers and various components. From Oral Pharmacotherapy for Male Sexual Dysfunction: A Guide to Clinical Management. Broderick Ga, ed. Totowa, NJ: Humana Press; 2005. Reprinted with permission.

Figure 2.

Molecular mechanism of penile smooth-muscle relaxation. Cyclic AMP (cAMP) and cyclic GMP (cGMP), the intracellular second messengers mediating smooth-muscle relaxation, activate their specific protein kinases, which phosphorylate certain proteins to cause opening of potassium channels, closing of calcium channels, and sequestration of intracellular calcium by the endoplasmic reticulum. The resultant fall in intracellular calcium leads to smooth-muscle relaxation. Sildenafil inhibits the action of phosphodiesterase type 5 (PDE-5), thus increasing the intracellular concentration of cGMP. Papaverine is a nonspecific phosphodiesterase inhibitor. GTP denotes guanosine triphosphate and eNOS denotes endothelial nitric oxide synthase. From Lue TF. Erectile dysfunction. N Engl J Med. 2000; 342:1802-1813. Copyright © 2000 Massachusetts Medical Society. All rights reserved.

Erectile dysfunction can be caused by organic or psychogenic factors. Organic factors include vascular, neurogenic, and hormonal causes. Erectile dysfunction following pelvic surgery is usually due to a neurogenic component secondary to damage to the cavernosal nerve.[19] As a consequence, the penile tissue undergoes an intense remodeling process characterized by a decrease in smooth-muscle cells and an increase in collagen synthesis that leads to reduced compliance of the CC and tunica albuginea during erection.[20]


Sexual response in both men and women can be divided into four phases on the basis of physiologic characteristics and subjective reports. These phases are excitement, plateau, orgasm, and resolution.[21,22] In the excitement phase, female sexual arousal is the final expression of a complex process involving sexual stimulation, ascending/ descending steady control by the central nervous system, and peripheral neurovascular changes in a normal hormonal enviroment.[23] Physiologically, this phase begins with the engorgement of the vaginal mucosa, causing thickening of the vaginal walls and transudation of fluid into the vagina. Orgasm is defined as an altered state of consciousness associated with primarily genital but also nongenital sensory input. A so-called "orgasmic platform" in women, potentially responsible for either the genital pleasure at the peak and a possible biological basis for the greater capacity for multiple orgasms, has been suggested as the result of genital sexual arousal.[24,25] Sensory trigger points have been advocated at the orgasmic platform level, including the clitoris and vagina. Any biological modification of these trigger points and areas can significantly affect a woman's orgasmic phase.

Female sexual dysfunction is a complex neurovascular phenomenon under psychologic and hormonal control. Various pelvic cancer pathology and/or subsequent treatment can affect each aspect of the female sexual cycle at different levels. An international consensus was established recently to develop a classification system of female sexual dysfunction. This classification system consists of four major categories: desire disorders, arousal disorders, orgasmic disorders, and sexual pain disorders.[1]


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