Neurogenic Bladder, Neurogenic Bowel, and Sexual Dysfunction in People With Spinal Cord Injury

Barbara T Benevento, Marca L Sipski


The purpose of this article is to review the literature related to the effects of spinal cord injuries on genitourinary, gastrointestinal, and sexual function. These important areas of function are profoundly affected by spinal cord injuries, with the effects of injury being dependent on the specific level and degree of neurologic dysfunction. Our ability to manage neurogenic bladder dysfunctions and neurogenic bowel dysfunctions has improved over the past few years; however, in general the techniques used have not significantly changed. In contrast, a significant amount of new information has been made available regarding the effects of specific neurologic injuries on sexual response, particularly female sexual response. Moreover, techniques to remediate erectile dysfunction and infertility in the male have vastly improved the fertility potential of men with spinal cord injuries. Further research is warranted in all of these areas.

One of the most important sequelae after spinal cord injury (SCI) is the loss of genitourinary1 and gastrointestinal function. In this article, we will briefly describe the anatomy, physiology, and management of bladder, bowel, and sexual dysfunction. Recent research will be reviewed, and recommendations for further research will be provided.

Neurogenic Bladder

Normally, the bladder stores urine until the proper time for voiding and then empties in a coordinated fashion.2 In order to understand the neurogenic bladder, it is useful to understand how the bladder is innervated and controlled by the brain and then examine how SCI affects normal bladder function.

The bladder's parasympathetic efferent nerve supply, which governs the contraction of the bladder, originates from the sacral cord at S2-S4 and travels to the bladder via the pelvic nerve. The effect of parasympathetic stimulation is detrusor contraction. The sympathetic efferent nerve, which increases bladder storage, originates at T11-L2 and travels to the bladder and urethra via the hypogastric nerve. The β-adrenergic receptors in the body of the bladder cause relaxation of smooth muscle, and the α receptors in the base of the bladder and urethra cause contraction of the smooth muscle. Somatic efferents originate from the sacral segments at S1-S4 and travel through the pudendal nerve and innervate the external urethral sphincter.14

The main coordination center is located in the pontine mesencephalic reticular formation.5 An intact pathway between the pontine and sacral micturition centers allows for coordinated voiding by relaxation of the urethral sphincter and contraction of the detrusor muscle. Volitional control of micturition is controlled by the medial frontal lobes and corpus callosum. In suprapontine lesions, micturition occurs, but it is involuntary.2,6

With SCI, central lesions can interrupt the pontine and sacral micturition centers. In addition, peripheral lesions can affect the parasympathetic supply to the detrusor muscle or the sympathetic supply to the bladder neck as well as somatic innervation to the external urethral sphincter.1,7 Usually, patients with SCI do not lose the cortical control of the pontine mesencephalic reticular formation unless there is concomitant head injury.1

In order to explain the different types of voiding dysfunction, several different classification systems have been described, which are based on site and extent of the neurologic lesion, urodynamic findings, and classification of bladder function.812 We believe that the most helpful method is to consider the dysfunction as falling into 1 of 2 categories: (1) failure to store and (2) failure to empty. These 2 categories are further subdivided based on whether the failure is due to a problem with the detrusor or due to the bladder outlet. Examples of failure to store would be detrusor hyperreflexia (or uninhibited bladder contractions) or an areflexic bladder outlet.813 In contrast, failure to empty may be due to an areflexic bladder or a sphincter that is unable to relax.2,3 Detrusor-sphincter dyssynergia—impaired coordination between bladder contraction and sphincter relaxation—is also a common finding in patients with SCIs. Any of these problems may occur at different stages of the acute and chronic period of SCI. Therefore, during the course of a patient's life, bladder management may have to change depending on the bladder dysfunction.

The goals of bladder management are to prevent upper and lower urinary tract complications, including hydronephrosis, renal calculi, bladder calculi, and vesicoureteral reflux.14 The type of voiding dysfunction, level of injury, and patient's ability to perform self-catheterizations, dressing and transfers. are considered in designing bladder management. Urodynamic evaluation is helpful in defining urologic problems associated with SCI. This test studies the filling and voiding phases of bladder function. In addition, the detrusor pressure, duration of detrusor contraction, and compliance of the detrusor can be measured. As spinal shock resolves by approximately 3 months after injury, detrusor activity is noted.15 This is often indicated by the presence of incontinence. Therefore, performing the urodynamic study after that time will provide the most useful information regarding the bladder dysfunction.1 In addition, cystoscopy may be performed to evaluate bladder and sphincter anatomy and pathology.

Bladder drainage is achieved through indwelling catheters, intermittent catheterizations, suprapubic catheters, condom sheath catheters, or a combination of these methods.1,2 We believe the choice of catheter or type of bladder drainage should be made on an individual basis, taking into account many factors such as patient preference, sex of the patient, level of injury, functional status, financial concerns, and the patient's desire for sexual intercourse. For example, in a person with a high cervical-level SCI, an indwelling catheter, in our opinion, is probably the most useful (at least during the acute phase), because this will allow the patient more independence than the use of other techniques. In a person with paraplegia who can be taught to self-catheterize, we believe that intermittent catheterization may be the first choice.

Pharmacologic management of specific bladder dysfunctions may also be required, and many medications are currently available. For instance, when there is a failure to store due to bladder dysfunction, anticholinergics such as oxybutynin and propantheline have an antispasmodic effect on the smooth muscle.16 Tricyclic antidepressants such as imipramine are thought to have a peripheral anticholinergic effect. These medications suppress uninhibited bladder contractions, increase bladder capacity, and increase urethral resistance.3,1618 Alpha adrenergics including ephedrine and phenylpropanolamine may be used for treatment of failure to store due to relaxation of the sphincter.3,18 In women with atrophy of the urethral epithelium, estrogen may improve the local mucosal seal.19 Supportive treatment with diapers or a condom sheath catheter may also be useful.

Patients with failure to empty due to bladder dysfunction may be treated with cholinergics such as bethanechol.20 People with a sphincter that is unable to relax and, therefore, failure to empty have been helped with α blockers such as Hytrin* and Minipress.,3

These medications, however, have side effects. This is especially true of the anticholinergic drugs, which can cause dry mouth and constipation.16,17 If these medications are required and these patients drink large amounts of liquids, an indwelling catheter may be preferred. In our opinion, patients who perform intermittent catheterization may require fluid restriction of approximately 2 L per day, and this may be difficult because of the side effects of the drugs.

Once catheters and medical management have been tried, surgical options also exist. In patients with incontinence caused by the detrusor hyperreflexia, the following methods have been suggested. An augmentation cystoplasty may increase bladder capacity and lower intravesical pressure.21 In this procedure, a portion of the bladder is removed and a larger segment of bowel is attached to the remaining bladder. Intermittent catheterization is then performed on a regular basis. There is often mucus in the urine from the bowel segment that was used to create the new bladder.3,2224 Denervation of the bladder such as cordectomy or rhizotomy has been tried and is sometimes successful.2527 Erectile dysfunction, however, may occur after the procedure. Neurostimulation for control of bladder function has also been used. The most widely used technique is to apply electrodes to the sacral anterior roots within the cauda equina.28,29 These techniques have often been accompanied by surgical division of the sacral posterior roots which reduces reflex incontinence29; however, concern for the effects of this procedure on sexual response have also recently been expressed.30

In those patients with incontinence due to incompetence of the sphincter, artificial sphincters may be implanted.31,32 These devices are usually not used in people with SCI, because upper urinary tract damage may result in hyperreflexia or increased intravesical pressure.

Other methods to aid in the treatment of incontinence are timed voiding, pelvic-floor exercises, and biofeedback.3 Valsalva manuevers, suprapubic tapping, Credé's method, and anal stretch aid in voiding in a patient with problems of urinary retention.1,3 External sphincterotomy via surgical procedure or laser is sometimes performed in patients with detrusor areflexia and detrusor-sphincter dyssynergia. Urethral stent placement has also been performed in patients with retention due to problems with failure to empty.33

Neurogenic Bowel

Bowel dysfunction is one of the most devastating sequelae of SCI, because it not only affects morbidity but it also can severely disrupt a person's quality of life. There are numerous gastrointestinal complications of bowel dysfunction, including ileus, gastric ulcers, gastroesophageal reflux, autonomic dysreflexia, pain, distention, diverticulosis, hemorrhoids, nausea, loss of appetite, impaction, constipation, diarrhea, and delayed or unplanned evacuation.3437 With proper care, however, these complications can be minimized. In order to better understand the neurogenic bowel, a brief review of normal anatomy and physiology is needed.

The colon is bounded proximally by the ileocecal valve and distally by the anal sphincter. The internal anal sphincter (IAS) is a continuous smooth muscle layer of the rectum at the end of the colon. The external anal sphincter (EAS) is a circumferential band of striated muscle that is continuous with the pelvic floor and located proximal to the anus. The puborectalis muscle loops around the rectum and maintains the anorectal angle by tethering the rectum toward the pubic bone.4,38 The puborectalis muscle is positioned like a sling around the posterior rectal wall and is attached to the pubic bone. When the puborectalis muscle contracts, it lifts the rectum upward and forms an angle between the rectum and anus.4,39,40 The EAS, IAS, and puborectalis muscle act together to maintain fecal continence. In the resting state, continence is maintained by the tonic activity of the IAS.4,41 To prevent incontinence with cough or Valsalva maneuver, the EAS and puborectalis muscle contract.4,38

The intrinsic nervous system of the gastrointestinal tract, which includes Auerbach's plexus, is situated in the colonic wall between the longitudinal and circular muscle layers. This nerve supply helps coordinate colonic wall movement and the advancement of stool through the colon. The extrinsic nervous system also innervates the colon and includes the parasympathetic, sympathetic, and somatic nerves.4 The vagus nerve provides parasympathetic innervation from the esophagus to the splenic flexure of the colon. The pelvic nerve carries parasympathetic fibers from S2-S4 to the descending colon and rectum. Some pelvic nerve branches travel proximally and innervate the transverse and ascending colon. Sympathetic innervation is supplied by the superior and inferior mesenteric (T9-T12) and hypogastric (T12-L2) nerves.4 The somatic pudendal nerve (S2-S4) innervates the pelvic floor.4,38,42

The colon absorbs fluids, electrolytes, and short-chain fatty acids; provides for growth of symbiotic bacteria; secretes mucus for lubrication of feces; and slowly propels stool toward the anus.4 The contents in the distal colon are retained until bowel evacuation. Transport of contents may take 12 to 30 hours from the ileocecal valve to the rectum.42,43

Small and large intestinal movements are mainly autonomous, with some spinal cord and minimal brain influence. Peristaltic waves travel both toward and away from the ileocecal valve in the ascending colon, but in the descending colon the waves travel mainly to push the contents to the anus.4,44

The motility of the colon is performed by 3 primary mechanisms: myogenic, chemical, and neurogenic.4,45 The myogenic transmission of signals occurs between enteric smooth muscle cells that are interconnected by gap junctions, which produces transmission from cell to cell. Most intestinal muscle displays autorhythmicity that causes colonic wall contractions.44

Chemical control is through the activity of neurotransmitters and hormones. The chemicals influence the promotion or inhibition of contractions through the action of the central nervous system, autonomic nervous system, or direct action on muscle cells.38,45,46

The local neurogenic mechanism of colonic control is the enteric nervous system, which coordinates all segmental motility and some propagated movement.46 The intestinal wall is stretched or dilated. The nerves in the myenteric plexus cause the muscles above the dilation to constrict and those below the dilation to relax, and this helps propel the contents caudally. The extrinsic nervous system including the vagus nerve, sacral parasympathetics, and pelvic nerve—all help increase colonic motility.

The gastrocolonic response or “gastrocolic reflex” is initiated by fatty or proteinaceous meal, which increases propulsive small intestine and colonic motility. The mechanism of this action is not fully understood.4,38

In the resting state, both anal sphincters are active and the anal-rectal canal is maintained in an acute angle by the puborectalis muscle. As the rectum distends, relaxation of the IAS occurs and the muscle tone in the EAS increases. Voluntary contraction of the EAS also helps to maintain continence. The IAS maintains continence of liquid and gas, and the EAS maintains continence of solids. Increased intra-abdominal pressure also causes the EAS to reflexively contract.4,39 Defecation occurs with relaxation of the puborectalis muscle and the EAS resulting from involuntary advancement of stool into the rectum.46 This creates a straighter anorectal tunnel for stool to pass, which is aided by peristalsis and increased intra-abdominal pressure.38

A neurogenic bowel occurs when there is a dysfunction of the colon due to lack of nervous control. The enteric nervous system remains intact after SCI; however, depending on the level of the injury, different bowel problems and complications may arise. Stiens et al38 described 2 main types of neurogenic bowel. The lower motor neuron (LMN) bowel syndrome or areflexic bowel results from a lesion affecting the parasympathetic cell bodies in the conus medullaris, the cauda equina, or the pelvic nerve. No spinal cord–mediated peristalsis occurs, and there is slow stool propulsion. Only the myenteric plexus coordinates segmental colonic peristalsis, and a dryer, rounder stool shape occurs. Due to the denervated EAS, there is increased risk for incontinence. The levator ani muscles lack tone, and this reduces the rectal angle and causes the lumen of the rectum to open. The LMN bowel syndrome produces constipation and a significant risk of incontinence due to the lax EAS.

A lesion above the conus medullaris causes an upper motor neuron (UMN) bowel syndrome or hyperreflexic bowel. There is increased colonic wall and anal tone. The voluntary control of the EAS is discontinued, and the sphincter remains tight thereby retaining stool. The nerve connections between the spinal cord and the colon, however, remain intact; therefore, there is reflex coordination and stool propulsion. The UMN bowel syndrome produces constipation and fecal retention at least in part due to the activity of the EAS.4,38,39

In designing a bowel program for a patient with SCI, a variety of factors must be considered. First, does the patient have UMN or LMN bowel dysfunction? A history is used to determine whether any gastrointestinal problems or any other medical conditions—such as diabetes, irritable bowel syndrome, lactose intolerance, inflammatory bowel disease, or rectal bleeding—existed before the SCI. These disorders may affect the choice of medications used in the bowel regimen. Medications frequently used by patients with SCI for other problems—such as anticholinergics for treatment of neurogenic bladder, antidepressants, narcotics, and antispasticity medications—may also affect the bowel. In addition, we believe the person's dietary habits and preferences as well as the amount of fluid intake allowed should be addressed as part of the bowel management. The diet should be nutritional and provide high-residue foods such as fruits, vegetables, grains, and cereals. Drinking fluids should be encouraged.4

A full physical examination including rectal examination should be performed to help devise a bowel regimen. A neurologic examination can reveal the extent of the nerve damage and the completeness of the SCI. The abdomen should be inspected for distention, increased abdominal muscle tone indicative of spasticity and bowel sounds. The rectal examination can provide information regarding external sphincter tone, stool in the rectal vault, and the presence of hemorrhoids or masses, and it assesses the tone and ability to produce voluntary contraction of the puborectalis muscles. We contend that it is also important to take into account the patient's strength in the upper and lower extremities; his or her sitting balance and ability to transfer; the length of the patient's arms, legs, and trunk; and the patient's weight. These factors will help determine whether the patient can perform his or her own bowel program or whether he or she will need assistance.4 Berkowitz et al47 found that 37% of all patients with SCI need assistance with bowel care. People with tetraplegia (59%) were more than 3 times as likely to need assistance as people with paraplegia (16%).4,47

Prolonged bed rest interferes with bowel motility. The seated position reduces the anorectal angle and facilitates defecation. If it is possible to perform the bowel program in the seated position, after taking into account all the previously mentioned factors, the seated position is preferred.

The time when the person conducts his or her bowel regimen will be determined by his or her lifestyle, and it is arranged around work, school, or other activities. Many people prefer to perform the bowel regimen in the morning and have the rest of the day free. Some people can be assisted only at certain times of the day, and that will determine when the bowel regimen is performed.

There are numerous medications used to aid in the management of the neurogenic bowel. The 4 main categories of medications are stool softeners, colonic stimulants, contact irritants, and bulk formers. An example of a stool softener is docusate sodium, which emulsifies fat in the gastrointestinal tract and, therefore, softens the stool. Senna tablets are colonic stimulants that stimulate Auerbach's plexus to induce peristalsis. Bisacodyl tablets and suppositories act as contact irritants in the mucosa of the colon and produce peristalsis. Psyllium is a type of bulk former.4,38,39

A usual bowel program will consist of a stool softener administered 3 times per day—2 senna tablets and a bisacodyl enema daily. The times that these medications will be given depends on the time of day the bowel program begins. Many people have had good results with this method; however, most times the medications will require adjustments in order to achieve proper and regular evacuation. In adjusting the medical regimen, the effects of other medications the patient is taking are considered as are the person's diet and the position in which the person performs the bowel program.4,38,39

For a reflexic bowel, the chemical stimulant is placed into the rectum with the patient in the upright or left lateral decubitus position, and digital stimulation is performed until evacuation. Digital stimulation increases peristalsis and relaxes the EAS. It is performed by inserting a gloved, lubricated finger into the rectum and slowly rotating the finger in a circular movement. Other assistive techniques such as the Valsalva maneuver, push-ups, abdominal massage, or leaning forward may also be used. A bowel care regimen for an areflexic bowel consists of performing gentle Valsalva maneuvers or manual evacuation in the upright or side-lying position.48

Medication management also depends, in part, on the type of bowel dysfunction. In a reflexic bowel, the medical regimen should work to produce a soft, formed stool that can be evacuated with rectal stimulation. In an areflexic bowel, firm, formed stool is required to allow the stool to be retained between bowel regimens and to be manually evacuated easily.4,38,39,43

A surgical approach to bowel management is the placement of a colostomy or ileostomy. The time spent in bowel care has been reported to decrease from 11 hours to 4 hours per week with ostomies, and fecal incontinence is prevented.4,49 Biofeedback has been used to treat fecal incontinence in people with some rectal sensation and voluntary anal sphincter contraction. Most patients with SCI do not meet these criteria, and, therefore, biofeedback does not appear to be beneficial.4 There is a strong social and sexual aspect of bowel management. Bowel accidents were noted to be the most socially distressing situation in people with SCIs, and bowel and bladder accidents were of primary concern when related to sexual activity.50,51

Neurogenic Sexual Function

Sexual Response

The impact of SCI on sexual response depends on the degree of injury and its location in the spinal cord.52 Furthermore, it depends on whether the person is male or female and what aspect of sexual response is being evaluated. Most of the information available about male sexual response is based on questionnaire studies,5254 whereas most of the data available about women comes from laboratory-based research.30,5559

Masters and Johnson60 provided a framework for studying human sexual response and divided its components into arousal, plateau, orgasm, and resolution. Each of the phases has particular genital and peripheral physiologic characteristics. When we discuss the topic of male sexual response, the components that most frequently come to mind include the occurrence of erections during the arousal phase and ejaculation during the orgasm phase. As may be expected, most of the literature pertaining to the impact of SCI on male sexual response relates to these 2 phenomena. Nevertheless, in both sexes, heart rate, blood pressure, and respiratory rate also progressively increase during the arousal, plateau, and orgasm phases of sexual response and then return to baseline levels during the resolution phase.60

In order to predict the impact of SCI on male erection, knowing the level and degree of a person's injury and whether the injury is in the UMN or LMN and is affecting the sacral reflex arc is critical.61,62 In addition, the status of the neurologic pathways that control erection determines function. Erectile function can occur 2 ways: (1) reflexively through sacral stimulation and a parasympathetic neurologic pathway and (2) psychogenically under control of the hypogastric plexus originating at T11-L2 and also involving the sacral segments.6365 Men with complete UMN injuries above the level of T11 can have reflex erections but not psychogenic erections, whereas men with complete LMN injuries will most likely not have reflex erections but may have psychogenic erections, depending on the degree of preserved neurologic function in the T11-L2 region of the spinal cord.66,67 Men with incomplete UMN injuries may retain the capacity for psychogenic function, depending on the degree of preserved neurologic function in the T11-L2 region of the spinal cord, and they should retain the capacity for reflexive erectile function. Men with a complete LMN injury should not experience reflex erections but may experience psychogenic erection, depending on the degree of preserved neurologic function affecting the T11-L2 region of the spinal cord.66,67

Ejaculation is a more complicated neurologic process and is more profoundly affected by SCI. Coordinated efforts of the sympathetic, parasympathetic, and somatic nervous systems result in the production of a man's ejaculate. In men with SCI, any of these neurologic pathways can be interrupted, depending on where the injury is located, and the result will often be a retrograde ejaculation in which semen is forced into the bladder instead of out the urethra. According to statistics on the effect of SCI on ejaculation, 4% of men with complete UMN lesions and 32% of men with incomplete UMN lesions retain the ability to ejaculate.52 In men with complete LMN SCIs, 18% are reported to ejaculate, and a greater likelihood of ejaculation is associated with the capacity for psychogenic erection. Seventy percent of men with incomplete LMN injuries reportedly can ejaculate.52 These estimates of how often men with SCI can ejaculate are based on ejaculation that occurs naturally through masturbation or sexual contact and without the use of augmentative techniques such as electroejaculation or penile vibratory stimulation.63 These stimulation techniques, which are relatively new and used primarily for fertility purposes, are able to produce ejaculation in a greater percentage of men than the above figures indicate.

Orgasm in men with SCI has only been studied by questionnaire.53,54 Nevertheless, the findings in these reports have been quite similar. Using self-defined definitions of orgasm, researchers in one study54 noted that 42% of men reported achieving orgasms, whereas researchers in another study53 indicated that 47% of men reported achieving orgasm. In addition, it was noted that 38% of men with complete SCIs reported that they had orgasms.53 Unfortunately, none of these reports provided detailed information about the feelings associated with orgasm.

In women, the arousal phase of sexual response is characterized by lubrication of the vagina; clitoral swelling; increases in heart rate, respiratory rate, and blood pressure; and other changes.60 Hypotheses have been made about how the sexual function of women with different types of injuries should be affected; these hypotheses were initially based on information regarding men with SCIs. Most of these effects have been confirmed in the laboratory. For women with complete UMN injuries affecting the sacral segments, the ability for reflex but not psychogenic lubrication should be maintained.68,69 This hypothesis has been tested in a laboratory-based analysis,56 and the results, although not conclusive, supported the hypothesis that lubrication occurs reflexively. For women with incomplete UMN injuries affecting the sacral segments, it is thought that they may retain the capacity for reflex lubrication and may maintain the capacity for psychogenic lubrication.68 Laboratory studies have shown that those women with greater ability to perceive a combination of light touch and pinprick sensation in the T11-L2 dermatomes will have a greater likelihood of achieving psychogenic lubrication.30 This holds true regardless of the level or degree of injury and regardless of whether the injury to the sacral segments is to the UMN or LMN.

Orgasm in women with SCIs has also been studied in laboratory settings.30,55 Although 100% of women without SCIs were able to stimulate themselves to orgasm, only 52% of women with SCIs were able to do likewise.55 Women with SCIs are less likely to achieve orgasms if they have a complete LMN injury affecting the sacral segments than if they have any other levels and degrees of injury.30 Autonomic responses, including blood pressure, heart rate, and respiratory rate, were generally similar between subjects with and without SCIs. Furthermore, at no time were unsafe blood pressure responses noted in women with SCI. Latency to orgasm was greater in women with SCIs than in women without SCI. Descriptions of orgasm were indistinguishable between women with and without SCI.30 Another group of researchers59 reported on the orgasms of 3 women with complete SCIs below T6 after a controlled type of stimulus. Based on the above research,30 it is hypothesized that an intact sacral reflex arc is needed to achieve orgasm and that orgasm may be a reflex response of the autonomic nervous system. Currently, a comprehensive assessment of the orgasms of men with SCIs is under way to determine whether the impact of neurologic injuries on sexual response will be similar to those of women.


Although men remain interested in sexual activity after SCI,53,54,70 their level of desire has been shown to decrease.53 Most men with SCIs resume sexual activity within 1 year of injury53; however, their frequency of sexual activity has been shown to decrease after injury. In one study,35 52% of men had sex 2 to 3 times per week before injury compared with 30% after injury; 48% of men had sex once a week or less prior to injury compared with 70% after the injury. Other researchers71 noted a decrease in the frequency of intercourse in men from 3 to 4 times per week to 1 to 2 times per week. Reasons for the decrease in the frequency of sexual activity have included fewer opportunities for sex,54 but the level and degree of injury have not been found to affect frequency of sexual activity.53 The types of sexual activities men engage in after SCI are similar, although they occur at a slightly different frequency, to those before their injuries. In one study,53 men reported the following frequencies of sexual activity before and after injury: intercourse=97% before injury and 61% after injury, kissing=97% before injury and 84% after injury, hugging=89% before injury and 79% after injury, and touching=87% before injury and 76% after injury. In addition, although 99% of men reported penile-vaginal intercourse as their favorite sexual activity before injury, only 16% of men indicated that this was true after injury; furthermore, after injury, most men preferred oral sex, kissing, and hugging.53 Sexual satisfaction has been shown to decrease after SCI.53,54,70,71

The sexuality of women with SCI received little attention until the 1990s. As in men, women's desire for sexual activity seems to decrease after injury. One group of researchers72 found that 46% of women with SCIs (N=231) indicated that sex was less important after injury, whereas other researchers73 found that 44% of women with SCIs (N=25) rated their level of desire as “none” to “low” after injury compared with 20% prior to injury. Frequency of sexual activity is also known to decrease in women with SCIs.72,74 Little difference has been noted in the sexual activities that women with SCI participate in after injury compared with the sexual activities they participate in before injury.72,73 A decrease in the frequency of masturbation, however, has been noted after injury.63 Preferred sexual activities after SCI have been reported to be kissing, hugging, and touching.73

Treatment of Sexual Dysfunction

Aside from studies examining treatment of erectile dysfunction, essentially no studies have focused on treatment of male or female sexual dysfunction after SCI. Although studies have been performed to determine whether there could be increases in the ability of men to ejaculate, these studies were performed with a medical focus rather than focusing on whether sexual pleasure improved.7578 Part of the reason may be that many people have decreased sexual desire after an SCI, and, therefore, they may not seek treatment for their inability to become aroused or have orgasms. In addition, the lack of available treatment methods may be part of the reason. Our comments, therefore, will focus on the remediation of erectile dysfunction, an area where much information is available.

Although many men with SCI are able to have some type of erectile function, many report that the quality of their erections is insufficient for intercourse.79 In addition, some men are unable to have erections. Therapies for remediation of erectile dysfunction have improved since the recommendations for “stuffing” the penis into the vagina that were still popular in the 1970s.

The penile prosthesis was the first reliable method developed to ensure adequate erection.80 Prostheses are available in both semirigid and malleable forms. These devices, however, are the most invasive treatment for erectile dysfunction and have been found to have a high rate of complications in men with SCIs. Complications include (1) erosion of the device due to a lack of sensation and (2) infections due to the patients' predisposition to infection. Researchers in one report80 noted that 25% of the men with SCI that they studied required removal of the device due to erosion or infection.

Another type of device to improve erectile function in men with SCIs is the vacuum erection device.81 Negative pressure produced by either manual pumping or battery operation is used to cause engorgement of the penile corpora. The erection is then maintained through the application of a constricting ring at the base of the penis. Although these devices have the advantage of being noninvasive, the resultant erection is not as aesthetically pleasing as that produced by other means. The penis may appear discolored due to the engorgement, surface blood vessels may bulge, the size of the penis may be wider than with a regular erection, and the penis tends to pivot at the junction where the constricting ring lies. The device also must not be used for more than 30 minutes, because the lack of blood flow can result in necrosis of the penile skin and other injuries. Furthermore, use of the device in conjunction with anticoagulation medication is contraindicated.81 As an alternative to the use of the pump, those men who are able to achieve a reflex erection may use the ring to maintain an erection. Men who use this method should observe the same precautions given for the use of the pump and the ring.

Injections of vasoactive drugs into the penis have also been used as a means to improve erectile function.82,83 This method is cosmetically superior to the use of a vacuum pump; however, some men dislike the idea of placing a needle in their penis, and this method certainly decreases spontaneity. Various medications, including phenoxybenzamine, phentolamine, papaverine, and prostaglandin E1, have been utilized to improve erectile function. Currently, prostaglandin E1 remains the only medication that is approved by the Food and Drug Administration (FDA) for this purpose. The documented side effects to the use of injection to achieve erections in men with SCIs include dysesthesias, priapism, seizures, and intracorporeal fibrosis.65,82,83

A new means to improve erectile function in men with SCIs occurred with the development and FDA approval of the drug sildenafil (Viagra).84 The drug has been shown to be efficacious in men with varying types of erectile dysfunction, including those resulting from SCIs.79 Adverse events occurred in 6% to 18 % of men and most commonly included headache, flushing, and dyspepsia.84 Use of the drug in men with SCIs has shown that it is generally safe and effective.66,85

Early after the FDA approval of sildenafil, concerns emerged, including cardiovascular dysfunction (which was temporally associated with use of the drug), priapism, and ocular effects.86 More recently in a randomized crossover trial using exercise echocardiography, it has been shown that, even in men with stable coronary artery disease, there were no effects of sildenafil on symptoms, exercise duration, presence or extent of exercise-induced ischemia.87 Due to potential drug interactions, the use of nitrates, either on a regular basis or intermittently, is an absolute contraindication to the use of the drug.86 Sildenafil is also contraindicated in men with a history of retinitis pigmentosa. Overall, the relatively young age of men with SCIs and their overall good health makes them generally good candidates for the drug. Furthermore, premarket studies are being conducted on several other oral medications designed to remedy erectile dysfunction.

In our opinion, remediation of sexual dysfunction in women with SCI should focus on the improvement of the physiologic changes brought on by SCI and in improving the subjective aspects of sexual response. We believe treatments should focus on improving the ability of women with SCI to become aroused and to achieve orgasm. A recent double-blind, placebo-controlled study of women with SCI indicated that sildenafil may improve female sexual arousal.88 Another recent study89 showed a beneficial effect of false positive feedback in improving subjective sexual arousal and genital arousal as measured by vaginal pulse amplitude. We recommend that future studies should focus on improving sexual responsiveness and satisfaction for women with SCIs and that similar studies should be performed for men with SCIs.


The impact of SCI on procreation is more severe for men than for women. The majority of men with SCI have poor sperm quality and ejaculatory dysfunction, making reproduction via sexual intercourse virtually impossible. Researchers have examined the reasons for this decline in sperm quality. The inability to control scrotal temperature was thought to contribute to the poor quality of sperm in men with SCIs64; however, this theory has recently been tested and disproved.90 Endocrine profiles and their relationship to semen quality also have been studied. Mean levels of gonadotropins were lower in men with SCI compared with men without SCI; moreover, the frequency of abnormal endocrine profliles was greater in men with SCI compared with men without SCI.91 In men with SCI, no semen parameter correlated with any hormone profile except in men with SCI who had abnormal follicle-stimulating hormone levels. All these men were azoospermic.91 The researchers felt that these abnormalities were probably not the only reason for poor sperm quality.

The seminal plasma of men with SCIs also was tested and found to inhibit the motility of the sperm of men without SCI.92 Therefore, it appears that the seminal plasma of men with SCIs contributes to the poor sperm motility that they exhibit. Furthermore, it was found that the level of reactive oxygen species in the semen of men with SCI were negatively correlated with sperm motility.93 In addition to poor sperm motility but unrelated to the level of their SCI, the semen of men with SCI has been found to have a significantly higher percentage of dead sperm than that of men without SCI.94 Because of the finding of a high percentage of dead sperm in men with SCI, a pathological mechanism for sperm cell death may exist. The timing of sperm retrieval was thought to be another factor possibly related to sperm quality. One research group95 noted that alterations in sperm count occur within weeks of SCI. Another group's96 analysis of 638 specimens from 125 men with SCI revealed an initial decline in semen quality, which probably occurs in the first few weeks after injury; however, they found no evidence for a progressive decline in semen quality in the years after injury.

Stimulation to obtain ejaculate for insemination of a partner is now routinely performed, usually through the use of penile vibratory stimulation or electroejaculation. For most men with SCIs, the process of penile vibratory stimulation is probably superior to that of electroejaculation because it is less invasive and the semen quality obtained is better.75 In addition, penile vibratory stimulation may be performed in a home or office setting. Optimal settings for penile vibratory stimulation have been determined76 and are an amplitude of 2.5 mm and a frequency of 100 Hz. Furthermore, it has been reported that there is no difference between high- or low-amplitude vibratory stimulation in the quality of the semen obtained.77

Not all men with SCIs are able to ejaculate with vibratory stimulation, and a neurologically intact lower lumbar spinal cord may be necessary for ejaculatory success.78 For those men unable to ejaculate with vibratory stimulation, the use of electroejaculation may be a viable option.64 The downside of electroejaculation is that it must always be performed in a clinic or office setting.

Once a semen specimen is obtained, insemination of a woman may occur. This may be performed via ovulation induction in combination with intrauterine insemination,97 in-vitro fertilization, gamete intrafallopian transfer, or intracytoplasmic sperm injection.64 These methods are listed in terms of increasing cost. Despite the procedures may need to be performed, the positive prognosis for men with SCIs to father children is one of the recent advances of medicine, and ongoing research will certainly continue to improve the probability for successful outcomes.

Unlike men with SCIs, the ability of women with SCIs to conceive is thought to be unchanged. Of the 231 women studied by Charlifue et al,72 60 experienced an average of 5 months of temporary amenorrhea after injury. After this time period, the women's fertility should have returned to normal levels; however, in the same group of subjects, the pregnancy rate was 0.34 pregnancy per person compared with 1.3 pregnancies per person before injury. Furthermore, those women who had higher and more complete neurological injuries were the least likely to become pregnant compared with those with the lowest degree of neurologic impairment. This may reflect the fact that women are avoiding having children because of the overall difficulties they may have caring for themselves after an SCI.

For those women who have SCIs and are interested in birth control, little research has examined their options. Only 4 of 70 women with SCIs who took birth control pills for an undetermined period of time developed thrombophlebitis98; however, this should not be taken as an overall approval for women with SCI to use birth control pills because of the known associations between both birth control pills and SCI with thrombophlebitis. Instead, in our opinion, the individual nuances of the woman's injury and her psychosocial status must be taken into account. For instance, those women who are unsure of the status of their sexual relationships should be counseled to use condoms. If they do not have good hand function and sensation, a diaphragm is not a reasonable choice. In addition, because pelvic inflammatory disease has been associated with intrauterine device use,99 women with SCIs and those who have probable urinary tract infections should use intrauterine devices with caution. The effects of levonorgestrel implants in women with SCIs are yet to be studied; however, this may prove to be a safe, appropriate means of contraception for women with SCIs.

A discussion of management of pregnancy in the woman with SCI is beyond the scope of this article. However, the reader is referred to a recent review100 for an excellent discussion of this topic.


  • Dr Sipski provided concept/idea, and both authors provided writing.

    This work was supported in part by R 01 HD 30149 from the National Institutes of Health to Dr Sipski.

  • * Abbott Laboratories Inc, Pharmaceutical Products Div, North Chicago, IL 60064.

  • Pfizer Inc, 235 E 42nd St, New York, NY 10017.

  • Received January 19, 1999.
  • Accepted January 15, 2002.


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