Management of Chronic Spinal Cord Dysfunction

Abstract

Purpose of Review:

Both acute and chronic spinal cord disorders present multisystem management problems to the clinician. This article highlights key issues associated with chronic spinal cord dysfunction.

Recent Findings:

Advances in symptomatic management for chronic spinal cord dysfunction include use of botulinum toxin to manage detrusor hyperreflexia, pregabalin for management of neuropathic pain, and intensive locomotor training for improved walking ability in incomplete spinal cord injuries.

Summary:

The care of spinal cord dysfunction has advanced significantly over the past 2 decades. Management and treatment of neurologic and non-neurologic complications of chronic myelopathies ensure that each patient will be able to maximize their functional independence and quality of life.

INTRODUCTION

Neurologists are frequently challenged with managing chronic medical and functional deficits associated with myelopathies (Case 11-1). While acute traumatic spinal cord injury is a relatively rare disorder in the United States (estimated 300,000 survivors in 2013),1 acquired myelopathies secondary to diseases are three to four times more prevalent.2 The few existing systematic studies comparing nontraumatic myelopathies with acute traumatic spinal cord injuries have consistently noted that outcomes are more related to level and completeness of lesion and age, rather than etiology.3–6 Most clinical observations presented in this section are derived from investigations in individuals with traumatic spinal cord injuries. However, the various medical and rehabilitative concepts are reasonably generalizable to patients with all types of chronic spinal cord dysfunction. The interested reader should consult the many helpful clinical practice guidelines for management of spinal cord injuries developed by The Consortium for Spinal Cord Medicine (www.pva.org).

Case 11-1

A 45-year-old man sustained a C7 American Spinal Injury Association (ASIA) complete spinal injury (ASIA A) while snowboarding. He was stabilized at a trauma center and subsequently transferred to a rehabilitation unit. Anticoagulation was started for deep venous thrombosis prophylaxis and was discontinued at 3 months. At the conclusion of inpatient rehabilitation, his neurologic examination was notable for a spastic quadriplegia with absent sensation below C7. Functionally, he was independent in level-surface transfers, manual wheelchair mobility, and basic activities of daily living. He was placed on baclofen 20 orally mg 3 times a day with modest control of symptomatic spasticity. Four months postinjury, he developed a pulmonary embolus secondary to a venous thrombosis in his leg. He was treated with warfarin for 6 months. Five months postinjury he began to note deep, nonlocalized pain below the level of injury. Spinal cord MRI showed no evidence of cystic transformation at the site of injury. He was treated unsuccessfully with gabapentin and was subsequently switched to pregabalin with 30% pain relief. Video urodynamic study revealed detrusor hyperactivity with high-pressure contractions; renal ultrasound was normal. His wife was assisting him with his bladder management, which was clean intermittent catheterization every 5 to 6 hours and long-acting oxybutynin to prevent occasional bladder leakage. He was interested in fertility. He had used vibratory stimulation unsuccessfully for ejaculation and had a semen analysis by electroejaculation with consideration of semen cryopreservation.

Comment. This case is representative of cervical traumatic spinal cord injury and demonstrates the need for multidisciplinary medical and rehabilitation interventions. The course reflects pitfalls (pulmonary embolus), challenges (below-level of neurologic injury neuropathic pain), and successes (effective bladder continence) that characterize management of spinal cord injury.

CARDIOPULMONARY AND AUTONOMIC COMPLICATIONS

Prophylactic anticoagulation for deep venous thrombosis with low molecular weight heparin should start as soon as possible following traumatic spinal cord injury. Although the duration of prophylactic anticoagulation remains controversial, a minimum of 3 months is recommended for paralyzed patients. While one series that studied rehabilitation patients and compared traumatic spinal cord injuries with nontraumatic myelopathies found a threefold increased incidence of deep venous thrombosis in the traumatic injuries,7 it is generally accepted that the incidence of deep venous thrombosis is not increased over the general population after 3 months.

Cardiovascular issues such as arrhythmias or fluctuating blood pressures are common after acute spinal cord injury, and orthostatic hypotension and reduced cardiac reflexes occur in chronic spinal cord injury. Autonomic dysfunction also disrupts normal temperature regulation, particularly with high cervical and high thoracic injuries, due to loss of sympathetic control of temperature and sweat regulation below the level of injury. Hyperthermia, hypothermia, or poikilothermia may be observed.8

Autonomic dysreflexia may complicate acute and, less commonly, chronic spinal cord injuries at or above the level of T6.9 Autonomic dysreflexia is usually associated with complete traumatic spinal cord injury, but has been reported in inflammatory disorders,10,11 spinal cord tumors,12 or neurosurgical interventions.13 Neurologists should be aware that noxious stimuli below the level of injury can trigger an exaggerated sympathetic response. Systolic blood pressures of 250 to 300 mg Hg and diastolic blood pressures of greater than 200 mm Hg have been reported, leading to hypertensive crisis complicated by intracranial hemorrhage and seizures. It is important to recognize that patients with chronic spinal cord injury frequently have low baseline blood pressures. Thus, normotensive blood pressure readings may indicate hypertension. The source of stimulation is usually bladder distention or bowel impaction, but bladder calculi, pressure sores, occult bone fractures, visceral disturbances, or sexual activity can also be triggers. Autonomic dysreflexia may complicate medical procedures such as cystoscopy or labor and delivery. The sympathetic activation is characterized by abnormal vasomotor regulation. Dangerous hypertension is associated with spinal cord injury at T6 or above, which blocks compensatory parasympathetic vasodilatation.9 Parasympathetic activation above the level of injury may also produce bradycardia, sweating, nasal congestion, and flushing.

Management of acute attacks includes immediately sitting the patient upright to orthostatically lower blood pressure and loosening tight-fitting clothing. Identification and removal or treatment of the inciting stimulus generally resolves the situation. The bladder should be investigated for an obstructed catheter or urinary tract infection. Especially given that myelopathies are associated with chronic constipation, fecal impaction should be assessed for on rectal examination. If antihypertensive agents are needed (systolic blood pressure greater than 150 mm Hg), short-acting agents such as topical or sublingual nitrates should be considered. Check that the patient has not taken a phosphodiesterase 5 inhibitor (eg, sildenafil) within 24 to 48 hours in order to avoid excessive hypotension. Other options include sublingual nifedipine or captopril, but there are limited data supporting the efficacy or safety of any specific treatment. In more severe cases, IV hydralazine or labetalol may be necessary. Prevention of autonomic dysreflexia rests on patient education and careful management of urinary tract issues associated with the neurogenic bladder. Adrenoceptor blockers such as prazosin or terazosin may be tried for prophylactic management.9

Coronary artery disease risk factors are elevated in patients with spinal cord injury. Depending on severity and neurologic level, these individuals experience the consequences of immobility and inactivity. Risk factors for coronary artery disease are similar to able-bodied individuals, and problems such as abnormal glucose metabolism and lipid profiles are more prevalent in the spinal cord injury population.14 Not surprisingly, an increased incidence of stroke has been reported in spinal cord injury.15 Development of an appropriate nutritional and exercise program is important.14 Exercise options such as swimming, hand-crank ergometry, or body-weight–supported treadmill walking16 can be considered. Depending on the severity and level of the injury, physiologic responses will be altered, thus, exercise programs should be supervised and monitored.

Disorders involving the cervical and thoracic spinal cord may affect respiratory muscles. Impaired cough and reduced ability to mobilize secretions increase the risk of pneumonia.17 Long-term compromise of pulmonary reserve places patients with chronic spinal cord injuries at greater risk for obstructive sleep apnea, ventilatory failure, and reduced exercise tolerance.17

Genitourinary Disorders

Myelopathies often produce bladder dysfunction (neurogenic bladder). Urologic evaluation is recommended for all patients with traumatic spinal cord injuries and should be seriously considered for patients with any myelopathy and a neurogenic bladder. Bladder control is complex, requiring the coordinated function of the cerebral cortex, pontine and sacral micturition centers, and the peripheral nervous system.17 Patients with complete spinal cord injuries rarely regain volitional bladder control, however, recovery or maintenance of bladder sensory function is a good prognostic sign for voluntary voiding, particularly in younger patients.18 Similarly, in many nontraumatic myelopathies, retained bladder sensory function is a favorable prognostic sign. Older patients with vascular diseases of the spinal cord are more likely to experience significant bladder dysfunction than patients with myelopathy associated with degenerative spine disease.19 In general, neurologic control of bladder function depends on the location and completeness of the lesion, rather than the underlying pathology.

The two major functions of the bladder are storage and emptying of urine, and the principal goal of bladder management is to maintain detrusor pressure within limits that preserve upper urinary tract (kidneys) integrity, avoid infections, and maintain continence. The most effective methods for assessing lower urinary tract (bladder and urethra) function in myelopathies are a clinical history, a voiding diary documenting symptoms (eg, urgency, frequency/volume of urination, and incontinence), and a urodynamic study. Although bladder dysfunction depends on the neurologic level of injury, detrusor hyperreflexia (spastic bladder) with or without sphincter dyssynergia is likely the most common problem encountered by neurologists who treat myelopathies. Typical symptoms are urgency and frequency that may be accompanied by episodic incontinence. Cauda equina injuries or injuries to the conus medullaris may result in chronic urinary retention due to atonic bladder and, in more severe cases, overflow incontinence or leakage due to urinary sphincter incompetence.

The cornerstone of treatment is clean intermittent catheterization, which is less likely to lead to infections compared with chronic indwelling catheters.20 Bladder volumes should be kept at less than 500 mL of urine. In selected patients, clean intermittent catheterization and adjustment of fluid intake can supplement voluntary voiding. In addition to posing an increased risk of infection, indwelling catheters increase the risk of epididymitis, prostatitis, urethral stricture, and possibly bladder cancer.21 Asymptomatic bacteriuria with or without pyuria should not be treated. Antimicrobial prophylaxis and cranberry juice are not effective.22 Symptomatic urinary tract infections should be treated promptly. A recent review of urologic follow-up after spinal cord injury suggested no specific monitoring for infections other than annual urinalysis, which is recommended for neurogenic bladders associated with myelopathy of any etiology. An annual renal ultrasound to detect upper tract problems and urinary tract lithiasis is also recommended.23

Pharmacologic interventions can be guided by urodynamic assessment of bladder and sphincter physiology. In patients with detrusor hyperreflexia or instability, anticholinergic medications,24 or tricyclic antidepressants can decrease bladder tone, inhibit involuntary bladder contractions, and reduce urinary frequency. Botulinum toxin injected into bladder musculature for treatment of neurogenic detrusor overactivity decreases urinary incontinence and improves quality of life in patients with multiple sclerosis (MS) and other causes of spinal cord dysfunction.25 In cauda equina lesions with reduced bladder or sphincter tone, cholinergic medications may facilitate bladder emptying, while α₁-adrenergic agents such as ephedrine promote bladder storage. Older men with myelopathies may have urinary tract outflow obstruction due to prostatic hypertrophy. α₁-Adrenergic receptor blockers reduce sphincter tone and promote bladder emptying. In detrusor sphincter dyssynergia, which is more typically seen in complete traumatic spinal cord injury rather than incomplete myelopathies, the bladder contracts against a closed sphincter, which may produce elevated intravesicular pressure with vesicoureteral reflux that can threaten upper urinary tract integrity (Figure 11-126). For patients with neurogenic bladders in whom satisfactory management cannot be achieved through medications or catheters, urologic surgical procedures or neural stimulation devices may be options.

Figure 11-1.

Detrusor pressure with simultaneous EMG of sphincter during slow infusion of fluid into bladder. In the healthy adult patient (upper graph), note the change in sphincter tone with starting and stopping of normal voluntary voiding. In the paraplegic patient (lower graph), there is abnormal increase in sphincter pressure with reflex voiding resulting in elevated detrusor pressures.

Modified from Fowler CJ, et al, Nat Rev Neurosci.26 © 2008 The Authors. www.nature.com/nrn/journal/v9/n6/abs/nrn2401.html.

Sexual dysfunction with spinal cord injury is an important factor affecting quality of life. An open and frank discussion regarding sexual issues is recommended.27 In men, libido, potency, and fertility are reduced, and a variety of treatment options are available including medications (eg, phosphodiesterase 5 inhibitors) and mechanical devices to achieve erections and ejaculation. In women with spinal cord dysfunction, libido and sexual response may be altered, but ovarian function and fertility are usually retained.28 The effects of skin and bowel/bladder care and medical comorbidities on sexual activity should be considered.

GASTROINTESTINAL COMPLICATIONS

While bowel dysfunction is common with myelopathies, the optimal management is uncertain. The majority of myelopathies in neurologic practice are incomplete injuries occurring above the level of the conus medullaris. Such lesions produce an upper motor neuron bowel syndrome characterized by increased colonic wall and anal sphincter tone, with a tendency toward constipation and fecal retention. Fortunately, most of these patients retain the ability to maintain continence and bowel evacuation. Conus medullaris or cauda equina lesions will also be marked by constipation, but sphincter tone may be compromised and bowel incontinence may be problematic. In either situation, the basic approach should be to promote regular and predictable bowel evacuation. For individuals who cannot be satisfactorily managed with diet alone, oral medications should be used judiciously. A bowel routine should be established with a convenient time for evacuation using a stimulant rectal suppository or digital stimulation. Optimal management for spinal cord injury–related constipation and fecal incontinence remains undetermined.29

Musculoskeletal Disorders

Myelopathies are usually characterized by impaired mobility. Muscle and connective tissue maintained in a shortened position for as little as 1 week will contract and stiffen. After several weeks, loose periarticular tissue enveloping a joint will reorganize, leading to reduced motion and function. The essential interventions to prevent development of contractures are unknown. A combination of positioning, range-of-motion exercises, and splinting has been recommended; however, stretching and ranging of joints for periods of up to 7 months have not demonstrated clinically meaningful short-term or long-term effects.30 Resting night splints or removable casting are frequently used to prevent upper extremity and ankle plantar flexion contractures, but their efficacy is also not well documented. While certain contractures may facilitate function, others will interfere with maintenance of hygiene or wheelchair seating and positioning. Surgical intervention may be required.

Osteoporosis due to immobility affects bones below the level of injury. Sclerostin, produced by osteocytes, appears to be a key mediator of bone loss immediately after paralysis and is a biomarker of osteoporosis in chronic spinal cord injury.31 Corticosteroids, which are used to treat some myelopathies, can contribute to osteoporosis. Patients receiving glucocorticoids should receive calcium (800 to 1200 mg/d) and vitamin D supplementation (more than 800 IU/d).32 Osteoporosis medications, such as bisphosphonates, slow bone loss, but do not seem to stimulate new bone formation. Effective treatments for increasing bone density include weight bearing, functional electrical stimulation, and vibration therapy.31

Heterotopic ossification refers to deposition of bone within soft tissue around peripheral joints. Large joints below the level of injury such as the hip are affected. Heterotopic ossification occurs in up to 50% of patients with traumatic spinal cord injury,33 but is much less common in nontraumatic myelopathies.34 Pain and decreased range of motion often precede the appearance of calcification. Triple-phase bone scan is the best diagnostic test. Early administration of indomethacin can prevent heterotopic ossification, and bisphosphonates may stop progression.33 Surgery may restore functional range of movement, but ossification is likely to recur.

Repetitive overuse of the arms for crutches or wheelchairs may lead to various injuries. Rotator cuff and other tendon injuries, compression neuropathies, bursitis, and osteoarthritis are commonly seen in late spinal cord injuries. Proper techniques for wheelchair transfers and specific exercise programs to minimize injuries and preserve joint function can be helpful. The prescription of power or power-assisted wheelchairs may postpone or prevent overuse injuries.35

PRESSURE ULCERS

Pressure sores occur when external pressure on skin and subcutaneous tissue is combined with distortion or shear. Patients with myelopathies and preserved sensation are less likely to develop pressure sores. Pressure on skin while in bed may reduce regional blood circulation. Relieving skin pressure over a bony prominence for 5 minutes every 2 hours will allow for adequate perfusion and prevent tissue breakdown. The best treatment for pressure ulcers is prevention. Patients at risk for ulcers need to learn techniques for pressure relief and maintenance of bowel and bladder hygiene. Transfers from bed to chair should be done with minimal shear, and pressure-relieving wheelchair cushions should be prescribed. Good perineal region hygiene is essential. Adequate nutrition must also be maintained.36

PAIN

Pain is common with both traumatic and nontraumatic spinal cord injury.37,38 Recent classifications have specifically divided spinal cord injury pain into nociceptive (pain arising from non-neural tissue injury or irritation) and neuropathic types of pain. Neuropathic pain is divided into at-level of neurologic injury pain and below-level of neurologic injury pain.38 In nontraumatic myelopathies, pain seems to be particularly common with malignant spinal cord disease. In one series of nontraumatic myelopathies, approximately 70% of patients with disorders such as vascular disease, spinal stenosis, malignant or benign tumors, and infections reported that pain was a problem in daily life.37

At-level neuropathic pain may arise in a segmental pattern from the spinal cord or roots and is typically described as burning, tingling, or pricking. Sensory deficits and allodynia or hyperalgesia occur within the pain distribution. Below-level neuropathic pain (at least three levels below normal sensation) is typically diffuse, nondermatomal, with variable intensity. In cases of incomplete injuries, allodynia and hyperalgesia may occur within the pain distribution. In traumatic spinal cord injury, late onset at-level neuropathic pain may be indicative of syrinx formation within an area of myelomalacia. In contrast, nociceptive pain (eg, musculoskeletal pain) is dull, aching, and well localized. Although neuropathic pain appears to be associated with neuronal hyperexcitability, mechanisms are poorly understood. Suggested etiologies include neuroplastic changes in the cord (eg, sprouting of primary afferents); increased levels of inflammatory mediators; changes in receptors or ion channels; and loss of inhibitory neurons within pain pathways.39

Treatments for spinal cord injury neuropathic pain are generally unsatisfactory.39 Tricyclic antidepressants, gabapentin, or mixed serotonin noradrenaline reuptake inhibitors are often recommended as first-line treatments. Opiates (including tramadol) may also provide relief. A recent large, multicentered randomized trial of pregabalin in patients with chronic below-level neuropathic spinal cord injury pain due to trauma reported improvements in duration-adjusted average change in pain, although a large proportion of patients did not achieve pain reduction of at least 30%.40 Intrathecal therapies and various neurostimulation techniques and neuroablation procedures have been tried without substantial benefit.

SPASTICITY

Approximately 65% to 78% of traumatic spinal cord injuries are associated with symptoms of spasticity.41 The relationship between spasticity and function may be complex. For example, while severe chronic spasticity can result in pain and dystonic posturing of paretic limbs, less severe spasticity may aid transfers or weight bearing. However, potential advantages may be offset by spasms that interfere with activities of daily living (eg, perineal hygiene or sleep).

Functional goals are essential for guiding treatment. Current evidence does not support routine treatment of spasticity,42 and management decisions should be individualized. Exclusion of possible exacerbating factors is an important first step in the evaluation. It is well known that common comorbidities with spinal cord injuries increase spasticity, such as infections, pressure ulcers, or other sources of noxious stimuli. Just as syrinx formation may be a source of late-onset pain after traumatic spinal cord injury, it may also cause unexplained increasing spasticity, thus, imaging of the affected area should be considered.

A variety of measures can reduce spasticity.42,43 Although its overall efficacy can be limited at a population level, physiotherapeutic approaches such as stretching and weight bearing can be beneficial in individuals.43 Oral medications are frequently used, despite limited evidence for their efficacy (Table 11-144). In addition, while studies have demonstrated reduction of clinical spasticity, less evidence exists for functional improvements,42 thus, therapeutic approaches should be chosen with careful consideration of adverse effects. Baclofen, a γ-aminobutyric acid (GABA) B receptor agonist, is the most commonly used oral medication. Tizanidine, a centrally acting α₂-adrenergic agonist, is another possibility. Both can have side effects such as drowsiness, cognitive slowing, and worsening weakness. Benzodiazepines, allosteric modulators of GABA A receptors, are an additional treatment choice. In certain patients, nocturnal use of medication can reduce spasms that interfere with sleep. Dantrolene sodium reduces calcium release from the sarcoplasmic reticulum and diffusely reduces muscle strength and, therefore, is generally reserved for individuals with more severe disability.

Table 11-1.

Oral Medications Commonly Used for Spasticity^a

Chemodenervation with injections of botulinum toxin and intrathecal delivery of baclofen via an implantable pump are two additional treatment modalities.42 Botulinum toxin is currently US Food and Drug Administration (FDA) approved as a treatment for spastic flexor muscles at the elbow, wrists, and fingers, and is likely also beneficial for spasms of the hip adductor muscles. The FDA has warned about the possibility of systemic effects from local injections, possibly related to inadvertent overdosing. Patients with refractory spasticity involving the trunk and lower extremities may be candidates for treatment with intrathecal baclofen. Intrathecal baclofen allows delivery of therapeutic, targeted doses of baclofen through a programmable pump. Such a method of delivery can increase overall efficacy while reducing side effects associated with oral administration. Although no randomized controlled trials exist, a meta-analysis of multiple case series supported intrathecal baclofen treatment.45 In nontraumatic myelopathies, a combined approach of botulinum toxin, intrathecal baclofen, and general rehabilitative measures may help to improve overall function.

PSYCHOSOCIAL ISSUES

Acute spinal cord injury is associated with increased psychological morbidity, substance abuse, and risk of suicide. Individuals with chronic spinal cord injury have an increased prevalence of depression, anxiety, and posttraumatic stress disorder, and their average life satisfaction is below that of the general population.46 However, subjective well-being after spinal cord injury is frequently better than might be expected after such a serious injury. Factors consistently associated with subjective well-being include perceived control of life, purpose in life, feelings of self-efficacy, and self-esteem. Various types of supportive psychotherapy have been tried with mixed results.46

NEUROLOGIC REHABILITATION

Rehabilitation goals, functional needs, and expectations are determined by the level and completeness of the injury (Table 11-247). While customized rehabilitation programs can be developed in a similar manner for both traumatic and nontraumatic spinal cord injury, the etiology of the injury can also be a factor. For example, a recent review suggested that infectious myelopathies (eg, epidural abscess) are associated with worse outcomes.48 In general, higher levels of injury require increased levels of assistance and achieve reduced functional independence. Injuries at the level of C5 to C8 are associated with increasingly greater levels of self-care and mobility. Injuries at or below T1 are typically associated with the ability to independently perform activities of daily living and mobility using wheelchairs. Injuries at or below L2 also have the potential for independent ambulation.

Table 11-2.

Expected Functional Recovery Following Complete Spinal Cord Injury by Spinal Level^a

A growing body of literature supports intensive locomotor training as a means of improving lower extremity function in incomplete spinal cord injury,49,50 which represents a marked departure from historical efforts that focused upon compensation using assistive devices. Animal studies over the past several decades have provided support for functional recovery after training. More recent studies in human subjects have also provided support for this approach.49,50 It is unclear, however, if particular training approaches are superior. For example, one popular method uses body-weight–supported treadmill training to facilitate task-specific rehabilitation. Recent work suggests that body-weight–supported treadmill training may not be more effective than traditional overground training.49 Thus, while strong evidence supports task-specific gait training after partial spinal cord injury, the specific approach can depend on provider and patient preferences.

FUTURE DIRECTIONS

Several promising therapeutic and rehabilitative methods exist for spinal cord injury patients. Perhaps the most promising is neuromodulation using electrical stimulation. For example, a recent report described motor improvements in patients with complete spinal cord injury after electrical stimulation coupled with rehabilitation.51 Stem cells also represent a promising treatment for spinal cord injury. A large body of preclinical literature suggests that stem cell–based therapies may improve recovery in animal models of spinal cord injury through a variety of mechanisms.52 Even while pilot translational trials using stem cells occur, a great deal of research has to be performed in order to broadly translate this to patients. Finally, brain-machine interfaces may allow the patients with the most severe spinal cord injury to control external devices using their “thoughts.”53 However, numerous challenges still exist that limit broader use of these approaches at present.

KEY POINTS

• Outcomes in nontraumatic myelopathies and acute traumatic spinal cord injuries are more related to level and completeness of lesion and age, rather than etiology.

• Autonomic dysreflexia occurs with spinal cord injury above T6. Bladder and bowel distention or bowel impaction are the most common stimuli that can trigger an unmodulated sympathetic response, leading to dangerous hypertension.

• Abnormal glucose metabolism and lipid profiles are more prevalent in the spinal cord injury population. Development of an appropriate nutritional and exercise program is important. Exercise options include swimming, hand-crank ergometry, or body-weight–supported treadmill walking.

• Clean intermittent catheterization is the cornerstone of treatment for a neurogenic bladder and is less likely to produce a urinary tract infection than an indwelling catheter. Only symptomatic infections should be treated. Prophylactic antibiotics are discouraged.

• Upper motor neuron bowel syndrome is characterized by constipation and fecal retention. With conus medullaris or cauda equina lesions, bowel incontinence may be problematic. Diet should be modified and oral medications used judiciously. Regular and predictable bowel evacuation needs to be promoted by establishing a convenient time for evacuation using a stimulant rectal suppository or digital stimulation.

• Interventions to prevent development of contractures are unknown. Positioning, range-of-motion exercises, and splinting has been recommended, but ranging of joints for up to 7 months has not demonstrated clinically meaningful short-term or long-term effects.

• Pressure sores occur when external pressure on skin and subcutaneous tissue is combined with distortion or shear. Relieving skin pressure over a bony prominence for 5 minutes every 2 hours will allow for adequate perfusion and prevent tissue breakdown.

• Pain is common in both traumatic and nontraumatic myelopathies. A recent study provided class 1 evidence for pregabalin 150 to 600 mg/d in treatment of pain due to spinal cord injury.

• Spasticity treatment should be guided by functional goals. Currently available oral medications may not be very effective and have limiting side effects. Local treatment with chemodenervation or intrathecal baclofen may be options.

• With chronic spinal cord injury there is an increased prevalence of depression, anxiety, and posttraumatic stress disorder. Average life satisfaction is below that of the general population. However, subjective well-being after spinal cord injury is frequently better than might be expected.

• Level and completeness of neurologic injury determine functional abilities. Patients with complete injuries at a C7 level have potential for independence in activities of daily living and wheelchair mobility; patients with injuries at L2 or below may ambulate independently.

• Neuromodulation, stem-cell therapy, and brain machine interface applications are promising future treatment options in the management of spinal cord injury.