Chronic Complications of Spinal Cord Injury and Disease - UpToDate

23/05/2017 Chronic complications of spinal cord injury and disease UpToDate
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Chronic complications of spinal cord injury and disease
Authors: Gary M Abrams, MD, Marc Wakasa, MD
Section Editor: Michael J Aminoff, MD, DSc
Deputy Editor: Janet L Wilterdink, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2017. | This topic last updated: Jul 15, 2014.
INTRODUCTION — Spinal cord injury (SCI) is a common event; in the United States, the incidence of
traumatic SCI is about 40 per million persons per year, with approximately 250,000 living survivors of
traumatic SCI in July 2005 [1]. The prevalence of nontraumatic SCI is unknown, but it is estimated that it is
three to four times greater than traumatic SCI [2]. SCI produces a wide variety of changes in systemic
physiology that can lead to a number of complications, which rival the neurologic deficits in their impact on
function and quality of life.
Medical complications after SCI are both common and severe. In the Model Spinal Cord Injury Systems
Database, rehospitalizations occurred in 55 percent of patients in the first year after SCI and continued at a
stable rate of about 37 percent per year over the next 20 years [3]. Genitourinary and respiratory
complications and pressure ulcers were the most common reasons for hospitalization. Increased patient age
and severity of the spinal cord lesion also impacted on the risk of complications requiring hospitalization.
This topic reviews the management of common complications of chronic SCI, whether due to trauma or other
conditions. Acute manifestations and complications of SCI are presented separately. (See "Acute traumatic
spinal cord injury" and "Disorders affecting the spinal cord".)
LIFE EXPECTANCY — Life expectancy is reduced among survivors of spinal cord injury (SCI). Mortality rates
are highest in the first year. For patients surviving at least one year after traumatic SCI, life expectancy is
approximately 90 percent of normal [1,4,5]. Higher neurologic level and severity of injury and older age at the
time of SCI negatively impact survival.
The most common causes of death after traumatic SCI are diseases of the respiratory system followed by
cardiovascular events [1,4]. In earlier decades (prior to 1972), urinary complications were the leading cause of
death. The risk of suicide is also increased among patients with SCI [5]. (See 'Psychiatric complications'
below.)
CARDIOVASCULAR COMPLICATIONS
Autonomic dysreflexia — Spinal cord injuries (SCI) above T6 may be complicated by a phenomenon known
as autonomic dysreflexia, a manifestation of the loss of coordinated autonomic responses to demands on
heart rate and vascular tone [6,7]. Uninhibited or exaggerated sympathetic responses to noxious stimuli below
the level of the injury lead to diffuse vasoconstriction and hypertension. A compensatory parasympathetic
response produces bradycardia and vasodilation above the level of the lesion, but this is not sufficient to
reduce elevated blood pressure. SCI lesions lower than T6 do not produce this complication, because intact
splanchnic innervation allows for compensatory dilatation of the splanchnic vascular bed.
The estimated frequency of this complication is quite variable, ranging from 20 to 70 percent of patients with
SCI lesions above T6 [6,7]. Autonomic dysreflexia is unusual within the first month of SCI but usually appears
within the first year [8,9].
Typical stimuli include bladder distention, bowel impaction, pressure sores, bone fracture, or occult visceral
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disturbances [6,7]. Sexual activity can be a trigger. Autonomic dysreflexia can also complicate medical
procedures, as well as labor and delivery. (See "Neurologic disorders complicating pregnancy", section on
'Spinal cord injury'.)
Common clinical manifestations are headache, diaphoresis, and increased blood pressure [8]. Flushing,
piloerection, blurred vision, nasal obstruction, anxiety, and nausea may also occur. Bradycardia is common;
however, some patients have tachycardia instead. The severity of attacks ranges from asymptomatic
hypertension to hypertensive crisis complicated by profound bradycardia and cardiac arrest or intracranial
hemorrhage and seizures. The severity of the SCI influences both the frequency and severity of attacks.
Management of acute attacks includes [6,8]:
● Measuring and monitoring blood pressure.
● Immediately sitting the patient upright to orthostatically lower blood pressure.
● Removal of tightfitting garments.
● Searching for and correcting noxious inciting stimuli. Bladder distension and fecal impaction are the most
common precipitants. Bladder catheterization and evaluation for urinary tract infection should be
undertaken; indwelling catheters should be checked for obstruction, and a rectal examination should be
performed.
● Prompt reduction of blood pressure with a rapidonset/shortduration agent, depending on the severity of
attack and response to above measures. Medications often used in this setting include nitrates (1 inch, 2
percent nitropaste), nifedipine (10 mg PO or SL), sublingual captopril (25 mg), intravenous hydralazine
(10 mg), and intravenous labetalol (10 mg). Nitrates should be avoided in patients who may be using
sildenafil for erectile dysfunction.
Recognition and avoidance of inciting stimuli are important in preventing attacks. Nifedipine, prazosin, and
terazosin have been reported to prevent an attack when administered prophylactically [6,7,1012].
Coronary artery disease — With improved longterm survival, coronary artery disease (CAD) has become
an increasingly important complication in SCI [4]. CAD risk factors, such as adverse lipid profile (low levels of
highdensity lipoproteins, elevated lowdensity lipoprotein cholesterol) and abnormal glucose metabolism
(impaired glucose tolerance, insulin resistance, and diabetes) are more prevalent in chronic SCI patients than
the ablebodied population [13]. Factors that contribute to the development of these disorders include
decreased muscle mass, increased fat, and inactivity [14]. Studies suggest that the prevalence of CAD is 3 to
10 times higher in SCI patients compared with the general population [13]. In addition, a nationwide cohort
study in Taiwan found that SCI was associated with an increased risk of stroke (HR = 2.9) [15].
CAD mortality also appears to be higher among SCI patients [4]. One contributing factor may be that SCI
lesions above the T5 level may lead to atypical presentations for cardiac ischemia; manifestations may include
autonomic dysreflexia or changes in spasticity rather than typical chest pain.
Risk factor management and treatment for CAD are similar to that of ablebodied individuals. (See "Overview
of the risk equivalents and established risk factors for cardiovascular disease".)
Exercise options for SCI patients include handcrank ergometry, hand cycling, swimming, and functional
electrical stimulation of muscles [16]. Body weightsupported treadmill training has been reported to improve
glucose regulation in incomplete SCI [17]. However, diminished sympathetic responses, reduced cardiac
output, impaired ventilation, and decreased muscle mass lead to reduced exercise capacity in chronic SCI
[13]. Physiologic responses to exercise, including increased heart rate, increased cardiac contractility, and
vasoregulation, are also impaired with higherlevel SCI.
Others — The autonomic nervous system dysfunction that results from SCI disrupts normal cardiovascular
homeostasis. With SCI above the T6 level, baseline blood pressure is usually reduced, and baseline heart
rate may be as low as 50 to 60 beats per minute [13,18]. This is generally not a clinical problem, but may
contribute to hemodynamic instability and exercise intolerance.
Orthostatic hypotension due to peripheral vasodilatation is more common in the first several months of SCI
and tends to dissipate with the development of muscle tone in the lower extremities [8]. However, it may also
occur in chronic SCI, especially with excessive bed rest and diminished fluid intake. Gradual position changes,
compression stockings, and abdominal binders decrease venous pooling and may improve orthostatic
tolerance. Occasionally, increased salt intake, alpha adrenergic agonists (midodrine), or mineralocorticoid
agents (fludrocortisone) may be required. (See "Treatment of orthostatic and postprandial hypotension".)
Acute cervical SCI is associated with a risk of cardiac arrhythmia due to excess vagal tone, as well as
complicating hypoxia, hypotension, and fluid and electrolyte imbalances. Arrhythmias are much less frequent
in chronic SCI. However, patients with complete cervical SCI appear to have an ongoing risk of
cardiopulmonary arrest [19,20].
PULMONARY COMPLICATIONS — Cervical and high thoracic spinal cord injury (SCI) affect respiratory
muscles. The severity of ventilatory failure and requirement for assisted ventilation depends on the level and
severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea and exercise intolerance. (See
"Respiratory physiologic changes following spinal cord injury" and "Respiratory complications in the adult
patient with chronic spinal cord injury", section on 'Respiratory insufficiency'.)
Because of impaired cough and difficulty mobilizing lung secretions, patients after SCI are also at increased
risk for pneumonia. Although the incidence of pneumonia is highest in the first year following SCI, these
patients remain at increased risk over their lifetime [21]. Older patients are at higher risk than younger
patients. Efforts to prevent pneumonia include chest physiotherapy and vaccination. (See "Respiratory
complications in the adult patient with chronic spinal cord injury", section on 'Pulmonary infection'.)
Deep venous thrombosis and pulmonary embolism remain common early complications of SCI despite
advances in awareness and treatment. Prophylactic use of lowmolecularweight heparin is the treatment of
choice for most patients with SCI. While there are no good clinical trial data to guide duration of treatment, we
suggest that it should be continued in paralyzed patients for at least three months after SCI, after which the
risk appears to approximate that of the general population [22]. Specific regimens are discussed separately.
(See "Prevention of venous thromboembolic disease in surgical patients".)
URINARY COMPLICATIONS — Spinal cord injury (SCI) produces bladder dysfunction, often referred to as
the neurogenic bladder. Other complications can result from this, including infections, vesicoureteral reflux,
renal failure, and renal calculi.
Urologic evaluation with regular followup is recommended for all patients after SCI; even ambulatory patients
with SCI may have bladder dysfunction that can lead to complications [23]. Complications such as
vesicoureteral reflux, renal failure, and nephrolithiasis may not produce symptoms, and if untreated, can have
serious consequences. The frequency and specific testing involved (serum creatinine, cystoscopy, urodynamic
studies, renal ultrasound) are not well defined but depend in part on the nature of the patient's urologic
problems and other risk factors [24,25].
Bladder dysfunction — SCI disrupts the two major functions of the bladder, storage and emptying of urine.
Bladder control is a complex activity requiring the coordinated function of the cerebral cortex, pontine and
sacral micturition centers, and peripheral nervous system [26]. (See "Anatomy and localization of spinal cord
disorders", section on 'Autonomic fibers'.) In SCI, the sensation for bladder fullness as well as motor control of
bladder and sphincter function are impaired. Depending on the acuity, level, and completeness of the spinal
cord lesion, a number of problems can result:
● Bladder or detrusor hyperactivity produces reflexive bladder emptying. Patients may be troubled by
bladder spasms as well as urgency and frequency, often with incontinence. Over time, this can lead to
decreased capacity of the bladder.
● Sphincter hyperactivity can impair complete emptying of the bladder.
● Detrusor sphincter dyssynergia, a combination of detrusor and sphincter hyperactivity, can lead to bladder
contractions against a closed sphincter, leading to elevated bladder pressures and vesicoureteral reflux.
● Bladder flaccidity is produced in lower motor neuron injuries affecting the cauda equina or conus
medullaris as well as with acute upper motor neuron injuries (spinal shock). This leads to chronic urinary
retention with overflow incontinence and incomplete emptying.
Most patients with incomplete SCI and all patients with complete SCI, regardless of the level of the lesion,
require assistance with bladder function [21]. Although there are no clinical trials that guide the longterm
management of bladder dysfunction in SCI, accumulated clinical experience has led to some management
strategies [27,28]. The efficacy of these approaches may be manifest by the declining incidence of urinary
tractrelated morbidity and mortality in SCI patients [4,21].
The goal of a SCI bladder program is to preserve renal function while eliminating urine at regular and socially
acceptable times, avoiding high bladder pressures, retention, incontinence, and infection. This should begin as
early as possible after SCI, with removal of the indwelling Foley catheter.
Clean technique intermittent catheterization (CIC) has a lower infection rate compared with the use of
indwelling catheters [21]. CIC is performed at regular intervals, usually every four hours. A bladder volume of
less than 500 cc of urine is targeted in order to avoid bladder distention, excessive intravesicular pressure,
and reflux, as well as to reduce the incidence of infections. The timing of CIC and the amount of fluid intake is
adjusted to reach this goal. A fluid intake restriction of two liters a day is common for patients with SCI. If
present, a sensation of fullness and attempt at voluntary voiding is encouraged prior to CIC, since some
incompletely injured persons will regain normal voiding function.
Intermittent urinary incontinence is expected. Condom catheters (for men) and adult diapers are important
shortterm interventions. After ruling out an infection and adjusting the frequency of CIC and fluid intake,
medications are considered. Urodynamic studies should be considered to assess physiology and guide
pharmacologic intervention [24]:
● Anticholinergic medications (eg, oxybutynin, tolterodine) decrease bladder tone, suppress bladder
contractions, and may reduce urinary frequency and incontinence. Tricyclic antidepressants such as
imipramine have the added side effect of increasing urethral resistance tone.
● Alpha adrenergic medications (ephedrine and phenylpropanolamine) can increase bladder storage in
patients with pathologic relaxation of the sphincter.
● Cholinergic medications (bethanechol) may help complete bladder emptying in those with hypotonic
bladders.
● Alphablockers (eg, prazosin, terazosin) help sphincter relaxation, lowering bladder pressures during
contraction. These can be prescribed for treatment of detrusor sphincter dyssynergia, but may aggravate
hypotension.
Most patients are managed with a combination of CIC and oral anticholinergic medications [29].
For patients unable to perform CIC and without available caregivers, a chronic indwelling catheter may be
necessary. This is associated with an increased risk of urinary tract infection (UTI) compared with CIC [30].
The indwelling catheter is changed every month to minimize infections. Oxybutynin chloride (5 mg bid) can
decrease catheterinduced bladder spasms. With indwelling catheters, there is an increased risk of prostatitis,
epididymitis, and urethral stricture. Suprapubic tube placement can help minimize the risks of infection and
stricture. A cystoscopy every two years is recommended to monitor for the increased incidence of bladder
cancer and stone development [24].
Studies of detrusor injections of botulinum toxin A in patients with detrusor hyperactivity suggest that this
treatment is safe and highly effective in controlling symptoms and improving quality of life [29,3134]. However,
the optimal dose has not been determined and longterm efficacy is unknown. There have been no
comparative studies with anticholinergic agents [35]. The use of botulinum toxin for the treatment of non
neurogenic lower urinary tract dysfunction is discussed separately. (See "Use of botulinum toxin for treatment
of nonneurogenic lower urinary tract conditions".)
Studies of implanted sacral nerve modulators show promise as a treatment for urinary incontinence following
SCI [36,37].
For patients with unsatisfactory response to medical and catheter management, other treatments, bladder
augmentation, urinary diversion, sphincterotomy, urethral stent, and electrical implantation devices can be
considered in selected cases [2,24].
Urinary tract infection — Urinary tract infections (UTI) are common in SCI, with an incidence of 2.5 episodes
per patient per year [38]. The urinary tract is the most frequent source of septicemia in SCI patients and has a
high mortality rate (15 percent) [38,39]. UTI is more common in women than men. Lowfrequency and high
volume catheterization increase the risk of UTI, as do indwelling catheters and assisted (as opposed to self)
intermittent catheterization [30,40,41].
Symptomatic UTI, as manifest by fever, autonomic dysreflexia, increased spasticity, foulsmelling urine,
incontinence, frequency, or dysuria, warrants prompt antibiotic treatment to avoid septicemia and other
complications. (See "Acute uncomplicated cystitis and pyelonephritis in women" and "Acute uncomplicated
cystitis and pyelonephritis in men" and "Acute complicated cystitis and pyelonephritis".)
Asymptomatic UTIs are not generally treated; nor is there a role for routine use of prophylactic antibiotics to
prevent UTI in SCI patients, despite the fact that asymptomatic bacteriuria is common after SCI and is
associated with a higher risk of symptomatic UTI [40]. A metaanalysis of published literature found that
antibiotic prophylaxis in patients with SCI reduced asymptomatic bacteriuria but not symptomatic infections,
and was associated with a twofold increase in the risk of drugresistant bacteria [42]. However, some
individuals with recurrent UTI may benefit from prophylactic antibiotic treatment, depending on the frequency
and clinical severity of the infections. In particular, the combination of frequent UTI and vesicoureteral reflux is
associated with a high risk of renal failure. (See "Recurrent urinary tract infection in women".)
Other methods of reducing the incidence of UTI are under investigation and include colonization of the urinary
tract with inert bacterial strains [43]. Cranberry juice is believed to reduce bacterial adherence to the
uroepithelium and thereby prevent UTI [44]. However, its efficacy is unproven, and the associated fluid and
caloric intake may be problematic in individuals with SCI. In two small clinical trials, a cranberry supplement
was found ineffective in reducing bacteriuria, pyuria, or UTI in patients with SCI [45,46].
Urinary calculi — Calculi in the kidney, ureter, or bladder are increased after SCI, especially in patients who
have recurrent UTIs, indwelling catheters, and immobilization hypercalciuria [21]. (See 'Bone metabolism'
below.) Because of altered bladder sensation, there may not be pain to alert the clinician to ureteral
obstruction. Other clinical symptoms such as increased limb spasticity and episodes of autonomic dysreflexia
should suggest this as a possible diagnosis (see 'Autonomic dysreflexia' above).
The diagnosis and treatment of urinary calculi is discussed separately. (See "Diagnosis and acute
management of suspected nephrolithiasis in adults" and "Options in the management of renal and ureteral
stones in adults".)
Vesicoureteral reflux — Impaired function of the vesicoureteral insertion may result from high bladder
pressures and recurrent UTI. The estimated incidence of this complication in SCI patients is as high as 25
percent [47,48]. Because persistent reflux is associated with a higher risk of pyelonephritis and renal
dysfunction, it represents a treatment imperative. If reflux persists despite the use of anticholinergic drugs and
increased frequency of catheterization, placement of an indwelling catheter or a surgical procedure may be
necessary. The use of oxybutynin may reduce phasic increases in bladder pressure caused by bladder
spasms with an indwelling catheter [49].
Renal insufficiency — The cumulative incidence of renal insufficiency increases with time since SCI and is
as high as 25 percent at 20 years [21,50,51]. Indwelling urethral catheters, vesicoureteral reflux, and
advanced age are associated with the development of renal failure.
SEXUAL DYSFUNCTION — Consequences of spinal cord injury (SCI) on sexual function include decreased
libido, impotence, and infertility [52].
● Male impotence occurs in 75 percent of patients with SCI [24]. Patients with complete as opposed to
incomplete injuries have the greatest incidence and severity of this complication. There are a variety of
treatment options for erectile dysfunction, including medications, assistive devices, and surgically
implanted prostheses. Sildenafil, vardenafil, and tadalafil have documented efficacy in SCI, but are
contraindicated (as are other phosphodiesterase5 inhibitors) if there is comorbid coronary artery disease
[5358]. (See "Treatment of male sexual dysfunction".)
● The prevalence of male infertility in SCI is high as a consequence of erectile dysfunction, ejaculatory
dysfunction, and/or poor sperm quality [25,52]. In general, male reproduction after SCI requires artificial
insemination. (See "Evaluation of male infertility" and "Treatment of male infertility".)
● Sexual responses in women may also be impaired after SCI, but ovulation and fertility are generally
unaffected [24,52]. The lower pregnancy rates among women with SCI as compared with the general
population are felt to reflect personal choice. Pregnancy in women with SCI is generally categorized as
high risk because of a high rate of complications including infections and autonomic dysreflexia. This is
discussed separately. (See "Neurologic disorders complicating pregnancy", section on 'Spinal cord
injury'.)
GASTROINTESTINAL COMPLICATIONS — Bowel dysfunction is common and disabling after spinal cord
injury (SCI) and significantly affects functional and quality of life outcomes [5961]. A multidimensional
program is frequently necessary to obtain the best results [62].
Two patterns of bowel dysfunction may occur [63]. With injuries above the conus medullaris, neural
connections between the spinal cord and bowel are maintained, resulting in hyperreflexic pelvic muscle
contraction and inability to voluntarily relax the external anal sphincter. This causes constipation and fecal
retention. A lower motor neuron or areflexic bowel occurs with injuries below the conus medullaris, leading to
slower transit, decreased sphincter tone, and constipation with frequent incontinence.
Because few studies have evaluated the management of this problem, recommendations are based on clinical
experience and expert opinion [63,64]. With a goal of predictable and timely bowel evacuation that avoids
fecal incontinence and impaction, a consistent, structured regimen is integrated into the patient's lifestyle as
early as possible after SCI, using their preinjury bowel pattern as a guide [8,52]. A typical routine may begin at
a regular time point each day (eg, 30 minutes after a meal) with insertion of a chemical stimulant rectal
suppository. After several minutes, digital stimulation with slow, gentle rotation of the finger for 15 to 60
seconds is repeated every 5 to 10 minutes, until stool evacuation is complete. Abdominal massage, deep
breathing, Valsalva maneuver, and forwardleaning position may assist evacuation [62].
Oral bowel medications (stool softener, docusate sodium; bowel stimulants, senna and bisacodyl; bulking
agents, psyllium) are often used during the initial phase of establishing a regular bowel pattern, and are then
slowly eliminated [63]. Chronic use of stimulant laxatives is associated with a number of side effects. (See
"Management of chronic constipation in adults", section on 'Other laxatives'.)
A regular diet is an important feature of the bowel program and should include adequate fiber intake (30 g)
and relatively lower amounts of dairy products and fat content [8,63]. Targets for fluid intake are often dictated
by the patient's bladder status, but if possible, should be high enough to produce 2 to 3 liters of urinary output
each day.
If constipation or impaction develops, a trial of enemas, laxatives, or bulkforming agents may be considered
[63]. Abdominal xrays should be considered to screen for evidence of obstruction. Diseases not related to the
SCI, particularly colorectal cancer, should be excluded. Prokinetic medications (eg, cisapride,
metoclopramide) are reserved for persistent, severe constipation that is unresponsive to modifications of the
bowel program [62]. Some patients with severe bowel dysfunction require a colostomy. Uncontrolled
observational studies suggest that regular transanal irrigation can reduce constipation and fecal incontinence
and improve quality of life in some patients with chronic bowel dysfunction following SCI [6567]. A new
therapeutic technology, sacral electrical stimulation, is under investigation and appears promising [62]. Details
regarding the treatment of constipation are discussed separately. (See "Management of chronic constipation
in adults".)
Hemorrhoids can be increased by the interventions (suppositories, enemas, digital stimulation) commonly
used in bowel programs for SCI. Treatment includes stool softeners, minimizing trauma, topical anti
inflammatory creams, and suppositories. Hemorrhoids causing persistent bleeding, pain, or autonomic
dysreflexia warrant surgical consultation. (See "Treatment of hemorrhoids".)
Serious abdominal complications (cholecystitis, upper gastrointestinal bleeding, pancreatitis, or appendicitis)
account for 10 percent of deaths following SCI, with the most significant risks during the first few months after
injury [18,68]. There is an increased prevalence of gallstones in patients with chronic SCI, perhaps in
relationship to denervation [69]. Sensory deficits resulting from SCI contribute to a delay in diagnosis and
increased mortality associated with these complications. Vague or nonspecific symptoms such as nausea,
anorexia, or autonomic dysreflexia should raise concern for occult abdominal processes [18].
The superior mesenteric artery syndrome is an unusual complication of SCI, usually in patients with cervical
cord injuries [70,71]. Weight loss leads to loss of the mesenteric fat pad and compression of the duodenum by
the superior mesenteric artery, leading to symptoms of small bowel obstruction. (See "Superior mesenteric
artery syndrome".)
BONE METABOLISM
Osteoporosis — After spinal cord injury (SCI), osteoporosis affects bones below the level of the injury and
increases the risk of lower extremity fractures. In one series of 41 men, after a median of 15 years after SCI,
61 percent had osteoporosis and 34 percent had had a fracture [72].
The pathogenesis of osteoporosis is unknown; neural factors as well as disuse are believed to play a role [73].
Biomarkers of bone resorption are increased, beginning as early as the first week after injury, while markers of
bone formation are normal or only minimally elevated [73,74]. Some studies suggest that about two years
after SCI, a new steady state level between bone resorption and formation is reestablished [73]. Older age,
higher spinal level of injury, lesser degrees of spasticity, and longer chronicity of the injury have been
inconsistently associated with higher degrees of observed bone loss [21,7377]. Rates of osteoporosis among
men and premenopausal women with SCI are similar; too few postmenopausal women with SCI have been
included in studies to know whether this population is at additional risk [25].
Occasionally, symptomatic hypercalcemia and hypercalciuria complicate early resorption of bone mass within
the first few months of SCI [8]. Manifestations can include nausea, vomiting, anorexia, lethargy, and polyuria.
There is an increased risk of nephrolithiasis [74]. Treatment is graded to severity of symptoms. Intravenous
pamidronate has been used for acute immobilization hypercalcemia after SCI [78,79]. (See "Clinical
manifestations of hypercalcemia" and "Treatment of hypercalcemia".)
Over time, patients with SCI develop a specific pattern of bone abnormalities, with marked loss of bone
density in the proximal tibia and femur, and relatively less bone loss in the spine [75,80]. The impact of weight
bearing on the spine during sitting and wheelchair use may contribute to this discrepancy [74]. Patients with
quadriparesis may also experience bone loss in the distal forearm [77].
In small observational and openlabel, randomized studies, treatment with bisphosphonates such as
tiludronate, etidronate, pamidronate, and alendronate has been shown to attenuate bone loss in patients with
SCI [8184]. In one small, doubleblind, randomized trial (31 patients), alendronate (70 mg weekly) was also
shown to prevent bone loss at the hip when administered within 10 days of acute SCI [85]. Functional
electrical stimulation has shown minimal and largely unsustained benefits in improving bone density [74,86
88].
Heterotopic ossification — Heterotopic ossification refers to the deposition of bone within the soft tissue
around peripheral joints. This occurs in up to half of SCI patients, beginning at a mean of 12 weeks after injury
[89]. Although heterotopic ossification is common after SCI, only 10 to 20 percent of patients have clinical
symptoms, with decreased range of motion and inflammatory symptoms in the affected joints. The large joints
below the level of injury are typically affected, most commonly the hip. The pathogenesis of this phenomenon
is incompletely understood, but it is believed to originate from osteoprogenitor stem cells lying dormant within
the affected soft tissues. With the proper stimulus (as with hip surgery, spinal cord injury, and stroke), these
stem cells may differentiate into osteoblasts that form osteoid and eventually bone. Heterotopic ossification in
the setting of total hip arthroplasty is discussed separately. In one casecontrol study of SCI patients,
heterotopic ossification was more common in patients with complete spinal cord lesions, more rostral injuries,
and also in those with associated thoracic trauma [90]. (See "Complications of total hip arthroplasty", section
on 'Heterotopic ossification'.)
Deep venous thrombosis, cellulitis, infection, hematoma, and tumor should be considered as alternative
diagnoses for localized pain in SCI patients. Because calcification may not appear for weeks after clinical
presentation, plain radiographs are of limited use in the early diagnosis. An elevated serum alkaline
phosphatase level can help differentiate early heterotopic ossification from other conditions, but is not a
specific finding [91]. The triple phase bone scan is the most reliable test for diagnosis.
Early administration of NSAIDs (indomethacin 75 mg daily for three weeks or rofecoxib 25 mg daily for four
weeks) after SCI appears to reduce the incidence of heterotopic calcification according to a 2010 systematic
review that included two randomized trials [9294]. Further research is required to identify which patients will
benefit from this intervention. Warfarin and pulse lowintensity electromagnetic field therapy may also be
useful in the prevention of heterotopic ossification, but a clinical role for these modalities for this indication is
not yet established.
The initial treatments of heterotopic ossification are passive rangeofmotion exercise, with the goal of
maintaining joint mobility, and nonsteroidal antiinflammatory drugs (NSAIDS). Bisphosphonates may also be
useful [92]. According to uncontrolled case series, etidronate (given intravenous for three days, followed by six
months of oral therapy) reduced swelling and retarded or halted progression of heterotopic ossification,
particularly if it was administered early, when bone scans were positive, but radiographs remained normal
[92,9597]. Radiotherapy also appeared to limit progression in one case series of 52 patients with heterotopic
ossification after SCI [92,98]. For refractory cases, surgery is a treatment option to allow functional range of
movement; however, the majority of patients experience recurrence after surgery [99]. A small retrospective
study found that intravenous pamidronate (a bisphosphonate) prevented recurrent heterotopic ossification in
patients undergoing excision surgery [89]. Reports of early resection in combination with drug and radiation
treatment also appear promising [100,101].
MUSCULOSKELETAL COMPLICATIONS — After spinal cord injury (SCI), muscle contractures can result
from reorganization of the collagen tissue matrix that occurs when the muscle lies in the shortened position for
an extended period of time. Both immobility and spasticity contribute to this occurrence [102]. Preventive
management is extremely important and should begin immediately after a SCI and continue for longterm
care:
● Positioning. While in bed, the patient should be positioned, using pillows to minimize flexion at the hip and
knee, and adduction and internal rotation at the shoulder. Wheelchair positioning should maintain normal
lumbar lordosis. Frequent repositioning prevents skin breakdown as well as contractures; these
complications often coexist [102].
● Rangeofmotion exercise. Paretic extremity joints should be exercised 5 to 20 minutes daily. The
intensity of exercises needed to prevent deformity varies among individuals, but the goal is maintenance
of full range. Any limitation warrants investigation for heterotopic ossification, fracture, hematoma,
infection, or thrombosis.
● Splinting. Upper extremity flexion contractures and ankle plantarflexion contractures can be prevented
with resting night splints or bivalve (removable) casting. The fitting and timing of splints must be adjusted
based on skin and pain tolerance.
The goal of these interventions is to induce prolonged muscle stretching of vulnerable muscles; however, their
efficacy in preventing contractures has not been documented [103]. Established contractures may require
surgical treatment.
Certain contractures can facilitate function. Patients with SCI at C6 level may gain improved functional hand
tenodesis with finger flexion contractures that enhance prehension with wrist extension. A slight elbow flexion
contracture can improve the mechanical advantage of a weakened biceps muscle.
Repetitive overuse injuries in the upper extremities are common in SCI patients, related to transfers and
wheelchair use. Rotator cuff and other tendon injuries, carpal tunnel syndrome, bursitis, and osteoarthritis are
common sequelae [104106]. The shoulders are most often affected (75 percent), followed by wrists, hands,
and elbows (53, 43, and 35 percent, respectively). Specific exercise programs to minimize injuries and
preserve joint function can be helpful, as can the use of power wheelchairs and ergonomic assessments [107].
(See "Overview of joint protection".)
PRESSURE ULCERS — Pressure ulcers result from tissue damage due to unrelieved pressure that typically
occurs over bony prominences. Shear, friction, poor nutrition, and changes in skin physiology below the level
of the lesion also contribute to the development of pressure ulcers [21]. Prevalence rates for pressure ulcers
in chronic spinal cord injury (SCI) are difficult to obtain, but have been estimated at approximately 30 percent
at 20 years following SCI [21,108]. Both the level and severity of SCI impact significantly on the risk of
developing a pressure ulcer.
Multiple pressure ulcers occur in more than onethird of patients [20]. The most common locations of pressure
ulcers in the SCI patient are [21]:
● Ischium – 31 percent
● Trochanter 26 percent
● Sacrum 18 percent
● Heel 5 percent
● Malleolus 4 percent
● Feet 2 percent
Preventative strategies include:
● Examining skin over areas most vulnerable to ulcer formation daily
● Avoiding immobility and excess moisture in susceptible regions
● Use of pressurerelieving wheelchairs, cushions, and other devices
● Maintenance of adequate nutritional intake and weight
Comprehensive treatment includes assessment of health status and status of the ulcer. An ulcer treatment
plan consists of cleansing, debridement, nutritional support, and management of tissue loads. The prevention
and treatment of pressure ulcers are discussed in detail separately. (See "Prevention of pressureinduced skin
and soft tissue injury" and "Clinical staging and management of pressureinduced skin and soft tissue injury".)
SPASTICITY — Spasticity is believed to result from disruption of descending inhibitory modulation of the
alpha motor neurons, producing hyperexcitability, which is manifest as increased muscle tone and spasms
[109,110]. Negative effects of spasticity include pain, decreased mobility, contractures, and muscle spasms, all
of which can interfere with sleep and activities of daily living. At the same time, spasticity has some positive
aspects: increased tone can facilitate some functional activities, including standing and transfers. Increased
muscle tone may also promote venous return, minimizing deep venous thrombosis and orthostatic
hypotension.
Abolishing spasticity is difficult and not necessarily desirable [110]. Treatment should be directed at minimizing
spasticity as it relates to functional impairment and should follow a graded approach, starting with the least
invasive approach. Nonpharmacologic treatments include physical therapy. Regular stretching and use of
braces can help maintain range of movement and prevent contractures [110]. (See 'Musculoskeletal
complications' above.)
Oral medications — Though often prescribed for spasticity, the evidence of efficacy for commonly used oral
medications is not substantial, side effects are often dose limiting, and the relative benefit of these treatments
has not been established [111]. With all medications, slow dose escalation may mitigate against adverse side
effects, which include sedation, dry mouth, dizziness, and weakness. Dosing guidelines and adverse effects of
these medications are summarized in the Table (table 1).
● Baclofen, a GABAB agonist, is the most commonly used oral medication for spasticity, despite the
paucity of evidencebased support for its efficacy [111113]. Although adverse effects of sedation and
weakness can be doselimiting, baclofen is safe for longterm use, without evidence of tolerance [110].
Abrupt discontinuation of baclofen is advised against because of potential withdrawal symptoms. (See
"Neuroleptic malignant syndrome", section on 'Other drugrelated syndromes'.)
● Tizanidine, a centrally acting alpha2 adrenergic agonist, was compared with placebo in one of the largest
studies of spasticity treatment in spinal cord injury (SCI) patients [114]. Among the 78 of 124 randomized
patients who completed the study, tizanidine produced a significant reduction in spasticity, but had no
effect on activities of daily living and other functional assessments. Sedation was the most common
limiting side effect [115].
● Diazepam, a GABAA agonist, is the most commonly used benzodiazepine for spasticity, often in
conjunction with baclofen or tizanidine [109,116]. Sedation, confusion, hypotension, and gastrointestinal
symptoms can be doselimiting. Diazepam or clonazepam may be particularly useful in controlling
nighttime spasms.
● Dantrolene sodium differs from other medications discussed in that it acts peripherally, inhibiting calcium
release from sarcoplasmic reticulum of the muscle [110]. More than the other agents used, it produces
weakness of both affected and unaffected muscles [113]. Its potential for hepatotoxicity requires liver
function test monitoring every three to six months [109].
● Less commonly used oral medications used for spasticity include clonidine, gabapentin, cannabinoids,
and cyproheptadine (table 1) [109,110,117119].
Intrathecal baclofen — Baclofen is centrally acting, but crosses the blood brain barrier ineffectively, limiting
its bioavailability when taken orally. Intrathecal baclofen allows for fourtimes the amount of baclofen to be
delivered to the spinal cord with 1 percent of the oral dose [18,110]. Treatment is administered by a surgically
implanted, computerprogrammed infusion pump with a catheter extending into the intrathecal space. In
general, patients undergo a trial of intrathecal baclofen infusions prior to pump implantation. Although
systemic side effects of baclofen are generally avoided with this approach, complications of intrathecal
baclofen therapy can include spinal fluid leaks, hemorrhage, infection, catheter dislodgement, and pump
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failure.
Two doubleblind crossover studies compared intrathecal baclofen infusion with saline placebo in patients
after SCI [120,121]. Patients treated with intrathecal baclofen had both reduced spasticity and improved
disability. This approach may also reduce pain associated with spasticity [122].
Injection techniques — Chemodenervation provides a localized treatment of spasticity within a muscle or
muscle group. Although systemic side effects associated with medications are avoided, the large number of
muscles involved in SCI limit the use of this approach for these patients. However, in some patients, targeted
relief of spasticity in certain muscle groups can improve ambulation and other specific functions. Agents
include botulinum toxin, phenol, and alcohol.
Botulinum toxin acts at the neuromuscular junction, preventing acetylcholine release. Treatment effects last a
few months, requiring repeated injections. Side effects include muscle weakness and injectionsite reactions,
but in general this treatment is safe and effective [123]. One randomized study compared botulinum toxin
injections to tizanidine for upper limb spasticity following stroke or traumatic brain injury [115]. Botulinum toxin
treatments were more effective in reducing tone and were associated with fewer adverse effects than
tizanidine. However, spasticity is not as yet an FDAapproved indication for botulinum toxin.
The US Food and Drug Administration has issued a warning about the possibility of lifethreatening systemic
adverse effects from local botulinum toxin injections. The warning was based on reports of severe difficulty
swallowing or breathing in several patients and occurred mostly in children with cerebral palsy receiving local
injections for limb spasticity. Some of these complications appear be caused by inadvertent overdosing,
because potency determinations expressed in "units" varied among botulinum toxin products. In response, the
FDA mandated changes in drug names that were designed to emphasize these differences in drug potency
and prevent medication errors [124]. Providers should be alert for the potential of systemic effects, including
dysphagia, dysphonia, weakness, or dyspnea, occurring up to several weeks after treatment.
Phenol and ethanol nerve blocks essentially superimpose a lower motor neuron lesion on the upper motor
neuron deficit [109,110]. Weakness, injection site pain, phlebitis, permanent nerve damage, and sensory
dysesthesia can be problematic complications of this procedure.
Surgery — Surgical destructive procedures, rhizotomy, myelotomy, cordotomy, and cordectomy are reserved
for refractory cases [18]. Orthopedic procedures involving the muscle or tendon can be used to treat
established contractures.
PAIN SYNDROMES — A significant number of patients develop a chronic pain syndrome several months to
years after spinal cord injury (SCI). Reported prevalences vary considerably. On average, twothirds of
patients suffer chronic pain and about onequarter to onethird of patients have severe pain that significantly
affects quality of life [113,125].
Neurogenic pain after SCI can be both spontaneous and stimulusevoked, is often poorly localized, and is
often described as burning, stabbing, or electrical in quality. Hyperesthesia is a common component. These
qualities can help distinguish neurogenic from musculoskeletal pain (usually dull, aching, and welllocalized)
that can result from a number of complications common to SCI patients. (See 'Musculoskeletal complications'
above.)
Although neurogenic pain appears to be associated with neuronal hyperexcitability, mechanisms are poorly
understood. Two types of neurogenic pain syndromes are recognized: atlevel pain (ie, pain in segments at
the level of SCI) and belowlevel pain. These are believed to have different neuroanatomic and
pathophysiologic bases, with injury to nerve roots and dorsal gray matter causing atlevel pain, and injury to
spinothalamic tracts and/or thalamic deafferentation responsible for belowlevel pain [126]. Development of at
level pain should provoke an evaluation for posttraumatic syringomyelia, with which it is associated. (See
'Syringomyelia' below.)
Medical treatments are often unsatisfactory; antidepressant, antiepileptic, and standard analgesic medications
are tried, often in combination:
● Antiepileptic drugs are believed to improve neuropathic pain by suppressing abnormal neuronal
hyperexcitability. Two randomized studies of pregabalin (150 to 600 mg daily) in patients with pain after
SCI have reported improvements in blinded assessments of pain scores, as well as in disturbed sleep,
anxiety, and depression [127,128]. Other randomized trials have studied lamotrigine, gabapentin,
valproate in SCI; with mixed evidence of efficacy [129132].
● Antidepressant medications are also used in a variety of central and peripheral neuropathic pain
syndromes. Randomized trials of trazodone and amitriptyline in SCI have not demonstrated efficacy [132
134].
● Opiates may provide relief in anecdotal reports, but side effects, tolerance, and dependence are
significant issues [135].
It is reasonable to believe that nonoral routes of administration may provide better efficacy with fewer side
effects; however, evidence supporting these therapies is somewhat limited in SCI. Therapies have included
intrathecal administration of morphine, clonidine, and baclofen [136,137].
Invasive treatments, including deep brain stimulation, motor cortex stimulation, cordotomy, and dorsal root
entry zone lesions have been tried, again without substantive evidence of success [113,138]. In the absence
of good therapies, it is not unreasonable to also consider nontraditional treatments such as acupuncture and
biofeedback [18].
Details regarding dosing regimens, side effects, and other aspects of chronic pain management are discussed
separately. (See "Overview of the treatment of chronic noncancer pain".)
NEUROLOGIC DETERIORATION
Syringomyelia — A delayed progressive intramedullary cystic degeneration complicates 3 to 4 percent of
traumatic spinal cord injury (SCI) as well as other acute myelopathies. The interval since SCI can vary from
several months to many years [139]. Postulated mechanisms include scarring with obstruction of CSF flow
and altered tissue compliance leading to expansion of the central canal and compression of surrounding cord
tissue [140]. Symptoms are consistent with a progressive myelopathy and include worsening motor, sensory,
bowel, and bladder deficits and pain [139]. Arachnoiditis, cord compression and/or a narrowed spinal canal,
and bony deformity, especially kyphosis, seem to be risk factors for progressive enlargement of the cyst and
neurologic deterioration [141144].
An asymptomatic syrinx is a common incidental finding on neuroimaging in SCI patients. This entity usually
has a benign prognosis, and likely represents a focal area of liquefaction necrosis of cord tissue.
Treatment is aimed at reducing expansile intracystic pressure and improving CSF flow [139]. Surgical
approaches include shunt placement, lysis of subarachnoid adhesions, cyst fenestration, and dural
augmentation. Extradural decompression is anecdotally reported to be helpful when there is significant bone
deformity and compression of the spinal canal with restriction of spinal fluid circulation [145,146].
Unfortunately, longterm treatment benefits are seen in less than half of patients, and shunt failure is common
[146,147]. Pain may be more responsive to intervention than are motor symptoms [148,149].
Progressive posttraumatic myelomalacic myelopathy — Also known as the marshy cord syndrome,
progressive posttraumatic myelomalacic myelopathy is a less frequent complication of SCI and is
characterized pathologically by microcysts, reactive gliosis, and meningeal thickening. Adhesions and cord
tethering appear to be causally related; surgical untethering and duraplasty with expansion of the
subarachnoid space can lead to clinical improvement [139,150].
PSYCHIATRIC COMPLICATIONS — Psychosocial complications associated with spinal cord injury (SCI)
include depression, suicide, drug addiction, and divorce [5,8].
Between 20 to 45 percent of patients are depressed after traumatic SCI [8,151]. This symptom often emerges
early on, within the first month after SCI, and is not closely tied to the severity of injury. Patients with SCI have
a four to five times higher rate of suicide compared to agematched population samples [5,152]. Suicide is a
leading cause of death in traumatic SCI patients younger than 55 years; 75 percent of suicides occur within
the first five years of injury [8]. Similar rates of depression and suicide are observed after transverse myelitis
[153].
Because of its high prevalence and serious consequences, patients with SCI should be regularly screened for
symptoms of depression. High levels of pain and lack of social support identify patients at high risk for
depression and suicidality [151].
Depression and anxiety following SCI should be treated; it should not be assumed that symptoms are a
"normal" reaction to the circumstances and do not require treatment [8]. Recommended interventions include
psychologic counseling, pharmacologic intervention, and peer support groups. (See "Unipolar depression in
adults: Assessment and diagnosis" and "Unipolar major depression in adults: Choosing initial treatment".)
THERMOREGULATORY DYSFUNCTION — Disrupted autonomic pathways following spinal cord injury (SCI)
can lead to impaired vasomotor and sudomotor responses in regions of insensate skin, reduced
thermoregulatory effector response for a given core temperature, and loss of skeletal muscle pump activity
from paralyzed limbs [154]. Consequences can include hyperthermia during exercise or high ambient heat
and hypothermia in lower ambient heat. There can be a blunted fever or a hypothermic response to infection.
Others have noted episodes of hyperthermia or hypothermia in the absence of infection or environmental
temperature change in SCI patients.
FUNCTIONAL DEFICITS — The level and completeness of the spinal cord injury (SCI) are the principal
determinants of the needs, goals, and expectations in functional abilities. Age, general health, body habitus,
concurrent injuries, spinal instrumentation, intelligence, and motivation also influence recovery [155].
Functional recovery after a SCI begins in the acute care setting as soon as the patient is medically stable with
rangeofmotion and resistive exercise, upright positioning, and transfer work. In the inpatient rehabilitation
setting, physical and occupational therapists experienced in SCI rehabilitation develop individualized programs
that emphasize strengthening, joint protection, and compensatory strategies, combined with creative use of
assistive devices and equipment to maximize function. There are no studies that suggest one form of therapy
is more effective than another; despite evolving technological advances, the simplest traditional approaches
are often the best [156,157].
The general expectations for functional recovery based on motor level are outlined in the Table (table 2) [158].
These assume an uncomplicated, complete SCI followed by appropriate rehabilitation interventions in a
healthy, motivated individual.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics”
and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th
grade reading level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer short, easytoread
materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed.
These articles are written at the 10th to 12th grade reading level and are best for patients who want indepth
information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or email
these topics to your patients. (You can also locate patient education articles on a variety of subjects by
searching on “patient info” and the keyword(s) of interest.)
● Basics topics (see "Patient education: Neurogenic bladder in adults (The Basics)" and "Patient education:
Paraplegia and quadriplegia (The Basics)")
SUMMARY AND RECOMMENDATIONS — Medical complications after spinal cord injury (SCI) are both
common and severe, contributing to a high rehospitalization rate and decreased life expectancy. (See 'Life
expectancy' above.)
● Autonomic dysreflexia can complicate SCI above T6. This is an exaggerated sympathetic response
characterized by headache, diaphoresis, and increased blood pressure that occurs with noxious stimuli
such as pain from bladder distension, constipation, or pressure sores. (See 'Autonomic dysreflexia'
above.)
● Patients with SCI also have an increased incidence of CAD. Hemodynamic instability and cardiac
arrhythmias can be problematic in the acute and subacute SCI and are less frequent problems in chronic
SCI. (See 'Cardiovascular complications' above.)
● The severity of ventilatory failure and requirement for assisted ventilation depends on the level and
severity of the SCI. Lesser degrees of ventilatory failure may produce dyspnea and exercise intolerance.
(See "Respiratory physiologic changes following spinal cord injury" and "Respiratory complications in the
adult patient with chronic spinal cord injury", section on 'Respiratory insufficiency'.)
● An increase risk of pneumonia is highest in the first year following SCI, but patients remain at increased
risk over their lifetime. (See "Respiratory complications in the adult patient with chronic spinal cord injury",
section on 'Pulmonary infection'.)
● Prophylactic use of lowmolecularweight heparin to prevent deep venous thrombosis and pulmonary
embolism should be continued for at least three months after SCI, after which the risk appears to
approximate that of the general population. (See "Prevention of venous thromboembolic disease in
surgical patients".)
● SCI produces bladder dysfunction, often referred to as the neurogenic bladder. Other complications can
result from this, including infections, vesicoureteral reflux, renal failure, and renal calculi. Clean
intermittent catheterization, supplemented by medications as needed is the usual initial treatment. Some
patients require a chronic indwelling catheter. Botulinum toxin and sacral nerve modulators are being
investigated as alternative treatment options. (See 'Urinary complications' above.)
● Sexual dysfunction after SCI can include decreased libido, impotence, and infertility. Erectile dysfunction
may respond to treatment with a phosphodiesterase5 inhibitor. (See 'Sexual dysfunction' above.)
● Bowel dysfunction after SCI usually requires treatment with a bowel evacuation protocol and a multi
dimensional approach. A regular diet that includes adequate fiber is an important part of management.
(See 'Gastrointestinal complications' above.)
● Osteoporosis affects bones below the level of the SCI and increases the risk of fracture. The role of
bisphosphonates in this setting is under investigation. (See 'Bone metabolism' above.)
● Positioning and mobilization can help ameliorate contractures and pressure ulcers after SCI. (See
'Musculoskeletal complications' above and 'Pressure ulcers' above.)
● Spasticity is common after SCI and has positive as well as negative effects. Treatment is empiric and is
aimed at minimizing pain while maximizing function. Options include oral medication, intrathecal baclofen,
botulinum toxin, and nerve blocks. Refractory spasticity may require surgery. (See 'Spasticity' above.)
● Neurogenic pain after SCI is often refractory but may respond to standard analgesic therapy, antiepileptic
drug therapy, and/or antidepressant therapy. (See 'Pain syndromes' above.)
● Depression frequently complicates SCI; patients are at high risk for suicidality and should be monitored.
(See 'Psychiatric complications' above.)
● Functional neurologic deficits are determined by the level and completeness of the SCI and are
ameliorated by appropriate rehabilitation interventions. If patients experience neurologic decline,
neuroimaging is indicated to exclude syringomyelia, posttraumatic myelomalacic myelopathy, or other
neurologic pathology. (See 'Functional deficits' above and 'Neurologic deterioration' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. National Spinal Cord Injury Statistical Center, Birmingham, AL. Annual Report for the Model Spinal Cord
Injury Care Systems, Birmingham, AL 2005.
2. McDonald JW, Sadowsky C. Spinalcord injury. Lancet 2002; 359:417.
3. Cardenas DD, Hoffman JM, Kirshblum S, McKinley W. Etiology and incidence of rehospitalization after
traumatic spinal cord injury: a multicenter analysis. Arch Phys Med Rehabil 2004; 85:1757.
4. Frankel HL, Coll JR, Charlifue SW, et al. Longterm survival in spinal cord injury: a fifty year
investigation. Spinal Cord 1998; 36:266.
5. Hagen EM, Lie SA, Rekand T, et al. Mortality after traumatic spinal cord injury: 50 years of followup. J
Neurol Neurosurg Psychiatry 2010; 81:368.
6. Bycroft J, Shergill IS, Chung EA, et al. Autonomic dysreflexia: a medical emergency. Postgrad Med J
2005; 81:232.
7. Karlsson AK. Autonomic dysreflexia. Spinal Cord 1999; 37:383.
8. Kirshblum SC, Priebe MM, Ho CH, et al. Spinal cord injury medicine. 3. Rehabilitation phase after acute
spinal cord injury. Arch Phys Med Rehabil 2007; 88:S62.
9. Helkowski WM, Ditunno JF Jr, Boninger M. Autonomic dysreflexia: incidence in persons with
neurologically complete and incomplete tetraplegia. J Spinal Cord Med 2003; 26:244.
10. Chancellor MB, Erhard MJ, Hirsch IH, Stass WE Jr. Prospective evaluation of terazosin for the treatment
of autonomic dysreflexia. J Urol 1994; 151:111.
11. Vaidyanathan S, Soni BM, Sett P, et al. Pathophysiology of autonomic dysreflexia: longterm treatment
with terazosin in adult and paediatric spinal cord injury patients manifesting recurrent dysreflexic
episodes. Spinal Cord 1998; 36:761.
12. Lindan R, Leffler EJ, Kedia KR. A comparison of the efficacy of an alphaIadrenergic blocker in the slow
calcium channel blocker in the control of autonomic dysreflexia. Paraplegia 1985; 23:34.
13. Myers J, Lee M, Kiratli J. Cardiovascular disease in spinal cord injury: an overview of prevalence, risk,
evaluation, and management. Am J Phys Med Rehabil 2007; 86:142.
14. Bauman WA, Spungen AM. Metabolic changes in persons after spinal cord injury. Phys Med Rehabil
Clin N Am 2000; 11:109.
15. Wu JC, Chen YC, Liu L, et al. Increased risk of stroke after spinal cord injury: a nationwide 4year follow
up cohort study. Neurology 2012; 78:1051.
16. Jacobs PL, Nash MS. Exercise recommendations for individuals with spinal cord injury. Sports Med
2004; 34:727.
17. Phillips SM, Stewart BG, Mahoney DJ, et al. Bodyweightsupport treadmill training improves blood
glucose regulation in persons with incomplete spinal cord injury. J Appl Physiol (1985) 2004; 97:716.
18. 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.
19. Franga DL, Hawkins ML, Medeiros RS, Adewumi D. Recurrent asystole resulting from high cervical
spinal cord injuries. Am Surg 2006; 72:525.
20. Chen D, Apple DF Jr, Hudson LM, Bode R. Medical complications during acute rehabilitation following
spinal cord injurycurrent experience of the Model Systems. Arch Phys Med Rehabil 1999; 80:1397.
21. McKinley WO, Jackson AB, Cardenas DD, DeVivo MJ. Longterm medical complications after traumatic
spinal cord injury: a regional model systems analysis. Arch Phys Med Rehabil 1999; 80:1402.
22. Ploumis A, Ponnappan RK, Maltenfort MG, et al. Thromboprophylaxis in patients with acute spinal
injuries: an evidencebased analysis. J Bone Joint Surg Am 2009; 91:2568.
23. Bellucci CH, Wöllner J, Gregorini F, et al. Acute spinal cord injurydo ambulatory patients need
urodynamic investigations? J Urol 2013; 189:1369.
24. Burns AS, Rivas DA, Ditunno JF. The management of neurogenic bladder and sexual dysfunction after
spinal cord injury. Spine (Phila Pa 1976) 2001; 26:S129.
25. Chiodo AE, Scelza WM, Kirshblum SC, et al. Spinal cord injury medicine. 5. Longterm medical issues
and health maintenance. Arch Phys Med Rehabil 2007; 88:S76.
26. Nesathurai S. Bladder management. In: The Rehabilitation of People with Spinal Cord Injury, Nesathurai
S (Ed), Arbuckle Academic Publishers, Boston 1999. p.39.
27. Jamison J, Maguire S, McCann J. Catheter policies for management of long term voiding problems in
adults with neurogenic bladder disorders. Cochrane Database Syst Rev 2011; :CD004375.
28. Cameron AP, Rodriguez GM, Schomer KG. Systematic review of urological followup after spinal cord
injury. J Urol 2012; 187:391.
29. Benarroch EE. Neural control of the bladder: recent advances and neurologic implications. Neurology
2010; 75:1839.
30. Shekelle PG, Morton SC, Clark KA, et al. Systematic review of risk factors for urinary tract infection in
adults with spinal cord dysfunction. J Spinal Cord Med 1999; 22:258.
31. Kalsi V, Gonzales G, Popat R, et al. Botulinum injections for the treatment of bladder symptoms of
multiple sclerosis. Ann Neurol 2007; 62:452.
32. Naumann M, So Y, Argoff CE, et al. Assessment: Botulinum neurotoxin in the treatment of autonomic
disorders and pain (an evidencebased review): report of the Therapeutics and Technology Assessment
Subcommittee of the American Academy of Neurology. Neurology 2008; 70:1707.
33. Gallien P, Reymann JM, Amarenco G, et al. Placebo controlled, randomised, double blind study of the
effects of botulinum A toxin on detrusor sphincter dyssynergia in multiple sclerosis patients. J Neurol
Neurosurg Psychiatry 2005; 76:1670.
34. Herschorn S, Gajewski J, Ethans K, et al. Efficacy of botulinum toxin A injection for neurogenic detrusor
overactivity and urinary incontinence: a randomized, doubleblind trial. J Urol 2011; 185:2229.
35. Duthie JB, Vincent M, Herbison GP, et al. Botulinum toxin injections for adults with overactive bladder
syndrome. Cochrane Database Syst Rev 2011; :CD005493.
36. Sievert KD, Amend B, Gakis G, et al. Early sacral neuromodulation prevents urinary incontinence after
complete spinal cord injury. Ann Neurol 2010; 67:74.
37. Peters KM, Kandagatla P, Killinger KA, et al. Clinical outcomes of sacral neuromodulation in patients
with neurologic conditions. Urology 2013; 81:738.
38. Siroky MB. Pathogenesis of bacteriuria and infection in the spinal cord injured patient. Am J Med 2002;
113 Suppl 1A:67S.
39. Waites KB, Canupp KC, Chen Y, et al. Bacteremia after spinal cord injury in initial versus subsequent
hospitalizations. J Spinal Cord Med 2001; 24:96.
40. Bakke A, Vollset SE. Risk factors for bacteriuria and clinical urinary tract infection in patients treated with
clean intermittent catheterization. J Urol 1993; 149:527.
41. Esclarín De Ruz A, García Leoni E, Herruzo Cabrera R. Epidemiology and risk factors for urinary tract
infection in patients with spinal cord injury. J Urol 2000; 164:1285.
42. Morton SC, Shekelle PG, Adams JL, et al. Antimicrobial prophylaxis for urinary tract infection in persons
with spinal cord dysfunction. Arch Phys Med Rehabil 2002; 83:129.
43. Hull R, Rudy D, Donovan W, et al. Urinary tract infection prophylaxis using Escherichia coli 83972 in
spinal cord injured patients. J Urol 2000; 163:872.
44. Reid G, Hsiehl J, Potter P, et al. Cranberry juice consumption may reduce biofilms on uroepithelial cells:
pilot study in spinal cord injured patients. Spinal Cord 2001; 39:26.
45. Linsenmeyer TA, Harrison B, Oakley A, et al. Evaluation of cranberry supplement for reduction of urinary
tract infections in individuals with neurogenic bladders secondary to spinal cord injury. A prospective,
doubleblinded, placebocontrolled, crossover study. J Spinal Cord Med 2004; 27:29.
46. Waites KB, Canupp KC, Armstrong S, DeVivo MJ. Effect of cranberry extract on bacteriuria and pyuria
in persons with neurogenic bladder secondary to spinal cord injury. J Spinal Cord Med 2004; 27:35.
47. Foley SJ, McFarlane JP, Shah PJ. Vesicoureteric reflux in adult patients with spinal injury. Br J Urol
1997; 79:888.
48. Ku JH, Choi WJ, Lee KY, et al. Complications of the upper urinary tract in patients with spinal cord injury:
a longterm followup study. Urol Res 2005; 33:435.
49. Kim YH, Bird ET, Priebe M, Boone TB. The role of oxybutynin in spinal cord injured patients with
indwelling catheters. J Urol 1997; 158:2083.
50. Weld KJ, Wall BM, Mangold TA, et al. Influences on renal function in chronic spinal cord injured patients.
J Urol 2000; 164:1490.
51. Giannantoni A, Scivoletto G, Di Stasi SM, et al. Clean intermittent catheterization and prevention of renal
disease in spinal cord injury patients. Spinal Cord 1998; 36:29.
52. Benevento BT, Sipski ML. Neurogenic bladder, neurogenic bowel, and sexual dysfunction in people with
spinal cord injury. Phys Ther 2002; 82:601.
53. Derry FA, Dinsmore WW, Fraser M, et al. Efficacy and safety of oral sildenafil (Viagra) in men with
erectile dysfunction caused by spinal cord injury. Neurology 1998; 51:1629.
54. Giuliano F, Hultling C, El Masry WS, et al. Randomized trial of sildenafil for the treatment of erectile
dysfunction in spinal cord injury. Sildenafil Study Group. Ann Neurol 1999; 46:15.
55. Maytom MC, Derry FA, Dinsmore WW, et al. A twopart pilot study of sildenafil (VIAGRA) in men with
erectile dysfunction caused by spinal cord injury. Spinal Cord 1999; 37:110.
56. Schmid DM, Schurch B, Hauri D. Sildenafil in the treatment of sexual dysfunction in spinal cordinjured
male patients. Eur Urol 2000; 38:184.
57. Giuliano F, SanchezRamos A, LöchnerErnst D, et al. Efficacy and safety of tadalafil in men with erectile
dysfunction following spinal cord injury. Arch Neurol 2007; 64:1584.
58. Giuliano F, RubioAurioles E, Kennelly M, et al. Vardenafil improves ejaculation success rates and self
confidence in men with erectile dysfunction due to spinal cord injury. Spine (Phila Pa 1976) 2008;
33:709.
59. Glickman S, Kamm MA. Bowel dysfunction in spinalcordinjury patients. Lancet 1996; 347:1651.
60. Levi R, Hultling C, Nash MS, Seiger A. The Stockholm spinal cord injury study: 1. Medical problems in a
regional SCI population. Paraplegia 1995; 33:308.
61. Stone JM, NinoMurcia M, Wolfe VA, Perkash I. Chronic gastrointestinal problems in spinal cord injury
patients: a prospective analysis. Am J Gastroenterol 1990; 85:1114.
62. Krassioukov A, Eng JJ, Claxton G, et al. Neurogenic bowel management after spinal cord injury: a
systematic review of the evidence. Spinal Cord 2010; 48:718.
63. Lynch AC, Antony A, Dobbs BR, Frizelle FA. Bowel dysfunction following spinal cord injury. Spinal Cord
2001; 39:193.
64. Coggrave M, Wiesel PH, Norton C. Management of faecal incontinence and constipation in adults with
central neurological diseases. Cochrane Database Syst Rev 2006; :CD002115.
65. Christensen P, Bazzocchi G, Coggrave M, et al. Outcome of transanal irrigation for bowel dysfunction in
patients with spinal cord injury. J Spinal Cord Med 2008; 31:560.
66. Del Popolo G, Mosiello G, Pilati C, et al. Treatment of neurogenic bowel dysfunction using transanal
irrigation: a multicenter Italian study. Spinal Cord 2008; 46:517.
67. Faaborg PM, Christensen P, Kvitsau B, et al. Longterm outcome and safety of transanal colonic
irrigation for neurogenic bowel dysfunction. Spinal Cord 2009; 47:545.
68. Strauther GR, Longo WE, Virgo KS, Johnson FE. Appendicitis in patients with previous spinal cord
injury. Am J Surg 1999; 178:403.
69. Moonka R, Stiens SA, Resnick WJ, et al. The prevalence and natural history of gallstones in spinal cord
injured patients. J Am Coll Surg 1999; 189:274.
70. Laffont I, Bensmail D, Rech C, et al. Late superior mesenteric artery syndrome in paraplegia: case report
and review. Spinal Cord 2002; 40:88.
71. Wilkinson R, Huang CT. Superior mesenteric artery syndrome in traumatic paraplegia: a case report and
literature review. Arch Phys Med Rehabil 2000; 81:991.
72. Lazo MG, Shirazi P, Sam M, et al. Osteoporosis and risk of fracture in men with spinal cord injury. Spinal
Cord 2001; 39:208.
73. Jiang SD, Dai LY, Jiang LS. Osteoporosis after spinal cord injury. Osteoporos Int 2006; 17:180.
74. Maïmoun L, Fattal C, Micallef JP, et al. Bone loss in spinal cordinjured patients: from physiopathology to
therapy. Spinal Cord 2006; 44:203.
75. Shojaei H, Soroush MR, Modirian E. Spinal cord injuryinduced osteoporosis in veterans. J Spinal Disord
Tech 2006; 19:114.
76. Garland DE, Adkins RH, Kushwaha V, Stewart C. Risk factors for osteoporosis at the knee in the spinal
cord injury population. J Spinal Cord Med 2004; 27:202.
77. Sabo D, Blaich S, Wenz W, et al. Osteoporosis in patients with paralysis after spinal cord injury. A cross
sectional study in 46 male patients with dualenergy Xray absorptiometry. Arch Orthop Trauma Surg
2001; 121:75.
78. Massagli TL, Cardenas DD. Immobilization hypercalcemia treatment with pamidronate disodium after
spinal cord injury. Arch Phys Med Rehabil 1999; 80:998.
79. Kedlaya D, Brandstater ME, Lee JK. Immobilization hypercalcemia in incomplete paraplegia: successful
treatment with pamidronate. Arch Phys Med Rehabil 1998; 79:222.
80. Reiter AL, Volk A, Vollmar J, et al. Changes of basic bone turnover parameters in shortterm and long
term patients with spinal cord injury. Eur Spine J 2007; 16:771.
81. Chappard D, Minaire P, Privat C, et al. Effects of tiludronate on bone loss in paraplegic patients. J Bone
Miner Res 1995; 10:112.
82. Pearson EG, Nance PW, Leslie WD, Ludwig S. Cyclical etidronate: its effect on bone density in patients
with acute spinal cord injury. Arch Phys Med Rehabil 1997; 78:269.
83. Nance PW, Schryvers O, Leslie W, et al. Intravenous pamidronate attenuates bone density loss after
acute spinal cord injury. Arch Phys Med Rehabil 1999; 80:243.
84. Zehnder Y, Risi S, Michel D, et al. Prevention of bone loss in paraplegics over 2 years with alendronate.
J Bone Miner Res 2004; 19:1067.
85. Gilchrist NL, Frampton CM, Acland RH, et al. Alendronate prevents bone loss in patients with acute
spinal cord injury: a randomized, doubleblind, placebocontrolled study. J Clin Endocrinol Metab 2007;
92:1385.
86. BeDell KK, Scremin AM, Perell KL, Kunkel CF. Effects of functional electrical stimulationinduced lower
extremity cycling on bone density of spinal cordinjured patients. Am J Phys Med Rehabil 1996; 75:29.
87. Clark JM, Jelbart M, Rischbieth H, et al. Physiological effects of lower extremity functional electrical
stimulation in early spinal cord injury: lack of efficacy to prevent bone loss. Spinal Cord 2007; 45:78.
88. Giangregorio L, McCartney N. Bone loss and muscle atrophy in spinal cord injury: epidemiology, fracture
prediction, and rehabilitation strategies. J Spinal Cord Med 2006; 29:489.
89. Schuetz P, Mueller B, ChristCrain M, et al. Aminobisphosphonates in heterotopic ossification: first
experience in five consecutive cases. Spinal Cord 2005; 43:604.
90. Citak M, Suero EM, Backhaus M, et al. Risk factors for heterotopic ossification in patients with spinal
cord injury: a casecontrol study of 264 patients. Spine (Phila Pa 1976) 2012; 37:1953.
91. Freebourn TM, Barber DB, Able AC. The treatment of immature heterotopic ossification in spinal cord
injury with combination surgery, radiation therapy and NSAID. Spinal Cord 1999; 37:50.
92. Teasell RW, Mehta S, Aubut JL, et al. A systematic review of the therapeutic interventions for
heterotopic ossification after spinal cord injury. Spinal Cord 2010; 48:512.
93. Banovac K, Williams JM, Patrick LD, Haniff YM. Prevention of heterotopic ossification after spinal cord
injury with indomethacin. Spinal Cord 2001; 39:370.
94. Banovac K, Williams JM, Patrick LD, Levi A. Prevention of heterotopic ossification after spinal cord injury
with COX2 selective inhibitor (rofecoxib). Spinal Cord 2004; 42:707.
95. Banovac K, Gonzalez F, Renfree KJ. Treatment of heterotopic ossification after spinal cord injury. J
Spinal Cord Med 1997; 20:60.
96. Banovac K, Gonzalez F, Wade N, Bowker JJ. Intravenous disodium etidronate therapy in spinal cord
injury patients with heterotopic ossification. Paraplegia 1993; 31:660.
97. Banovac K. The effect of etidronate on late development of heterotopic ossification after spinal cord
injury. J Spinal Cord Med 2000; 23:40.
98. SautterBihl ML, Hültenschmidt B, Liebermeister E, Nanassy A. Fractionated and singledose
radiotherapy for heterotopic bone formation in patients with spinal cord injury. A phaseI/II study.
Strahlenther Onkol 2001; 177:200.
99. Stover SL, Niemann KM, Tulloss JR. Experience with surgical resection of heterotopic bone in spinal
cord injury patients. Clin Orthop Relat Res 1991; :71.
100. McAuliffe JA, Wolfson AH. Early excision of heterotopic ossification about the elbow followed by
radiation therapy. J Bone Joint Surg Am 1997; 79:749.
101. SautterBihl ML, Liebermeister E, Nanassy A. Radiotherapy as a local treatment option for heterotopic
ossifications in patients with spinal cord injury. Spinal Cord 2000; 38:33.
102. Dalyan M, Sherman A, Cardenas DD. Factors associated with contractures in acute spinal cord injury.
Spinal Cord 1998; 36:405.
103. Harvey LA, Herbert RD. Muscle stretching for treatment and prevention of contracture in people with
spinal cord injury. Spinal Cord 2002; 40:1.
104. Gellman H, Sie I, Waters RL. Late complications of the weightbearing upper extremity in the paraplegic
patient. Clin Orthop Relat Res 1988; :132.
105. Hastings J, Goldstein B. Paraplegia and the shoulder. Phys Med Rehabil Clin N Am 2004; 15:vii, 699.
106. Sinnott KA, Milburn P, McNaughton H. Factors associated with thoracic spinal cord injury, lesion level
and rotator cuff disorders. Spinal Cord 2000; 38:748.
107. Paralyzed Veterans of America Consortium for Spinal Cord Medicine. Preservation of upper limb
function following spinal cord injury: a clinical practice guideline for healthcare professionals. J Spinal
Cord Med 2005; 28:434.
108. Yarkony, GM, Heinemann, AW. Pressure ulcers. In: Spinal cord injury: Clinical outcomes from the model
systems, Stover, SL, DeLisa, JA, Whiteneck, GG, (Eds), Aspen Publishing, Gaithersburg, MD 1995.
p.100.
109. Satkunam LE. Rehabilitation medicine: 3. Management of adult spasticity. CMAJ 2003; 169:1173.
110. Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord 2005; 43:577.
111. Taricco M, Adone R, Pagliacci C, Telaro E. Pharmacological interventions for spasticity following spinal
cord injury. Cochrane Database Syst Rev 2000; :CD001131.
112. Burke D, Gillies JD, Lance JW. An objective assessment of a gamma aminobutyric acid derivative in the
control of spasticity. Proc Aust Assoc Neurol 1971; 8:131.
113. Burchiel KJ, Hsu FP. Pain and spasticity after spinal cord injury: mechanisms and treatment. Spine
(Phila Pa 1976) 2001; 26:S146.
114. Nance PW. A comparison of clonidine, cyproheptadine and baclofen in spastic spinal cord injured
patients. J Am Paraplegia Soc 1994; 17:150.
115. Simpson DM, Gracies JM, Yablon SA, et al. Botulinum neurotoxin versus tizanidine in upper limb
spasticity: a placebocontrolled study. J Neurol Neurosurg Psychiatry 2009; 80:380.
116. Corbett M, Frankel HL, Michaelis L. A double blind, crossover trial of Valium in the treatment of
spasticity. Paraplegia 1972; 10:19.
117. Gruenthal M, Mueller M, Olson WL, et al. Gabapentin for the treatment of spasticity in patients with
spinal cord injury. Spinal Cord 1997; 35:686.
118. Stewart JE, Barbeau H, Gauthier S. Modulation of locomotor patterns and spasticity with clonidine in
spinal cord injured patients. Can J Neurol Sci 1991; 18:321.
119. Norman KE, Pépin A, Barbeau H. Effects of drugs on walking after spinal cord injury. Spinal Cord 1998;
36:699.
120. Penn RD, Savoy SM, Corcos D, et al. Intrathecal baclofen for severe spinal spasticity. N Engl J Med
1989; 320:1517.
121. Hugenholtz H, Nelson RF, Dehoux E, Bickerton R. Intrathecal baclofen for intractable spinal spasticitya
doubleblind crossover comparison with placebo in 6 patients. Can J Neurol Sci 1992; 19:188.
122. McClelland S 3rd, Bethoux FA, Boulis NM, et al. Intrathecal baclofen for spasticityrelated pain in
amyotrophic lateral sclerosis: efficacy and factors associated with pain relief. Muscle Nerve 2008;
37:396.
123. Simpson DM, Gracies JM, Graham HK, et al. Assessment: Botulinum neurotoxin for the treatment of
spasticity (an evidencebased review): report of the Therapeutics and Technology Assessment
Subcommittee of the American Academy of Neurology. Neurology 2008; 70:1691.
124. U.S. Food and Drug Administration. Information for healthcare professionals: OnabotulinumtoxinA
(marketed as Botox/Botox Cosmetic), AbobotulinumtoxinA (marketed as Dysport) and
RimabotulinumtoxinB (marketed as Myobloc). Available at:
www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/DrugSafetyIn
formationforHeathcareProfessionals/ucm174949.htm (Accessed on August 5, 2009).
125. Siddall PJ, Loeser JD. Pain following spinal cord injury. Spinal Cord 2001; 39:63.
126. Wasner G, Lee BB, Engel S, McLachlan E. Residual spinothalamic tract pathways predict development
of central pain after spinal cord injury. Brain 2008; 131:2387.
127. Siddall PJ, Cousins MJ, Otte A, et al. Pregabalin in central neuropathic pain associated with spinal cord
injury: a placebocontrolled trial. Neurology 2006; 67:1792.
128. Cardenas DD, Nieshoff EC, Suda K, et al. A randomized trial of pregabalin in patients with neuropathic
pain due to spinal cord injury. Neurology 2013; 80:533.
129. Drewes AM, Andreasen A, Poulsen LH. Valproate for treatment of chronic central pain after spinal cord
injury. A doubleblind crossover study. Paraplegia 1994; 32:565.
130. Finnerup NB, Sindrup SH, Bach FW, et al. Lamotrigine in spinal cord injury pain: a randomized
controlled trial. Pain 2002; 96:375.
131. Tai Q, Kirshblum S, Chen B, et al. Gabapentin in the treatment of neuropathic pain after spinal cord
injury: a prospective, randomized, doubleblind, crossover trial. J Spinal Cord Med 2002; 25:100.
132. Finnerup NB, Jensen TS. Spinal cord injury painmechanisms and treatment. Eur J Neurol 2004; 11:73.
133. Davidoff G, Guarracini M, Roth E, et al. Trazodone hydrochloride in the treatment of dysesthetic pain in
traumatic myelopathy: a randomized, doubleblind, placebocontrolled study. Pain 1987; 29:151.
134. Cardenas DD, Warms CA, Turner JA, et al. Efficacy of amitriptyline for relief of pain in spinal cord injury:
results of a randomized controlled trial. Pain 2002; 96:365.
135. Cardenas DD, Jensen MP. Treatments for chronic pain in persons with spinal cord injury: A survey study.
J Spinal Cord Med 2006; 29:109.
136. 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.
137. Herman RM, D'Luzansky SC, Ippolito R. Intrathecal baclofen suppresses central pain in patients with
spinal lesions. A pilot study. Clin J Pain 1992; 8:338.
138. Denkers MR, Biagi HL, Ann O'Brien M, et al. Dorsal root entry zone lesioning used to treat central
neuropathic pain in patients with traumatic spinal cord injury: a systematic review. Spine (Phila Pa 1976)
2002; 27:E177.
139. Lee TT, Alameda GJ, Camilo E, Green BA. Surgical treatment of posttraumatic myelopathy associated
with syringomyelia. Spine (Phila Pa 1976) 2001; 26:S119.
140. Brodbelt AR, Stoodley MA. Posttraumatic syringomyelia: a review. J Clin Neurosci 2003; 10:401.
141. Schurch B, Wichmann W, Rossier AB. Posttraumatic syringomyelia (cystic myelopathy): a prospective
study of 449 patients with spinal cord injury. J Neurol Neurosurg Psychiatry 1996; 60:61.
142. Abel R, Gerner HJ, Smit C, Meiners T. Residual deformity of the spinal canal in patients with traumatic
paraplegia and secondary changes of the spinal cord. Spinal Cord 1999; 37:14.
143. Vannemreddy SS, Rowed DW, Bharatwal N. Posttraumatic syringomyelia: predisposing factors. Br J
Neurosurg 2002; 16:276.
144. PerrouinVerbe B, LenneAurier K, Robert R, et al. Posttraumatic syringomyelia and posttraumatic
spinal canal stenosis: a direct relationship: review of 75 patients with a spinal cord injury. Spinal Cord
1998; 36:137.
145. Holly LT, Johnson JP, Masciopinto JE, Batzdorf U. Treatment of posttraumatic syringomyelia with
extradural decompressive surgery. Neurosurg Focus 2000; 8:E8.
146. Sgouros S, Williams B. Management and outcome of posttraumatic syringomyelia. J Neurosurg 1996;
85:197.
147. Batzdorf U, Klekamp J, Johnson JP. A critical appraisal of syrinx cavity shunting procedures. J
Neurosurg 1998; 89:382.
148. Kramer KM, Levine AM. Posttraumatic syringomyelia: a review of 21 cases. Clin Orthop Relat Res 1997;
:190.
149. Carroll AM, Brackenridge P. Posttraumatic syringomyelia: a review of the cases presenting in a regional
spinal injuries unit in the north east of England over a 5year period. Spine (Phila Pa 1976) 2005;
30:1206.
150. Lee TT, Alameda GJ, Gromelski EB, Green BA. Outcome after surgical treatment of progressive
posttraumatic cystic myelopathy. J Neurosurg 2000; 92:149.
151. North NT. The psychological effects of spinal cord injury: a review. Spinal Cord 1999; 37:671.
152. DeVivo MJ, Black KJ, Richards JS, Stover SL. Suicide following spinal cord injury. Paraplegia 1991;
29:620.
153. Kaplin AI, Krishnan C, Deshpande DM, et al. Diagnosis and management of acute myelopathies.
Neurologist 2005; 11:2.
154. Krassioukov AV, Karlsson AK, Wecht JM, et al. Assessment of autonomic dysfunction following spinal
cord injury: rationale for additions to International Standards for Neurological Assessment. J Rehabil Res
Dev 2007; 44:103.
155. Yarkony GM, Roth EJ, Heinemann AW, Lovell LL. Spinal cord injury rehabilitation outcome: the impact of
age. J Clin Epidemiol 1988; 41:173.
156. Kirshblum S. New rehabilitation interventions in spinal cord injury. J Spinal Cord Med 2004; 27:342.
157. Mehrholz J, Kugler J, Pohl M. Locomotor training for walking after spinal cord injury. Cochrane Database
Syst Rev 2012; 11:CD006676.
158. Braddom R. Physical medicine and rehabilitation, 2nd, WB Saunders Company, Philadelphia 2000.
p.1236.
Topic 4839 Version 9.0
GRAPHICS
Oral medications commonly used for spasticity
Starting dose Maximum dose Adverse effects
Baclofen 5 mg, three times 80 mg daily, in Muscle weakness, sedation, dizziness, withdrawal

daily divided doses syndrome
Tizanidine 2 mg daily 36 mg daily in Sedation, weakness, dizziness, reversible elevation of

divided doses transaminase
Diazepam 2 mg twice daily 40 to 60 mg daily, in Sedation, cognitive impairment, dizziness, potential for

or 5 mg at hs divided doses dependence and withdrawal syndrome
Dantrolene 25 mg 100 mg, four times Potentially irreversible hepatotoxicity requires regular

daily monitoring, weakness, sedation
Clonidine 0.05 mg, twice 0.1 mg, four times Hypotension, bradycardia, dizziness, constipation

daily daily
Gabapentin 100 mg three 3600 mg daily in Sedation, dizziness

times daily divided doses
Graphic 63526 Version 1.0
Expected functional recovery following complete spinal cord injury by spinal
level
Spinal
Activities of daily living Mobility/locomotion
level
C1C4 Feeding possible with balanced forearm orthoses Operate power chair with tongue, chin, or breath

Computer access by tongue, breath, voice controller
controls
Weight shifts with power tilt and recline chair
Mouth stick use
C5 Drink from cup, feed with static splints and setup Propel chair with hand rim projections short
Oral/facial hygiene, writing, typing with equipment distances on smooth surfaces
Dressing upper body possible Power chair with hand controller
Sidetoside weight shifts
C6 Feed, dress upper body with setup Bed mobility with equipment
Dressing lower body possible Level surface transfers with assistance
Forward weight shifts Propel indoors with coated hand rims
C7 Independent feeding, dressing, bathing with Independent bed mobility, level surface transfers
adaptive equipment, builtup utensils Wheelchair use outdoors (power chair for school
or work)
C8 Independent in feeding, dressing, bathing Propel chair, including curbs and wheelies
Bowel and bladder care with setup Wheelchairtocar transfers
T1 Independent in all selfcare Transfer from floor to wheelchair
T2L1 Stand with braces for exercise
L2 Potential for swingto gait with long leg braces
indoors
Use of forearm crutches
L3 Potential for community ambulation
Potential for ambulation with short leg braces
L4S1 Potential for ambulation without assistive devices
Reproduced with permission from: Physical Medicine and Rehabilitation, 2nd ed, Randall Braddom (ED), WB Saunders
Company, 2000. Copyright © 2000 Elsevier.
Graphic 73350 Version 3.0
Contributor Disclosures
Gary M Abrams, MD Nothing to disclose Marc Wakasa, MD Nothing to disclose Michael J Aminoff, MD,
DSc Equity Ownership/Stock Options: Trust, which is independently managed by a financial company. The
portfolio may include medical or drug companies. Janet L Wilterdink, MD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multilevel review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform
to UpToDate standards of evidence.
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Chronic Complications of Spinal Cord Injury and Disease - UpToDate

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Starting dose Maximum dose Adverse effects

Baclofen 5 mg, three times 80 mg daily, in Muscle weakness, sedation, dizziness, withdrawal

Tizanidine 2 mg daily 36 mg daily in Sedation, weakness, dizziness, reversible elevation of

Diazepam 2 mg twice daily 40 to 60 mg daily, in Sedation, cognitive impairment, dizziness, potential for

Dantrolene 25 mg 100 mg, four times Potentially irreversible hepatotoxicity requires regular

Clonidine 0.05 mg, twice 0.1 mg, four times Hypotension, bradycardia, dizziness, constipation

Gabapentin 100 mg three 3600 mg daily in Sedation, dizziness

C1C4 Feeding possible with balanced forearm orthoses Operate power chair with tongue, chin, or breath

You might also like

Chronic Complications of Spinal Cord Injury and Disease - UpToDate

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Document Information

Copyright

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Chronic Complications of Spinal Cord Injury and Disease - UpToDate

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23/05/2017 Chronic complications of spinal cord injury and disease ­ UpToDate

Starting dose Maximum dose Adverse effects

Baclofen 5 mg, three times 80 mg daily, in Muscle weakness, sedation, dizziness, withdrawal

Tizanidine 2 mg daily 36 mg daily in Sedation, weakness, dizziness, reversible elevation of

Diazepam 2 mg twice daily 40 to 60 mg daily, in Sedation, cognitive impairment, dizziness, potential for

Dantrolene 25 mg 100 mg, four times Potentially irreversible hepatotoxicity requires regular

Clonidine 0.05 mg, twice 0.1 mg, four times Hypotension, bradycardia, dizziness, constipation

Gabapentin 100 mg three 3600 mg daily in Sedation, dizziness

C1­C4 Feeding possible with balanced forearm orthoses Operate power chair with tongue, chin, or breath

You might also like

23/05/2017 Chronic complications of spinal cord injury and disease UpToDate

C1C4 Feeding possible with balanced forearm orthoses Operate power chair with tongue, chin, or breath