Rehabilitative Management of Complications of Spinal Cord Injury

Much has changed over the past severaldecades in the field of spinal cord injury (SCI)care. Improved acute and chronic medicalmanagement of patients with SCIs and earlierimplementation of aggressive rehabilitationhave not only resulted in a dramatic increasein patient survival but also have led to adecrease in morbidity from common medicalcomplications.

Predicting extent of neurologic recovery is crucial. The most accurate and standardized method is clinical neurologic examination using the International Standards for Neurological Classification of Spinal Cord Injury.¹

The most important factors in predicting degree of neurologic recovery are assessing the neurologic level and motor strength at 1 month after injury and whether injury is complete or incomplete. Although incomplete injuries often have favorable outcomes, more than 95% of injuries classified as complete will remain complete. Most motor recovery occurs within the first 6 months after injury, although additional recovery will occur for up to 2 years but at a slower pace.²

SCIs are associated with a number of medical complications. Certain complications are unique to the level and type of neurologic injury. Interventions have been established that manage both the complication and also restore function as part of the rehabilitation process.

COMPLICATIONS AND MANAGEMENT

Pulmonary complications. Cervical and upper thoracic SCIs are usually associated with impaired pulmonary function. Atelectasis, pneumonia, and mucous plugging are the most common causes of morbidity in patients with these types of injuries. Pneumonia remains the leading cause of death in SCI.³

Patients with high (C1 through C3) tetraplegia require mechanical ventilation because of bilateral diaphragm paralysis. Tetraplegia at C4 to C5 is associated with partial diaphragmatic and abdominal wall dysfunction, leading to paradoxical breathing. These patients have restrictive patterns of pulmonary function, including reduced chest wall and lung compliance and decreased all-lung volumes except residual volume.⁴ Increased parasympathetic activity causes bronchial constriction and increased mucus production, leading to atelectasis. The presence of a gastrostomy tube and gastroesophageal reflux are risk factors for recurrent aspiration.⁵

Management of pulmonary complications in SCI and rehabilitation of pulmonary function include pulmonary toilet through suctioning, postural drainage, chest percussion and vibration; respiratory strengthening exercises; assisted cough ("quad cough"); incentive spirometry; and ß-agonist therapy.⁶

Patients with complete C3 to C4 injuries can be successfully weaned from mechanical ventilation. This can be achieved by intermittent mandatory ventilation, pressure support ventilation, or progressive ventilator-free breathing.⁷

Glossopharyngeal breathing also is an important technique. It consists of gulping a mouthful of air into the lungs through the outward movement of the glottis. It assists both inspiratory and expiratory effort and is useful in the case of ventilator failure, allowing the patient to sustain alveolar ventilation for some time.⁶

For patients with an SCI above C3 and intact phrenic nerves, an implantable functional electrical stimulation (FES) system, which produces diaphragmatic contractions by phrenic nerve stimulation, could be a consideration. Benefits of this system include improved speech, reduction of respiratory tract infections, improved level of comfort, and psychological well-being. However, the risks of the surgical procedure, postimplantation complications, and high cost remain limiting factors to use of the FES system in this patient population.^8,9

Cardiovascular complications. The higher the SCI lesion, the more severe the cardiovascular problems are. An SCI at or above T6 causes autonomic imbalance between intact parasympathetic innervation and impaired sympathetic response, resulting in exaggerated or hyperreflexic sympathetic reaction.

In the acute phase after SCI, patients experience neurogenic shock, which presents as hypotension, bradycardia, and hypothermia. Hypovolemic shock is often an associated complication of multiple trauma. Management should include careful fluid resuscitation and awareness of neurogenic pulmonary edema risk.

Orthostatic hypotension is best treated by prevention. Preventive strategies include the use of compression garments, such as abdominal binders, elastic stockings, and elastic bandage wrapping of lower extremities, and gradual mobilization of the patient during transfer activities. Some patients will require pharmacologic management with a-adrenergic agonist drugs, such as ephedrine and midodrine (ProAmatine). These agents cause an increase in vascular tone and elevation of blood pressure through contraction of arterial and venous vascular bed. Fludrocortisone promotes sodium and water retention, thereby producing intravascular volume expansion.

Bradycardia is usually present within the first few months after SCI as a result of an unopposed effect on the vagus nerve and disruption of cardiosympathetic factors.

Procedures that stimulate abnormal vagal response include suctioning, insertion of nasogastric tube, and rapid change in position. Usually, bradycardia in SCI patients does not require specific treatment; however, if it becomes severe and persistent, atropine or permanent-demand pacemakers may be required.¹⁰

Compromise of the autonomic pathways to the hypothalamus results in impaired thermoregulation in tetraplegic patients. Patients become poikilothermic-- that is, their body temperature assumes that of the environment. Extreme temperatures should be avoided. Whenever possible, patients should be in an environment with climate control systems.¹¹

One of the most significant cardiovascular complications of SCI is autonomic dysreflexia (AD). It is potentially a life-threatening condition that results in massive and uninhibited reflex sympathetic discharges in patients with injuries above T6. AD is triggered by various noxious stimuli below the level of neurologic injury. The most common are bladder overdistention, urinary tract infection, and bladder or renal calculi. Fecal impaction is the second most common trigger of AD. Other GI stimuli include bowel distention, gas- troesophageal reflux, gallstones, gastric ulcers, hemorrhoids, and any acute abdominal pathology.¹²

The most common symptoms of AD are significant hypertension, pounding headache, bradycardia, profuse sweating and flushing of the skin above the level of the injury, blurred vision, nasal congestion, and anxiety and apprehension. Hypertension, in particular, can lead to intracranial hemorrhage, seizures, myocardial infarction, and death. AD therefore should be treated as a medical emergency. The patient who is in a supine position must be immediately seated upright and all constrictive clothing must be removed or loosened. Cause of noxious stimuli should be identified, beginning with the urinary system.

If the patient requires bladder catheterization, an instillation of 2% lidocaine should be introduced through the urethra before catheterization to avoid additional stimuli caused by advancement of the catheter. If the patient has an indwelling catheter, it needs to be checked for kinking and blockage. If it is not draining, it is best to remove the catheter and catheterize the bladder.

In management of fecal impaction, the rectal wall should be lubricated with lidocaine gel, allowing up to 5 minutes before performing a gentle rectal examination. If stool is present, it needs to be gently removed.

If symptoms of AD continue and blood pressure remains elevated, pharmacologic management should be considered. Antihypertensive therapy using agents with rapid onset and short duration is useful while additional causes of AD are being identified. Topical and sublingual nitrates and nifedipine are the initial drugs of choice. In using a topical nitrate, apply an inch of 2% nitroglycerin paste to the chest above the level of injury. Topical application of nitroglycerin has the advantage of easy removal if blood pressure falls precipitously. When using nifedipine, administer as a bite-and-swallow 10-mg dose. If needed, the dose can be repeated in 15-minute increments until blood pressure is controlled. Other agents, such as phenoxybenzamine (Dybenzyline), diazoxide, mecamylamine (Inversine), and hydralazine also can be used. For severe episodes of AD, intravenous drip of sodium nitroprusside under close monitoring is effective.¹²

As with many other complications after SCI, prevention is the best management. The patient and his or her family need to be educated about the early symptoms and appropriate initial management of AD.

Thromboembolism. Deep venous thrombosis (DVT) and pulmonary embolism (PE) are common complications after SCI. Risk for DVT is greatest within the first 2 weeks after injury. Contributory factors include obesity, trauma to the pelvis and lower extremities, congestive heart failure, history of malignancy, and previous occurrence of thromboembolism.

Diagnosis of PE is frequently delayed in patients with SCI secondary to a nonspecific presentation, although clinical suspicion of PE should be high in this population because it is associated with a high mortality rate. Given that thromboembolism presents a significant challenge in patients with SCIs, early implementation of preventive measures is critical.

Guidelines developed by the Consortium for Spinal Cord Medicine recommend initiation of prophylaxis within 72 hours after injury.¹³ Management includes use of pneumatic compression sleeves for the first 2 weeks after injury and use of either low molecular weight or unfractionated heparin.

For uncomplicated complete and incomplete motor paraplegia, anticoagulation therapy should continue for 8 weeks. Paraplegic patients with complications and all tetraplegic patients should receive 12 weeks prophylaxis, according to the guidelines.

Placement of vena cava filters is somewhat controversial. It is indicated for high-risk patients, defined as those with a previous history of PE and extensive chest and lower extremity injuries, and for patients with contraindications to anticoagulation prophylaxis. The most significant complications of filters include thrombosis, perforation, and migration.

Neurogenic bladder. Even though mortality associated with renal complications after SCI has decreased over the past few decades, morbidity secondary to a neurogenic bladder remains high and contributes to over 30% of readmissions to acute care hospitals.¹⁴ Impaired bladder function after SCI significantly correlates with perceived quality of life in patients.¹⁵

Goals of neurogenic bladder management are to achieve adequate urine storage without incontinence, effective bladder emptying, and maintenance of low in- travesical pressure. Sustained high detrusor pressure causes deterioration of the upper urinary tract with hydronephrosis and subsequent renal failure.

Urinary tract surveillance is essential in all patients with SCIs and has contributed significantly to reduction in mortality and morbidity in this population. Baseline studies are recommended within 3 months after injury and should include renal ultrasonography, renal MRI, urodynamic testing, and measurement of serum creatinine, and 24-hour urinary creatinine clearance.^14,16 Subsequently, annual evaluations during the first 3 to 5 years after injury are appropriate. Intravenous pyelograms should be reserved for cases of renal calculi, obstruction or suspicion of tumor, or other lesions. Cystoscopy is recommended for patients with recurrent episodes of hematuria, frequent urinary tract infections (UTIs), bladder stones, and a long-term indwelling catheter.

The rehabilitation program for management of the neurogenic bladder is based on premorbid urologic history, physical examination, type of neurologic bladder dysfunction, and patient's functional abilities, especially to hand function and dexterity. The patient's cognitive status and lifestyle and the availability of a support system should be taken into consideration. It is crucial that the patient and caregivers receive appropriate education regarding bladder physiology, catheterization techniques, catheter management, and potential complications.

Immediately after the injury, bladder management is best achieved by placement of an indwelling urethral catheter to ensure adequate hydration and electrolyte balance. Once the medical condition is stabilized, an intermittent catheterization program should be initiated as part of long-term management.

Many patients are able to achieve adequate bladder emptying through reflex voiding. However, a risk of vesicoureteral reflux is associated with this mechanism. Hydronephrosis can result because of sustained elevation of detrusor pressure. Urodynamic studies become instrumental in assess- ing reflex voiding and provide critical guidelines in management.

Physicians must keep in mind that prolonged use of an indwelling catheter contributes to acute and chronic recurrent UTIs, urethral erosions and fistulas, and stone formation, and presents a significant risk of squamous cell carcinoma. Kidney stones will develop within 5 years in 34% of patients who have a past diagnosis of kidney stones.¹⁷ Urine screening for BLCA-4, a tissue matrix protein found in the nucleus of cancerous cells in the bladder, may be warranted; the 5-year mortality from bladder cancer is about 40%.¹⁸

UTIs are the most frequent medical complication of neurogenic bladder, affecting 80.4% of patients with spinal cord injury.¹⁶ Because of the high frequency of infection with resistant organisms, urinalysis with Gram stain, urine culture, and sensitivity testing should be obtained whenever possible before initiation of antibiotic therapy.

Uncomplicated UTIs can be treated with oral antibiotics such as quinolones, trimethoprim/sulfamethoxazole, and nitrofurantoin. Recommended duration of treatment is 7 to 14 days. Current consensus stipulates that asymptomatic bacteriuria does not require routine treatment with antibiotics in otherwise healthy per- sons with SCI.¹⁴ Presence of pyuria may be an indication for treatment even though pyuria usually is a poor indicator of tissue invasion. Prophylactic use of antibiotics in patients with SCIs has not been shown to be particularly useful in preventing recurrent UTIs; however, this is an area of ongoing discussion in clinical practice. Use of urine acidifiers is controversial but may be warranted in some cases.¹⁹

Anticholinergic drugs that block parasympathetic postganglionic receptors, such as oxybutynin, tolterodine, hyoscyamine, imipramine, and propantheline, are indicated for patients with detrusor hyperreflexia. Extended-release formulations are preferred because they have a better adverse-effect profile than regular formulations.

For patients with significant detrusor-sphincter dyssynergia, a-adrenergic antagonists, such as terazosin, tamsulosin (Flomax), prazosin, and phenoxybenzamine, reduce internal sphincter tone. Anti-spasticity drugs such as baclofen (Lioresal), diazepam, and dantrolene (Dantrium) might be of value in those with severe spasticity of perineal muscles. Botulinum toxin A (Botox) injected in the detrusor muscle or sphincter has been shown to be effective as well.²⁰ Nonpharmacologic options for detrusor hyperreflexia include surgery or laser sphincterotomy, which can result in a 70% to 90% improvement in bladder emptying, and stent placement at the level of the proximal urethra to reduce resistance to urinary outflow.²¹

Urinary diversion, augmentation cystoplasty, detrusor myomectomy, and continent and incontinent urostomies are more complex alternative surgical procedures. They are usually reserved for patients who have persistent and progressive hydronephrosis or recurrent pyelonephritis or for those in whom all other forms of therapy have failed.²²

For the hyporeflexic bladder, pharmacologic management is limited. Bethanechol, a cholinergic agonist, has limited effect on detrusor contractility. a-Adrenergic agonists such as ephedrine, pseudoephedrine, and phenylpropanolamine can increase sphincter resistance. These drugs, have limited use because of lack of effectiveness and adverse effects, including blood pressure elevation, tremor, cardiac arrhythmia and palpitations, anxiety, and insomnia.

A bladder neuroprosthesis (VoCare System) is available for more advanced management of hyperreflexic neurogenic bladder. It is based on the principle of functional electrical stimulation of the detrusor to initiate micturition on demand.²³ It is an implantable FES system for patients with complete SCI above sacral spinal cord segments. Implantation of the system requires intact peripheral innervation to the bladder, additional L3 to S2 laminectomy, and S2 to S5 dorsal selective rhizotomy to eliminate the afferent pathway of voiding reflex. Benefits include voiding on demand, increased bladder capacity, elimination of incontinence, improved bladder emptying, and reduced UTIs, decreased episodes of AD, and prevention of upper urinary tract complications.

Disadvantages of the system are the need for major surgery, loss of reflex erection and ejaculation, permanent damage to dorsal roots, and high cost. This system is better suited for women with complete paraplegia who are not dependent on a wheelchair for mobility and activities of daily living.

Neurogenic bowel. For many patients with SCI, bowel incontinence and constipation are sources of continued inconvenience, frustration, and a major psychosocial limiting factor. Rehabilitation goals include achievement of predictable bowel evacuation without bowel accidents and prevention of GI complications. A bowel program is largely based on neurologic level of injury and consists of a combination of diet, oral pharmacotherapy, procedures to facilitate defecation, and adequate levels of physical activity.²⁴

In suprasacral lesions, bowel dysfunction is of a hyperreflexic type with overactive segmental peristalsis, poor propulsive peristalsis, hyperactive holding reflex, and prolonged colonic transit. These impairments produce fecal retention and colon distention with constipation. Lesions at or below the conus medullaris cause loss of colonic reflex, poor peristalsis, flaccid external anal sphincter, and high risk of incontinence.

The most common complication associated with neurogenic bowel in the acute stage after SCI is paralytic ileus, which usually resolves spontaneously. Patients who have chronic SCIs frequently present with partial bowel obstruction and fecal impaction. Impaction requires complete evacuation of the bowel with oral osmotic or saline stimulants and enemas along with pulsed irrigation to enhance stool evacuation.

For most patients, bowel evacuation every other day is adequate. Bowel routine should be performed shortly after mealtime to capitalize on the natural gastrocolic reflex. Mechanical and chemical rectal stimulation (suppositories, enemas and/or digital manipulation) are used for hyperreflexic bowel, and manual evacuation is usually necessary for areflexic bowel.

Diet should include adequate fiber (20 to 30 g/d) and adequate fluids (2000 to 3000 mL/d). Oral medications are frequently necessary to facilitate a bowel program. These include stool softeners, bulk forming agents, colonic irritants or stimulant laxatives, and prokinetic agents.

When long-term use of stimulant laxatives is required, osmotic laxatives are preferred because of their low incidence of tolerance and lack of association with colon damage. For patients with SCI who have repeated fecal impactions and an excessively long bowel routine time, a permanent ileostomy or colostomy is the best in- terventional option.

Musculoskeletal complications. Acute paralysis and immobilization secondary to SCI leads to increased bone resorption. This can cause significant elevation of serum calcium levels and can present as an acute medical emergency, especially in male adolescents and young adults, who usually have large active bone mass.²⁵ Clinically, these patients experience acute onset of abdominal pain, nausea, and vomiting; behavior changes; and progressive lethargy. These symptoms usually occur when serum calcium levels exceed 12 mg/dL. Untreated hypercalcemia can cause nephrocalcinosis, urolithiasis, and renal failure.

Management of clinically symptomatic hypercalcemia includes adequate hydration; thiazide diuretics to facilitate calcium excretion; and medications that reduce bone resorption by suppressing osteoclastic activity, such as calcitonin, mitomycin, and bisphosphonates. Intravenous pamidronate (Aredia), 60 to 90 mg adminis-tered over 4 hours, also is usually effective.²⁶

Osteoporosis. The causes of osteoporosis after SCI are multifactorial and include immobilization, significant increase in osteoclastic bone activity with only slight increase in osteoblastic activity, parathyroid hormone suppression secondary to increased serum ionized calcium and probable vitamin D deficiency, reduced absorption of calcium from the GI tract, and loss of active muscle traction on bone.^27,28 Osteoporosis causes additional functional impairment and carries a high risk of fractures and morbidity.

Approximately 30% of bone loss occurs within the first 4 months after SCI, and bone loss continues significantly over the next 2 to 3 years, reaching in excess of a 50% decline of total bone content in the distal bones of the lower extremities within 10 years after the injury. Bone density of the spine remains preserved because the spine is subject to functional weight bearing for patients who spend most of their time in a wheelchair.^27,29

Quantifying the severity of osteoporosis and monitoring it over time is important. The most commonly used test is bone density dual-energy x-ray absorptiometry. No effective prevention and treatment of osteoporosis after SCI has been established to date. Data on bisphosphonates, especially alendronate (Fosamax), however, are promising.³⁰ The parathyroid hormone teriparatide (Forteo), which promotes new bone formation, might be of benefit. Calcium and vitamin D supplementation also should be considered.

From the rehabilitation standpoint, a number of therapies are useful when they are introduced early and are continued with consistency and increasing intensity for months after the injury. These include early mobilization; weight- bearing exercises, such as use of the standing frame, ambulation with lower extremity orthoses, and treadmill walking using partial body weight-supported systems; and robotic devices that produce a reciprocating gait pattern. FES also has been shown to have positive effect on bone loss retardation. It can be used with a bicycle ergometer or ambulation devices.^31,32

Spasticity. Spasticity is one of the most common clinical problems encountered by patients with SCIs. It results from loss of suprasegmental inhibition and selective increase in motor neuron excitability. It leads to joint and muscle contractures and skin breakdown, contributes to muscle fibrosis and atrophy, may cause pain, interferes with sleep, interferes with sexual function, and causes difficulties in mobility and self-care.

Clinical evaluation and assessment of effectiveness of interventions for spasticity are difficult because muscle tone fluctuates throughout the day and because management depends on the patient's level of activity and participation in an exercise program and on the patient's concomitant medical problems and their environmental conditions. The Ashworth and the Modified Ashworth Scales are the most commonly used measurements to quantify spasticity.³³

Management includes avoidance of noxious stimuli, proper positioning in the bed and wheelchair, joint range of motion and stretching exercises, application of superficial heat or cold, biofeedback, FES, splinting, serial casting, and use of orthotic devices.³⁴

Severe spasticity and spasms should be treated with systemic medications. Traditional oral therapies include the g-aminobutyric acid agonists baclofen and diazepam and the a-adrenergic agonists tizanidine and clonidine (Catapres). Among peripherally acting agents, dantrolene sodium produces a direct effect on muscle by inhibiting calcium reuptake into the sarcoplasmic reticulum.

Patients with SCI who demonstrate poor response to oral medications or experience severe adverse effects are candidates for intrathecal baclofen infusion therapy.³⁵ Patients with severe localized spasticity respond well to nerve blocks and intramuscular injection with botulinum toxin A.^33,36

Surgical treatment, which is usually destructive and includes techniques such as neurectomy, rhizotomy, and myelotomy, should be avoided especially, since significant progress is being made in the field of neurologic restoration of the spinal cord. Orthopedic surgical procedures, such as tendon release, tendon transfers, and tenotomies, may be useful with other therapeutic interventions.

Heterotopic ossification (HO). HO is a formation of mature bone in the soft tissue surrounding joints below the neurologic level of injury. The incidence rate of HO is 16% to 53%. The most common location is in the hip region followed by the knee, shoulder, and elbow. Clinically, HO presents with loss of range of motion, swelling, tenderness, erythema, and pain. Differential diagnosis includes DVT, cellulitis, abscess, fracture, and hematoma.³⁷ Positive triple-phase bone scan will usually confirm the diagnosis.

Once the diagnosis of HO is made, treatment should be initiated with oral etidronate (Didronel) and NSAIDs. Intravenous etidronate at a dosage of 300 mg/d for the first 3 days followed by oral therapy has been shown to be more effective in reducing early symptoms and inhibiting the mineralization process than oral etidronate alone.³⁸

Surgical intervention is appropriate in a small group (3% to 5%) of patients who represent the most severe cases. Unfortunately, recurrence of HO after surgical resection is high. Physical therapy must be integrated in the treatment program and should include gentle range of motion and stretching exercises and use of dynamic and static splinting.

Pain. The prevalence rate of pain after SCI ranges from 81% at 1 year after injury to 83% at 25 years after injury. A third of patients experience severe pain.³⁹ Presence of pain at 6 weeks is the most significant predictive factor for presence of pain at 1 year after the injury. It is frequently associated with depression, increased stress, poor morale, and self-perceived poor health status.⁴⁰ Pain is more prominent among paraplegics than tetraplegics and is more severe in incomplete injuries than in complete injuries and in injuries caused by gunshot wounds than in those associated with traumatic SCIs.

Central pain is the most common pain associated with SCI. It is usually persistent and refractory to conventional therapeutic interventions, such as NSAIDs and muscle relaxants. Tricyclic antidepressants generally are not effective either. Recent data suggest that gabapentin (Neurontin), a calcium channel blocking antiepileptic drug, may be effective.⁴¹ Opioids and benzodiazepines, baclofen, clonidine, and tizanidine may provide some relief. Intravenous ketamine, intrathecal morphine, and oral lamotrigine also have been shown to reduce neuropathic pain.^42,43

Although limited success has been seen with transcutaneous electrical nerve stimulation and implanted dorsal column electrical stimulators, FES has been reported to improve pain as a secondary outcome through reduction of spasticity, increased level of activity, and overall improved physical conditioning.⁴⁴

As for the neurosurgical approach, the dorsal root entry zone microcoagulation procedure was shown to have some effect in reducing radicular and central pain at the neurologic level of injury; however, results have been disappointing in alleviating central pain below the level of the injury.⁴⁵

Among the upper extremities, the shoulder is the most common site of pain. Pain usually is associated with rotator cuff pathology, bicipital tendinitis, shoulder subluxation, acromion-clavicular joint pathology, and myofascial pain.⁴⁶ Preventive measures such as proper positioning, early mobilization exercises, supportive splinting and bracing, proper transfer skills, and proper wheelchair sitting arrangements are important.

REHABILITATION CONSIDERATIONS

The goal of rehabilitation therapy for patients with SCIs is optimization of function in mobility, self-care, and activities of daily liv- ing. Traditionally, this has been achieved through strength and endurance training, prevention of musculoskeletal complications, utilization of static and dynamic orthoses, use of adaptive equipment, and assistive devices to enhance functional performance.

Compared with able-bodied persons, patients with SCIs have impaired cardiovascular response to exercise. The reduced CNS vasoconstrictor efferent output results in decreased venous return and reduction of end-diastolic ventricular volume. At the same time, heart rate and myocardial contractility are only marginally increased. This results in reduced cardiac performance and contributes to exercise intolerance.⁴⁷

In recent years, the use of body weight supported treadmill training (BWSTT) to facilitate restoration of walking has received significant attention. Evolving evidence suggests that BWSTT in combination with FES induces a locomotor pattern and improves ambulation in patients with incomplete SCIs. Standing and walking also can be achieved through use of orthoses and FES.^48,49 Certain available FES systems, such as the FREEHAND (implanted) and the Bionic Glove (external), have proved useful in restoring grasp and hold functions.^50,51 Furthermore, innovations in wheelchair designs are allowing patients greater mobility and improved community access.⁵²

SUMMARY

Many advances have been made in medical and rehabilitative care of patients with SCIs during the past several decades. Understanding of spinal cord regeneration potentials is expanding, although curative therapies have yet to be discovered. The best we can do for patients is to ensure comprehensive and timely management of their medical issues and focus on preventive and health maintenance issues, especially since the SCI population is surviving longer.

REFERENCES1. DeVivo MJ, Go BK, Jackson AB. Overview of the national spinal cord injury statistical center database. J Spinal Cord Med. 2002;24:335-338.
2. American Spinal Injury Association. International Standards for Neurologic and Functional Classification of Spinal Cord Injury, Revised 2002. Chicago: ASIA; 2002.
3. DeVivo MJ, Black KJ, Stover SL. Causes of death during the first 12 years after spinal cord injury. Arch Phys Med Rehabil. 1993;74:248-254.
4. Anke A. Lung volumes in tetraplegic patients according to cervical spinal cord injury level. Scand J Rehabil Med. 1993;25:73-77.
5. Lemons VR, Wagner FC Jr. Respiratory complications after cervical spinal cord injury. Spine. 1994;19:2315-2320.
6. Braun SR, Giovannoni R, O'Connor M. Improving the cough in patients with spinal cord injury. Am J Phys Med. 1984;63:1-10.
7. Bach JR. Pulmonary perspectives: the assisted cough in neuromuscular disease. Chest. 1997;14: 4-6.
8. Glenn WW, Brouillette RT, Dents B, et al. Fundamental considerations in pacing of the diaphragm for chronic ventilatory insufficiency: a multi-center study. Pacing Clin Electrophysiol. 1988;11:2121-2127.
9. Dobelle WH. 200 cases with a new breathing pacemaker dispel myths about diaphragm pacing. ASAIO J. 1994;40:M244-M252.
10. McKinley WO, Gittler MS, Kirshblum SC, et al. Spinal cord injury medicine, 2: medical complications after spinal cord injury: identification and management. Arch Phys Med Rehabil. 2002; 83:S58-S64, S90-S98.
11. Menard MR, Hahn G. Acute and chronic hypothermia in a man with spinal cord injury: environmental and pharmacologic causes. Arch Phys Med Rehabil. 1991;72:421-424.
12. Acute management of autonomic dysreflexia: individuals with spinal cord injury presenting to healthcare facilities. J Spinal Cord Med. 2002;25 (suppl 1):S67-S88.
13.Prevention of Thromboembolism in Spinal Cord Injury. 2nd ed. Washington, DC: Paralyzed Veterans of America; 1999.
14. Kirshblum SC, Groah SL, McKinley WO, et al. Spinal cord injury medicine, 1: etiology, classification and acute medical management. Arch Phys Med Rehabil. 2002;83(3, suppl 1):S50-S57, S90-S98.
15. Hicken BL, Putzke JD, Richards JS. Bladder management and quality of life after spinal cord injury. Am J Phys Med Rehabil. 2001;80:916-922.
16. The prevention and management of urinary tract infections among people with spinal cord injuries. National Institute on Disability and Rehabilitation Research consensus statement. January 27-29, 1992. J Am Paraplegia Soc. 1992;15:194-204.
17. Chen Y, DeVivo MJ, Stover SL, Lloyd LK. Recurrent kidney stone: a 25-year follow-up study in persons with spinal cord injury. Urology. 2002;60: 228-232.
18. Konety BR, Nguyen TT, Brenes G, et al. Clinical usefulness of the novel marker BLCA-4 for the detection of bladder cancer. J Urol. 2000;164: 634-639.
19. Linsenmeyer TA, Harrison B, Oakley A, et al. Evaluation of cranberry supplement for reduction of urinary tract infection in individuals with neurogenic bladders secondary to spinal cord injury. J Spinal Cord Med. 2004;27:29-34.
20. Dykstra DD, Sidi AA. Treatment of detrusor-sphincter dyssynergia with Botulinum A toxin: a double-blind study. Arch Phys Med Rehabil. 1990; 71:24-26.
21. Ricottone AR, Pranikoff K, Steinmetz JR, Constantino G. Long-term follow-up of sphincterotomy in the treatment of autonomic dysreflexia. Neuroural Urodyn. 1995;14:43-46.
22. Gudziak MR, Tiguert R, Puri K, et al. Management of neurogenic bladder dysfunction with incontinent ileovesicostomy. Urology. 1999;54: 1008-1011.
23. Jezernik S, Craggs M, Grill WM, et al. Electrical stimulation for the treatment of bladder dysfunction: current status and future possibilities. Neural Res. 2002;24:413-430.
24. Clinical practice guidelines: neurogenic bowel management in adults with spinal cord injury. Spinal Cord Medicine Consortium. J Spinal Cord Med. 1998;21:248-293.
25. Maynard FM. Immobilization hypercalcemia following spinal cord injury. Arch Phys Med Rehabil. 1986;67:41-44.
26. Nance PW, Schryvvers O, Leslie W, et al. Intravenous pamidronate attenuates bone density loss after acute spinal cord injury. Arch Phys Med Rehabil. 1999;80:243-251.
27. Consensus development conference: diagnosis, prophylaxis, and treatment of osteoporosis. Am J Med. 1993;94:646-650.
28. Demirel G, Yilmaz H, Paker N, Onel S. Osteoporosis after spinal cord injury. Spinal Cord. 1998; 36:822-825.
29. Frey-Rindova P, de Briun ED, Stussi E, et al. Bone mineral density in upper and lower extremities during 12 months after spinal cord injury measured by peripheral quantitative computed tomography. Spinal Cord. 2000;38:26-32.
30. Moran de Brito CM, Battistella LR, Satio ET, et al. Effect of alendronate on bone mineral density in spinal cord injury patients: a pilot study. Spinal Cord. 2005;43:341-348.
31. BeDell KK, Scremin AM, Perrell KL, Kunkel CF. Effects of functional electrical stimulation-induced lower extremity cycling on bone density of spinal cord injury patients. Am J Phys Med Rehabil. 1996;75:29-34.
32. Belanger M, Stein RB, Wheeler GD, et al. Electrical stimulation: can it increase muscle strength and reverse osteopenia in spinal cord injured individuals? Arch Phys Med Rehabil. 2000;8: 1090-1098.
33.Spasticity: Diagnosis and Treatment. New York: Worldwide Education and Awareness for Movement Disorders (WE MOVE); 1995.
34. Priebe MM, Sherwood AM, Thornby JI, et al. Clinical assessment of spasticity in spinal cord injury: a multidimensional problem. Arch Phys Med Rehabil. 1996;77:713-716.
35. Penn RD, Kroin JS. Continuous intrathecal baclofen for severe spasticity. Lancet. 1985;2:125-127.
36. Glen MB. Nerve blocks for treatment of spasticity. Phys Med Rehabil. 1994;8:481-505.
37. Banovac K, Gonzalez F. Evaluation and management of heterotopic ossification in patients with spinal cord injury. Spinal Cord. 1997;35:158-162.
38. Banovac K, Sherman AL, Estores IM. Prevention and treatment of heterotopic ossification after spinal cord injury. J Spinal Cord Med. 2004;27:376-382.
39. Cardenas DD, Bryce NT, Shem K, et al. Gender and minority differences in the pain experience of people with spinal cord injury. Arch Phys Med Rehabil. 2004;85:1774-1781.
40. Bryce TN, Ragnarsson KT. Pain management in persons with spinal cord disorders. In: Lin V, ed. Spinal Cord Medicine. New York: Demos; 2001.
41. Levendoglu F, Ogun CO, Ozerbil O, et al. Gabapentin is a first line drug for the treatment of neuropathic pain in spinal cord injury. Spine. 2004;29:743-751.
42. Siddall PJ, Molloy AR, Walker S, et al. The efficacy of intrathecal morphine and clonidine in the treatment of pain after spinal cord injury. Anesth Analg. 2000;91:1493-498.
43. Finnerup NB, Sindrup SH, Bach FW, et al. Lamotrigine in spinal cord injury pain: a randomized controlled trial. Pain. 2000;96:375-388.
44. Glaser RM. Functional neuromuscular stimulation: exercise conditioning of spinal cord injured patients. Int J Sports Med. 1994;15:142-148.
45. Nashold BS, Bullitt E. Dorsal root entry zone lesions to control central pain in paraplegics. J Neurosurg. 1981;55:414-419.
46. Dalyan M, Cardenas DD, Gerard B. Upper extremity pain after spinal cord injury. Spinal Cord. 1999;37:191-195.
47. Figoni S. Exercise responses and tetraplegia. Med Sci Sports Exerc. 1993;25:433-441.
48. Postans NJ, Hasler JP, Granat MH, Maxwell DJ. Functional electrical stimulation to augment partial weight bearing supported treadmill training for patients with acute incomplete spinal cord injury: a pilot study. Arch Phys Med Rehabil. 2004; 85:604-610.
49. Field-Fote EC. Combined use of body weight support, functional electrical stimulation, and treadmill training to improve walking ability in individuals with chronic incomplete spinal cord injury. Arch Phys Med Rehabil. 2001;82:818-824.
50. Keith MW, Peckham PH, Thrope GB, et al. Implantable functional FNS in the tetraplegic hand. J Hand Surg Am. 1989;14:524-530.
51. Prochazka A, Gauthier M, Wieler M, Kenwell Z. The bionic glove: an electrical stimulator garment that provides controlled grasp and hand opening in quadriplegia. Arch Phys Med Rehabil. 1997;78:608-614.
52. Boninger ML, Souza AL, Cooper RA, et al. Propulsion patterns and pushrim biomechanics in manual wheelchair propulsion. Arch Phys Med Rehabil. 2002;83:718-723.