Phys Med Rehabil Clin N Am

18 (2007) 651–679

Spinal Cord Injury: A Comprehensive

Review
Fernando Branco, MDa,*,
Diana D. Cardenas, MD, MHAb,
Jelena N. Svircev, MDc,d
a
2833 26th Street, Fort Lauderdale, FL 33305, USA
b
Department of Rehabilitation Medicine, University of Miami Miller School of Medicine,
P.O. Box 016960 (D-461), CRB 958, Miami, FL 33101, USA
c
Department of Veterans Affairs, Puget Sound Health Care System, Seattle, WA, USA
d
Department of Rehabilitation Medicine, University of Washington, 1660 South Columbian
Way-SCI 128, Seattle WA 98108, USA

Spinal cord injury (SCI) results in multiorgan system dysfunction. In the

past, SCI portended reduced survival and diminished quality of life. How-
ever, with increasing awareness and advances in the management of compli-
cations resulting from SCI, individuals are living longer and more satisfying
lives. This article summarizes major interventions and advances in the man-
agement of patients who have SCI. Fundamental principles of SCI are re-
viewed by organ system and key points are highlighted.

Spinal cord injury epidemiology

The annual incidence of SCI in developed countries is estimated at 15 to
40 cases per million population [1]. In the United States, approximately
12,000 new injuries occur per year, with 5000 of those injured dying before
arrival at a hospital or during the hospitalization.
The prevalence of SCI is estimated to be 253,000 persons, ranging from
225,000 to 296,000 [2,3]. Men sustain SCI approximately four times more
often than women. Although this 4:1 gender ratio has remained constant
over the past 3 decades, a slight trend has been seen toward more women
having injuries, increasing from 18.2% in the 1970s to 21.8% in the 2000s
[4]. From 2000 to 2003, the average age of injury was 38 years [4]. This

* Corresponding author.
E-mail address: brancof@bellsouth.net (F. Branco).

1047-9651/07/$ - see front matter Ó 2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.pmr.2007.07.010 pmr.theclinics.com
652 BRANCO et al

increase is believed to be caused by the increasing age of the general

population.
At 67.4%, Whites compromise the larger proportion of those injured, fol-
lowed by African Americans making up 19.4%, Hispanic-Latino with
10.1%, and Other contributing 3.2% [4].
Motor vehicle crashes continue to be the most common cause of SCI
(45.6%), followed by falls (19.6%), violence (17.8%), sports (10.7%), and
other causes (6.3%) [4].
Since 2000, the most frequent neurologic category of injury is incomplete
tetraplegia (34.1%), followed by complete paraplegia (23.0%), complete tet-
raplegia (18.3%), and incomplete paraplegia (18.5%) [2]. In persons who
have motor and sensory complete injuries, mortality rates are higher for
those who have higher tetraplegia (C1-3) than for mid (C4-5) and low
(C6-8) injuries. Those who have low tetraplegia have a higher mortality
than individuals who have paraplegia.

Functional and clinical anatomy

The spinal cord serves as the relay tract that transfers motor information
from the brain to the periphery, and receives sensory information distally
and brings it centrally. It is protected and supported by meningeal coverings
(the dura and pia mater), ligaments, and bony vertebrae (7 cervical, 12 tho-
racic, 5 lumbar, and 5 sacral). Blood supply to the spinal cord is provided by
a single anterior spinal artery that supplies the anterior two thirds of cord,
and two posterior spinal arteries that supply the posterior one third of the
cord. Radicular arteries support the anterior and posterior spinal arteries.
The artery of Adamkiewicz, a large lumbar radicular artery, supplies the
midthoracic cord (T8-L1 vertebral level) and can be disrupted through in-
jury to the thoracoabdominal aorta [5].
The spinal cord lies within the spinal canal of the vertebrae and is contin-
uous with the medulla. It extends rostrally from the base of the foramen
magnum to the distal L2 vertebra, where it ends as a conical structure
known as the conus medullaris. Below the L2 level, nerve fibers of the
cord continue as the cauda equina.
Thirty-one pairs of nerve roots extend from the spinal cord: 8 cervical,
12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. The nerves numbered
1 through 7 exit above the corresponding vertebrae, and the eighth cervical
nerve slips between the seventh cervical and first thoracic vertebrae. For the
thoracic and lumbar sections, each of the numbered nerves exits below the
corresponding numbered vertebrae. Because the spinal cord is shorter than
the spinal canal, the segments of the cord do not correspond below the cer-
vical level. Therefore, the cervical vertebrae contain the cervical nerve seg-
ments, the thoracic vertebrae contain both the thoracic and lumbar nerve
segments, and the top lumbar vertebrae contain the sacral nerve segments.
 SPINAL CORD INJURY 653

For example, fractures at the T11-L1 vertebral level can affect the L1-S5
cord segments (Fig. 1).
A cross-section of the cord reveals gray and white matter. The central
gray matter may be divided into three horns: the posterior (dorsal) horn
contains projections of cell bodies of sensory fibers from dorsal root ganglia,
the lateral (intermediate) horn carries sympathetic neurons, and the anterior
(ventral) horn contains motor neurons (Fig. 2).
The surrounding white matter is divided into three main columns or
tracts: posterior (dorsal) column carrying sensory information, lateral

Fig. 1. Spinal cord peripheral nerve anatomy. (Reprinted from Netter Anatomy Illustration
Collection, Ó Elsevier Inc. All rights reserved.)
654 BRANCO et al

Fig. 2. Spinal cord tracts. (Reprinted from Netter Anatomy Illustration Collection, Ó Elsevier
Inc. All rights reserved.)

column relaying sensory and motor information, and anterior (ventral) col-
umn carrying primarily motor information (see Fig. 2).
Key tracts include (see Fig. 2) the dorsal columns (fasciculus gracilis and
fasciculus cuneatus), which carry information for proprioception, vibration,
and light touch; anterolateral spinothalamic tracts, which carry information
 SPINAL CORD INJURY 655

for pain and temperature (lateral), and touch and pressure (anterior); and
the corticospinal tract, which carries motor information.

Spinal cord injury examination

The International Standards for Neurological Classification of Spinal
Cord Injury [6], guidelines created by the Neurological Standards Commit-
tee of the American Spinal Injury Association (ASIA) are widely used to
classify spinal cord injuries. The Standards detail a neurologic examination
testing 10 key muscle group (5 upper extremity and 5 lower extremity) sen-
sations (light touch and pin prick) in 28 key dermatomes, and a rectal exam-
ination testing sensation and voluntary sphincter contraction (see Fig. 2).
Motor examination is performed by manual testing of 10 key muscle
groups on the right and left sides of the body (Table 1). Most muscles
have multiple spinal segment innervation. The key muscles selected are
innervated primarily by two segments, and the most rostral segment is
assigned for every key muscle [6]. With the patient in supine position, con-
ventional muscle grading (0–5) is assigned to each muscle. The motor level
of injury is defined by the lowest key muscle that has a grade of at least 3/5,
provided that the key muscles above that level are graded 5/5 [6].
Sensation is tested for light touch and pinprick. Light touch is performed
using a cotton wisp, with sensation graded on a scale of 0 to 2 (0 ¼ absent;
1 ¼ altered; 2 ¼ normal). The face serves as normal. The examiner then tests
each of the 26 dermatomes on both sides of the body and records the grade
of sensation. Pinprick is tested using a safety pin, with sensation also graded
on a scale of 0 to 2 (0 ¼ absent or cannot distinguish sharp or dull; 1 ¼ al-
tered but can differentiate sharp from dull; 2 ¼ normal). Similar to the light-
touch portion of the examination, the face serves as a normal reference and
each of the 28 key dermatomes on the right and left sides of the body are
tested and recorded. The sensory level of injury is defined as the most caudal
segment of the spinal cord, with normal sensory function on both right and

Table 1
Motor levels and key muscles
Motor level Muscles
C5 Elbow flexors
C6 Wrist extensors
C7 Elbow extensors
C8 Finger flexors
T1 Finger abductors
L2 Hip flexors
L3 Knee extensors
L4 Ankle dorsiflexors
L5 Long toe extensors
S1 Ankle dorsiflexors
656 BRANCO et al

left sides of the body. Muscles or sensory areas not able to be tested are re-
corded as ‘‘not tested.’’
A neurologic level of injury is defined as the most caudal spinal cord seg-
ment with normal muscle testing and sensation. For dermatomes not cov-
ered by muscles (C1-C4, T2-L1, S1-S4-S5), the sensory level is used to
identify the level of injury [6].
A rectal examination is performed to document the presence or absence
of intact voluntary sphincter control and deep anal sensation. Results are
recorded as ‘‘yes’’ or ‘‘no.’’ The presence of deep anal sensation may be
the only indicator of an incomplete SCI.
A complete injury is defined as the absence of sensory and motor function
in the lowest sacral segment. An incomplete injury is defined as partial pres-
ervation of sensory or motor function in the lowest sacral segments. The
zone of partial preservation is used only with complete injuries and for doc-
umenting dermatomes and myotomes caudal to the neurologic level of in-
jury that remain partially innervated. The zone of partial preservation is
recorded for motor and sensation for the right and left sides.
The ASIA Impairment Scale (AIS) is used to grade the degree of impair-
ment, and is defined as follows [6]:
 Complete injury:
AIS A; absence of sensory and motor function at lowest sacral seg-
ment S4/5
 Incomplete injuries:
AIS B: sensory but no motor function below the neurologic level of in-
jury, including the sacral segments S4/5
AIS C: Motor function is preserved below the neurologic level and
more than half of key muscles graded show strength of less than
3/5
AIS D: Motor function is preserved below the neurologic level and
more than half of the key muscles graded show strength greater
than or equal to 3
AIS E: Normal sensory and motor strength

Acute spinal cord injury treatment

Comprehensive medical treatment for the person who sustains an SCI be-
gins at the scene of the injury. Recognition of the potential for further cord
injury has led to the widespread use of immediate spine immobilization for
all SCIs or suspected SCIs. The main objectives of surgery are to decom-
press the spinal canal and achieve mechanical stability. An anterior or a pos-
terior approach to decompression may be chosen. Instrumentation may be
used to stabilize or augment a fusion. The surgeon determines the exact ap-
proach, which depends partly on the mechanism of injury. Flexion injuries
may be associated with posterior spinal ligamentous disruption, which may
 SPINAL CORD INJURY 657

not be apparent on plain radiographs but is with MRI [7]. Imaging generally
includes CT scans and plain films, and often MRI. Bone is better visualized
with CT than MRI, but MRI is better for showing cord and ligamentous
tissue damage. In SCI from gunshot wounds, surgical treatment is rarely in-
dicated unless progressive neural injury is present.
The Jefferson fracture is a C1 (atlas) posterior ring burst fracture caused
by axial load with hyperextension. C2 (axis) odontoid fractures are classified
according to anatomic location of the fracture, and treatment depends on
the type of injury. Subluxation of the axis on the C3 vertebra associated
with a fracture is termed a Hangman’s Fracture [8]. After surgical stabiliza-
tion, most patients who have cervical injuries are immobilized with an
orthosis for 8 to 12 weeks. In thoracolumbar injuries, a thoracic lumbar
sacral orthosis (TLSO) is often used for 3 to 6 months according to surgeon
recommendations. A recent report suggests that shorter periods of immobi-
lization suffice after internal fixation [9].

Spinal orthoses
Cervical orthosis
The cervical spine has the most range of all the spine segments (eg, occi-
put/C1, flexion/extension; C1-C2 (atlantoaxial), rotation. Various orthoses
are used in SCI. The Soft cervical collar is the most commonly used collar
and is mainly used for cervical muscle strain relief. It is made of a firm
foam material covered with cotton and causes minimal immobilization
(Fig. 3) [10,11]. The Philadelphia collar is foam-reinforced and provides
chin, occipital and upper chest support with minimal control of rotation
and lateral bending. It is commonly used after cervical surgery and stable
cervical fractures (Fig. 4) [10,11]. The Aspen collar is similar to the Philadel-
phia collar but offers slightly greater stability of lateral bending and rotation
than a soft collar (Fig. 5) [11]. The Miami J collar is hard plastic with cloth
pads and a tracheostomy cutout. It enables the best control of all move-
ments [11]. The Sternal Occipital Mandibular Immobilizer (SOMI) provides
rigid chest support and has adjustable chin and occipital portions. It offers
only moderate restraint of lateral bending and rotation, and is applied su-
pine (Fig. 6) [11]. The Minerva brace is a cervical–thoracic brace with a chest
plate and headband that provides immobilization from C1 to T1 (Fig. 7) [11]
and the Halo vest is a cranial–thoracic brace with cranial fixation pins that
provides maximal restriction of range of motion. Pin complications are com-
mon (eg, loosening, pain, infection, skin breakdown) (Fig. 8) [10,11].

Thoracic, lumbar, and sacral orthoses

The lumbosacral corset has molded plastic or metal stays, and is used
mainly for acute or chronic pain, with minimal immobilization (Fig. 9) [10].
658 BRANCO et al

Fig. 3. Soft cervical collar. (Reprinted from Netter Anatomy Illustration Collection, Ó Elsevier
Inc. All rights reserved.)

The Taylor brace is a TLSO that is mainly used for counteracting kyphosis
(Fig. 10) [10,11]. The Knight Taylor brace is a TLSO that provides moderate
limitation of flexion/extension and lateral flexion and hyperextends the tho-
racic spine for bracing stable fractures and providing stability postsurgery
(see Fig. 10) [10,11]. The Jewett brace is a hyperextension TLSO that provides
a three-point system to facilitate thoracic hyperextension, an anterior pad on
 SPINAL CORD INJURY 659

Fig. 4. Philadelphia collar. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida; with
permission.)

the sternum and pubic symphysis, and a posterior pad on the thoracolumbar
junction, and permits limited flexion (Fig. 11) [10,11]. The Cruciform Anterior
Spinal Hyperextension (CASH) brace is also used for kyphosis. It consists of
an anterior cross bar with pads at the four ends, and adjusts from the back. It is
harder to use than the Jewett brace (Fig. 12) [10,11]. The Milwaukee brace is
a cervical TLSO with lateral pads in noncircumferential arrangement. It is
used mainly for idiopathic scoliosis and designed to cause active and passive
forces to correct the curvatures (Fig. 13) [11].
Pharmacologic treatment of acute SCI is currently limited. Standard care
using methylprednisolone during the acute phase is controversial [12]. An-
other compound is GM1 ganglioside, which can promote neurite outgrowth,
regeneration, and sprouting [13]. Activated macrophages, when injected in
the spinal cord, can be associated with improved motor recovery in rats
[14], but the ProCord clinical trial, which began in 2003, was suspended.

Bladder management
The primary components of the voiding mechanism include the bladder
(detrusor) muscle, bladder neck, urethra, periurethral muscles, and striated
pelvic floor muscles, including the levator ani and endopelvic fascia. Three
660 BRANCO et al

Fig. 5. Aspen cervical collar. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida;
with permission.)

smooth muscles layers interweave to form the detrusor. The fibers of the
three layers continue to form the bladder neck. The urethra is composed
of smooth muscle fibers descending from the bladder neck and striated mus-
cles extending from the pelvic floor muscles (Fig. 14).
Control of the bladder is regulated by neural circuits in the brain and spi-
nal cord that coordinate smooth muscles in the bladder wall and striated
muscle in the urethral sphincter. The detrusor is innervated by the parasym-
pathetic fibers arising from the anterior gray columns of the sacral second,
third, and fourth segments. The nerve fibers pass through the pelvic splanch-
nic nerves, continue as the pelvic nerve, and synapse at the ganglion located
in the bladder wall. The postganglionic nerves secrete acetylcholine at the
motor nerve endings. The bladder wall is supplied with muscarinic M2
and M3 receptors, which respond to parasympathetic stimulation with con-
traction. Sympathetic nerve supply to the bladder originates from cells in the
lateral gray columns of the thoracic and lumbar spinal cord at the thoracic
10 to lumbar 2 levels. The nerves synapse at the sympathetic trunk located in
the paravertebral region. The postganglionic fibers continue as the hypogas-
tric nerve, traverse the bladder, and release norepinephrine. a-Adrenergic
 SPINAL CORD INJURY 661

Fig. 6. Sternal Occipital Mandibular Immobilizer cervical brace. (Courtesy of Lexel Publishing
Company, Inc., Tampa, Florida; with permission.)

receptors, which respond to norepinephrine by stimulating contraction, pre-

dominate in the bladder neck and proximal urethra. b-Adrenergic receptors
prevail in the detrusor and respond by relaxing under the influence of nor-
epinephrine. The fibers of the somatic pudendal nerve (S2-S4) originate in
the anterior gray columns of the sacral segments and innervate the striated
pelvic floor and external urethra.
Coordination of micturition in the intact urinary system requires precise
communication among the parasympathetic, sympathetic, and somatic ner-
vous systems to function properly. This coordination is achieved through
a local bladder reflex arc mediated by cortical micturition centers. The cor-
tical centers offer volitional control of micturition, inhibit uninhibited con-
tractions, and maintain sufficient bladder capacity. Urine collects in the
bladder and provides direct feedback by way of autonomic nerves, which
maintain control through cortical awareness. Micturition is initiated on vol-
untary active bladder contraction.
This regulation is impaired in individuals who have SCI, possibly caus-
ing several neurogenic dysfunctions, which can be classified into two
662 BRANCO et al

Fig. 7. Minerva cervical brace. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida;
with permission.)

categories: the hyperreflexic/spastic bladder and the areflexic/flaccid or hy-

pocontractile bladder. With the hyperreflexic/spastic bladder, when the co-
ordination of bladder contraction and external urinary sphincter relaxation
is lost, a pattern of simultaneous reflex contractile activity known as detru-
sor–sphincter dyssynergia occurs. Reflex micturition is possible but often
results in elevated bladder pressures. With the areflexic/flaccid or hypocon-
tractile bladder, a S2-S4 lesion results in no reflex voiding.
Pharmacologic treatment can be used to improve urinary continence. An-
ticholinergic drugs bind to muscarinic receptors in the bladder. Medications,
including oxybutynin hydrochloride, hyoscyamine, and propantheline bro-
mide, are used to decrease detrusor contractility and increase bladder com-
pliance. Side effects are dry mouth, decreased sweating, and constipation.
Cholinergic agents (bethanechol) can be helpful in managing detrusor are-
flexia through increasing detrusor activity.
Alpha-antagonists (prazosin, terazosin, doxazosin) can be considered if
decreased bladder neck resistance is suspected. Side effects may include hy-
potension and dizziness. Adrenergic agonists (ephedrine) are rarely used to
increase urethral resistance.
Surgery can be used to facilitate management of the neurogenic bladder.
Surgeries for hyperreflexic bladder include bladder augmentation with or
without urinary diversion (eg, continent ileal conduit diversion,
 SPINAL CORD INJURY 663

Fig. 8. Halo vest. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida; with
permission.)

catheterization through an abdominal stoma) or cystoplasty and detrusor

myectomy. In instances of areflexic bladder, outlet resistance may be en-
hanced with artificial sphincters or bladder neck procedures. Additionally,
artificial urinary sphincters, periurethral injections, and fascial slings have
been used to achieve continence.
New strategies are arising to manage the hyperreflexic bladder. Electrode
stimulation involves surgical posterior rhizotomy of the sacral nerve roots
and electrode placement at the anterior nerve roots. Stimulation of the an-
terior roots causes contraction of the detrusor and sphincter, leading to
voiding. Injections with botulinum toxin have been used to control detrusor
hyperactivity [15]. The toxin inhibits release of acetylcholine from presynap-
tic nerve terminals, resulting in paralysis in the affected muscles.
Goals for bladder management in individuals who have SCI include ef-
fective bladder emptying while maintaining safe vesicular pressures during
urine storage and voiding. Hyperreflexic bladders are managed with inter-
mittent catheterization in individuals who have sufficient hand dexterity,
or with indwelling urethral or suprapubic catheter in persons who have in-
sufficient finger dexterity. Bladder volumes should be maintained at less
than 500 mL. Intermittent catheterization performed at home by someone
other than the patient has been shown to result in increased urinary tract
infections compared with indwelling catheter or self–intermittent
664 BRANCO et al

Fig. 9. Lumbosacral orthosis. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida;
with permission.)

catheterization or condom catheter use [16]. The Valsalva or Credé maneu-

ver (abdominal external pressure to mechanically push urine out) can be
used in cases of an areflexic bladder or pelvic floor denervation, but is
more effective on women. The Credé maneuver should be used with cau-
tion, because it may theoretically lead to ureteral reflux [16]. Voluntary
voiding may be performed if postvoid residuals remain in acceptable ranges
(approximately !100 mL urine).
A yearly urologic examination is recommended for individuals who have
chronic SCI, although no consensus exists on the frequency or examination
components [17]. Components of the examination may include evaluation of
the upper tract (eg, renal scan, ultrasound, CT scan, intravenous pyelogram)
and lower tract (eg, urodynamics, cystogram, cystoscopy).

Neurogenic bowel
Neurogenic bowel is a common consequence of SCI. Gastrointestinal
consequences of neurogenic bowel dysfunction include pain, bloating, nau-
sea, anorexia, autonomic dysreflexia, ileus, gastroesophageal reflux, gastric
ulcers, constipation, diarrhea, hemorrhoids, diverticulosis/diverticulitis,
impaction, and stool incontinence [18].
 SPINAL CORD INJURY 665

Fig. 10. Knight Taylor orthosis. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida;
with permission.)

The external anal sphincter (EAS) is a circular band of striated muscle that
is continuous with the pelvic floor and proximal to the anus [19]. The pubor-
ectalis muscle loops around the rectum and maintains the anorectal angle
through securing the rectum to the pubic bone [19]. Together, the internal
anal sphincter, EAS, and puborectalis muscle maintain fecal continence.
The gastrointestinal tract is under primary control of the enteric nervous
system. The two main plexi are the myenteric (Auerbach’s) and submucosal
(Meissner’s) plexi. The myenteric plexus provides motor innervation to the
two muscular layers and secretomotor innervation to the mucosa [20]. The
submucosal plexus plays a secretory role [20]. This network of neurons re-
tains contact with the central nervous system through the afferent and effer-
ent extrinsic neurons of the sympathetic and parasympathetic nervous
system (see Fig. 14).
The extrinsic nervous system modulates the intrinsic reflexes and coordi-
nates gut activity with the body. It consists of the parasympathetic, sympa-
thetic, and somatic nerves [19]. The vagus nerve provides parasympathetic
innervation from the esophagus to the splenic flexure. The pelvic nerve car-
ries parasympathetic fibers from the distal spinal cord segments S2-S4 to the
descending colon and rectum. Sympathetic innervation originates from the
superior and inferior mesenteric (T9-T12) and hypogastric (T12-L3) nerves
[19]. The EAS and pelvic floor receive somatic innervation by way of the
pudendal nerve (S2-S4) [19] (see Fig. 14).
666 BRANCO et al

Fig. 11. Jewett orthosis. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida; with
permission.)

Motility of the colon is performed through three primary mechanisms:

myogenic, chemical, and neurogenic. Myogenic transmission of signals oc-
curs between smooth muscle cells connected through gap junctions and pro-
duces transmission between cells [19]. Chemical control is modulated by
neurotransmitters, including acetylcholine, norepinephrine, substance P,
vasoactive intestinal peptide, serotonin, and somatostatin [20]. The neuro-
genic mechanism of colonic motility is regulated by the enteric nervous sys-
tem and modulated by the extrinsic nervous system.
Generally, two main types of neurogenic bowel have been discussed:
upper motor neuron and lower motor neuron bowel syndromes [19]. Upper
motor neuron bowel syndrome or hyperreflexic bowel involves lesions above
the conus medullaris, resulting in a bowel with increased colonic and anal
tone. Voluntary control of the EAS is absent and the sphincter remains tight
and retains stool. However, as the nerve connections between the spinal
cord and colon remain intact, reflex coordination and stool propulsion oc-
cur. Upper motor neuron neurogenic bowels produce constipation and fecal
retention caused by EAS activity. Lower motor neuron bowel syndrome, or
 SPINAL CORD INJURY 667

Fig. 12. Cruciform Anterior Spinal Hyperextension orthosis. (Courtesy of Lexel Publishing
Company, Inc., Tampa, Florida; with permission.)

areflexic bowel, results from a lesion affecting the conus medullaris, cauda
equine, or pelvic nerves. Constipation is the result of slow stool propulsion.
A recent study noted three different neuropathophysiologic bowel patterns
characterized by more specific neurologic levels [21]. Constipation was associ-
ated with incapacity to increase intra-abdominal pressure and absence of anal
relaxation during defecation in individuals who had injuries above T7. Indi-
viduals who had lesions below T7 and intact spinal sacral reflexes were most
challenged by obstructive defecation as the primary cause of constipation.
Prolonged colonic transit time was the primary cause of constipation in pa-
tients who had lesions below T7 and absent spinal sacral reflexes.
The four main categories of medications used in the management of
neurogenic bowel [18,19] are stool softeners, colonic stimulants, contact
irritants, and bulk formers. Stool softeners, such as docusate sodium,
emulsify fat in the intestine, thereby softening the stool. Senna, a colonic
stimulant, activates the myenteric plexus to induce peristalsis. Contact irri-
tants, such as bisacodyl suppositories, are placed in direct contact with the
668 BRANCO et al

Fig. 13. Milwaukee brace. (Courtesy of Lexel Publishing Company, Inc., Tampa, Florida; with
permission.)

colonic mucosa and produce peristalsis. Psyllium is a bulk former that pro-
motes propulsive activity from increased colonic wall distension [20].
Individuals who have upper motor neuron bowel syndrome can take ad-
vantage of the rectocolic reflex to facilitate defecation [20]. Digital stimulation
can trigger a reflex wave of rectal peristalsis. An intact rectoanal inhibitory re-
flex leads to internal anal sphincter relaxation and defecation.
Persons who have lower motor neuron bowel syndrome have areflexic
bowels and reduced sphincter tone. The increased sphincter pressure pro-
duced by the Valsalva maneuver is reduced, leading to increased risk for un-
planned bowel evacuations [19,20]. As anorectal reflexes often yield
insufficient results in defecation, stool may require manual evacuation.
Alternative approaches to bowel management include surgical bowel revi-
sions, such as colostomies, ileostomies [18], or antegrade continence enema
 SPINAL CORD INJURY 669

Fig. 14. Parasympathetic and sympathetic tracts. (Courtesy of Lexel Publishing Company, Inc.,
Tampa, Florida; with permission.)

(ACE) procedures [20]. Anterior sacral nerve root stimulators have been used
for bladder emptying, but often can be used to initiate defecation [20].

Sexuality and fertility issues

The site of the spinal cord lesion and the extent of injury are key deter-
minants of sexual function. The genital organs are under both autonomic
(parasympathetic/sympathetic) and somatic (sensory/motor) neural regula-
tion. Several regions of the brain, such as the limbic system and the hypo-
thalamus, also contribute to sexual function. The parasympathetic visceral
efferent fibers arise from neurons in the second through fourth segments
of the sacral cord. Preganglionic sympathetic fibers arise from the eleventh
thoracic to the second lumbar spinal segments to synapse on sympathetic
chain ganglia, and subsequently onto the pelvic plexus through the hypogas-
tric nerve. Parasympathetic stimulation is responsible for erections. Erection
can also be achieved through nonadrenergic, noncholinergic neurons when
mediated by nitric oxide. Ejaculation is a more complex process than
670 BRANCO et al

erection and involves certain sympathetic, parasympathetic, and somatic

nerves. Sympathetic stimulation is responsible for seminal emission by in-
ducing the contraction of the prostate and seminal vesicles while simulta-
neously causing closure of the bladder neck. Ejaculation occurs when
projectile movement of the sperm occurs from clonic contractions of the is-
chiocavernosus and bulbospongiosus. If the bladder neck fails to close dur-
ing ejaculation, retrograde ejaculation may occur. Ejaculation in men who
have lower motor neuron or incomplete injuries can occur naturally with
sexual contact, but men who have complete injuries above T10 will most of-
ten need to use additional stimulation, such as vibrostimulation. Although
men who have complete SCI often have impaired ability to achieve orgasm,
as many as 38% have reported the ability to achieve orgasm.

Interventions for erectile dysfunction in men

Penile prosthesis and mechanical methods
Penile prosthesis consists of malleable rods or inflatable cylinders that are
implanted into the spongy tissue of the corpora cavernosum. These devices de-
stroy much of the tissue and are not recommended unless other less-invasive
methods do not suffice. Complications are common and the rate of prosthesis
infection can be as high as 16.5% in patients who have SCI [22,23].
Vacuum-assisted devices (VEDs) are used in association with a constriction
band (a ring placed around the base of the penis to keep it engorged). Compli-
cations can occur with excessive vacuum, causing a penile hematoma.

Pharmacologic interventions
Intracavernous penile injections are widely accepted as an effective treat-
ment for the restoration of erectile function in men who have SCI. They can
be highly effective in producing an erection in patients who have psycho-
genic or neurogenic erectile dysfunction. Papaverine alone had good results
in 98 of 101 patients who had SCI [24]. Prostaglandin E1 (PGE1) is gener-
ally the preferred drug [25–27]. The only medication that has been success-
fully used transurethrally is alprostadil [28].
Oral medications for erectile dysfunction include sildenafil. In the past few
years, several authors studied sildenafil in patients who had SCI, showing pos-
itive results with 100-mg dosages [29,30]. However, because of its potential for
hypotension, sildenafil is generally started at 25 mg rather than 100 mg.
Nitrates are contraindicated with sildenafil and the newer drugs, tadalafil
and vardenafil. Tadalafil and vardenafil are longer acting than sildenafil.
Tadalafil is effective up to 36 hours after dosing, but one study showed that
patients preferred to start treatment with sildenafil [30]. Vardenafil is a potent
and highly selective oral phosphodiesterase type 5 (PDS5) inhibitor. It was
found to significantly improve erectile and ejaculatory function in a random-
ized controlled trial of 418 men who had SCI and erectile dysfunction [31].
 SPINAL CORD INJURY 671

Early studies of semen produced with natural ejaculation show generally re-
duced sperm counts and motility. However, multiple studies using vibrostimu-
lation and the technique of electroejaculation showed mostly normal sperm
counts, although still lower motility.

Treatment of female sexual dysfunction

Treatment of female sexual dysfunction has traditionally relied on cogni-
tive behavioral therapies. Testosterone has recently been used to treat hypo-
active sexual desire and multiple studies have confirmed its efficacy [32]. The
use of topical alprostadil has been shown to increase clitoral blood flow [33]
and a small pilot study showed increased subjective and physiologic arousal
during visual sexual stimulation [34]. The use of sildenafil has also been ad-
vocated in small clinical studies to improve female sexual arousal [35,36];
however, its efficacy has not been confirmed in large-scale clinical trials.
Pregnancy for women who have SCI is always high risk because of increased
urinary tract infections, deep venous thrombosis, pressure ulcers, spasticity,
autonomic dysreflexia, and premature delivery [37].

Medical complications
Autonomic dysreflexia manifests with acute elevation of blood pressure
associated with headache, sweating, piloerection, nasal congestion, and
sometimes reflex bradycardia (see Fig. 14). Autonomic dysreflexia typically
only affects patients who have a lesion at or above the T6 level [38], although
it has been observed in patients who have lesions below this level. Estimates
of the prevalence of autonomic dysreflexia vary widely, but generally ap-
proximately 50% of those at risk will experience at least one episode. Auto-
nomic dysreflexia usually does not occur during spinal shock.
The pathophysiology of autonomic dysreflexia is related to loss of bal-
ance of the sympathetic and parasympathetic nervous systems caused by
the spinal cord lesion. Stimuli from below the level of the lesion produce a re-
flex sympathetic discharge. This response is normally modulated by inhibi-
tory signals from the brain; however, because of the spinal cord lesion, the
signals are blocked. Patients experience symptoms of sympathetic overload,
including headache, piloerection, and hypertension caused by vasoconstric-
tion. The baroreceptors at the carotid sinus and aortic arch detect the in-
creased blood pressure and trigger a parasympathetic response above the
level of the lesion. Reflex vasodilation leads to the sweating and flushing
of the face and trunk.
Triggering factors include bladder distension (80%), bowel impaction
(15%), pressure ulcers, ingrown toenails, occult fracture, soft tissue injury,
other intra-abdominal pathology (eg, cholecystitis, appendicitis, gastric
ulcers, gallstones, hemorrhoids), epididymitis, testicular torsion, acute
672 BRANCO et al

urinary tract infection, nephrolithiasis, heterotopic bone formation, deep

venous thrombosis, sexual intercourse, childbirth, and tight clothing.
Autonomic dysreflexia can cause intracerebral and subarachnoid hemor-
rhage, ischemic stroke, retinal hemorrhage, seizures, cardiac dysrhythmias,
and rarely even death. Therefore, every effort should be made to begin treat-
ment as soon as possible. The Clinical Practice Guidelines published by the
Consortium for Spinal Cord Medicine describes an algorithm for treatment
[39]. In general, acute management includes finding and removing the nox-
ious stimulus (bladder or bowel distension), positioning the patient upright,
and loosening tight clothing. If systolic blood pressure rises above 150 mm Hg,
treatment with nitropaste should be considered, and then hydralazine, if
needed [40]. If episodes are recurrent, prazosin or terazosin should be con-
sidered [39].
Heterotopic ossification is the pathologic ossification occurring within
soft tissue planes surrounding neurologically affected joints in individuals
who have central nervous system injury. Heterotopic ossification is not an
intra-articular process but occurs in the connective tissue between the mus-
cle planes. It is important to differentiate heterotopic ossification from myo-
sitis ossificans, which is the consequence of deep muscle hemorrhage after
trauma, usually not related to joints. Heterotopic ossification is present in
16% to 53% of all patients who have SCI but only 10% result in significant
functional limitations (most commonly within the first 4 months) [41]. Risk
factors include neurologically complete injuries, pressure ulcers, spasticity,
and age between 20 to 30 years. Most common sites include hip (most com-
mon), knee, shoulder, and elbow. Diagnosis can be determined with triple
phase bone scan (2–3 months postinjury), alkaline phosphatase (elevated
acutely, peak value at 10 weeks), and radiographs (earliest finding 1 month
after injury).
If the bone scan is positive 4 weeks postinjury, acute treatment with etidr-
onate should be given intravenously for 3 days (300 mg/d) and orally for
6 months (20 mg/kg/d) [42]. Other treatments include indomethacin and,
in refractory cases, radiation therapy [43]. Range of motion exercises should
be instituted or continued to help prevent ankylosis [44]. Surgical treatment
may be necessary if the heterotopic ossification interferes with function
(eg, sitting at 90 ) but is associated with recurrence. Prophylaxis can be per-
formed with etidronate or indomethacin (62% reduction in heterotopic
ossification).
Pulmonary complications, such as pulmonary embolism, pneumonia, and
respiratory failure, are the leading cause of death. Deep venous thrombosis
has potential lethal consequences, such as pulmonary embolism. General
risk factors include stasis (paralysis and loss of venous muscle pumping), hy-
percoagulable state, extremity injury, previous thrombosis, cancer, heart
failure, obesity, and age older than 70 years. The incidence of deep venous
thrombosis in patients who have acute SCI can be as high as 40%. Acute
deep venous thromboses are frequently asymptomatic, but can include
 SPINAL CORD INJURY 673

increased thigh and calf circumference, pain if sensate, and low-grade fever.
Diagnosis is made with venous duplex ultrasound (noninvasive, high sensi-
tivity), but the gold standard is contrast venography (invasive, high sensitiv-
ity). Impedance plethysmography (thrombi above knee), MRI (pelvic veins),
and D-dimer (complementary test) are also used. There is a lower risk of em-
bolization if the thrombus is located below the knee. Diagnosis of pulmo-
nary embolism is through ventilation and perfusion (V/Q) scan or helical
CT. The gold standard is pulmonary angiography (invasive; only if V/Q
or helical CT scan negative and high clinical suspicion is present). D-dimer
has 85% sensitivity and 65% specificity in patients who have no SCI [45,46].
Prophylaxis includes compression hose or pneumatic devices for at least
the first 2 weeks and minimizing immobility. Patients at high risk should re-
ceive low-molecular weight heparin, such as enoxaparin or dalteparin. The
therapeutic dose of enoxaparin is 1 mg/kg subcutaneously every day, and
that of dalteparin is 100 IU/kg subcutaneously twice a day or 200 IU/kg
once a day. If other risk factors are present (eg, lower limb fracture, prior
thrombosis, cancer, heart failure, obesity, age O70 years), low-molecular
weight heparin should be continued for 12 weeks or until discharge [47].
Cervical and high SCI cause paralysis of respiratory muscles (diaphragm,
scalene, sternocleidomastoid, external intercostals) below the level of injury,
resulting in a weak cough mechanism and difficulty mobilizing lung secre-
tions, and increasing the risk for developing atelectasis and pneumonia
[48]. Patients who have vital capacity less than 10 to 5 mL/kg are at greatest
risk. Abdominal or quad cough requires a forceful upward compression of
the abdomen above the umbilicus at the end of the inspiration to simulate
a cough and increase the peak cough flow by 15% to 33% [49].

Spasticity
Spasticity is defined as an abnormal, velocity-dependent increase in re-
sistance to passive movement of peripheral joints caused by increased mus-
cle activity [50]. Spasticity is caused by the hyperexcitability of alpha
motoneurons within the spinal cord secondary to loss of descending inhib-
itory influences. A common clinical assessment tool is the Modified Ash-
worth Scale, with a score from 0 to 4 (0 ¼ no increased tone; 1 ¼
slight catch on range of motion; 2 ¼ moderate tone, easy range of motion;
3 ¼ marked tone, difficult range of motion; 4 ¼ rigid, in flexion or exten-
sion) [51]. Treatment mainstay is stretching of spastic muscles (range of
motion exercises). Proper positioning and orthoses can also be used. Phar-
macologic treatment typically begins with oral baclofen (structural analog
of gamma-aminobutyric acid), with adverse effects including fatigue, dizzi-
ness, and seizures with abrupt withdrawal. Intrathecal baclofen has also
been used [52]. Diazepam and other benzodiazepines should be avoided
because they can cause dependency. Tizanidine (central a-adrenergic
674 BRANCO et al

agonist) is another option, with adverse effects including sedation and liver
function abnormalities. Dantrolene sodium has a peripheral rather than
central action, but it can cause hepatotoxicity. Treatment options for spas-
ticity that cannot be managed with oral medications include intrathecal
baclofen; percutaneous nerve blocks with phenol, alcohol, or Botox; and
neurosurgical procedures. Intrathecal baclofen is also efficacious but re-
quires a strong commitment by the patient to refill the pump.

Pain after spinal cord injury

Chronic pain is a significant problem for many individuals who have
SCI. Recent data from the national Model Spinal Cord Injury Systems in-
dicate a pain prevalence ranging from 81% at 1 year after injury to 82.7%
at 25 years [53]. The pain can originate above the lesion from musculoskel-
etal injury, mainly caused by overuse injuries. Neuropathic pain may de-
velop at or below the level of the lesions and is more refractory to
treatment than musculoskeletal pain [54]. The types of medications used
for chronic pain include anticonvulsants, antidepressants, and opioids. Al-
ternative pain treatments are also commonly used by persons who have
SCI and chronic pain.

Spinal cord injury functional outcomes

Complete spinal cord injury
With complete tetraplegia, if patients remain complete motor and sen-
sory more than 1 month postinjury, they have little chance for functional
recovery of the lower extremities [55]. Accurately predicting recovery of
the upper extremities is, therefore, crucial in predicting a patient’s antici-
pated functional independence. Functional motor strength has been de-
fined as the ability to move a joint through full range of motion against
gravity (grade 3–5 motor strength with manual muscle testing) [55,56]. If
initial upper-extremity muscle strength testing at a given motor level shows
grade 0–2/5 strength, the patient has a 70% to 97% chance that the mus-
cle will increase in strength to 3/5 or greater within 2 years after injury,
thereby gaining one motor level [57]. However, if muscle strength was
grade 0/5 at 1 month postinjury, the patient has only a 24% chance of re-
covering a functional level.
In complete paraplegia, 73% of patients did not change neurologic level
of injury at 1 year [58]. In muscles with initial grades of 1–2/5, approxi-
mately 70% recovered to grade 3/5 within 1 year. In 3% to 7% of cases,
muscles with grade 0/5 at initial testing progressed to grade 3/5 or greater
in 1 year. Most motor recovery occurs in the first 6 months after injury.
After this initial period, improvement plateaus with minimal functional
recovery beyond 12 months postinjury.
 SPINAL CORD INJURY
675
Fig. 15. American Spinal Injury Association examination. (Courtesy of the American Spinal Injury Association, Atlanta, Georgia; with permission.)
676 BRANCO et al

Incomplete spinal cord injury

More than 90% of incomplete injuries gained at least one motor level in
the upper extremities. When initial motor testing showed 0–2/5 strength, the
muscle recovered to a grade 3/5 or better within 2 years. With incomplete
paraplegia, 85% of muscles that were grades 1–2/5 at 30 days postinjury
achieved 3/5 or greater strength within 1 year [59].

Ambulation potential
To ambulate in the community, patients must have pelvic control and
at least grade 3/5 strength in both hip flexors and one knee extensor
[60]. Patients who have complete tetraplegia are unable to ambulate in
the community. Only 5% of people who have complete paraplegia will
have sufficient motor recovery to permit community ambulation [61]. Pa-
tients who have incomplete tetraplegia and incomplete paraplegia can of-
ten ambulate at the community level with or without assistive devices. This
ability frequently depends on age, with less-optimistic ambulatory goals in
older patients. Reports have shown that 91% of patients who have ASIA
C tetraplegia and are younger than 50 years become ambulatory on dis-
charge from acute rehabilitation [62], compared with 42% of patients
who are older than 50 years. All patients who had ASIA D tetraplegia
were able to ambulate on discharge. Patients who have incomplete para-
plegia have similar potential for ambulation; 76% of individuals who
had incomplete paraplegia were able to ambulate at the community level
1 year postinjury (Fig. 15).

Functional outcomes
Although the degree of independence anticipated for patients at each
level of injury can be predicted [63], their age, contributing medical con-
ditions, and social circumstances must be considered. Triceps innervation
provides elbow extension and facilitates stability in transfers. Therefore,
the C7 level is particularly important for independent living [64]. In ex-
ceptional situations, a young and particularly motivated individual who
has a C6 complete injury may be able to live independently. Patients
who have paraplegia at any level are predicted to be able to live
independently.

Summary
SCI is probably one of the most complex clinical syndromes that any
physician can encounter. It is a catastrophic condition and involves clinical
consequences in almost every organ system. Improvement in early treatment
and prevention of complications have increased the survival rate of individ-
uals who have SCI. Initial inpatient rehabilitation of patients is critical to
 SPINAL CORD INJURY 677

their future health and well-being. Inpatient rehabilitation is when patients

begin to learn and practice the skills necessary for daily living and begin the
psychological adjustment necessary to become a productive member of so-
ciety. Although a cure has been elusive, much research is in progress and
a breakthrough is hoped to be forthcoming that will move the recovery of
SCI to the next level.

References
[1] Sekhon L, Fehlings M. Epidemiology, demographics, and pathophysiology of acute spinal
cord injury. Spine 2001;26(Suppl 24):S2–12.
[2] Spinal cord injury: facts and figures at a glance. J Spinal Cord Med 2006;29(5):591–2.
[3] Lasfargues JE, Custis D, Morrone F, et al. A model for estimating spinal cord injury in the
United States. Paraplegia 1995;33:62–8.
[4] Jackson A, Dijkers M, Devivo M, et al. A demographic profile of new traumatic spinal
cord injuries: change and stability over 30 years. Arch Phys Med Rehabil 2004;85(11):
1740–8.
[5] Bryce Thomas N, Ragnarsonsson, Stein Adam B. Spinal cord injury Chapter 56. In:
Randall L. Braddom, editor. Physical medicine and rehabilitation. 3rd edition. 2006.
p. 1285–349.
[6] American Spinal Cord Injury Association and the International Medical Society of Paraple-
gia. International Standards for Neurological Classification of Spinal Cord Injury, revised
2000, Chicago.
[7] Eismont FJ, Arena MJ, Green BA. Extrusion of an intervertebral disc associated with trau-
matic subluxation or dislocation of cervical facets: case report. J Bone Joint Surg 1991;
73:1555–60.
[8] Bono CM, Vives MJ, Kauffman CP. Cervical injuries: indications and options for surgery.
Spinal Cord Medicine 2002;9:131–41.
[9] Apple DF, Perez M. Prospective study of orthotic use after operative stabilization of trau-
matic thoracic and lumbar fractures. Top Spinal Cord Inj Rehabil 2006;12(2):77–82.
[10] Redford J, Ogle A, Robinson R. PM&R Secrets, Spinal Orthoses Chapter 107, 1997. p. 570–
573.
[11] O&P Desk Reference, Lexel Publishing Company, Inc., 1995.
[12] Coleman WP, Benzel D, Cahil DW, et al. A critical appraisal of the reporting of the National
Acute Spinal Cord Injury Studies (II and III) of methylprednisolone in acute spinal cord
injury. J Spinal Disord 2000;13:185–99.
[13] Gorio A, Ferrari G, Fusco M, et al. Gangliosides and their effects on rearranging peripheral
and central neural pathways. Cent Nerv Syst Trauma 1984;1:29–37.
[14] Rapalino O, Lazarov-Spiegler O, Agranov E, et al. Implantation of stimulated homologous
macrophages results in partial recovery of paraplegic rats. Nat Med 1998;4:814–21.
[15] Schurch B, Stohrer M, Kramer G. Botulinum toxin-A to treat detrusor hyperreflexia in spi-
nal cord injured patients. J Urol 2000;164:692–7.
[16] Cardenas DD, Mayo ME. Bacteriuria with Fever after Spinal Cord Injury. Arch Phys Med
Rehabil 1987;68(5):291–3.
[17] Consortium for Spinal Cord Medicine Clinical Practice Guidelines. Bladder management for
adults with spinal cord injury: a clinical practice guideline for health-care providers. 2006.
p. 15–6.
[18] Benevento BT, Sipski ML. Neurogenic bladder, neurogenic bowel, and sexual dysfunction in
people with spinal cord injury. Phys Ther 2002;82:601–12.
[19] Consortium for spinal cord medicine: neurogenic bowel management in adults with spinal
cord injury. Washington, DC: Paralyzed Veterans of America; 1998.
678 BRANCO et al

[20] Lynch AC, Antony A, Dobbs BR, et al. Bowel dysfunction following spinal cord injury. Spi-
nal Cord 2001;39:193–203.
[21] Valles M, Vidal J, Clave P, et al. Bowel dysfunction in patients with motor complete spinal
cord injury: clinical, neurological, and pathophysiological associations. Am J Gastroenterol
2006;101:2290–9.
[22] Carson CC, Roberston CN. Late hematogenous infection of penile prosthesis. J Urol
139:50–2.
[23] Kappor VK, Chahal AS, Jyoti SP, et al. Intracavernous papaverine for impotence in spinal
cord injured patients. Paraplegia 1993;31(10):675–7.
[24] Beretta G, Zanollo A, Ascani L, et al. Prostaglandin E1 in the therapy of erectile deficiency.
Acta Eur Fertil 1989;20(5):305–8.
[25] Linet OI, Ogrinc FG. Efficacy and safety of intracavernosal alprostadil in men with erectile
dysfunction. N Engl J Med 1996;334:873–7.
[26] Tang SF, Chu NK, Wong MK. Intracavernous injection of prostaglandin E1 in spinal cord
injured patients with erectile dysfunction. Paraplegia 1995;33(12):731–3.
[27] Wethman P, Rajfer J. MUSE therapy: preliminary clinical observations. Urol 1997;50(5):
809–11.
[28] Schmid DM, Schurch B, Hauri D. Sildenafil in the treatment of sexual dysfunction in spinal
cord-injured male patients. Eur Urol 2000;38(2):184–93.
[29] 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. Annals of Neurology
1999;46(1):15–21.
[30] Govier F, Potempa AJ, Kaufman J, et al. A multicenter, randomized, double-blind, cross-
over study of patient preference for tadalafil 20 mg or sildenafil citrate 50 mg during initiation
of treatment for erectile dysfunction. Clin Ther 2003;11:2709–23.
[31] Giuliano F, Rubio-Aurioles E, Kennelly M, et al. Vardenafil Study Group. Efficacy and safety
of vardenafil in men with erectile dysfunction caused by spinal cord injury. 2006;66(2):210–16.
[32] Becher EF, Bechara A, Casabe A. Clitoral hemodynamic changes after a topical application
of alprostadil. J Sex Marital Ther 2001;27:405–10.
[33] Islam A, Mitachel J, Rosen R, et al. Topical alprostadil in the treatment of female sexual
arousal disorder: a pilot study. J Sex Marital Ther 2001;27:531–40.
[34] Berman JR, Berman LA, Lin H, et al. Effect of sildenafil on subjective and physiologic pa-
rameters of the female sexual response in women with sexual arousal disorder.
[35] Sipski ML, Alexander CJ, Rosen RC, et al. Sildenafil effects on sexual and cardiovascular
responses in women with spinal cord injury. Urology 2000;55:812–5.
[36] Ducharme SH, Gill KM. Sexuality and disability. In: Diamant L, Mc Anulty R, editors. The
psychology of sexual orientation, behavior and identity: a handbook. Westport (CT): Green-
wood Press; 1995. p. 348–409.
[37] Baker ER, Cardenas DD, Benedetti TJ. Risks associated with pregnancy in spinal cord in-
jured women. Obstet Gynecol 1992;80(3):425–8.
[38] Snow JC, Sideropoulos HP, Kripke BJ, et al. Autonomic hyperreflexia during cystoscopy in
patients with high spinal cord injuries. Paraplegia 1978;15:327–32.
[39] Consortium for Spinal Cord Medicine. Acute management of autonomic dysreflexia: indi-
viduals with spinal cord injury presenting to health care facilities. Washington, DC: Para-
lyzed Veterans of America; 1997.
[40] James J, Cardenas DD. Spinal cord injury. In: Garrison SJ, editor. Handbook of physical
medicine and rehabilitation. 2nd edition. Philadelphia: Lippincott, Williams & Wilkins;
2003. p. 270–95.
[41] Maynard FM, Karunas RS, Adkins AH, et al. Management of the neuromusculoskeletal
systems. Spinal cord injury, clinical outcomes from the model systems. Gaithersburg
(MD): Aspen; 1995. p. 145–69.
[42] Banovac K, Estores I, Sherman A, et al. Prevention and treatment of heterotopic ossification
after spinal cord injury. J Spinal Cord Med 2004;27(4):376–82.
 SPINAL CORD INJURY 679

[43] Schaeffer M, Sosner J. Heterotopic ossification: treatment of established bone with radiation
therapy. Arch Phys Med Rehabil 1995;76:284–6.
[44] Cardenas DD. Current concepts of rehabilitation of spinal cord injury patients.
[45] Consortium for Spinal Cord Medicine. Prevention of thromboembolism in spinal cord
injury; 1997.
[46] Green LA. Deep vein thrombosis and pulmonary embolism. Presented at the Programs and
abstracts of the American Academy of Family Physicians 2005 Scientific Assembly. San
Francisco (CA), September 28-October 2, 2005.
[47] Consortium for Spinal Cord Medicine. Prevention of thromboembolism in spinal cord in-
jury. 2nd edition. Washington, DC: Paralyzed Veterans of America; 1999.
[48] Jackson AB, Groomes TE. Incidence of respiratory complications following spinal cord in-
jury. Arch Phys Med Rehabil 1999;75:270–5.
[49] Jaeger RJ, Turba RM, Yarkony GM, et al. Cough in spinal cord injured patients: compar-
ison of three methods to produce cough. Arch Phys Med Rehabil 1993;74:1358–61.
[50] Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Koella WP, editors. Spastic-
ity: disordered motor control. Chicago: Year Book Medical Publishers; 1980. p. 485–94.
[51] Bohannon RW, Smith MB. Interrater reliability of a modified Ashworth scale of muscle
spasticity. Phys Ther 1987;67:206–7.
[52] Hsieh J, Penn R. Intrathecal Baclofen in the treatment of adult spasticity. Neurosurg Focus
2006;21(2).
[53] Cardenas DD, Bryce TN, Shem K, et al. Gender and minority differences in the pain expe-
rience of people with spinal cord injury. Arch Phys Med Rehabil 2004;85:1774–81.
[54] Cardenas DD, Jensen MP. Treatments for chronic pain in persons with spinal cord injury:
a survey study. J Spinal Cord Med 2006;29:109–17.
[55] Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery following complete
tetraplegia. Arch Phys Med Rehabil 1993;74:242–7.
[56] Burns AS, Ditunno JF. Establishing prognosis and maximizing functional outcomes after
spinal cord injury. Spine 2001;26:S137–45.
[57] Ditunno JF, Cohen ME, Hauck WW, et al. Recovery of upper-extremity strength in com-
plete and incomplete tetraplegia: a multi center study. Arch Phys Med Rehabil 2000;81:
389–93.
[58] Waters RL, Yakura JS, Adkins RH, et al. Recovery following complete paraplegia. Arch
Phys Med Rehabil 1992;73:784–9.
[59] Waters RL, Adkins RH, Yakura JS, et al. Motor and sensory recovery following incomplete
paraplegia. Arch Phys Med Rehabil 1994;75:67–72.
[60] Waters RL, Adkins R, Yakura J, et al. Prediction of ambulatory performance based on
motor scores derived from standards of the American Spinal Injury Association. Arch
Phys Med Rehabil 1994;75:756–60.
[61] Waters RL, Adkins R, Yakura J, et al. Functional and neurologic recovery following acute
SCI. J Spinal Cord Med 1998;21:195–9.
[62] Burns SP, Golding DG, Rolle WA, et al. Recovery of ambulation potential in motor-incom-
plete tetraplegia. Arch Phys Med Rehabil 1997;78:1169–72.
[63] Consortium for Spinal Cord Medicine. Outcomes following traumatic spinal cord injury:
clinical practice guidelines for health-care professionals. Washington, DC: Paralyzed Vet-
erans of America; 1999.
[64] Gittler MS, McKinley WO, Stiens SA, et al. Spinal cord injury medicine: 3. Rehabilitation
Outcomes. Arch Phys Med Rehabil 2002;83(Suppl 1):S65–71.