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Spinal Cord Injury Rehabilitation

Kresimir Banovac, MD, PhD
Andrew L. Sherman, MD

Spinal cord injury (SCI) is a catastrophic event that results in

impairments that affect almost every aspect of a persons
bodily function. SCI is virtually unmatched in the level of
devastation it brings to a persons life and the social and financial cost it levies to society. SCI plunges the injured person,
most often a young previously healthy individual, into a world
of emergency care, intensive medical and surgical care, and
total dependency. The SCI patient then arrives on the rehabilitation unit and is expected to relearn the most basic of bodily
functions despite seeing slow or no neurologic recovery.
Finally, the SCI patient is expected to learn to perform once
simple and now complex tasks of daily living independently
so that he or she can return home in increasingly shorter
amounts of time.
SCI is defined as an injury to the spinal cord that partially
or completely interrupts the three main functions of the cord:
motor, sensory, and reflex activities. Before World War I, SCI
inevitably resulted in early death. Egyptian physicians long
ago labeled SCI as an ailment not to be treated at all because
they feared the pharaoh would kill them if they let a patient
die under their care.1 However, advances in treatment that
began during World War II and have progressed since have
allowed many persons with SCI to live much longer. Today in
many cases, patients with SCI can expect to live an almost
normal lifespan. As a result, the numbers of persons alive
today with SCI in the United States has increased to more than

In 1970 the first federally funded Model Spinal Cord Injury
Care Systems (MSCICS) were developed. Currently there are
14 such centers (there were 18 before funding was cut) as
designated by the National Institute on Disability and Rehabilitation Research (NIDDR). Each center represents a comprehensive interdisciplinary service delivery integrating all
aspects of care for the SCI patient from the initial injury to
lifelong follow-up. The model centers are based on the principles set forth by Sir Ludwig Guttman, a British physician

who pioneered advances in the care of SCI patients during

World War II1:
1. Transfer of the SCI patient to a specialized unit as soon
after injury as possible.
2. Unit management by a physician who is knowledgeable
and dedicated to spinal care.
3. A team of allied health professionals who are trained in the
intricacies of spinal cord problems.
4. A commitment to vocational pursuits.
5. An emphasis on psychosocial and recreational needs.
6. Provision for follow-up care for the lifetime of the individual.
The 14 MSCICS centers and 8 previously designated centers
have been contributing clinical information to a national database following a jointly agreed-upon protocol. They have been
able to report results on the basis of an estimated 13% of all
SCI injuries in the United States occurring since 1973. The
database contains information on about 25,000 spinal cord
injured persons.3 The end result is a wealth of information
regarding injury trends from 1973 to1998 and some recent
updates that include information through the year 2004. The
data not only allow physicians to know the current status of
SCI patients but also give physicians the ability to spot trends
in the demographic data. These changes in the demographics
of SCI have allowed rehabilitation programs and centers to
change with the times to reduce the cost and ultimately
improve the quality of medical rehabilitative care for their
patients with SCI.4

Incidence, Race, Age, and Gender

On the basis of information from the national database, there
are approximately 11,000 new cases (40 per million in the U.S.
population) each year. However, this number is based on older
data from the 1970s. The prevalence is estimated to be 225,000
to 296,000 persons and growing.3 The recently updated
national SCI Statistical Center statistics put the prevalence at

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84 Spinal Cord Injury Rehabilitation 1465

Life Expectance
Life expectancies for persons with SCI that were so low
many years ago continue to steadily increase. Mortality rates,
however, while improving, continue to be highest during the
first year after injury. Complete injuries still have lower ultimate survival rates than incomplete injuries. The degree of
neurologic impairment, as measured by the Frankel Grade or
the American Spinal Injury Association (ASIA) Impairment
Scale, and level of injury were significantly correlated with
mortality risk. For example, the average life expectancy of a
20-year-old who suffers complete paraplegia is 66 years. This
compares with 61 years for a C5 to C8 SCI, 57 years for a C1
to C4 SCI, and 43 years for a ventilator-dependent patient.
This compares with the normal life expectancy in the general
population of 77 years and in a patient with incomplete SCI
of 72 years.5 The factors that can increase life expectancy are
favorable circumstances for good health, community integration, and higher income.6

Many years ago, the leading cause of death among persons
with SCI was renal failure. Pulmonary embolus (PE) usually
in the first few weeks after injury, and most often associated
with a deep vein thrombosis (DVT), was another frequent
cause of death. Advances in urologic management, DVT and
PE prevention, and early mobilization have reduced the
number of early deaths. Today, renal failure rarely occurs in
the acute SCI setting. Because more SCI patients live not only
through their first year after injury but also survive to old age,
cardiovascular disease has become a more frequent cause of
death (Fig. 841). Nash and colleagues7 demonstrated that SCI
is an independent risk factor for developing multiple risks for


First year
After first year





em lmo
bo na
lu ry










Between 1973 and 2004, 66% of patients were Caucasian,

21% were African American, and 9.7% were Hispanic.3
Cervical injuries resulting in tetraplegia occur in 54% of
SCI patients. Lumbar and thoracic injuries causing paraplegia
comprise the rest (45%). A few (1%) were discharged as
normal or indeterminate. Since 1990, the numbers of
patients with complete SCI has been higher than incomplete
injuries (56% vs. 44%).3 Since 2000, however, the most frequent injury has been incomplete tetraplegia (34.7), followed
by incomplete paraplegia (23.0), complete tetraplegia (18.5),
and complete paraplegia (18.5).
SCI affects young adults most often. Population-based data
show the highest incidence, nearly 51.6% of injuries, occurs in
the 16- to 30-year age group.3 However, the most recent trends
suggest that SCI is occurring with increasing frequency in
older persons. The result is that the fastest growing population
of new SCI patients is older than 60 years of age. Since 1990,
the incidence of SCI in persons older than 60 has increased to
12% from 4.5% in the 1970s.3 The average age at SCI has
increased from 28.7 to 38.9 as of 2007. Additionally, while SCI
is an injury that occurs primarily in males (81.6% since 1973),
some centers are reporting increasing numbers of females suffering SCI.

FIGURE 841 Cause of death after spinal cord injury.

cardiovascular disease such as increased cholesterol. Respiratory illness, particularly pneumonia, is now the leading cause
of death among older SCI patients with cervical injuries.8 The
cause of death in persons with paraplegia is more varied. In
addition to heart disease, cancer, suicide, and septicemia are
the leading causes.

The causes of spinal cord injury are typically divided into
traumatic and nontraumatic. The top five causes of traumatic
SCI in males are auto accidents, falls, gunshot wounds, diving,
and motorcycle accidents.3 The top three remain the same in
women, but the final two are medical causes and diving3 (Fig.
The major trend is that violent injuries have decreased from
20% in the 1990s to 9.8% in 2000s.3 Geographic variations
occur depending on the state or city. In the older SCI patients,
in addition to falls, nontraumatic causes of SCI such as cancer,
vascular injuries, and infection make up a larger proportion
of injuries.
Etiology is also reported in terms of major groups.
Figure 843 illustrates the frequency that each of these
groups causes SCI.

Classification of Spinal Cord Injury

The spinal cord has three basic physiologic functions. The
ascending tracts in the cord receive sensory information from
the somatic and visceral receptors through dorsal root ganglia
and transmit this information to higher centers. The descending tracts receive signals from higher centers and ultimately

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% patients






FIGURE 842 Etiology of spinal cord injury by gender of patients. (Adapted

with permission from Jackson AB, Dijkers M, DeVivo MJ, Poczatek RB: A
demographic profile of new traumatic spinal cord injuries: Change and
stability over 30 years. Arch Phys Med Rehab 85:1740-1748, 2004.)

transmit these signals to target sites via the ventral roots. The
other basic function of the spinal cord is to modulate these
signals via a variety of local mechanisms.
Assessment, treatment, and classification of spinal cord
injury flow directly from the anatomy, physiology, and topography of the spinal cord. Classification or grouping of patients
allows the rehabilitation physician to predict the outcome and
ultimate function in a majority of patients on the basis of
others with similar injuries. This allows the rehabilitation team
to design a rehabilitation program appropriate for individual


SCI patients to give them the best opportunity to maximize

their potential functional outcome.
The most accurate way to assess a patient who has suffered
an SCI is to perform a standardized physical examination as
outlined by the American Spinal Injury Association. The neurologic examination includes two key componentsthe motor
and sensory examination with required and optional elements. The result allows the clinician to compile a score and
determination of the completeness of injury. The neurologic
level is also determined by rules set forth in the ASIA examination. From these data a functional classification is assigned
to each patient. This information can then be used to design
each patients rehabilitation program and predict his or her
functional outcome on the basis of previous patients with
similar injury classifications.
Two assessment tools are used in the evaluation of patients
after SCI.9 One is the neurologic classification of SCI using the
ASIA impairment scale. The other is the functional score, or
Functional Independence Measure (FIM) score.
The ASIA impairment scale measures the degree of completeness of injury using categories from A to E (Table 841).
Complete paralysis is defined as the absence of sensory and
motor function in the lowest sacral segments and incomplete
paralysis as preservation of sensation below the level of the
injury including the lowest sacral segments. Sacral sparing is
defined as voluntary anal contraction or presence of dull touch
and pinprick sensation in the rectal and perianal area.
In addition to the ASIA impairment scale is a scoring
system that measures the strength of each muscle on a 6-point
scale (0 to 5) and sensation for pinprick and dull touch on a
3-point scale (0 to 2). The motor level of SCI is defined as the
lowest normal motor segment that has a grade 3 or more,
providing the muscles above that level are graded as a 5. The
motor level best reflects the severity of impairment and disability during rehabilitation.
FIM score is a widely accepted functional assessment tool
and is currently used as an indicator of function in patients
with SCI. FIM is an 18-item scale. There are two categories of
items, motor and cognitive. Individual items in each category
score from 1 to 7, from total assistance to complete

TABLE 841 American Spinal Injury Association (ASIA) Impairment Scale


FIGURE 843 Etiology of spinal cord injury. (Adapted with permission from
Jackson AB, Dijkers M, DeVivo MJ, Poczatek RB: A demographic profile of
new traumatic spinal cord injuries: Change and stability over 30 years. Arch
Phys Med Rehab 85:1740-1748, 2004.)

Scale Grade


CompleteNo motor or sensory function is preserved

in the sacral segments S4-5.

IncompleteSensory but not motor function is

preserved below the neurologic level and includes the
sacral segments S4-5.

IncompleteMotor function is preserved below the

neurologic level, and more than half of key muscles
below the neurologic level have a muscle grade less
than 3.

IncompleteMotor function is preserved below the

neurologic level, and at least half the key muscles
below the neurologic level have a muscle grade of 3 or

NormalMotor and sensory function is normal.

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84 Spinal Cord Injury Rehabilitation 1467

Clinical Syndromes
In addition to classifying patients on the basis of their individual motor and sensory injury levels, the following specific
clinical syndromes have been identified in the literature:
central cord, anterior cord, posterior cord, Brown-Squard,
conus medullaris, and cauda equina syndromes.10,11

BOX 841 Functional Independence Measure (FIM) Scale

Motor Items
Dressing upper body
Dressing lower body
Sphincter Control
Bladder management
Bowel management
Bed, chair transfer
Toilet transfer
Tub, shower transfer

FIM Scale Level of Function Scoring

Central Cord Syndrome

The most common type of incomplete SCI in the elderly,
central cord syndrome also carries with it a relatively favorable
prognosis for recovery. The mechanism of injury is usually
hyperextension of an already stenotic cervical canal producing
central hematomyelia.12 Because the lumbar and sacral motor
tracts are located in the periphery of the white matter, the
syndrome is characterized by motor weakness of the upper
extremities greater than the lower extremities and sacral
sparing. Recovery occurs more favorably in younger patients.
Between 87% and 97% of patients younger than 50 will eventually ambulate, versus 31% to 41% of those older than 50.
Hand intrinsic function is last to recover, usually incompletely
in all ages.

Anterior Cord Syndrome

This is an injury to the anterior two thirds of the spinal cord
including both gray and white matter. The posterior columns
are preserved. The mechanism of injury is either due to thoracic fractures with retropulsion of disc or bone fragments or
lesions of the anterior spinal artery. The resulting SCI is most
commonly complete paralysis with spasticity. In the lower
extremities deep pressure and proprioception are preserved.
However, the prognosis for motor recovery is relatively poor.13

Posterior Cord Syndrome

The least common incomplete SCI is characterized by absence
of position sense. There is usually preservation of pain, temperature, and touch. Motor function is impaired in varied

Brown-Squard Syndrome
This injury occurs with a literal or functional hemisection of
the spinal cord. The most common cause is a bullet or knife
wound. The classic presentation is ipsilateral loss of motor
function, ipsilateral loss of dorsal column sensation, and

7Complete independence
6Modified independence
Modified Dependence
4Minimal assist
3Moderate assist
Complete Dependence
2Maximal assist
1Total assist

contralateral loss of pain and temperature below the level of

the lesion. Overall, these patients have the greatest potential
for functional outcome and ambulation (75% to 90%).14 Bowel
and bladder continence is regained in 82% and 89%,

Conus Medullaris, Epiconus, and Cauda Equina

Patients with these lesions present with similar motor and
sensory deficits but are also different in a few distinct ways.
Patients present with patchy lower extremity weakness, saddle
anesthesia, and incontinence of stool. Urinary retention is
more common than incontinence. Lesions of the cauda equina
are clearly lower motor neuron with decreased lower extremity motor tone, absent lower extremity and bulbocavernosus
reflexes, flaccid bladder, and asymmetric weakness. High
conus (epiconus) lesions may have upper motor neuron
(UMN) findings mixed with the lower motor neuron
Cauda equina lesions carry a much more favorable prognosis for functional motor and sensory recovery, especially
when surgical/medical treatment occurs promptly. Bowel,
bladder, and sexual function return less frequently, often
leading to adjustment and psychologic difficulties. The longterm difficulties in patients with cauda injuries are compounded by a high incidence of severe neuropathic lower
extremity pain not usually seen in conus injuries. Thus patients
recovering from cauda equina injuries may have long-term

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independence. There are 13 items of motor scoring important

in determination of self-care, sphincter control, and mobility
(Box 841). Scores falling below 6 indicate that the patient
requires another person for assistance. Many rehabilitation
units now use FIM scores to measure patient outcomes.
Quality assurance units use these data from groups of patients
to draw inferences on the effectiveness of the rehabilitation



physical and emotional disabilities despite their seemingly

normal outward appearance even after successful physical

Therapy Approaches
As stated earlier, rehabilitation of the SCI patient begins from
the moment of injury. Quick response, transfer to a level I
trauma center, and prompt medical and surgical treatment
results in a minimizing of medical complications and preservation of neurologic function. In the acute hospital setting,
important recommendations given on consultation with the
SCI specialist include treatment of neurogenic bowel and
bladder, prophylaxis of DVT and PE, prophylaxis of gastric
ulcer, preventing atelectasis and pneumonia via proper pulmonary management, and preventing skin ulcers with proper
positioning in bed and turning every 2 hours. Physical and
occupational therapies are initiated in the acute hospital unit
once the spine is stabilized. Range of motion (ROM) is performed to the shoulders, hips, elbows, and heel cords. ROM
should be performed twice daily to prevent joint contractures
and can be taught to family members. Splints are made for the
upper extremities for the same reason. The patient begins to
build tolerance to sitting and is taught weight shifting to
prevent pressure ulcers. The goal is to achieve medical stability
so that the injured patient can be admitted as quickly as possible to a multidisciplinary inpatient rehabilitation hospital
that specializes in SCI treatment.
Once the acute treatment is completed and the patient is
deemed medically stable, the rehabilitation course is assisted
with the quickest possible transfer to the rehabilitation unit.
In cases of high tetraplegia, medical stability may be achieved
while the patient is still on a ventilator. The result of a shorter
length of stay in the acute hospital and quicker move to rehabilitation is to lower the cost to the health care system and
improve the ability of patients to quickly see functional
Moving patients quickly through rehabilitation has some
negative consequences, too. Sometimes patients do not have a
chance to psychologically adjust to their injury fully. Additionally, shorter lengths of stay have also moved to the rehabilitation hospital.
Unfortunately, these shorter lengths of stay that are often
forced on patients and rehabilitation providers by insurance
company mandates continue a trend that patients will need to
complete their physical, functional, and psychologic rehabilitation as outpatients. Therefore it is imperative then that the
rehabilitation be focused and aggressive to accomplish as
much as possible in a shorter amount of time. The challenge
is to provide SCI patients with the highest quality rehabilitative care despite these imposed constraints so that they leave
the hospital with the highest possible outcome.
On the rehabilitation unit, the SCI patient begins a new
journey. The basic skills of mobility, self-care, and bladder/
bowel functions are relearned regardless of the severity of the
injurysometimes quickly but other times painfully slowly.
Patients try to achieve independence in each area, although

sometimes only modified or partial independence is possible.

The level of neurologic injury best predicts the level of independence and mobility each patient can achieve,15 even though
individual differences occur. SCI patients use a significant
time in rehabilitation to review a variety of handbooks and
computer programs to become educated on their injury. Most
patients also receive counseling for emotional and psychologic
adjustment, discover initial vocational options for their future,
and participate in recreational and leisure activities that ease
their reintegration into society. A subset of SCI patients who
suffered concurrent head trauma receives cognitive testing
and retraining. Another subset of SCI patients who remain on
ventilators receives breathing and communication training.
Finally, each patient is discharged to the most independent
living situation possible. Usually they can only go home after
multiple modifications are built and after a myriad of adaptive
equipment is prescribed.
Because the tasks of rehabilitation can be so daunting and
involve so much of the whole person with all organ systems
including the psychosocial system affected, only a dedicated
multidisciplinary team can accomplish a successful comprehensive rehabilitation. Each member of the multiple rehabilitation disciplines functions together as a team to optimize
each patients outcome.16 Historically the leader of the team
has been the rehabilitation physician, or physiatrist, who
would create the rehabilitation goals, lead weekly team meetings, and decide when the program is complete. More recently,
most rehabilitation programs have shifted to a more patientcentered approach with the interdisciplinary team working
toward goals set forth together.17 All disciplines focus their
treatments on the patient, so teamwork and treatment overlap
are encouraged. With this approach the patient, and often his
or her family, is intimately involved in deciding the direction
of the rehabilitation and the date of discharge. The individual
disciplines are listed in Table 842.18
Recent advances in rehabilitation techniques have led to
both increased functional outcomes and decreased lengths of
stay. One of the most influential advances has been in surgical
stabilization. Historically, large bulky cervical braces including
halos dominated rehabilitation units. Now, better internal
fixation has allowed patients to come onto the rehabilitation
units almost immediately after surgery and usually with only
a hard collar.19 The less intrusive bracing allows patients to
progress more quickly in their mobility training.
Newer medications have also allowed SCI patients to progress more quickly. Patients who were having difficulty with
postural hypotension can get upright sooner and for longer
time periods. Other medications have decreased the incidence
of DVT, pulmonary embolism, and spasticity. Those SCI
patients slowed by neuropathic pain now benefit from new
pain medications and procedures. Aggressive percussive lung
treatments have decreased the incidence of pneumonia and
down time on the unit.
The functional rehabilitation program begins with a comprehensive assessment of medical impairments, functional
deficits, and environmental setup. Then, on the basis of the
findings, appropriate goals can be set and a treatment approach
to reach those goals can be initiated and completed. Persons

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84 Spinal Cord Injury Rehabilitation 1469

Bed mobility
Transfer training
Wheelchair training
Functional mobility
Bathing and grooming
Neurogenic bladder management
Neurogenic bowel management
Assistive devices
Home and environment modifications
Many advances in therapy techniques have improved treatment offered to SCI patients in rehabilitation. Functional electrical stimulation (FES) has been applied to patients both in
the acute rehabilitation setting and later in the outpatient
setting to upper and lower extremities.20 Assisted or weighted

TABLE 842 Interdisciplinary Team




Medical care, coordination of rehabilitation,

team leader

Rehabilitation nurse

Daily care, medication, education, reinforce

skills, transfers

Physical therapist

Gross motor skills, transfers, mobility

(wheelchair, standing, ambulation)

Occupational therapist

Fine motor skills, activities of daily living (e.g.,

feeding, dressing, bathing)

Recreational therapist

Leisure activities, community reintegration,

assistive technology use

Social worker

Obtain community resources; assist with

disposition planning; communicate with
insurance companies

Speech therapist

Assess cognitive status; provide

communication, swallowing, and cognitive

Respiratory therapist

Manage patients on respirator; provide

respiratory treatments


Design and fabricate upper/lower extremity

braces and prosthesis; fit spine braces

Vocational counselor

Test skills and interest; recommend training

and assist with placement


Wheelchair procurement and fitting, adaptive


standing and walking, even with patients with complete injuries, is now being tried in a few centers with promising early
results.21 Technology and equipment innovation has influenced greatly the quality of care SCI patients receive. Power
wheelchairs now have standing options, more rugged wheels,
and automatic pressure relief. Manual chairs are now fitted
with more advanced cushions, sport options, and powerassist wheels. Most cars and vans are outfitted with hand
controls. Finally, computerized environmental control units
and voice-activated systems have improved independence and
freedom for patients with high-level tetraplegia.
Because shorter lengths of stay have moved patients home
sooner, the majority of rehabilitation gains often occur in the
outpatient setting. Patients with chronic SCI, some years
after their injury, are even seeing benefits from renewed
or prolonged rehabilitation. Jacobs and colleagues22 showed
improvements in cardiovascular status after circuit strength
training in SCI patients. Competitive sports for patients with
disabilities offer not only physical but also psychologic benefits. Technology has also fueled growth in the rehabilitative
treatment of SCI patients long after injury. Tendon transfers
had been coupled with the freehand implant to improve
hand function in many tetraplegic patients.23 Bladder implants
or injections of botulinum toxin may reduce incontinence,24
intrathecal baclofen pumps reduce malignant spasticity,25 and
FES implants have allowed for limited amounts of standing
and ambulation.26 All of these devices can increase functional
independence in the appropriate SCI candidate but also
require postplacement rehabilitation training.27

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with complete SCI share the common situation that in most

cases their impairment remains static or permanent.
Therapists may choose from a number of treatment
approaches to achieve the goal of functional independence or
achieving maximum function. More than one different type
of approach may also be used if felt appropriate by the therapist. Additionally, although therapy sessions and tasks are
divided by discipline (e.g., transfer training by physical
therapy, activities of daily living [ADL] to occupational
therapy), all therapists must use expertise from other specialists on the team to maximize functional restoration and
treatment. Within that framework, treatment can be either
restorative or compensatory. The goal of restorative treatment
is simply to reverse the disability, even if the impairment
cannot be reversed. The individual is encouraged to perform
the ADL task the same way as before the injury. Compensatory treatment aims to reverse the disability and even the
handicap by finding other means of traversing the divide
created by the impairment without directly restoring the function. Either way, the functional task gets done independently
or at least with the least dependence possible leading to the
point of discharge.
The choice of which method to use depends on the underlying condition of the patient. Most persons with complete
SCI may gain one or two levels of neurologic function but are
unlikely to gain any more neurologic return in their immediate future. Therefore therapists most often use compensatory
strategies to create independent function. However, persons
with incomplete SCI may see tremendous neurologic recovery
over time and are more appropriate for restorative therapy
immediately. Therefore therapists must carefully observe their
patient and try to project the amount and speed of the recovery. If recovery is occurring quickly, restorative treatment
strategies are more appropriate. One example would be
employing standing balance strategies at the kitchen even
when the patient cannot yet ambulate but should in the near
future. Areas of focus on the inpatient rehabilitation stay are
as follows:



Medical Management
Rehabilitation should begin as soon as possible after SCI.
The most important medical aspects in the acute period of
rehabilitation include neurogenic bowel and bladder care,
pulmonary management, thromboembolic and gastric ulcer
prevention, and proper positioning in bed. If early medical
complications can be prevented, the rehabilitation course is
assisted and the cost of care is significantly reduced.

Neurogenic Bowel Dysfunction

Neurogenic bowel dysfunction is common after SCI and has
the potential to influence the social, emotional, and physical
well-being of patients. Establishment of an effective bowel
program during rehabilitation can minimize the development
of disability related to neurogenic bowel. The goal is to control
severe constipation, promote regularity, and prevent involuntary bowel movements. Two types of neurogenic bowel dysfunction after SCI exist: reflexic and areflexic.28
Reflexic or UMN bowel dysfunction is seen in patients with
SCI above the conus medullaris. Voluntary control of bowel is
lost in these patients, but conus-mediated reflex activity and
intestinal peristalsis are intact. The external anal sphincter
becomes spastic because of the spasticity of the pelvic floor
preventing stool evacuation. Stool accumulates in the colon
unless reflex defecation is triggered. Bowel care in these
patients includes (1) nutritional changes with increased fiber
and fluid intake, (2) oral medication (lubricants and cathartics), (3) rectal chemical stimulation (suppositories or enema),
and (4) mechanical digital stimulation.29
Areflexic or lower motor neuron (LMN) bowel dysfunction
is a result of lesions at or below the conus medullaris. Voluntary control of bowel is lost, as well as sacral reflex activity.
The external anal sphincter becomes atonic and flaccid, which
increases the risk of fecal incontinence. Management of LMN
bowel dysfunction includes (1) diet with fiber and some fluid
restriction, (2) oral medication (bulk-forming agent), and (3)
mechanical digital removal of stool.29

Neurogenic Bladder Dysfunction

Urosepsis was the leading cause of death before introduction
of intermittent catheterization (IC).30 Urologic problems are
the most common complications of SCI. The rate of urinary
tract infections (UTIs) is 50% to 80% in the first year postinjury. The goal of bladder management during rehabilitation is
to establish an effective and safe method of emptying the
bladder and avoiding incontinence. Two types of neurogenic
bladder dysfunction exist: reflexic and areflexic.
Reflexic or UMN bladder is secondary to lesions above
conus medullaris. It is characterized by (1) incontinence secondary to conus-mediated reflex contractions of the bladder
detrusor muscle, (2) spastic external urethral sphincter, and
(3) detrusor/sphincter dyssynergia.
Areflexic or LMN bladder occurs in lesions below the
conus medullaris. This condition is characterized by (1)

denervated external urethral sphincter and (2) flaccid detrusor muscle leading to overflow or stress incontinence.
Management of neurogenic bladder after SCI is similar for
both types. The routine recommendations are based on clinical practice guidelines prepared by the Consortium for Spinal
Cord Medicine31:

Management of fluid intake to maintain daily urine output

between 1.5 and 2L
Intermittent catheterization using clean or sterile
Indwelling catheter for patients with poor hand control and
lack of attendant care
Suprapubic catheter for, most commonly, patients with urethral lesions
External (condom) catheter for male patients with UMN
bladder with reflex voiding
Surgery. The two circumstances when surgery is indicated
in management of neurogenic bladder after SCI are (1) to
correct the failure to store or (2) to correct the failure to
empty urine. The most commonly performed corrective
procedures are augmentation of small capacity bladder with
intestine and sphincterotomy. The most frequent method of
bladder management at discharge from SCI rehabilitation
centers is intermittent catheterization (59%); however, a
relatively high number of patients were discharged with
indwelling catheters (13%).4

Spasticity is seen frequently in patients after SCI. In 37% of
patients the spasticity is significant and requires chronic
therapy. Spasticity may interfere with function, daily activities,
and sleep. The severity of spasticity during rehabilitation in
SCI patients varies. It has been reported that patients with
cervical and upper thoracic injuries have a higher incidence
of spasticity than patients with lower spine injuries.32 The
underlying processes involved in pathogenesis of hyperactive
reflexes are multifactorial and involve both inhibitory and
excitatory neurotransmitters. The role of neurotransmitters in
spasticity is not fully understood; therefore the therapy is generally symptomatic. Immediately after SCI there is a short
period (2 to 3 weeks) of areflexia that is followed by a gradual
occurrence of increased muscle tone below the level of injury.
In mild to moderately severe cases, ROM and static stretching
can be used to treat spasticity during rehabilitation. Medication is usually indicated for severe and chronic spasticity. The
different drugs that can be used for spasticity are in order (1)
baclofen, (2) benzodiazepines, (3) tizanidine, and (4) dantrolene. Baclofen is a GABA agonist, a major inhibitory
neurotransmitter in the central nervous system (CNS). The
starting dose is 5mg three times per day and increased slowly
to avoid side effects. The standard maximum dose is 80mg/
day divided either into TID or QID dosing (although some
practitioners will go higher). For refractory and severe spasticity, baclofen can be given by intrathecal pump, which will

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84 Spinal Cord Injury Rehabilitation 1471

Cardiovascular Complications
The primary mechanisms underlying cardiovascular abnormalities are related to the disruption of sympathetic control
located in the cervical cord. The most frequent symptoms are
orthostatic hypotension (68%) and bradycardia (71%).33 Autonomic dysreflexia develops in patients with SCI above the T6
spinal segment.
Orthostatic hypotension after SCI is caused by passive vasodilatation below the level of injury, while bradycardia is due
to uninhibited parasympathetic tone. Frequent associated
clinical findings are weakness, dizziness, blurred vision, and
fainting during positional changes. The majority of patients
gradually develops adaptation to hypotension and may tolerate orthostasis for an extended period of time. During the
period of rehabilitation, different measures such as elastic
stockings, abdominal binders, and slow mobilization from the
bed can be effective. Also, in early periods after SCI, medication may be indicated. Two oral agents with different mechanisms of action can be used: midodrine and fludrocortisone.
Midodrine is an alpha-1 adrenergic agonist (ProAmatine); it
is the first-choice drug. Fludrocortisone (Florinef), a mineralocorticosteroid, enhances renal resorption of sodium and
may be used as an alternative.
Autonomic dysreflexia (AD) is a serious complication after
SCI34. It is characterized by a sudden onset of pounding headache, increase of blood pressure, and bradycardia. AD occurs
in patients with SCI above the T6 spine segment. These
patients have interrupted central inhibitory control of the
thoracic sympathetic system. Therefore, various peripheral
noxious stimuli below the injury (i.e. bladder distension, pressure ulcers, ingrown toenails, UTI, constipation, etc.) may
lead to overstimulation of the sympathetic system. AD may
have different causes, however it is most commonly related to
bladder or bowel distension34. Treatment of AD includes
immediate repositioning of patient in a sitting position and
loosening of clothing or constrictive devices to allow a pooling
of blood into the lower extremities. The placement of an

indwelling catheter should be performed early because the

most common cause of autonomic dysreflexia is bladder distension. If after the catheterization systolic blood pressure
remains elevated over 150mmHg, an antihypertensive agent
with rapid onset and short duration (i.e., nitrates or nifedipine) is recommended34. If bowel distension or impaction is
suspected, antihypertensive medication needs to be administered prior to rectal examination for stool.
The incidence of thromboembolism is high in the acute
stage of SCI. The routine screening for deep vein thrombosis
(DVT) showed positive results in 47% to 100% of patients.35
Studies based on clinical parameters estimated a lower incidence of DVT in acute SCI. The incidence of clinically diagnosed DVT was 11.4% in 1996, which was significantly
reduced to 5.2% in 1998. The decline in the incidence of DVT
is most likely the result of introduction of low molecular
weight heparin (LMWH).36 Prevention of thromboembolism
starts after injury and continues throughout rehabilitation.
Current methods for prevention of thromboembolism used
in the SCI patients are mechanical (compression hose, boots,
pneumatic devices), pharmacologic (unfractionated heparin,
LMWH, warfarin), and inferior vena cava filter. A consortium organized by Paralyzed Veterans of America in 199735
recommended mechanical prevention for the first 2 weeks
following injury. In patients with motor complete SCI, pharmacologic prevention with unfractionated heparin or LMWH
is recommended for a minimum of 8 weeks or until discharge
from the rehabilitation center. Patients with motor complete
injuries and risk factors such as obesity, heart failure, cancer,
lower extremity fractures, previous DVT, or age older than 70
may need their prevention extended after discharge. The
most recent recommendation for the prevention of thromboembolism in the rehabilitation phase of patients with SCI is
based on the sixth ACCP consensus in 2001.37 LMWH or
full-dose oral anticoagulation with warfarin was the initial
recommended method with IVCF recommended in patients
who failed or have contraindications to anticoagulation.
Treatment of thromboembolism in patients with SCI
does not differ from treatment currently used in non-SCI

Respiratory Complications
Respiratory complications are the most common early and late
causes of death after SCI. Figure 844 shows the most common
respiratory complications in patients with different levels of
SCI.38 Pneumonia is the most common complication in highlevel injuries, whereas atelectasis is seen in all groups of
patients in similar frequency regardless of level of injury.
Smith and coworkers found in more than 18,000 veterans with
SCI a steady rate of visits for acute respiratory infection,
without a declining trend in frequency.39
There are several factors important in genesis of ventilatory
abnormalities after SCI40 such as (1) restrictive ventilatory
dysfunction as a result of muscle paralysis, (2) inability to
cough, which is due primarily to paralysis of abdominal and
intercostal muscles, and (3) hypersecretion of mucus. Overproduction of mucus (about 1L/day) is due to absent

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reduce the therapeutic dose 100 times and will also markedly
decrease sedative side effects of the drug on the CNS.
Benzodiazepines assist the effect of endogenous GABA,
and they are a second-choice medication in treatment of spasticity because their sedative CNS side effects exceed that of
baclofen. Tizanidine is an alpha-adrenergic receptor agonist
with effects similar to noradrenaline. Noradrenaline belongs
to the group of inhibitory neurotransmitters that prevent
release of excitatory amino acids from nerve terminals. Tizanidine blocks hyperactive spinal reflexes and, similar to other
antispastic medication, has a sedative effect on the CNS. Dantrolene has no effects on the CNS, acting directly on skeletal
muscle cells, where it inhibits contraction of myofibrils. The
inhibitory effect of dantrolene is due to blockade of endoplasmatic release of calcium. Neurolytic nerve blocks and surgery
(dorsal rhizotomy) are additional therapeutic modalities in
treatment of spasticity. Although these therapies have not
been used frequently in recent years, they are indicated for
severe spasticity unresponsive to medication.



The management of pressure ulcers requires a multidisciplinary team approach. It is also important to provide sufficient nutritional support, treatment of comorbid conditions,
and special support surfaces (cushions and mattresses). Two
types of mattresses, static (foam, gel, air, or water) and dynamic
(air pump with alternating pressure), are used to reduce pressure on the ulcer. Medical treatment may include enzymatic
dbridement and moist wound dressing changes with various
products (transparent membranes, hydrogels, foams, alginates, etc.). Surgical repair is recommended when the ulcers
are too large and only if nutritional and medical conditions of
the patient are satisfactory.



% patients





Heterotopic Ossification




FIGURE 844 Respiratory complications after spinal cord injury. (Adapted

with permission from Jackson AB, Grooms TE: Incidence of respiratory
complications following spinal cord injury. Arch Phys Med Rehab 75:270275, 1994.)

sympathetic outflow and unopposed parasympathetic tone

that also leads to bronchoconstriction.
The neurologic level of injury mainly determines the
management of respiratory complications after SCI. Patients
with cervical injuries from C1 to C3 frequently need mech
anical ventilation. Patients with C4 to C7 and upper thoracic
injuries often require the following treatments during
rehabilitation: (1) bronchodilators (beta-adrenergic agonists
and/or anticholinergics), (2) mucolytic agents, and (3) chest
Later in the phase of rehabilitation and with the return of
peripheral sympathetic tone, there is a decrease of mucus production. At this stage respiratory treatments are focused on
assisted cough and prevention of respiratory complications.
All patients with cervical and high thoracic injuries need
yearly vaccination for influenza and every 5 years for

Pressure Ulcers
SCI causes profound changes in the structure and physiology
of the skin, which leaves patients susceptible to the development of pressure ulcers. The incidence of pressure sores after
SCI is high, with approximately 50% of chronic patients with
SCI developing a pressure ulcer in their lifetime. Pressure
ulcers are seen on the sacrum in 26%, ischium in 23%, heel in
12%, and trochanter in 10% of chronic SCI patients.41 Several
factors are responsible for the development of pressure ulcers
after SCI, but most important is prolonged pressure over a
bone prominence. The cornerstones in the prevention of pressure ulcers are regular daily inspection of skin and the performance of pressure relief techniques.

Heterotopic ossification (HO) is another early complication

after SCI. Often occurring in the first month of rehabilitation,
HO is often a cause of fever of unknown origin. The incidence of HO after SCI is about 50%.42,43 The etiology of HO is
unknown. The pathology of HO is characterized by bone
growth in extra-articular tissue of paralyzed extremities.
Clinically, in the acute stage of HO the most common findings are swelling, fever, and reduction in ROM of affected
joint(s). The level of creatine phosphokinase (CPK) in serum
in the early stage may indicate the severity of muscle involvement. In the chronic stage, HO may limit the functional
status of the patient. Diagnosis of HO in the early stages is
based on a positive three-phase bone scintigraphy with 99m
Tc diphosphonate. Prevention of HO with indomethacin in
patients with SCI is effective if started early (3 to 4 weeks)
after injury.44 Etidronate is often prescribed to treat HO in the
acute stage along with aggressive joint motion by a physical
therapist. Only when the heterotopic bone is mature up to 1
year after the onset can surgical resection be considered.

Osteoporosis and Fractures

In patients with SCI there is a significant bone loss in paralyzed limbs in the early period after injury. The most severely
involved skeletal regions are the distal femur and proximal
tibia. Bone densitometric studies showed that patients with
complete paralysis might have bone loss of 30% in the first 3
months.45 In later periods bone loss will continue at a slower
rate, reaching a new steady state after 2 years. At the final
stages bone mineral loss can be about 30% in the femoral shaft
and 50% in the proximal tibia.46 Patients who actually suffer
fractures were found to have even higher bone loss; about 40%
in femoral shaft and 70% in proximal tibia. Presently there is
no cure for osteoporosis after SCI. Many different preventive
programs for bone loss have been evaluated. So far, all preventive measures have shown some positive effect on bone mass,
but the effects are transient and the bone loss resumes as soon
as the intervention stops. The incidence of lower extremity
fractures after SCI is about 1% to 2% per year. Lower limb
fractures are most often treated using a nonsurgical approach
with the goal of maintaining functional independence. Use of

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84 Spinal Cord Injury Rehabilitation 1473

Pain prevalence is stable over time ranging from 81% at 1

year after injury to 83% at 25 years.47 Approximately 90% of
patients with SCI have a delayed onset of pain, and many
of them are not finding an adequate pain relief from
commonly used medication.48 Nepomuceno and colleagues49
described the negative impact of pain on the life of patients
with SCI. Thirty-seven percent of patients with cervical injuries and 23% of patients with lower level of SCI reported
that if they had the chance, they would trade pain for loss of
bladder, bowel, or sexual function. Most patients describe
pain as stable or controlled, while the others report that pain
increased their disability. Of the different classifications of
pain after SCI, the most commonly described are central
neuropathic and musculoskeletal pain.50,51 Clinical differentiation between central neuropathic and musculoskeletal pain
is shown in Table 843.
Several mechanisms have been proposed in the pathogenesis of central pain, but the causes still remain uncertain. In
contrast, musculoskeletal pain is most commonly due to spine
injury or overuse of joint, tendon, or ligament structures.
Treatment measures depend on which type of pain is being
treated. There is no known cure for central pain. The most
effective strategy in the management of central pain involves
an interdisciplinary approach. However, only partial pain
relief can be expected. The treatment strategies follow:
1. Nonpharmacologic (transcutaneous electrical nerve stimulation, aerobic and anaerobic exercise, recreational activity,
massage, acupuncture, heat or cold)
2. Pharmacologic
Guidelines from the World Health Organization for the
treatment of malignant pain can be applied in these patients:
(1) Nonopioid analgesics (nonsteroidal anti-inflammatory
drug [NSAIDs], acetaminophen) adjuvant (tricyclic antidepressants, selective serotonin reuptake inhibitor, anticonvulsants); (2) opioid for moderate pain (oxycodone,
codeine, hydrocodone) nonopioid adjuvant; and (3)
opioid for severe pain (hydromorphone, morphine, fentanyl) nonopioid adjuvant.
3. Psychosocial/Biofeedback
4. Surgical (nerve blocks, dorsal root entry zone, dorsal
column stimulator)
Musculoskeletal pain can be treated with mild analgesic,
NSAIDs, passive ROM, and trigger point injections.

Outcomes of Rehabilitation
Length of Stay
In general, patients with tetraplegia need a longer period for
rehabilitation than patients with paraplegia. Similarly, patients





Burning, tingling,
sharp, shooting

Not related

Anesthetic area


Dull, aching


Above level of injury

with complete paralysis require a longer stay at rehabilitation

centers than with incomplete paralysis. Recent statistical analysis showed that time needed for acute care has not changed
during the past 20 years; however, significant changes were
found in the length of stay (LOS) at the rehabilitation centers
(Fig. 845). Figure 845 illustrates results from a database
derived from the National database.5 A dramatic reduction of
LOS was documented at rehabilitation centers across the
country from 1977 to 2000. The average length of stay was 106
days in 1977, 90 days in 1987, 51 days in 1997, and 39 in 2004. The
changes in the LOS of patients after SCI can mainly be attributed
to measures that managed care instituted in the early 1990s.

Discharge Disposition
The changes in the length of stay of patients at rehabilitation
centers had some effect on the discharge disposition of these
patients. The results from the national database4 obtained in
1997 showed that the majority of patients were still discharged
home (91.2%); however, the percent of patients discharged to
skilled nursing homes also increased (5.3%) as compared with
2.8% in 1990.

Gain of Motor Function

The outcomes of motor function are determined by the previously discussed ASIA standard evaluation by using the ASIA

Acute care




TABLE 843 Characteristics of Pain after Spinal Cord Injury








Years of admission
FIGURE 845 Length of stay of patients after spinal cord injury in
rehabilitation centers. (Adapted with permission from Fiedler IG, Laud PW,
Maiman DJ, Apple DF: Economics of managed care in spinal cord injury.
Arch Phys Med Rehab 80:1441-1449, 1999.)

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splints and early mobilization are generally allowed initially in

a supervised setting.



% patients

B, C, or D. Usually neurologic return of motor function

starts in the first month after injury but may continue up to
24 months. Despite recent advances in pharmacologic treatment of spinal cord injury, prognosis for recovery of patients
with initial ASIA A remains poor. The prognosis for motor
function recovery of patients with ASIA B designation is
intermediate. One third of these patients remain unchanged,
one third converts to ASIA C, and one third to ASIA D or
E. In the group of patients with ASIA C designation, 70%
will convert to ASIA D. Patients with initial ASIA D
designation showed functional improvement to E in 4%,
whereas 96% of these patients remained in the D category.
Even after 5 years from traumatic SCI, results are not very
different. Kirshblum and colleagues53 found that only 4.5% of
patients with motor complete paralysis regained some motor
or sensory recovery.



Functional Independence (Charting ADL

Improvement Objectively)

ASIA score after 1 year

FIGURE 846 The changes in motor function after spinal cord injury. The
American Spinal Injury Association (ASIA) scale is used to grade motor
function. For ASIA scoring see text. (Adapted with permission from Marino
RJ, Ditunno J, Donovan WH, Maynard F: Neurological recovery after spinal
cord injury. Arch Phys Med Rehab 80:1031-1396, 1999.)

system and data obtained from the national database.52 The

outcomes of motor function were related to rehabilitation and
neurologic recovery and shown in Figure 846. As illustrated
in Figure 846, about 10% to 15% of patients diagnosed as
complete (ASIA A) will convert in 1 year to incomplete ASIA

Year #1


FIM score







Neurologic level
FIGURE 847 Functional independence measure (FIM) of spinal cord injury
patients at admission and discharge from rehabilitation center and 1 year
thereafter (YR-1). For FIM scoring see text. (Adapted with permission from
Hall KM, Cohen ME, Wright J, etal: Characteristics of the functional
independence measure in traumatic spinal cord injury. Arch Phys Med
Rehab 80:1471-1476, 1999.)

Currently the most widely used validated ADL evaluation

scale is the functional independence measure (FIM).54 The
FIM instrument evaluates nine areas of self-care and can be
applied multiple times throughout the course of treatment
not only to provide a baseline of function but also to chart
improvement in these key areas. The areas that the FIM reports
on are self-feeding; grooming; bathing; dressing upper and
lower body; toileting; and transfer to the toilet, tub, or shower.
The FIM has demonstrated a high degree of inter-relater
reliability.55After the SCI patient leaves the hospital, the FIM
can be continued in a self-reporting form (FIM-SR). Masedo
and colleagues found the FIM-SR motor scales and total
FIM-SR score to be reliable and valid measures of perceived
functional independence in individuals with SCI.56
Figure 847 shows the results from the national database
on FIM scores.57 The data were obtained on admission and
discharge from rehabilitation and at the follow-up after 1 year.
There is a marked difference in FIM motor scores from admission to discharge from rehabilitation in all neurologic groups
of patients. The greatest improvements are seen in patients
with lower cervical and thoracolumbar injuries. There was
little change in FIM scores in all categories of patients beyond
discharge from rehabilitation. Figure 847 illustrates mean
FIM motor scores for each neurologic group of patients and
indicates that a score of 78 (13 motor items with scores of 6),
correlating with functional independence, is reached only in
patients with thoracolumbar injuries.
Despite the advantages that using a validated comprehensive ADL measure creates, there are significant limitations.
Specifically, the FIM is not specific to SCI but is a general
measure of any rehabilitation diagnosis. Thus some aspects
critical to SCI function such as mastery of the environment
and respiratory function are not charted.
Therefore the Spinal Cord Independence Measure (SCIM
III, revised three times) created a new, more comprehensive
measure applicable to persons with paraplegia and tetraplegia,
complete and incomplete.58 Itzkovich and colleagues59 found
total agreement between raters was above 80% in most SCIM

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84 Spinal Cord Injury Rehabilitation 1475

III tasks. They also found the SCIM III was more responsive
to changes than FIM in the subscales of respiration and
sphincter management and mobility indoors and outdoors.
The measure is now undergoing final studies to see if it is more
sensitive or specific for SCI-injured persons than other measures while maintaining the practicality of the FIM.

Community Integration
Community integration of patients with SCI starts during
inpatient rehabilitation and continues after discharge from
rehabilitation center. The involvement of human services plays
a major role in assisting patients in the community. Figure
848 depicts the three aspects of community integration after
SCI: functional independence, social integration, and occupation. Data obtained from the national database61 indicate high
levels of social integration in all neurologic groups of patients
after SCI. The lowest median score of community integration
was found in occupation, as discussed in the paragraph earlier.
Community and athletic groups increase the levels of community integration. Activities that injured persons used to
participate in can be modified for the wheelchair athlete or
participant, increasing the quality of life for those injured. The
sports include sailing programs, diving programs, wheelchair
basketball teams, skiing, rugby, marathon racing, and Paralympic competitions.
In general, the analysis of demographic data indicates that
survivors of SCI with less severe neurologic injury, of younger
age, of Caucasian ethnicity, and more education will achieve
greater community integration.

Reintegration into the Environment

As a part of most inpatient rehabilitation treatment programs,
the home evaluation and home visit are highly anticipated.
The feeling that the home visit must mean the end of the
inpatient portion of rehabilitation is near excites and further
motivates the SCI patient to reach his or her goals and participate fully. However, evaluating the home environment as early
as possible in the rehabilitation process is also important so
that appropriate goals can be set and needed modifications can
begin earlier.62


% patients

More than half (57.4%) of those persons with SCI admitted to

a model system reported being employed at the time of their
injury. The postinjury employment picture is better among
persons with paraplegia than among their tetraplegic counterparts. By postinjury year 10, 32.4% of persons with paraplegia
are employed, whereas 24.2% of those with tetraplegia are
employed during the same year. National data from Model
System Spinal Cord Centers revealed that the rate of employment of SCI patients is approximately 27% after rehabilitation.60 Similar results were found for both genders, 24.1% in
female patients and 27.7% in male patients. Important factors
in obtaining employment after SCI were age, severity of injury,
and educational level before injury.





Physical independence
Social integration





All D

Neurologic level
FIGURE 848 Community integration after spinal cord injury. Each
neurologic group included patients with the American Spinal Injury
Association scale A, B, and C. (Adapted with permission from Whiteneck G,
Tate D, Charlifue S: Predicting community integration after spinal cord injury
from demographic and injury characteristics. Arch Phys Med Rehab
80:1485-1491, 1999.)

The environmental evaluation begins with a family history

(who is in the home), vocational history, and leisure history.
These are the components of the patients lifestyle that allow
the therapist to create a roadmap of where the injured patient
was and where he or she needs to get back to, and even beyond,
to maximize function. In certain cases the therapist may find
that the SCI patient was not functioning at optimal levels
even before the injury due to psychiatric illness or other
The second component of the evaluation concerns the
home structure itself. The therapist must create a picture of
the home and environment that will allow for an understanding of what impediments might exist and what might pose a
barrier to maximizing function. Through knowing the individual limitations of the patient, the therapist can set therapy
goals that may also involve making modifications to the home
and environment to maximize function.63 Ultimately, by marrying the functional abilities of each injured patient to the
environment that he or she is going to live within, the interdisciplinary rehabilitation team can help to maximize the
quality of life of each SCI patient.

1. Rehabilitation of the SCI patient begins from the moment of
injury and continues throughout the life of the patient.
2. The life expectancy of SCI patients continues to increase with
improved medical and rehabilitative care.

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3. Surgical advances have resulted in SCI patients being
transferred more quickly to rehabilitation with improved
functional abilities.
4. Shorter length of stay in the rehabilitation unit has reduced
inpatient cost but led to an increased need for prolonged
outpatient rehabilitation.

6. Future of rehabilitation. Two trends will continue into the

future. The first is shorter length of inpatient stays, leading to
increased importance and focus on outpatient rehabilitation.
The second is the introduction of neurotechnology to
supplement general strength rehabilitation, improve
function, and even allow assisted ambulation.

5. Technological advances have impacted SCI patients by

improving their mobility, function, and fitness.


1. As patients with SCI live longer, the frequency that they will
develop cardiovascular and other medical problems
associated with aging is increasing.

1. Kirshblum S, Campangnolo DL, and DeLisa JA (eds): Spinal

Cord Medicine. Philadelphia, Lippincott, Williams, and Wilkins,
The most recent comprehensive textbook written specifically
for physicians specializing in SCI medicine.

2. On average, patients with SCI have higher cholesterol levels

and reduced levels of fitness compared with able body
persons of similar age. This can be improved with exercise
3. The increase in elderly patients with multiple comorbidities
suffering SCI has led to an increase in medical complexity
seen on rehabilitation units.
4. Many patients who suffer SCI do not have adequate insurance
coverage to meet their complex medical, rehabilitation, and
equipment needs.
5. Much of the new technology designed for patients with SCI is
expensive and not available currently for the majority of
patients who could benefit.
1. Timing of rehabilitation. Rehabilitation and rehabilitation
planning can start immediately when the patient arrives into
the acute care system. Accurate assessment of the
neurologic level allows for initiation of treatment that can
minimize deficits and allow for maximum functional
2. Minimize medical complications. As early as possible,
rehabilitation should be started to prevent complications of
immobility and provide the patient with the tools to succeed
later in rehabilitation when the medical condition fully
3. Optimize teamwork. Rehabilitation of the spinal cordinjured
patient requires all members of the interdisciplinary team to
work together in a coordinated fashion. Creating achievable
short- and long-term goals will allow patients to work to
achieve their optimum function.
4. Demographics. As more elderly patients suffer spinal cord
injuries, many from nontraumatic causes, specialized
rehabilitation programs will need to be created to address
their unique medical and functional needs.
5. Pain. Chronic pain, neuropathic related to spinal cord injury,
or musculoskeletal related to acute or repetitive trauma, is
often the chief identified problem that spinal cordinjured
patients identify. Optimal treatment of pain improves
rehabilitation participation and optimizes function and
quality of life.

2. Archives of Physical Medicine and Rehabilitation, Vol 80, Nov

Entire issue devoted to reviewing SCI model systems data
and outcomes in patients with SCI.
3. Geerts WH, Heit JA, Clagett GT, et al: Prevention of venous
thromboembolism. Chest 119:132S-175S, 2001.
The most recent consensus definition of DVT prevention
after SCI.
4. Consortium for Spinal Cord Medicine: Acute Management of
Acute Autonomic Dysreflexia. J Spinal Cord Med 25:S67-S88,
This is considered as a guideline in the management of
autonomic dysreflexia.
5. Consortium Spinal Cord Consensus: Pressure Ulcer
Prevention and Treatment Following Spinal Cord Injury. J
Spinal Cord Med 24:S39-S101, 2001.
An excellent source of information with recommendation for
prevention and treatment of pressure ulcers.

1. Apple DF Jr: Spinal Cord Injury Rehabilitation. In Rothman RH,
Simeone FA (eds): The Spine. Philadelphia, WB Saunders, 1998,
pp 1225-1246.
2. DeVivo MJ: Epidemiology of Traumatic Spinal Cord Injury. In
Kirshblum S, Campagnolo DL, DeLisa JA (eds): Spinal Cord
Medicine. Philadelphia, Lippincott, Williams, and Wilkins, 2002,
pp 69-81.
3. Jackson AB, Dijkers M, DeVivo MJ, Poczatek RB: A Demographic Profile of New Traumatic Spinal Cord Injuries: Change
and Stability over 30 Years. Arch Phys Med Rehab 85:1740-1748,
4. Lammertse DP, Jackson AB, Sipski ML: Research from Model
Spinal Cord Injury Systems: Findings from the Current 5-Year
Grant Cycle. Arch Phys Med Rehab 85:1737-1739, 2004.
5. Facts and figures at a glance from National Spinal Cord Injury
Statistical Center, Birmingham, Alabama. J Spinal Cord Med
June, 2006.
6. Krause JS, DeVivo MJ, Jackson AB: Health status, community
integration, and economic risk factors for mortality after spinal
cord injury. Arch Phys Med Rehab 28:1764-1773, 2004.

Downloaded from at ClinicalKey Global Flex Package Trial June 07, 2016.
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84 Spinal Cord Injury Rehabilitation 1477

26. Yarkony GM, Roth EJ, Cybulski GR, et al: Neuromuscular stimulation in spinal cord injury: restoration of functional movement
of the extremities. Arch Phys Med Rehabil 73:78-86, 1992.

8. Frankel HL, Coll JR, Charlifue SW, et al: Long term survival in
spinal cord injury: A fifty-year investigation. Spinal Cord 36:266274, 1998.

27. Moynahan M, Mullin C, Cohn J, et al: Home use of a functional

electrical stimulation system for standing and mobility in adolescents with spinal cord injury. Arch Phys Med and Rehabil
77:1005-1013, 1996.

9. Kirshblum S, Donovan WH: Neurologic assessment and classification of traumatic spinal cord injury. In Kirshblum S, Campagnolo DL, DeLisa JA (eds): Spinal Cord Medicine. Philadelphia,
Lippincott, Williams, and Wilkins, 2002, pp 82-95.
10. Bing R: Compendium of regional diagnosis in affection of the
brain and spinal cord. ed 2. New York, Rebman, 1911.
11. Schneider RC, Cherry GR, Patek H: Syndrome of acute central
cervical spinal cord injury with special reference to mechanisms
involved in hyper-extension injuries of the cervical spine. J Neurosurg 11:546-577, 1954.
12. Quencer RM, Bunge RP, Egnor M, et al: Acute traumatic central
cord syndrome: MRI pathological correlations. Neuroradiology
34:85-94, 1992.
13. Cheshire WP, Santos CC, Massey EW, et al: Spinal cord infarction: etiology and outcome. Neurology 47:321-330, 1996.
14. Roth EJ, Park T, Pang T, et al: Traumatic cervical Brown-Squard
and Brown-Squard plus syndromes: The spectrum of presentations and outcomes. Paraplegia 29:582-589, 1991.
15. Kirshblum SC, OConnor KC: Predicting neurologic recovery in
traumatic cervical spinal cord injury. Arch Phys Med Rehabil
79:1456-1466, 1998.
16. Ragnarsson KT, Gordon WA: Rehabilitation after spinal cord
injury: the team approach. Phys Med Rehabil Clin North Am
3:853-878, 1992.
17. Zigler JE, Atkins MS, Resnik, CD, et al: Rehabilitation. In Levie
AM, Eismont FJ, Garfin SR, Zigler JE (eds): Spine Trauma. Philadelphia: WB Saunders, 1998, pp 567-596.
18. Banovac K, Fertel D, Bauerlein J: Principles of Rehabilitation
Medicine. In Humes D (ed): Kellys Textbook of Internal Medicine. ed 4. Philadelphia, Lippincott Williams and Wilkins, 2000,
pp 308-313.

28. Stiens SA, Bergman SB, Goetz LL: Neurogenic bowel dysfunction after spinal cord injury: Clinical evaluation and rehabilitation management. Arch Phys Med Rehab 78:S86-S102, 1997.
29. Consortium for Spinal Cord Medicine: Neurogenic Bowel Management in Adults with Spinal Cord Injury. Washington, DC,
Paralyzed Veterans of America, 1998.
30. Guttman L, Frankel H: The value of intermittent catheterization
in the early management of traumatic paraplegia and tetraplegia.
Paraplegia 4:63-84, 1966/1967.
31. Consortium for Spinal Cord Medicine: Bladder management for
adults with SCI. J Spinal Cord Med 29:532-567, 2006.
32. Maynard FM, Karunas R, Waring WW: Epidemiology of spasticity following traumatic spinal cord injury. Arch Phys Med Rehab
71:566-569, 1990.
33. Lehman KG, Lane JG, Piepmeier JM, Batsford WP: Cardiovascular abnormalities accompanying acute spinal cord injury in
humans: Incidence, time course and severity. J Am Coll Cardiol
10:46-52, 1987.
34. Consortium for Spinal Cord Medicine: Acute Management of
Acute Autonomic Dysreflexia. J Spinal Cord Med 25:S67-S88,
35. Consortium for Spinal Cord Medicine: Prevention of Thromboembolism in Spinal Cord Injury. Washington, DC, Paralyzed
Veterans of America, 1997.
36. Chen D, Apple DF, Hudson LM, Bode R: Medical complications
during acute rehabilitation following spinal cord injuryCurrent
experience of the Model Systems. Arch Phys Med Rehab 80:13971402, 1997.
37. Geerts WH, Heit JA, Clagett GT, et al: Prevention of venous
thromboembolism. Chest 119:132S-175S, 2001.

19. Askins V, Eismont FJ: Efficacy of five cervical orthoses in restricting cervical motion: a comparison study. Spine 22:1193-1198,

38. Jackson AB, Grooms TE: Incidence of respiratory complications

following spinal cord injury. Arch Phys Med Rehab 75:270-275,

20. Stein RB, Chong SL, James KB, et al: Electrical stimulation for
therapy and mobility after spinal cord injury. Prog Brain Res.
137:27-34, 2002.

39. Smith BM, Evans CT, Kurichi JE, et al: Acute respiratory tract
infection visits of veterans with spinal cord injury and disorders:
Rates, trends, and risk factors. J Spinal Cord Med 30:355-361,

21. Field-Foote EC, Tepavac D: Improved intralimb coordination in

people with incomplete spinal cord injury following training
with body weight support and electrical stimulation. Physical
Therapy 82:707-715, 2002.
22. Jacobs PL, Nash MS, Rusinowski JW: Circuit training provides
cardiorepiratory and strength benefits in persons with paraplegia. Med Sci Sports Exerc 33:711-717, 2001.
23. Kilgore KL, Peckham PH, Keith MW, et al: An implanted upperextremity neuroprosthesis follow-up of five patients. J Bone Joint
Surg 79A:533-541, 1997.

40. Lanig IS, Peterson WP: The respiratory system in spinal cord
injury. Phys Med Rehab Clin North Am 11:29-37, 2000.
41. Consortium Spinal Cord Consensus: Pressure Ulcer Prevention
and Treatment Following Spinal Cord Injury. J Spinal Cord Med
24:S39-S101, 2001
42. Banovac K, Renfree KJ, Hornicek FJ: Heterotopic ossification
after brain and spinal cord injuries. Clin Rev Phys Rehab Med
10:223-256, 1998

24. Creasey GH: Electrical stimulation of sacral roots for micturition

after spinal cord injury. Urol Clin North Am 20:505-515, 1993.

43. Van Kuijuk AA, Geuts ACH, van Kupperelt HJM: Neurogenic
heterotopic ossification after spinal cord injury. Spinal Cord
40:313-326, 2002.

25. Coffey RJ, Cahill D, Steers W, et al: Intrathecal baclofen for

intractable spasticity of spinal origin: results of a long term
multi-center study. J Neurosurg 78:226-232, 1993.

44. Banovac K, Williams JM, Patrick LD, et al: Prevention of heterotopic ossification after spinal cord injury with indomethacin.
Spinal Cord 39:370-374, 2001.

Downloaded from at ClinicalKey Global Flex Package Trial June 07, 2016.
For personal use only. No other uses without permission. Copyright 2016. Elsevier Inc. All rights reserved.


7. Nash MS, Jacobs PL, Mendez AJ, et al: Circuit resistance training
improves the atherogenic lipid profiles of persons with chronic
paraplegia. J Spinal Cord Med 24:2-9, 2001.



45. Garland DE, Stewart CA, Adkins RH, et al: Osteoporosis after
spinal cord injury. J Ortho Res 10:371-378, 1992.
46. Biering-Sorensen F, Bohr H, Schaadt O: Bone mineral content of
the lumbar spine and lower extremities years after spinal cord
lesion. Paraplegia 26:293-301, 1988.
47. Cardenas DD, Bryce TN, Shem K, et al: Gender and Minority
Differences in the pain experience of people with spinal cord
injury. Arch Phys Med Rehab 85:1774-1781, 2004.
48. Cardenas DD, Jansen MP: Treatment of chronic pain in persons
with spinal cord injuries: A survey study. J Spinal Cord Med
29:109-117, 2006.
49. Nepomuceno C, Fine PR, Scott Richards J, et al: Pain in patients
with spinal cord injury. Arch Phys Med Rehab 60:605-609, 1979.
50. Siddal PJ, Taylor DA, Cousins MJ: Classification of pain following spinal cord injury. Spinal Cord 35:69-75, 1997.
51. Cardenas DD, Turner JA, Warms CA, Marshall HM: Classification of chronic pain associated with spinal cord injuries. Arch
Phys Med Rehabil 83:1708-1714, 2002.

56. Masedo AI, Hanley M, Jensen MP, et al: Reliability and validity
of a self-report FIM (FIM-SR) in persons with amputation or
spinal cord injury and chronic pain. Am J Phys Med Rehabil
84:167-176, 2005.
57. Hall KM, Cohen ME, Wright J, et al: Characteristics of the functional independence measure in traumatic spinal cord injury.
Arch Phys Med Rehab 80:1471-1476, 1999.
58. Catz A, Greenberg E, Itzkovich M, et al: A new instrument for
outcome assessment in rehabilitation medicine: Spinal cord
injury ability realization measurement index. Arch Phys Med
Rehabil 85:399-404, 2004.
59. Itzkovich M, Gelernter I, Biering-Sorensen F, et al: The Spinal
Cord Independence Measure (SCIM) version III: Reliability and
validity in a multi-center international study. Disabil Rehabil
29:1926-1933, 2007.
60. Stuart Krause J, Kewman D, DeVivo MJ, et al: Employment
after spinal cord injury. Arch Phys Med Rehab 80:1492-1500,

52. Marino RJ, Ditunno J, Donovan WH, Maynard F: Neurological

recovery after spinal cord injury. Arch Phys Med Rehab 80:10311396, 1999.

61. Whiteneck G, Tate D, Charlifue S: Predicting community integration after spinal cord injury from demographic and injury
characteristics. Arch Phys Med Rehab 80:1485-1491, 1999.

53. Kirshblum S, Millis S, McKinley W, Tulsky D: Late neurologic

recovery after traumatic spinal cord injury. Arch Phys Med
Rehab 28:1811-1817, 2004.

62. Culler KH: Home management. In Crepeau EB, Cohn ES, Schell
BAB (eds): Willard and Spackmans Occupational Therapy. Philadelphia, Lippincott Williams & Wilkins; 2003, pp 534-541.

54. McKinley W, Santos K, Meade M, Brooke K: Incidence and outcomes of spinal cord injury clinical syndromes. J Spinal Cord
Med 30:215-224, 2007.

63. Cooper BA, Cohen U, Hasselkus BR: Barrier free design: A

review and critique of the occupational therapy perspective. Am
J Occupational Ther 45:344-350, 1991.

55. Ottenbacher KJ, Hsu Y, Granger CV, Fiedler RC: The reliability
of the functional independence measure: a quantitative review.
Arch Phys Med Rehabil 77:1226-1232, 1996.

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