Whenever possible, individuals who are at risk for pressure ulcer development or who are being treated for a pressure ulcer should be referred to a registered dietitian for assessment and intervention as necessary. 

Recommendations for prevention or treatment of a pressure ulcer would include eating a well balanced, nutritionally complete diet with appropriate calories, proteins, micronutrients (vitamins and minerals) and fluids.

Prevention studies are focusing on skin vs. muscle stimulation, dynamic vs. long-term effects and surface vs. implanted devices.  One effect under investigation is the ability of electrical stimulation to change blood flow to skin and muscle.  It is believed that by increasing regional blood flow, tissue health would be enhanced assisting with pressure ulcer prevention.

SCIRE found limited (level 4) evidence that electrical stimulation may decrease ischial pressures and increase blood flow to tissues.

Figure 2. Electrical stimulation set-up for pressure ulcer prevention

For more information, please see: Electrical Stimulation.

Teaching individuals with spinal cord injuries to shift their weight regularly while seated is a common and intuitive recommendation for pressure ulcer preventionas it is hypothesized that this relieves pressure on at risk tissues and allows for recovery of blood flow and oxygenation.  Several techniques have been suggested depending on the physical and cognitive status of the individual and include a lateral, forward lean or vertical push up.  When a manual weight shift cannot be performed the use of a power tilt feature has been recommended.

SCIRE found level 3 evidence that 1-2 minutes of pressure relief must be sustained to raise tissue oxygen to unloaded levels and level 4 evidence to support position changes to reduce pressure at the ischial sites and that forward flexion is an effective method of pressure relief.

Figure 3a: Tilt System

Figure 3b: Pressure Relief technique

Source: Copyright © 2010 by University of Washington/MSKTC

For more information, please see: Pressure Relief Practices.

Pressure ulcer prevention education programs for individuals with SCI provide knowledge and emphasize behaviours intended to reduce the risk of pressure ulcer occurrence

SCIRE found level 1 evidence that providing enhanced pressure ulcer education and structured follow-up results in a significantly longer time before recurrence of pressure ulcers especially in those individuals with no previous history of pressure ulcer surgery.

Providing enhanced pressure ulcer prevention education is effective at helping individuals with SCI gain and retain this knowledge (Level 4).

For more information, please see: Pressure Ulcer Prevention Education.

Cushion Type
 

47% of pressure ulcers occur at the ischial tuberosities or sacrum and are therefore more likely to have been initiated while seated.  See Figure 4 for areas where bones are close to the surface (called "bony prominences") and areas that are under the most pressure are at greatest risk for developing pressure ulcers.  Provision of a wheelchair cushion that relieves and redistributes pressure and reduces risk of pressure ulcer formation is an important prevention recommendation.  Historically, cushion design has been based on the belief that sitting interface pressure should be distributed evenly to reduce areas of high pressure underneath bony prominences.

SCIRE found level 3 evidence that various cushions or seating systems (e.g. dynamic versus static) are associated with potentially beneficial reduction in seating interface pressure or pressure ulcer risk factors like skin temperature. Conclusions from studies state that no one cushion is suitable for all individuals with SCI and cushion selection should be based on a combination of pressure mapping results, clinical knowledge of prescriber, individual characteristics and preference.

Lumbar Support Thickness

The addition of lumbar support to wheelchairs had a minimal effect on reducing highest seated buttock pressure at the ischial tuberosities of subjects with chronic ≥ 3 years SCI.

Figure 4. Areas where bones are close to the surface (called "bony prominences") and areas that are under the most pressure are at greatest risk for developing pressure ulcers.

Source: Copyright © 2010 by University of Washington/MSKTC

For more information, please see: Cushion Selection and Lumbar Support.

The incorporation of seating clinics into both the inpatient and outpatient rehabilitation program has been shown to reduce the incidence of pressure ulcers and readmission rates due to pressure ulcers

SCIRE found Level 2 evidence that attendance at a Specialized Seating Assessment (SSA) clinic did improve individual’s skin management abilities and that early attendance was optimal.

For more information, please see: Specialized Seating Clinics.

SCIRE found limited level 4 evidence indicated when behavioural contingencies (i.e. financial rewards) were introduced, positive behaviours resulted.  For some, participants results were sustainable once behavioural contingencies were withdrawn.

For more information, please see: Behavioural Contingencies.

Telerehabilitation Approaches to Pressure Ulcer Prevention

SCIRE found insufficient support for the use of telerehabilitation in delivery of cost effective prevention strategies and early pressure ulcer identification and treatment.

For more information, please see: Telerehabilitation.

A major challenge for recently discharged SCI consumers is continuation of specialized care in the community.In general, outpatients are followed up by family physicians or general rehabilitation facilities that do not specialize in SCI.  In addition, the concept of aging with an SCI is a relatively new phenomenon and many facilities are not equipped to adequately manage common secondary complications such as bladder and bowel issues, pressure ulcers, and osteoporosis. Also, in some jurisdictions initial rehabilitation hospital stays have become shorter in recent years. Consequently rehospitalisation following rehabilitation among persons with SCI remains high.

There are several proposed models to these dilemmas is the development of outpatient SCI-specific rehabilitation facilities intended to ease the transition between inpatient care and community reintegration. The purpose of these interventions is to prevent secondary complications from occurring such as pressure ulcers and urinary tract infections, as well as to increase knowledge of and access to community resources.

SCIRE found level 4 evidence using a non-controlled post-test design that a nurse-led outpatient clinic may be effective in preventing secondary complications of SCI. A case series design that transitional rehabilitation may increase the use of community resources and provide more opportunity to interact with family.  A targeted education program may improve knowledge and acquisition of community resources (Level 4).

Figure 1a. Phasic stretch reflex.  This picture shows reflex pathways that may underlie hyperactive phasic stretch reflexes of spasticity. 

Figure 1b.  Tonic stretch reflex arc.  This picture shows reflex pathways that may underlie hyperactive tonic stretch reflexes of spasticity.

Figure 1c.  Cutaneomuscular (flexor withdrawal) reflex.  This picture shows reflex pathways that may underlie the hyperactive cutaneomuscular reflex of spasticity.

The Ashworth Measure of Spasticity

A 5-point nominal scale using subjective clinical assessment of tone ranging from 0 – “no increases in tone” to 4 – “limb rigid in flexion or extension [abduction/adduction]”. An additional grade was added (1+) for the Modified Ashworth (MAS) to enhance sensitivity and accommodate hemiplegic patients who typically graded at the lower end of the scale.  Clinical examination is performed on a relaxed supine patient. The muscle is assessed by rating the resistance to passive range of motion (ROM) about a single joint.

The Penn Spasm Frequency Scale (PSFS)

A self report measure of the frequency or reported muscle spasms which is commonly used to quantify spasticity. The PSFS is a 2 component self-report scale developed to augment clinical ratings of spasticity and provide a more comprehensive understanding of an individual’s spasticity status. The first component is a 5 point scale assessing the frequency with which spasms occur ranging from “0 = No spasms” to “4 = Spontaneous spasms occurring more than ten times per hour”. The second component is a 3 point scale assessing the severity of spasms ranging from “1 = Mild” to “3 = Severe”. The second component is not answered if the person indicates they have no spasms in part 1.  Patients report their perceptions of spasticity with regards to frequency and severity.

Surface Electromyography (sEMG)

A noninvasive technique used to measure muscle activity (both voluntary and involuntary) in individuals with neuromuscular diseases  Surface electrodes are placed on the skin overlying the muscles of interest.  Patients are instructed to voluntarily activate lower limb muscles to provide either maximal muscle strength or to perform simple movements (e.g. ankle flexion/extension).  

For more information, please see: Ashworth Measure of Spasticity, Penn Spasm Frequency Scale (PSFS), Surface Electromyography (sEMG).

Typical clinical approaches to spasticity include rhythmic passive movements, muscle stretch, active exercise interventions, electrical stimulation, and ongoing (TENS) transcutaneous electrical nerve stimulation.

In addition different resaerchers have examined other treatment options including: penile vibration and rectal probe stimulation, other forms of afferent stimulation which may not be appropriate for routine clinical practice.

Individuals with severe spasticity may chose to undergo more invase surgical options such as spinal cord stimulation and dorsal longitudinal T-myelotomy.

Self-stretching, regular physiotherapy and physical activities affect spasticity and should be considered as a therapeutic approach prior to antispastic medication and surgical procedures. Therapies based on physical interventions are advantageous as they generally have fewer related adverse events although they also typically have short-lasting effects.

Hydrotherapy and Stretching

Short-term reduction in spasticity may result from hydrotherapy (Level 2), rhythmic, passive movements and externally applied forces or passive muscle stretch (Level 4).

There is no evidence describing the length and time course of the treatment effect related to spasticity for hydrotherapy. 

FES-Assisted Walking

SCIRE foundlevel 4 evidence that a program of FES-assisted walking acts to reduce ankle spasticity in the short-term (i.e., 24 hours).  There is no evidence describing the length and time course of the treatment effect related to spasticity for FES-assisted walking. 

Surface Muscle Stimulation

Single treatment of surface muscle stimulation reduces local muscle spasticity with agonist stimulation more effective than stimulation to the antagonist (Level 2).  There is conflicting evidence for how long the effects of a single treatment of electrical stimulation on muscle spasticity persist, although they appear to be relatively short lasting (i.e., 6 hours).  Based on a single pre-post study, there is no evidence that a long-term program of muscle stimulation has an effect on reducing muscle spasticity and may even increase local muscle spasticity.

Transcutaneous Electrical Nerve Stimulation

TENS, is focused on stimulating large, low threshold afferent nerves so as to alter motor-neuron excitability and thereby reduce spasticity.

SCIRE foundlevel 1 evidence from a single RCT that an ongoing program of TENS acts to reduce spasticity as demonstrated by clinical and electrophysiological measures for up to 24 hours.  A single treatment of TENS acts to reduce spasticity but to a lesser degree than that seen with ongoing programs of TENS. This evidence is muted somewhat by conflicting results with a null result (level 2) compared with 2 positive results (level 4).

Hippotherapy

Physical, occupational and speech therapists use hippotherapy, which uses the movement of the horse, for clients who have movement dysfunction. There is level 2 evidence from a single study supported by level 4 evidence from another studythat hippotherapy may reduce lower limb muscle spasticity immediately following an individual session.

Figure 1. Hippotherapy may result in short-term reductions in spasticity.

Neurofacilitation Techniques and Baclofen

SCIRE found limited level 1 evidence that a combination of a 6 week course of neural facilitation techniques (Bobath, Rood and Brunnstrom approaches) and Baclofen may reduce lower limb muscle spasticity with a concomitant increase in ADL independence. However, the results of this study should be assessed with caution, since the positive effects may be due to baclofen alone.

For more information, please see: Passive Movement or Stretching, Active Movement, Direct Muscle Electrical Stimulation and Various Forms of Afferent Stimulation.

Summary - American Spinal Injury Association: International Standards for Neurological Classification of Spinal Cord Injury (ASIA)

Practicality

Interpretability

The AIS scores are clearly defined and understood by most clinicians.  The AIS (5 point ordinal scale) classifies individuals from “A” (complete SCI) to “E” (normal sensory and motor function).  Preservation of function in the sacral segments (S4-S5) is key for determining the AIS.

Acceptability

The assessment is generally well tolerated although sensory testing can be problem with severe hypersensitivity and testing for voluntary anal contraction can result in the stimulation of a bowel movement.

Feasibility

Takes approximately 20 minutes to conduct/score. Training is mandatory and no specialized equipment is required.

Summary

Table 1.  ASIA Psychometric Summary:

For more information, please see: American Spinal Injury Association: International Standards for Neurological Classification of Spinal Cord Injury.

UMN bowel syndrome, or hyperreflexic bowel, is characterized by increased colonic wall and anal tone.Voluntary (cortical) control of the external anal sphincter is disrupted while the sphincter remains tight, thereby promoting retention of stool.  However, the nerve connections between the spinal cord below the level of the lesion and the colon remain intact; therefore, there is preserved reflex coordination and stool propulsion. The UMN bowel syndrome is typically associated with constipation and fecal retention at least in part due to external anal sphincter activity.  Stool evacuation in these individuals occurs by means of reflex activity caused by a stimulus introduced into the rectum, such as an irritant suppository or digital stimulation.

LMN bowel syndrome, or areflexic bowel, is characterized by the loss of centrally-mediated (spinal cord) peristalsis and slow stool propulsion.  A segmental colonic peristalsis occurs only due to the activity of the intrinsic myenteric plexus, resulting in the production of drier and round- shaped stool.  LMN bowel syndrome is commonly associated with constipation and a significant risk of incontinence due to the atonic external anal sphincter and lack of control over the levator ani muscle that causes the lumen of the rectum to open.

Causes and symptoms of bowel dysfunction are shown in Figure 2.  Completeness of Injury also has a significant impact on bowel function in individuals with SCI.  Those with an incomplete injury may retain the sensation of rectal fullness and ability to evacuate bowels so no specific bowel program may be required.

Figure 2.Causes and symptoms of bowel dysfunction.

Physical character of stool is the pivotal variable that can shift the balance in either direction.  Small, hard stool shifts the fulcrum to the left and more pressure is required to evacuate.  Soft, bulky stool causes the fulcrum to shift the opposite way.

Figure 3. Balance of forces favoring continence or bowel evacuation.  Physical character of stool is the pivotal variable that can shift the balance in either direction.  Small, hard stool shifts the fulcrum to the left and more pressure is required to evacuate.  Soft, bulky stool causes the fulcrum to shift the opposite way.

The Consortium for Spinal Cord Medicine developed guidelines for neurogenic bowel management.  A comprehensive evaluation of bowel function, impairment, and possible problems is recommended at the onset of SCI and at least once annually.  The evaluation may include a patient history, physical exam, an assessment of the ability of the individual or his caregiver to perform procedures safely and effectively, as well as of the bowel program design, assistive techniques/devices used, and the patient’s diet. Bowel programs should be initiated during acute care and continued throughout life, unless full recovery of bowel function returns.  Differences in bowel programs for reflexic and areflexic bowels include type of rectal stimulant, consistency of stool, and frequency of bowel care.

Improving the movement of stool through the GI tract is the most important part of any bowel management protocol following SCI.  An array of interventions, as components of a bowel routine, is recommended for the management of neurogenic bowel following SCI. These include dietary recommendations, anorectal/perianal stimulation, timing the performance of the bowel routine with food intake (thus taking advantage of gastro-colonic and recto-colonic reflexes), and a variety of pharmacological agents.

The step-wise management recommended for fecal impaction is first manual evacuation, then if not successful, oral stimulants, and finally oil retention enemas. To minimize the development of hemorrhoids, oral agents (to maintain soft-formed stool), minimize straining during bowel efforts, and minimal physical trauma during anal stimulation are recommended. Once hemorrhoids have developed, topical anti-inflammatory creams or suppositories are suggested as early treatment.

For more information, please see: Multi-Faceted Bowel Management Program.

Soluble dietary fibres mix with water in the intestine to form a gel-like substance, which acts as a trap to collect certain body wastes and then move them out of the body. Insoluble fibers absorb and hold water, producing uniform stool and helping to push content of the gut through the digestive system quickly. Insoluble fibers promote regularity and treat constipation.

The Consortium for Spinal Cord Medicine recommends an initial diet with no less than 15 grams of fiber daily. The most common source of dietary fiber is bran.  It is not recommended to place individuals with SCI on high fiber diets.

SCIRE found limited (level 4) evidence that indicates high fiber diets may increase colonic transit time.

For more information, please see: Dietary Fibre.

SCIRE found limited (level 4) evidence that digital rectal stimulation increases motility in the left colon. This involves inserting finger into rectum, rotating finger slowly for 15-30 seconds and then removing (may be repeated twice at 5 minute intervals, if needed). Figure 4 shows digital rectal stimulation.

Figure 4. Digital rectal stimulation.  From Memorial University of Newfoundland (2010).

The above flash video provides directions for self digital rectal stimulation.

"Graphic reproduced with permission of SCI-U (Go to
http://www.spinalcordconnections.ca/Spotlight/Spotlight-Content-1.aspx to
see eLearning modules about SCI)

Sacral Anterior Root Stimulation

There is moderate (level 2) evidence that supports the use of sacral anterior root stimulation to reduce severe constipation in complete injuries. Figure 5 shows sacral anterior root stimulation.

Figure 5. Sacral anterior root stimulation organization where an implant sends electrical signals through electrodes to the nerves that lead to the bladder and bowel. The user controls the implant with the external control box. This is about the size of a personal stereo/CD player. 

Sacral Anterior Root Stimulator" web page for the case studies, from where it was used:
Duke of Cornwall Spinal Treatment Centre.  (2009).  Sacral Anterior Root Stimulator.  Retrieved from http://www.spinalinjurycentre.org.uk/information/006.asp?UType=1&CType=1

Electrical Stimulation of the Abdominal Wall Muscles

There is strong (level 1) evidence that electrical stimulation of the abdominal wall muscles can improve bowel management for individuals with tetraplegia.  Figure 6 shows electrode placement for anterior electrical stimulation.

Figure 6. Schematic showing electrode placement for anterior electrical stimulation

Pulse water irrigation consists of supplying intermittent, rapid pulses of warm water into the rectum to break up stool impactions and to stimulate peristalsis. The Peristeen Anal Irrigation system consists of a rectal balloon catheter, a manual pump, and a water container. The catheter is inserted into the rectum and the balloon inflated to hold the catheter in place while a tap water enema is administered with the manual pump.

SCIRE found limited (level 4) evidence that supports using pulsed water irrigation (intermittent rapid pulses) to remove stool in individuals with SCI. 

There is strong (level 1) evidence that supports the use of transanal irrigation (Peristeen Anal Irrigation system) over conservative bowel treatment.

For more information, please see: Irrigation Techniques.

The procedure consists of re-implanting the appendix into the cecum and bringing the other end to the abdominal wall, thus forming an appendicostomy. Consequently, a catheter can be introduced to the patient through the stoma and an enema administered.

SCIRE found limited (level 4) evidence that the Malone Antegrade Continence Enema and Enema Continence Catheter successfully treat the neurogenic bowel.   Figure 7 shows the Malone antegrade continence enema procedure.

Figure 7. The Malone antegrade continence enema procedure provides a catheterizable channel through which antegrade colonic washout can be performed. (Reprinted with permission from Malone PSJ. Malone procedure for antegrade continence enemas. In: Spitz L, and Coran AG, eds. Rob & Smith’s Operative Surgery: Pediatric Surgery. 5th ed. London: Chapman & Hall Medical; 1995:459–467.)

For more information, please see: Malone Antegrade Continence Enema and Enema Continence Catheter.

There is limited (level 4) evidence that colostomy reduces the number of hours spent on bowel care and simplifies bowel care routines.    Figure 8 shows a colostomy.

Figure 8. A colostomy creates an opening on the abdomen (stoma) for the drainage of feces from the large intestine.  Colostomies are usually performed after the diseased colon has been removed.  The proximal end of the healthy colon is then brought out to the skin of the abdominal wall, where it is sutured in place. An adhesive drainage bag is placed around the opening. The abdominal incision is then closed.  From Medical Illustration© 2010 Nucleus Medical Media, Inc. 
 

For more information, please see: Colostomy.

Figure 10. Pathways for the control of urinary function.

Detrusor Overactivity Associated with Sphincter Dysynergia (DESD)

This type of dysfunction tends to be seen in those with injuries of the spinal cord affecting the upper motor neurons (i.e. often in people with L1 spinal level lesions or above.) In these cases, the lack of coordination of the sphincter and the detrusor is caused by the spinal cord lesion not allowing coordination by the pons. Both the detrusor and the sphincter are overactive due to lack of control and descending inhibition from the pons and cortex, and both sphincter and detrusor contract reflexively when stretched. The detrusor becomes small capacity, reflexively contracting at small volumes, and contracting against an overactive sphincter, causing high pressures in the bladder. This leads to incontinence (when the detrusor contracts hard enough to overcome the sphincter contraction), incomplete emptying (due to the sphincter co-contraction), and reflux (due to the high bladder pressures) with resultant recurrent bladder infections, stones, hydronephrosis, pyelonephritis, and renal failure.

Detrusor Areflexia

Flaccid bladderresults from injury to the sacral cord or cauda equina giving a lower motor neuron lesion and evidenced by areflexic detrusor.  This loss of detrusor muscle tone prevents bladder emptying and leads to bladder wall damage from over-filling, urine reflux and an increase in infection risk due to stasis. The sphincter tone also tends to be flaccid, at least the external sphincter, causing incontinence, especially with maneuvers that increase intraabdominal pressure (so-called “Valsalva” maneuvers). These maneuvers include sneezing, coughing, but more importantly for the SCI individual, straining during transfers. Internal sphincter tone may be intact due to the higher origin of the sympathetic innervation, thus complete emptying, even with externally applied suprapubic pressure, may be difficult.  Compared to DESD, patients with detrusor areflexia comprise a much smaller proportion of a SCI practice and there is very little literature examining the effectiveness of interventions in which these patients comprise a significant proportion of the subject pool. Therefore, in the present review the focus is on the literature addressing DESD therapy. In some cases, individual papers may include persons with detrusor areflexia and individual treatments or management methods may still be appropriate for and applied to those with an areflexic bladder.

The neurological physical examination should focus on the abdomen, external genitalia, and perineal skin.  The sensory exam should focus on determining the level of injury in patients with SCI.  The motor examination helps to establish the level of injury and degree of completeness in patients with SCI.  Upper tract tests which evaluate renal anatomy include abdominal x-ray, intravenous peylogram and renal ultrasound.  For more detailed imaging, an abdominal computed tomography can be used.  For evaluation of 24 – hour renal function include a 24 –hour urine creatinine clearance and quantitative renal scan.  Tests which evaluate the lower tracts include cystogram, cystoscopy and urodynamics. 

Urodynamics is defined as the study of normal and abnormal factors in the storage, transport and emptying of urine from the bladder and urethra by an appropriate method.  The water fill urodynamic study has a filling phase, where water is being infused into the bladder.  Bladder sensation, bladder capacity, bladder wall compliance and bladder stability can be evaluated.  In the voiding phase (when a person told to void, or person with neurogenic bladder has an uninhibited contraction and voiding begins) evaluate leak point pressure, maximum voiding pressure, urethral sphincter activity, flow rate, voided value and PVR.  Initial testing is often done 3 -6 moths post injury or whenever bladder comes out of spinal shock. 

Figure 11.Water fill urodynamic set-up.  Simultaneous monitoring of various urodynamic parameters is shown.  Intravesical pressure minus intrabdominal pressure will produce the detrusor pressure (P_det). (A) Intravesical pressure (P_ves). (B) Urethral sphincter pressure (P_ur). (C) Urethral sphincter electromyography. (D) Intraabdominal pressure (p_abd).

Figure 12.  Anatomical classification of the neurogenic bladder

Figure 12.  Schematic representation of various voiding patterns. (A). Normal.  (B). Uninhibited contractions occur with filling.  The sphincter is attempting to inhibit contractions.  Patient has a normal voiding phase.   (C). No bladder contractions.  Rises in bladder pressure are due to rises in abdominal pressure (D).  Uninhibited contractions occur with simultaneous sphincter contractions (i.e.detrusor sphincter dysnergia). (P_abd, intrabdominal pressure; P_ur urethral sphincter pressure; P_ves, intravesical pressure).

Figure 13a. Appearance of normal urodynamic study.  Cytometrogram is shown. Bladder filling is sensed at approximately 200 ml.  The external urethral sphincter is then activated to maintain continence.  At bladder capacity (400 – 500 ml) when bladder voiding is consciously initiated the bladder contracts generating intravesical pressures of 40 – 80 cm H₂0 and the external sphincter relaxes in a coordinated fashion to allow for complete bladder emptying.

Figure 13b. Urodynamic study characteristic of detrusor hypereflexia with sphincter dyssnergia.  Bladder contraction occurs at low bladder volumes.  The urethral sphincter contract as well instead of relaxing during bladder contraction, resulting in extremely high intravesical pressures (greater than 100 cm H₂0) and incomplete bladder emptying.

Figure 13c. Urodynamic study characteristic of detrusor and urethral sphincter reflexia.  Minimal or no bladder contractions are generated, even with bladder filling to high bladder volumes (greater than 500 ml.)  There is minimal urethral sphincter activity during bladder filling.

Table 2. Bladder Dysfunction based on Lesion Location

A.  Anticholinergic Therapy for SCI-Related Detrusor Hyperactivity

The body of the detrusor is smooth muscle that contains muscarinic receptors that are triggered by acetylcholine to cause contraction of the muscle. To relax the detrusor and allow it to fill with higher volumes under lower pressure, anticholinergics may be used.

Propiverine

Propiverine has both anticholinergic and calcium channel blocking properties thus decreases involuntary smooth muscle contractions. SCIRE found 15mg tid administration of propiverine over 2 weeks yielded significant improvement of SCI detrusor hyperreflexia represented by increased maximal cystometric bladder capacity.  

Oxybutynin

Oxybutynin is an anticholinergic agent used extensively clinically to treat overactive bladder, yet few studies have been performed on the neurogenic population with this medication.  Newer versions of oxybutynin in longer acting forms have sparked renewed interest in this medication with the hopes to decrease side effects seen with the short acting oxybutynin.  

Controlled-release oxybutynin was efficacious for SCI individuals with detrusor hyperreflexia as reflected by significantly increased bladder volume with decreased mean number of voids per 24 hours (Level 4).  However, post-void residual volumes, nocturia and weekly incontinence episodes did not change significantly.  Although oxybutynin is commonly chosen to treat overactive bladder, it is accompanied by annoying side effects such as dry mouth. 

Tolterodine

A newer anticholinergic, tolterodine, causes less dry mouth and has also been shown to be efficacious for the treatment of neurogenic bladder dysfunction.  Tolterodine has been shown to be significantly better at increasing intermittent catheterization (IC) volumes (p<0.0005) and reducing incontinence (p<0.001) but was similar in its effects on cystometric bladder capacity when compared to placebo.  

Trospium Chloride

Trospium chloride is an anticholinergic medication that is reported not to cross the blood-brain barrier.  Highly significant (p<0.001) responses were found in favour of trospium chloride vs placebo for increased  bladder capacity and compliance, and decreased bladder pressure with low side effects and no effect on flow rate and residual urine volumes. SCIRE found that tolterodine improved reflex volumes, cystometric capacity, and maximum detrusor pressures.

For more information, please see: Anticholinergic Therapy.

B.   Muscle Deinnervation Therapy for SCI-Related Detrusor Hyperactivity

Botulinum Toxin

Botulinum toxin is a chemo-denervation agent that blocks the presynaptic release of acetylcholine when injected into the muscle. A promising emerging use is for neurogenic detrusor overactivity treatment in individuals with SCI. The advantage of botulinum toxin over systemic drug administration of medications such as anti-cholinergics is the treatment of discrete portions of the dysfunctional voiding process. Application of botulinum toxin focally to the detrusor directs the drug to the area of need and avoids systemic side effects.

SCIRE found significant decrease in incontinence and a significant drop in maximum detrusor pressure post botulinum toxin detrusor wall injection.

A different form of botulinum toxin A, Dysport, was found to improve continence, cystometric capacity, and decrease pressure.

For more information, please see:Toxin Therapy.

C.   Decreased Sensory Input – Detrusor Analgesics

Capsaicin

The use of capsaicin (CAP), a vanilloid, as a topical temporary analgesic is not uncommon as evidenced by over-the-counter ointments available for purchase in local pharmacies.  Localized and reversible antinociception by capsaicin is a result of induced C-fibre conduction and subsequent neuropeptide release inactivation.  Although C-fibers are not involved in normal voiding, neuroplastic changes to C-fiber bladder afferent growth account for injury emergent C-fiber mediated voiding reflex (i.e., spinal detrusor hyperreflexia). 

SCIRE found strong (level 1) evidence in support of the ability of CAP to improve bladder function (decrease frequency and leakages) by increasing bladder capacity.  However, there was a significant side effect of causing autonomic dysreflexia in a small number of patients following CAP.

Resiniferatoxin

Resiniferatoxin (RTX) is another vanilloid which has been studied for its similar beneficial effects, with less irritation to the bladder and thus better tolerated.  By chemically decreasing C-fiber bladder afferent influence with intravesical vanilloids (i.e., CAP, RTX) bladder contractility is decreased and bladder capacity is increased.  RTX was similarly effective in increasing bladder capacity when compared to CAP.   

SCIRE found RTX was responsible for significantly increased volume of first involuntary detrusor contraction, maximum cystometric capacity, decreased urinary frequency (p=0.01) and incontinence (p=0.03) with similar side effects as compared to placebo.

Nociception/orphanin phenylalanine glutamine (N/OFG)

Nociception/orphanin phenylalanine glutamine (N/OFG) is a heptadecapeptide that acts on sensory innvervation of the lower urinary tract in a similar fashion to CAP and RTX. It activates the G protein coupled receptor nociceptin orphan peptide and thus has an inhibitory effect on the micturition reflex in the rat.  The authors conclude that this inhibition of the micturition reflex supports nociceptin orphan peptide receptor agonists as a possible new treatment for neurogenic bladders of SCI patients.

For more information, please see: Toxin Therapy.

Electrical Stimulation to Enhance Bladder Volumes

Electrical stimulation, most notably anterior sacral root stimulation, has been used to enhance bladder volume and induce voiding. Typically, this approach has involved concomitant dorsal sacral rhizotomy and implantation of a sacral nerve stimulator. The combined effect of this is a more compliant bladder with more storage capacity under lower pressure and triggered voiding resulting in reduced incontinence.

For more information, please see: Electrical Stimulation.

Surgical Augmentation of the Bladder to Enhance Volume

Bladder augmentation or augmentation cystoplasty is a surgical repair to the bladder typically suggested when conservative approaches such as anticholinergics with intermittent catheterization have failed to create an adequate bladder volume under low pressure for storage.

SCIRE foundlevel 4 evidence that surgical augmentation of bladder (ileocystoplasty) may result in enhanced bladder capacity under lower filling pressure and improved continence in persons with SCI who previously did not respond well to conservative approaches for overactive bladder.

Extraperitoneal (vs intraperitoneal) augmentation enterocystoplasty produces equivocal postoperative continence with easier early postoperative recovery (Level 3).

Figure 14.

Augmentation cytoplasty: a 30 cm segment of small bowel is opened and reconstructed as a U-shaped patch and then sewn into the bivalve bladder.

For more information, please see: Surgical Augmentation.

The low level of efferent sympathetic nervous activity and the loss of the reflex vasoconstriction following SCI are the two major causes of OH.  The decrease in blood pressure following the change to an upright position in individuals with SCI may be related to excessive pooling of blood in the abdominal viscera and lower extremities. This decrease is compounded by the loss of lower extremity muscle function post-SCI that is known to be important in counteracting venous pooling in the upright position. The reduced ventricular filling and emptying ultimately lead to a reduction in cardiac output, and thus, arterial pressure (provided the reductions in cardiac output are marked). Unloading of the arterial baroreceptors induces a reflexic reduction in cardiac parasympathetic (vagal) activity. As a result, tachycardia may occur, although this is usually insufficient to compensate for decreased stroke volume.  A reduction in cardiac output results and in turn, arterial blood pressure is reduced. Subsequently, pooling of blood in the lower extremities and decreased blood pressure results in reduced cerebral flow, which presents as a number of signs and symptoms.  Figure 2. shows factors which lead to orthostatic hypotension post SCI.

In addition to central causes of OH following SCI, there is also some evidence suggesting peripheral contributions. For example, upregulation of the potent vasodilator nitric oxide (NO) could potentially contribute to the orthostatic intolerance in this population. Several other factors may predispose individuals with SCI to OH, including low plasma volume, hyponatremia, and cardiovascular deconditioning due to prolonged bed-rest.

Figure 3.  Factors which lead to orthostatic hypotension post SCI

Figure 4.  Deep Vein Thrombosis:  This medical exhibit illustrates the process of clot formation in the deep veins of the leg.  From Medical Illustration© 2010 Nucleus Medical Media, Inc.

Bracing (alone) in SCI

There are several devices available for bracing the legs in persons with complete SCI to support standing and walking. SCIRE foundlimited level 4 evidence that bracing alone results in significant gains in functional ambulation for people with complete SCI.  However, this patient does not have a complete lesion and it must be noted that for people with incomplete SCI, bracing (AFO-use) alone during walking can enhance gait speed and endurance when compared with walking without an AFO.

Bracing Combined with FES in SCI

Hybrid systems combine conventional bracing with FES to activate large lower extremity muscles in the hopes of improving the gait pattern, reduce upper extremity exertion and improve trunk and hip stability.  Regarding this case, there is some indication that a combination of bracing and FES provides greater ambulatory function than either approach alone in incomplete SCI.

Figure 7a. Modular ankle-foot orthosis

Figure 7b. Knee ankle foot orthosis

For more information, please see:BracingandBracing with FES.

Depression post SCI is a function of difficulties coping with the multiple environmental, social and health-related problems that follow.

Musculoskeletal or Mechanical Pain

Musculoskeletal or mechanical pain occurs at or above the level of the lesionand is due to changes in bone, tendons or joints.  This is referred to as nociceptive pain caused by a variety of noxious stimuli to normally innervated parts of the body. Overuse of remaining functional muscles after spinal cord injury or those recruited for unaccustomed activity may be of primary importance in some patients.

Central or Neuropathic Dysesthetic Pain

"Central" dysesthesia or "deafferentation" pain is the most common type of pain experienced below the level of SCI and is generally characterized as a burning, aching and/or tingling sensation.  In many cases this dysesthetic or deafferentation pain has defied a pathophysiological explanation.  Excluding radicular pain, all other pains of paraplegia are central or deafferentation in origin.  This pain is most often perceived in a generalized manner below the level of the lesion, often as a diffuse burning type of pain.  Burning pain is reportedly most common with lesions at the lumbar levels.

One study refers to this pain as Central Dysesthetic Pain (CDP) and found dissociative sensory loss and absence of spinothalamic-anterolateral functions, with varying degrees of dorsal column function preservation present almost exclusively in incomplete SCI patients.  CDP takes weeks or months to appear and is often associated with recovery of some spinal cord function.  Paradoxically CDPis often characterized by complete loss of temperature, pinprick, and pain perception below the level of the lesion.  It rarely occurs in spinal cord Injuries with complete sensory loss or loss of both sensory and motor functions below the level of the lesion. 

Borderzone or Segmental Pain

Individuals with SCI frequently experience a band of pain and hyperalgesia at the border zone between diminished or abnormal and preserved sensation.  In the more recent literature, this segmental pain is further described as occurring at or just above the level of sensory loss in the cutaneous transition zone from the area of impaired/lost sensation to areas of normal sensation, involving at least one to three dermatomes and is often associated with spontaneous painful tingling or burning sensations in the same area.   Pain can be triggered by stroking and/or touching the skin in adjacent painful dermatomes.  Segmental pain is generally symmetrical although a partial spinal cord injury with asymmetrical neurological involvement will produce asymmetries.  This pain has also been described as "neuropathic at level pain"