The sequelae of spinal cord injury (SCI) can affect every major organ system. Nevertheless, the full impact of SCI on voiding and sexual function is underappreciated by many clinicians. Altered micturition and sexual function can significantly impact the quality of life for the patient. In addition, failure to address these issues can lead to significant morbidity and mortality. In the past, renal failure was the leading cause of death in patients with SCI. 17 With modern urologic care, this is no longer the case. What follows in this article is a comprehensive review of the physiologic alterations in bladder and sexual function after SCI and the therapeutic interventions available to clinicians.
Neurogenic Bladder Dysfunction After Spinal Cord Injury
Anatomy and Physiology of Normal Voiding
The lower urinary tract includes structures such as the bladder, internal sphincter, external sphincter, and urethra (Figure 1). The bladder (detrusor) is composed of the base (trigone), the body, and the neck. The bladder is composed of smooth muscle. The trigone is a triangular area demarcated superiorly and laterally by the ureteral orifices and inferiorly by the internal urethral orifice. The internal sphincter is also composed of smooth muscle and is located at the junction of the bladder neck and urethra. The external sphincter is striated muscle and surrounds the urethra.
Afferent input travels to the sacral (S2–S4) spinal cord through the pelvic nerve (Figure 2). Efferent, parasympathetic input to the bladder is also carried by the pelvic nerve (S2–S4). Detrusor contractions are primarily mediated by parasympathetic stimulation. In response to bladder distention, afferent fibers of the pelvic nerve are thought to initiate voiding. Experimentally, administration of acetylcholine or electrical stimulation of the predominantly parasympathetic pelvic nerve can also elicit contractions. 6,12,34,36
Sympathetic input to the bladder originates in the intermedial lateral cell column of the spinal cord (T10–L2) and travels via the hypogastric nerves (Figure 2). The sympathetic nervous system has little role in sensory function. Somatic innervation to the striated external sphincter originates in the sacral (S2–S4) spinal cord and reaches the bladder through the pudendal nerves (Figure 2).
The bladder has two primary functions: storage of urine (filling) and emptying (voiding). Sympathetic innervation promotes the storage of urine. α-Adrenergic receptors are present in both the bladder neck and proximal urethra (internal sphincter). Stimulation of these receptors leads to closure of the above structures. β-Adrenergic receptors are dispersed throughout the body of the bladder, and their role is to promote bladder relaxation. 2,18,22,47,77 Under normal circumstances the bladder has the ability to increase volume with only small changes in intravesical pressure. 27
Normal voiding requires the successful coordination of a series of events including sudden relaxation of the striated muscle of the urethra and pelvic floor, initiation of the detrusor contraction, reduction of urethral pressures mediated by relaxation of the internal and external sphincters, and widening of the bladder neck. Two critical structures involved in this process are the pontine micturition center and the sacral micturition center (Figure 2). As bladder volume increases, afferent input to the spinal cord increases until a threshold is reached. At this point reflexive voiding is initiated through contraction of the detrusor. The sacral micturition center (S2–S4) is primarily responsible for this local reflex arc.
In the neurologically intact individual, reflexive detrusor contractions are accompanied by several well-timed events mediated by the pontine micturition center. Cessation of efferent pudendal nerve firing leads to the relaxation of the striated external urinary sphincter and pelvic floor. 4 Simultaneously, sympathetic activity is suppressed, which results in the cessation of the inhibitory effects of sympathetic stimulation (see Urine Storage). The activity of both the pontine and sacral micturition centers can be suppressed by the cerebral cortex.
Physiologic Alterations After SCI
Bladder dysfunction after SCI can be classified into two syndromes: lower motor neuron (LMN) and upper motor neuron (UMN). In the LMN syndrome, injury to sacral (S2–S4) anterior horn cells or their associated axons leads to impaired motor output to the bladder and decreased or absent detrusor contractility (flaccidity). The UMN syndrome is characterized by disruption of the descending spinal pathways, which influence or modify input to the sacral micturition center. This is manifested by the loss of cortical inhibition of sacral reflex arcs.
In the immediate period after SCI the distinction between LMN and UMN bladder dysfunction can be clouded by the presence of “spinal shock.” The term “spinal shock” is used by most clinicians to describe the transient loss or depression of neural activity below an acute spinal cord lesion. It occurs in all animals after spinal cord transection, and it is thought to be caused by the sudden, abrupt interruption of all descending excitatory influences. 9 The average duration of spinal shock in humans is about 3 weeks. 9 Initial bladder flaccidity is commonly the result of this process.
Because of the issue of spinal shock and the need for aggressive fluid replacement, the patient with acute SCI is best managed with an indwelling catheter. When the patient is medically stable and daily urine output is approximately ≤2 L, consideration can be given to discontinuing the indwelling catheter and initiating a bladder program as outlined below. In most cases this is best done after transfer to an appropriate rehabilitation facility.
Upper Motor Neuron Syndrome
Bladder dysfunction in the majority of SCIs (i.e., neurologic levels above approximately S1–S2) can be categorized as UMN dysfunction. Complete patients can be expected to have involuntary, reflexive emptying with filling of the bladder. In comparison, many incomplete patients will have detrusor disinhibition (hyperreflexia) resulting in urge incontinence. Often intermittent catheterization is required until the patient’s bladder emerges from spinal shock.
With these injuries communication between the pontine (brain stem) micturition center and the sacral micturition center is disrupted. This can lead to the impaired coordination of detrusor contractions with accompanying events such as relaxation of the bladder neck, internal sphincter, and external sphincter. 43,82 The terms used to describe this phenomenon are bladder–sphincter or detrusor–sphincter dyssynergia.
The end result is that the bladder reflexively contracts against an outlet obstruction because of a closed bladder neck, internal sphincter, or external sphincter. In turn, this leads to elevated bladder pressures with micturition. Elevated pressures can lead to vesicoureteral reflux. 44,56 Voiding pressure should be less than 60 cm H2O and filling pressure should be less than 40 cm H2O. 44,59 Over time elevated detrusor pressures can predispose the SCI patient to hydronephrosis, recurrent pyelonephritis, and progressive deterioration in renal function. 59
When the SCI patient starts to exhibit the return of reflexive voiding, urodynamic studies should be performed to exclude the possibility of occult bladder–sphincter dyssynergia. If reflexive voiding fails to return by 6 months in a patient expected to have a UMN syndrome, urodynamic testing should also be performed. 39 Urodynamic testing can include the following components: cystometrography, electromyography, urethral pressure profiling, and fluoroscopy. Cystometrography provides information about pressure–volume relationships in the bladder. Electromyography, using needle or surface electrodes, clarifies the function of the external sphincter and its coordination with detrusor function. Urethral pressure profiling gives information about resistance to outflow. Fluoroscopy allows actual visualization of the bladder during voiding. An elevated voiding pressure in the face of increased sphincter electromyography activity during a detrusor contraction is diagnostic of detrusor–sphincter dyssynergia. 10,43
Treatment Strategies for the Upper Motor Neuron Bladder
The presence of bladder–sphincter dyssynergia requires intervention to prevent long-term complications such as ureteral reflux. Management strategies focus on achieving adequate drainage, low-pressure urine storage, and low-pressure voiding (Table 1). After any therapeutic intervention, follow-up testing should be performed to confirm that bladder pressures have been effectively lowered. In women and men, reflexive contractions can be suppressed with anticholinergic agents such as oxybutynin chloride and tolterodine tartrate. In some cases, anticholinergic suppression has been further augmented by the addition of tricyclic antidepressants.
If medications alone fail to work, bladder augmentation can facilitate low-pressure storage. Bladder emptying can then safely be accomplished with intermittent catheterization. Many patients with motor levels of C7 and below can be taught to perform self-catheterization. Bladder augmentation procedures with urinary diversion can sometimes facilitate intermittent catheterization via an easier to reach abdominal stoma.
In men, another option is to use pharmacologic agents such as α-blockers (i.e., prazosin, terazosin, doxazosin, tamsulosin) to reduce resistance to outflow at the α-adrenergically innervated bladder neck and internal sphincter. This can lower peak bladder pressures during contractions and allow the patient to safely use a condom (external) catheter and collection bag attached to the leg. Transurethral and transperineal injections of botulinum A toxin have also been to used to treat dyssynergia by lowering resistance to urine outflow. 19,20,57,62,63,64,67 Botulinum A toxin paralyzes muscle by blocking the release of acetylcholine at the neuromuscular junction. Disadvantages of botulinum A include expense and the fact that it has to be periodically repeated. It has also been suggested that baclofen (Lioresal), used for extremity hypertonia, can also reduce resistance to outflow by decreasing spasticity of striated pelvic floor muscles. 56
Alternatively, outlet obstruction can be reduced by transurethral sphincterotomy or placement of a urethral stent. Surgical and other invasive procedures should be viewed as irreversible, and patients should be counseled accordingly. Afterwards, reflexive voiding can then be managed by wearing a condom (external) catheter.
For SCI patients without significant dyssynergia but with detrusor hyperreflexia, resulting urge incontinence has been traditionally treated with systemic anticholinergic agents. Relatively new pharmacologic interventions include intravesical capsaicin and botulinum toxin A. Capsaicin or its potent analog resiniferatoxin works by desensitizing afferent c-fibers through the depletion of substance P as well as other mechanisms. 53 In chronic SCI the c-fibers are thought to mediate the afferent limb of the micturition reflex. These properties make capsaicin and resiniferatoxin ideally suited for the incomplete patient with urge incontinence secondary to detrusor hyperreflexia. 13,31,37,53,67 Alternatively, botulinum A toxin has been directly injected into the detrusor body, under cystoscopic guidance, with promising results. 65,66
Another increasingly popular approach to the management of UMN bladder dysfunction is the use of electric stimulation. The NeuroControl VOCARE Bladder System (NeuroControl Corp., Valley View, OH) is an implantable device currently available in the United States. First, a posterior rhizotomy of the sacral nerve roots is performed to prevent reflex incontinence. Electrodes are then attached to the anterior nerve roots. Electrical stimulation of these roots causes simultaneous contraction of the detrusor and sphincters. Because the striated-muscle external sphincter fatigues before the smooth-muscle detrusor, voiding occurs in short spurts when the sphincter intermittently relaxes. The device can also improve rectal evacuation and has been approved by the Federal Drug Administration for bowel management alone.
Long-term management with an indwelling catheter should be the choice of last resort. It can increase the risk for recurrent bladder infections and bladder stones. Nevertheless, it is sometimes indicated in the patient who lacks the manual dexterity to perform intermittent catheterization and does not have additional assistance available. This is more commonly an issue in women because the option of an external catheter is unavailable and intermittent catheterization is made more difficult by anatomic considerations. In men who will require a long-term indwelling catheter, consideration should be given to converting to a suprapubic catheter to prevent complications such as improper insertion and placement, urethral strictures and fistulas, and urethral erosions. Indwelling catheters should be replaced every 3–4 weeks.
Lower Motor Neuron Syndrome
Spinal cord injuries that present with LMN bladder dysfunction include conus medullaris and cauda equina injuries. These injuries interrupt the local reflex arc, which consists of afferent input from the detrusor, the sacral micturition center (S2–S4), and efferent input to the detrusor. The end result is detrusor areflexia (hypocontractility). Other clinical findings that accompany detrusor areflexia include saddle anesthesia, reduced anal sphincter tone, loss of voluntary sphincter control, and absence of the bulbocavernosus reflex.
Long-term bladder management of this patient population is fairly straightforward and ideally consists of intermittent, clean self-catheterization timed to regularly empty the bladder and prevent periods of overdistention (Table 1). In the hospital sterile technique is often used to minimize infection risk. If intermittent catheterization is not possible, adequate drainage can be achieved with a chronic, indwelling catheter.
Other Genitourinary Issues After Spinal Cord Injury
Recurrent UTIs are a common problem in SCI patients. The first point that should be emphasized is that all SCI patients with indwelling catheters become colonized with bacteria. This in itself does not warrant treatment unless the patient is clinically symptomatic or there is laboratory evidence of tissue invasion such as significant pyuria (≥8–10 white blood cells per high power field, by urine analysis).
The most effective method of preventing recurrent UTIs is adequate bladder drainage and emptying. 54 In addition, recurrent UTIs can be a manifestation of underlying pathology such as kidney or bladder stones, poor hygiene, and detrusor–sphincter dyssynergia with outlet obstruction. Evaluation should exclude the possibility of underlying causes. Prophylactic antibiotics should be avoided because they only serve to promote colonization with resistant organisms.
Patients with SCI are also at increased risk for renal and bladder calculi secondary to factors such as hypercalciuria, recurrent UTIs, and indwelling catheters. 8,16,45,48 Stones in the urinary tract can present with increased lower limb spasticity, recurrent UTIs, or refractory autonomic dysreflexia. Calcified stones can often be visualized with abdominal plain films, but ultrasound remains the gold standard for diagnosis. Bladder calculi can also be directly visualized with endoscopy.
In susceptible patients overdistention can lead to the potentially life-threatening condition of autonomic dysreflexia. 28 To prevent this condition, most patients are advised to perform self-catheterization every 6 hours. The goal is to keep catheterization volumes less than 500 mL in men and less than 400 mL in women to minimize the risk of urinary tract infections (UTIs) and other complications.
Long-Term Screening and Follow-up
The American Paraplegia Society has recently published guidelines for the urological evaluation of patients with SCI. 39 Annual follow-up is recommended for the first 5 to 10 years after injury. If the patient continues to do well, the follow-up interval can be reduced to every other year. Serum creatinine should be evaluated initially and then every 1 to 2 years. The upper (kidneys, ureters) and lower (bladder, urethra) urinary tracts should also be assessed initially and then annually for the first 5 to 10 years and afterwards every other year. This could be accomplished with periodic nuclear renal scans and plain abdominal radiographs. The plain films allow visualization of some calcified calculi. The renal scan is probably the most effective test with the fewest adverse effects for monitoring renal function. 24,32,33,40 A decrease of more than 20% in renal plasma flow warrants further investigation. 56
Other studies (intravenous pyelography, renal ultrasound, computerized tomography) can be used if anatomic abnormalities are suspected. Urodynamics should be performed at the same intervals as upper and lower urinary tract screening. Annual cystoscopy is recommended in those with an indwelling suprapubic or urethral catheter. As many as 5% of patients may develop squamous cell carcinoma after 5 to 10 years with an indwelling catheter. 23,29
Sexual Dysfunction After Spinal Cord Injury
Physiology of Sexual Function
There are three vascular structures in the penis: the corpus spongiosum and the paired corpora cavernosa. The corpora cavernosa lie dorsally. There are communications between the paired corpora cavernosa allowing free exchange of nutrients and pharmacologic agents. The corpus spongiosum surrounds the urethra and lies ventrally and centrally within the penis. The glans of the penis is a distal expansion of the corpus spongiosum. The corporal bodies consist of endothelium-lined sinusoidal spaces invested with smooth muscle. The three vascular structures become rigid when engorged with blood.
In the female the clitoris has vascular structures analogous to those found in the penis. The erectile bodies consist of two crura clitoridi and the glans clitoridis with overlying skin and prepuce. The glans is situated superiorly at the fused termination of the crura.
The pudendal nerves (S2–S4) relay afferent, somatic sensory fibers from the genitalia in men and women. The pelvic nerves (S2–S4) supply parasympathetic input to the genitals. Sympathetic fibers (T10–L2) exit the sympathetic chains to the hypogastric plexus and then travel in the hypogastric nerves to the genital structures.
The autonomic nervous system plays a key role in the initiation and maintenance of an erection. It is generally thought that parasympathetic stimulation initiates the erectile response. With parasympathetic input, blood flow from the internal pudendal artery increases to the penis. Lacunar spaces in the corporal structures dilate and blood is shunted into the erectile tissues. Superficial venules become compressed by expanding lacunas, thereby decreasing venous outflow. With continued parasympathetic inflow, penile rigidity is maintained throughout intercourse. 73
The analogous response in women includes engorgement and swelling of the labia and clitoris as well as lubrication of the vagina. As early as 1863, it was known that electrical stimulation of the pelvic nerve produced an erection in dogs. 21 Sympathetic stimulation can also mediate erections, but the mechanism is less clear. Accordingly, ablation of the pelvic parasympathetic system does not totally abolish erectile capability.
In contrast to erection, the major neurologic stimulus for ejaculation is the sympathetic nervous system. In men, this leads to peristaltic waves in the smooth muscle of the ampulla, seminal vesicles, and prostate. Rhythmic contractions of the bulbocavernosus, ischiocavernosus, and pelvic musculature then result in antegrade delivery of semen to the urethral meatus. The bladder neck also closes preventing retrograde ejaculation. In women, there are rhythmic contractions of the uterus, fallopian tubes, paraurethral glands, and pelvic floor musculature.
The incidence of impotence after SCI approximates 75%. 76 Incomplete patients are more likely to achieve erections sufficient for sexual intercourse than complete patients. 27 Also, patients with UMN lesions have more frequent erections than those with LMN lesions. 27 In one study 92% of SCI patients with UMN lesions were able to achieve some degree of reflexogenic erection. 11 These reflex erections may be of short duration and insufficient for intercourse.
Erections in SCI patients are classified into two categories: psychogenic and reflexogenic. Reflex erections are parasympathetically mediated through a local sacral (S2–S4) reflex arc. They tend to occur in patients with UMN lesions. LMN lesions can interrupt the sacral reflex arc and prevent erections in response to tactile stimulation. In comparison, psychogenic erections are thought to be mediated by sympathetic pathways that exit the spinal cord at T10–T12. Patients with LMN lesions who are unable to achieve reflex erections can often have psychogenic erections.
There is little available literature on sexual dysfunction in women with SCI. 3,68,69,79,80 Vaginal lubrication and engorgement occur in response to direct stimulation if the sacral reflex arc is intact and to psychogenic stimulation with LMN lesions. 69,70,72 The ability to achieve orgasm is significantly decreased in women with SCI (<50%) when compared with able-bodied controls (100%). 72 In addition, only 17% of women with complete LMN lesions achieved orgasm compared with 59% of women with other neurologic levels. The role of pharmacologic agents, such as sildenafil, are just starting to be evaluated in women with SCI. 71
Treatment of Sexual Dysfunction After Spinal Cord Injury
Providing adequate counseling and information to patients about the nature and impact of their SCI is the first step in successfully addressing sexual dysfunction. This involves concepts such as bladder emptying before sexual stimulation and the prevention of autonomic dysreflexia. Counseling can also help the patient foster a healthy body image and transition to again viewing oneself as a sexual being. 1 It is often helpful to include sexual partners in counseling sessions.
Treatment options for erectile dysfunction include surgical procedures, vacuum devices, and pharmacologic interventions. Surgical treatment involves the implantation of various prostheses. The use of such devices has declined because of new treatment alternatives and complications such as skin breakdown and foreign body infections. 30,60 They should be avoided in patients with indwelling urethral or suprapubic catheters because of increased infection risk. One indication for prosthesis implantation that is not related to sexual dysfunction is to facilitate the use of a condom catheter. 26,55
Vacuum suction devices use negative pressure to promote inflow of blood into the penis. A constriction band is then placed at the base of the penis to maintain the resulting erection. Contraindications to the use of such a device include pharmacologic anticoagulation and blood dyscrasias. 58
The intracorporeal injection of vasoactive substances can promote blood flow into the penis resulting in an erection. 78,81 Specific agents include papaverine, phentolamine, and prostaglandin E1. Prostaglandin E1 can also be administered intraurethrally. 5 Careful dose titration is essential to avoid priapism. If priapism occurs, it can be reversed with the intracorporeal injection of epinephrine. 41 Long-term side effects include penile fibrosis and scarring. 35
Sildenafil has rapidly become the treatment of choice as several studies have documented its efficacy in the SCI population. 15,25,42,61 In response to appropriate neurologic input, nitrous oxide is released in erectile tissue, leading to the production of cyclic guanosine monophosphate. Cyclic guanosine monophosphate is the chemical messenger that mediates relaxation of corporal smooth muscle leading to vascular engorgement and erection. Viagra locally increases levels of cyclic guanosine monophosphate by inhibiting Type 5 (cyclic guanosine monophosphate–specific) phosphodiesterase, the enzyme that catabolizes cyclic guanosine monophosphate. Its use is contraindicated in patients with coronary artery disease who might require the use of nitrates because it can significantly potentiate the effects of these medications.
Ovulation and fertility are generally unaffected in women with SCI. 7 In men infertility may be caused by erectile dysfunction, ejaculatory dysfunction, poor sperm quality, or a combination of all three. 52 Ejaculation is seen in less than 10% of cases. 52 The rate of ejaculation during penile–vaginal intercourse is even less clear. Spontaneous procreation without medical intervention is rare. 74
The primary factor for poor sperm quality is decreased motility. 14 The reasons for this remain unclear. Possible theories include recurrent urinary infections, type of bladder management, stasis of prostatic fluid, testicular hyperthermia, abnormal testicular histology, changes in the hypothalamic–pituitary testicular axis, sperm antibodies, and long-term use of various medications. 38,46 There is also evidence that method of bladder management might be particularly important. 50,52
The current mainstays of treatment for male infertility because of SCI are electroejaculation and vibratory stimulation. With electroejaculation, ejaculation is induced using electrical stimulation via a rectal probe. Seminal emission can be induced in nearly 100% of patients with specimens suitable for insemination in 70% to 90% of cases. 52 Vibratory stimulation is less invasive than electroejaculation and has a success rate of 81% in SCI patients with levels above T10. 51 The procedure involves applying vibratory stimulation to the penis in a standardized fashion. 75 Nearly all patients who fail vibratory stimulation will still respond to electroejaculation. 52 Once sperm is obtained, intrauterine insemination, rather than vaginal insemination, should be used. 52 If intrauterine insemination fails, in vitro fertilization with or without intracytoplasmic injection can be used.
The last three decades have elucidated many of the mechanisms responsible for the morbidity and mortality associated with bladder and sexual dysfunction after SCI. With proper management urinary continence can be safely achieved and renal deterioration can be effectively prevented. Furthermore, there are many therapeutic interventions currently available to treat SCI-related erectile dysfunction and infertility. Today, patients with SCI should be expected to resume healthy sexual relationships. This includes becoming parents if so desired. The end result is a significant improvement in the quality of life compared with that several decades ago.
- Bladder dysfunction after spinal cord injury can be classified into two main syndromes: upper motor neuron (UMN) and lower motor neuron (LMN).
- Appropriate management depends on the syndrome present: UMN vs. LMN.
- Ongoing structured surveillance is required to prevent secondary complications.
- Erectile dysfunction and diminished fertility are common in men after spinal cord injury.
- Current treatment options make it possible for virtually all individuals with spinal cord injury to resume sexual intercourse and reproduce if desired.
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