CHAPTER 49
SPINAL CORD INJURY
Thomas N. Bryce
Historical Perspective
Before the mid-part of the twentieth century, injury to the
spinal cord was synonymous with death, either instantly
or after a period of great suffering.
The Edwin Smith Surgical Papyrus, written almost 5000
years ago, contains descriptions of cases of cervical spinal
cord injury (SCI), among other traumatic injuries, along
with recommended treatments. With regard to the cases of
cervical SCI, the author noted that those cases represent
“an ailment not to be treated.”44 During the early nine-
teenth century, Lord Nelson, the Admiral of the British
Fleet, received a gunshot wound to his chest during the
Battle of Trafalgar. He was taken immediately to the ship’s
surgeon to whom he noted, “All power of motion and
feeling below my chest are gone.” The surgeon’s reply was,
“My lord, unhappily for our Country, nothing can be done
for you.” Later in the century, the president of the United
States, James A. Garfield, experienced a gunshot wound
to the conus medullaris, he did not survive more than 3
months.46
During the early part of the twentieth century, the prog-
nosis for surviving SCI remained poor. During World War
I, 80% of all American soldiers with SCI died within 2
weeks, the 20% surviving longer having incomplete inju-
ries. The mortality of British soldiers who sustained SCI at
this time was better than that of the Americans; however,
an estimated 80% were also dead by 3 years.
During the 1930s and 1940s, management of SCI finally
started to change when a few individuals, beginning with
Donald Monro in the United States and followed by Sir
Ludwig Guttman in the United Kingdom, both neurosur-
geons, began to comprehensively address the whole person
with SCI. They not only began programs to teach people
with SCI self-care and mobility with a goal of reintegrating
into society but also addressed all the organ systems
involved with SCI (e.g., neurologic, skeletal, urologic) to
prevent complications. Each developed SCI units, which
became models for comprehensive centers around the
globe over succeeding decades.
Model Systems of Care
The difference in outcomes for people with SCI, when
admitted to a dedicated SCI rehabilitation unit, was noticed
by the leaders of health care at the same time that special
trauma systems were being developed in the United States
to treat injured people. The trauma systems required that
injured people be handled at the scene of accident by well-
trained emergency medical technicians using state-of-the-
art equipment and transportation vehicles. The patients
were subsequently to be triaged to a specially designated
trauma center, which met strict criteria for emergency and
acute trauma care, rather than taking them to the nearest
hospital. The success of disease-specific units and trauma
systems highlighted that inadequate training, experience,
and number of staff, as well as lack of appropriate facilities
and equipment, not only placed the life of a person with
SCI at risk but often resulted in development of complica-
tions and poor functional outcomes. It was therefore
hypothesized that if optimal care was provided from the
very onset of major disabling injury and for as long as
primary and secondary medical problems and disability
last, functional outcomes would be improved and the cost
of care would be reduced.
Based on this hypothesis, the U.S. government began to
fund several SCI Model Systems of Care beginning in 1970.
In 2014, there were 14 such systems funded by the National
Institute on Disability and Rehabilitation Research
(NIDRR), U.S. Department of Education. Each funded
system had to meet four basic requirements. First, it had
to have several integrated clinical components: emergency
medical services; a level 1 trauma center; comprehensive
rehabilitation services for both inpatients and outpatients,
including vocational and job placement services; and life-
long follow-up and health maintenance programs. Second,
each funded system had to collect data on all patients
served and forward these to a National SCI Model System
Database. Third, each system was required to conduct
research consistent with NIDRR-announced priorities.
Fourth, each system had to disseminate the research and
demonstration findings as widely as possible to the appro-
priate audiences.
As a result, the SCI Model Systems have been instrumen-
tal in developing standards of care and new treatments,
and conducting epidemiologic, health services, and out-
comes research, as well as producing thousands of publica-
tions and training materials. The National SCI Database
has been in existence since 1973 and includes data regard-
ing approximately 30,000 people with SCI.88
Subspecialty of Spinal Cord
Injury Medicine
Most physicians providing nonsurgical care for people
with SCI in the United States have been physiatrists. In the
past, most such physicians developed their special knowl-
edge over a lengthy period by providing care rather than
by specific training. A creation of a subspecialty of SCI
medicine was first advocated in the late 1970s and gained
1095
1096 SECTION 4 Issues in Specific Diagnoses
momentum in the early 1990s. Through the concerted
efforts of many individuals and organizations, the Ameri-
can Board of Medical Specialties gave its approval in 1995
for such a subspecialty be established. After successfully
completing an Accreditation Council for Graduate Medical
Education-accredited SCI Medicine fellowship and passing
a written examination administered by the American Board
of Physical Medicine and Rehabilitation (ABPMR), indi-
viduals receive SCI medicine subspecialty certification
through the ABPMR. Several hundred individuals have
been certified in the subspecialty since the first examina-
tion was held in 1999.
Epidemiology
Incidence and Prevalence
The recorded annual incidence of traumatic SCI is the
highest in North America of all the developed regions of
the world that have documented the problem. The inci-
dence in the United States is approximately 56 cases per
million population (or approximately 17,500 per year),
whereas in Canada it is 53 cases per million.90 In other
developed regions of the world, the incidence is consider-
ably lower varying from 24 to 19 cases per million in Spain
and France, respectively, to between 12 and 14 cases per
million within The Netherlands, Qatar, Ireland, Finland,
and Australia.14
The exact number of people with SCI currently alive in
the United States (prevalence) is a matter of dispute;
however, given the similar incidences of SCI in Canada and
the United States, an estimate of the prevalence based on
data from Canada14, where the prevalence is approximately
1298 cases per million, leads one to conclude there are
over 430,000 individuals in the United States living
with SCI, based on an estimated U.S. population of 317
million.111
Similar to the incidence data, the prevalence of trau-
matic SCI in other regions of the world is considerably
lower ranging from a prevalence of 681 cases per million
in Australia to 280 cases per million in Finland.14
Age at Time of Injury, Gender, and
Marital Status
The incidence of traumatic SCI is bimodal being highest
among young adults and older individuals (>65 years).90
In the United States, the incidence of traumatic SCI in
older adults (>65 years) approaches 90 cases per million.
Furthermore, there is an increasing incidence of traumatic
SCI in older adults that is not seen in any other age group
throughout the world.90 The mean age at injury has
increased from 29 years in the 1970s in the United States
to 42 years in the 2000s, exceeding slightly the increase in
median age of the U.S. general population during this
time.38,89 The majority of traumatic SCI occurs in males,
70% to 80% overall depending on the database queried.88,90
The ratio of male to female SCI is equal up until the age
of 5 years after which the ratio begins to favor males,
exceeding 80% for those between 16 and 20 years. However
with age, especially in those older than 65 years, the ratio
narrows again, with women accounting for 44% of SCI
cases after the age of 65 years.
For those married at the time of SCI, the divorce rate is
increased after SCI, as compared with that in the general
population, especially during the first 3 postinjury years.
The annual marriage rate is also lower for single individu-
als with SCI than for individuals without SCI.37
Causes of Spinal Cord Injury
The most common causes of SCI worldwide in descending
order of incidence are transport crashes, falls, violence, and
sports. This does vary among regions of the world, with
transport crashes responsible for approximately 50% of
cases in Europe and 40% of cases in North America, South
East Asia, and the Mediterranean. Falls are responsible for
approximately 30% of cases in North America and Europe
but over 40% in South East Asia and the Mediterranean.
Although transport crashes remain a significant cause of
SCI in all age groups, falls are the most common cause of
SCI in those above the age of 60 years. High falls (from
>1 m) are more common in younger people, whereas low
falls (from <1 m) are more common for those older than
45 years.14 SCI in older individuals is often related to cervi-
cal spinal stenosis and is caused by a relatively minor
trauma, such as a fall at home or in the street, or a low-
velocity motor vehicle collision. Violence as a cause is also
disparate in its presence, being responsible for approxi-
mately 14% of cases in the United States but less than 2%
in Canada and Australia.14
The etiologies for children parallel those etiologies of
younger adults with the exception of a greater percentage
of injuries, over 30%, related to sports, with diving being
the most common sports-related cause.13 Sports lead to
more SCI in boys than in girls only after the age of 13 years.
Among those younger than 1 year of age who develop
traumatic SCI, medical and surgical causes are most
common, whereas for all those younger than 5 years of age,
transport crashes account for approximately 65% of cases.
Unique causes of SCI in children include lap belt injuries,
birth injury, child abuse injuries, and craniovertebral junc-
tion injuries.
Children younger than 8 years have significantly higher
incidences of SCI without radiologic abnormalities
(SCIWORA), delayed onset of neurologic deficits (ranging
from 0.5 hour to 4 days), and more neurologically com-
plete lesions than those of older children and adults.115
Among children younger than 10 years, SCIWORA is seen
in 60%, but only in 20% of those who are older.115
Neonatal SCI is reported to occur in 1 of 60,000 births
and is usually associated with breech presentations leading
most commonly to a lower cervical or upper thoracic cord
lesion.91 Upper cervical SCI, however, is associated with a
cephalic presentation and delivery.
Neurologic Level and Extent of
Neurologic Deficit
According to both the National SCI Database (14 Model
Systems of Care in the United States) and the Nationwide
Emergency Department Sample (NEDS) Database (980
hospital-based emergency departments in 29 states of the
 CHAPTER 49 Spinal Cord Injury 1097

Table 49-1 Life Expectancy (Years) for People with Spinal Cord Injury Surviving at Least 24 Hours Postinjury
Not Ventilator Dependent
Current Age Motor Functional, Tetraplegia Tetraplegia Ventilator dependent,
(years) No SCI Any Level Paraplegia C5-C8 C1-C4 Any Level
10 70 62 54 49 44 26
20 59 52 45 40 35 19
30 50 43 36 31 28 14
40 40 34 27 23 20 8
50 31 25 19 16 13 4
60 23 18 13 10 8 2
70 15 11 7 5 4 0.5
80 9 6 3 2 1 0.0
From National Spinal Cord Injury Statistical Center: 2012 Annual statistical report for the spinal cord injury model systems—complete public version, Birmingham, 2013, University of Alabama
at Birmingham.
SCI, Spinal cord injury.

United States), tetraplegia is more common than paraple- BOX 49-1

gia accounting for 52% to 57% of SCI cases.88,100 The per- Most Common Primary Causes of Death
centages of cases that are complete injuries, 29% and 11%
of SCI cases in the National SCI and NEDS databases, Diseases of the respiratory system 22%
respectively, are notably different.88,100 This is unsurprising Infective and parasitic diseases 12%
given the composition of the contributing centers to each Neoplasms 10%
database. Hypertensive and ischemic heart disease 10%
Nevertheless, older individuals are more likely to have Other heart disease 9%
incomplete neurologic lesions, which is especially true for Unintentional injuries 7%
Diseases of digestive system 5%
lesions in the cervical region. Cerebrovascular disease 4%
Diseases of pulmonary circulation 4%
Life Expectancy, Morbidity, and Suicides 4%
Causes of Death From National Spinal Cord Injury Statistical Center: 2012 Annual
Life expectancy for people with SCI remains below that of statistical report for the spinal cord injury model systems—complete public
version, Birmingham, 2013, University of Alabama at Birmingham.
people without SCI. People with SCI are two to five times
more likely to die prematurely.14 The mortality rate is
highest during the first postinjury year but declines signifi-
cantly thereafter. Significant predictors of mortality include
level and completeness of injury, age at time of injury, and insufficiency, pulmonary embolism (PE), renal stones, and
requiring a ventilator for respiration. Additional factors gastrointestinal bleeding.99
that affect longevity after the first postinjury year include
low life satisfaction, poor health, emotional distress, func-
tional dependency, and poor adjustment to disability.72 Anatomy, Mechanics, and
The National Spinal Cord Injury Statistical Center website Syndromes of Traumatic Injury
provides annual updates on life expectancy after the onset
of SCI, based on neurologic level and ventilatory depen- Because the bony vertebral column elongates more than
dency (Table 49-1). These life expectancy estimates do not the spinal cord during embryologic development, the
include many important variables that can also signifi- spinal cord terminates at the level of the L1-L2 interverte-
cantly affect survival, such as gender, ethnicity, medical bral disk. As a result of natural variation, the spinal cord
comorbidities, access to medical and nursing care, and termination can be as high as the T12 or as low as the L3
social support. vertebral body. The individual spinal cord segments do not
Diseases of the respiratory system, especially pneumo- line up with the corresponding bony levels of the same
nia, are the leading cause of death both during the first number (Figure 49-1). This is especially evident in the
postinjury year and during subsequent years (Box 49-1). lower thoracic and lumbar spine, where the L1-L5 spinal
The second most common cause of death, “other heart segments are adjacent to the T11-T12 vertebrae, and the
disease,” is thought to reflect deaths that are apparently S1-S5 spinal segments are adjacent to the L1 vertebra. This
caused by heart attacks in younger people without appar- concept can also be used when evaluating radiologic
ent underlying heart or vascular disease and cardiac studies to correlate the neurologic level of injury (NLI) to
dysrhythmia.37 the appropriate bony level of damage (e.g., a T11 burst
After SCI, older individuals (>65 years) have higher fracture with cord compression would be expected to cause
rates of complications, including pneumonia, respiratory an NLI at L1 or L2 rather than at T11).
1098 SECTION 4 Issues in Specific Diagnoses

Spinal
cord

L1

1 Subarachnoid
C1 C1 space
C1

Filum Dural
terminale space

7 8 C7
1
1 T1
C8
2
T1
3 Epidural
4 space
5
T5 6 T5 FIGURE 49-2 A sagittal schematic showing the relationship between the
7 dura, subarachnoid space, and the epidural space. (Redrawn from Pansky B:
Review of gross anatomy, ed 5, New York, 1984, Macmillan, with permission of
8 Macmillan.)
9

T10 10
11

12 T10

1
L1
2 L1

3 Cauda equina

4 Filum terminale
5 L5
L5 1
Sacrum
2
S1

Coccyx
FIGURE 49-1 A sagittal schematic showing the relationship between the
numbered segments of the spinal cord and the corresponding numbered
vertebral bodies. (Redrawn from Pansky B, Allen D, Budd G: Review of neuro-
science, ed 2, New York, 1998, McGraw-Hill, with permission of McGraw-Hill.)

The tapered end of the spinal cord, which contains

the sacral cord segments, is called the conus medullaris.
The collection of long lumbar and sacral roots found
in the canal, distal to the conus medullaris, is called the
cauda equina, because it resembles a horse’s tail. The
meninges of the spinal cord include the pia mater, a vas-
cular membrane covering the spinal cord, the arachnoid
membrane, and the dura mater. The subarachnoid space,
also called the intrathecal space, contains cerebrospinal
fluid (CSF). The CSF pushes the arachnoid directly against
the dura mater. The caudal margin of the dura mater and
arachnoid, the inferior extent of the intrathecal space, is
the second sacral vertebrae (Figure 49-2). The spinal epi-
dural space is located between the dura mater and the
periosteum of the vertebral bodies, and contains an inter-
nal vertebral venous plexus, fat, and loose areolar tissue.
A cross-sectional view of the spinal cord (Figure 49-3)
reveals a central butterfly-shaped region of gray matter
FIGURE 49-3 Normal spinal cord.The corticospinal and spinothalamic tracts
are outlined in the upper diagram, adjacent to the gray matter of the spinal
cord. (Redrawn from Tator C: Classification of spinal cord injury based on neu-
rological presentation. In Narayan R, Wilberger J, Povlishock J, editors: Neuro-
trauma, New York, 1996, McGraw-Hill, with permission of McGraw-Hill.)
consisting of neuronal cell bodies, their processes, support-
ing glial cells, and small blood vessels surrounded by white
matter consisting of neuronal fiber tracts and supporting
glial cells. The gray matter is subdivided into two horns on
each side called the anterior (ventral) and posterior (dorsal)
horns. The posterior horn contains cell bodies of sensory
neurons, whereas the anterior horn contains cell bodies of
interneurons and motor neurons.

The white matter is subdivided into three columns on
each side called the anterior, lateral, and posterior columns.
The columns are further subdivided into tracts. The gracilis
tract, located in the medial posterior column, contains
fibers from the T7-S5 dermatomes that relay touch, vibra-
tion, and position sense. The cuneatus tract, located in the
lateral posterior column rostral to T6, contains fibers from
dermatomes above T7 that relay touch, vibration, and posi-
tion sense. These tracts, comprising the posterior columns,
ascend ipsilaterally to the medulla. The lateral spinotha-
lamic tract, located peripherally in the lateral column, con-
tains fibers that relay pain and temperature sensations; this
tract ascends contralaterally to the thalamus. The lateral
corticospinal tract is located centrally and posteriorly in
the lateral column. This tract contains fibers, most of which
emanate from the motor cortex, that are responsible for
voluntary and reflex movement. Approximately 90% of the
corticospinal fibers cross midline in the caudal medulla,
forming the pyramidal decussations, and descend contra-
laterally in the lateral corticospinal tract to terminate on
interneurons and alpha and gamma motor neurons in the
spinal cord. The remaining corticospinal fibers, located in
the medial anterior column, do not cross midline in the
medulla but descend ipsilaterally in the anterior cortico-
spinal tract. These fibers ultimately cross midline segmen-
tally near their terminations on interneurons and alpha
and gamma motor neurons in the spinal cord. A Brown-
Séquard syndrome refers to an injury of the spinal cord in
which one side is damaged more than the other (Figure
49-4), resulting in relatively greater ipsilateral weakness
and position sense loss, but with contralateral pain and
temperature sensation loss.
FIGURE 49-4 Brown-Séquard syndrome. A burst fracture with posterior
displacement of bone fragments compresses one side of the spinal cord.
(Redrawn from Tator C: Classification of spinal cord injury based on neurological
presentation. In Narayan R, Wilberger J, Povlishock J, editors: Neurotrauma, New
York, 1996, McGraw-Hill, with permission of McGraw-Hill.)
CHAPTER 49 Spinal Cord Injury 1099
A corticospinal neuron is known as an upper motor
neuron (UMN). The motor neuron to which it synapses in
the spinal cord, which exits the spinal cord to innervate
muscle, is known as a lower motor neuron (LMN). If
damage to the UMNs and LMNs within the spinal cord is
localized to a few segmental levels anywhere rostral to the
conus medullaris (discussed later), a constellation of signs
and symptoms develops, often called the UMN syndrome.
This includes loss of voluntary movement, spasticity,
hyperreflexia, clonus, and development of Babinski sign.
If, in addition, there is damage to a significant number of
LMNs below the level of injury, loss of voluntary move-
ment occurs without the subsequent development of the
other components of the UMN syndrome. Examples of
this, defined as LMN injuries, include an SCI caused by an
extensive vascular insult to the spinal cord, an injury occur-
ring at the conus medullaris, or an injury occurring at the
cauda equina. The conus medullaris syndrome refers to an
injury of the sacral spinal cord and the lumbar nerve roots
within the spinal canal (Figure 49-5), resulting in an are-
flexic bladder, bowel, and lower limbs. Conus medullaris
lesions localized to the proximal sacral cord can occasion-
ally show a preserved sacral reflex, such as the bulbocaver-
nosus (BC) reflex. The cauda equina syndrome refers to an
injury to the lumbosacral roots within the spinal canal
(Figure 49-6), resulting in an areflexic bladder, bowel, and
lower limbs.
After an acute UMN-predominant SCI, initial develop-
ment of the UMN syndrome is delayed by a process called
spinal shock, whereby there is a transient suppression and
gradual return of reflex activity below the level of injury.
Ditunno et al.42 have proposed a four-phase model of
spinal shock. During phase 1, occurring 0 to 24 hours
postinjury, there is motor neuron hyperpolarization, mani-
festing clinically as hyporeflexia. During phase 2, occurring
on days 1 to 3 postinjury, there is denervation supersensi-
tivity and receptor upregulation, manifesting clinically
T12
L1
FIGURE 49-5 Conus medullaris syndrome. A burst fracture of T12 with
posterior displacement of bone fragments compresses the conus medullaris.
(Redrawn from Tator C: Classification of spinal cord injury based on neurological
presentation. In Narayan R, Wilberger J, Povlishock J, editors: Neurotrauma, New
York, 1996, McGraw-Hill, with permission of McGraw-Hill.)
1100 SECTION 4 Issues in Specific Diagnoses

Basilar artery

Vertebral
artery Anterior
spinal
Radicular artery
artery
C5 Cervical
C7 area

Radicular T1
artery

Thoracic
Intercostal T6 area
artery

T12

Lumbosacral
Artery of lumbar
area
enlargement

FIGURE 49-6 Cauda equina syndrome. A central disk herniation at L4-L5

compresses the cauda equina. Note how the roots of L5 and S1 are spared.
(Redrawn from Tator C: Classification of spinal cord injury based on neurological
presentation. In Narayan R, Wilberger J, Povlishock J, editors: Neurotrauma, New
York, 1996, McGraw-Hill, with permission of McGraw-Hill.)

with reflex return. During phase 3, occurring 1 to 4 weeks
postinjury, there is interneuron synapse growth, manifest-
ing clinically as early hyperreflexia. And finally, during
phase 4, occurring 1 to 12 months postinjury, there is long
axon synapse growth, manifesting clinically as late
hyperreflexia.
Blood is supplied to the spinal cord through two poste-
rior spinal arteries, a single anterior spinal artery, and
several segmental radicular arteries (Figure 49-7). The pos-
terior spinal arteries branch from the vertebral arteries and
travel along the posterior surface of the spinal cord to
supply the posterior one third of the spinal cord. Two
anterior spinal arteries also branch from the vertebral arter-
ies, but these quickly unite to form a single artery that
travels along the anterior surface of the spinal cord to
supply the anterior two thirds of the spinal cord. The ante-
rior spinal artery and the posterior spinal arteries are
dependent on contributions from the segmental radicular
arteries along the spinal cord to maintain an adequate
blood supply to the spinal cord. The segmental radicular
arteries travel through the intervertebral foramina from the
aorta and divide into anterior and posterior branches that
eventually anastomose with their respective spinal arteries.
These radicular arteries are not all identical in size or dis-
tribution. In the upper thoracic region between T1 and T4,
there is little overlap between radicular arterial supplies.
Between T12 and L2, there is an anterior radicular artery
that is more dominant than its neighbors, called the artery
of Adamkiewicz. This artery, usually found on the left side
of the body, is an important blood supply to the caudal
two thirds of the spinal cord. On reaching the anterior
Artery of
Adamkiewicz
(major anterior
radicular artery)
Anterior view
FIGURE 49-7 The spinal cord blood supply. (Redrawn from Pansky B, Allen
D, Budd G: Review of neuroscience, ed 2, New York, 1998, McGraw-Hill, with
permission of McGraw-Hill.)
surface of the spinal cord, the artery of Adamkiewicz
divides into a small ascending and larger descending
branch. The latter travels down to the level of the conus
medullaris, where it forms an anastomotic circle with the
terminal branches of the posterior spinal arteries. The
regions between T1 and T4, and T12 and L2 are areas par-
ticularly prone to ischemic damage, because of the impor-
tance of individual radicular arteries. The ischemic damage
often affects the anterior portion of the spinal cord more
than the posterior portion because of the nature of the
single anterior and dual posterior blood supplies. In this
situation the corticospinal and spinothalamic tracts are
affected, whereas the gracilis tract is often spared. This
leads to a syndrome of paraplegia, with loss of pain and
temperature sensation, and relative sparing of touch and
position sensation, called the anterior cord syndrome
(Figure 49-8).
Pathophysiology of Acute Spinal Cord Injury
The mechanical damage caused at the moment of impact,
called the primary injury to the spinal cord, starts a
sequence of pathologic events collectively referred to as

FIGURE 49-8 Anterior cord syndrome. A large disk herniation compresses
the anterior aspect of the spinal cord, leaving the dorsal columns intact.
(Redrawn from Tator C: Classification of spinal cord injury based on neurological
presentation. In Narayan R, Wilberger J, Povlishock J, editors: Neurotrauma, New
York, 1996, McGraw-Hill, with permission of McGraw-Hill.)
secondary injury. These secondary changes begin within
seconds of the primary injury and continue for several
weeks thereafter.123
Mechanical disruption of the spinal cord vasculature
leads to the development of microhemorrhages in the gray
and white matter, interstitial edema, and the release of
coagulation factors and vasoactive amines. This latter
release promotes thrombosis and vasospasm of the micro-
vasculature of the spinal cord causing tissue hypoxia and
impaired neuronal homeostasis. At the cellular level, there
are changes in ion concentrations, peroxidation of mem-
brane lipids, formation of free radicals, and release of toxic
excitatory neurotransmitters.123
In response to injury, neutrophils initially migrate to the
site of injury, where they can contribute to cellular injury
by producing lysosomal enzymes and oxygen radicals.
These are followed by macrophages that phagocytose cell
debris.96 Demyelination of white matter tracts begins
within 24 hours of injury and increases thereafter, with
Wallerian degeneration occurring by 3 weeks.118
Spinal Mechanics and Stability
There is no universally accepted definition of spinal stabil-
ity. White and Panjabi121 defined clinical instability as “the
loss of the ability of the spine under physiologic loads to
maintain relationships between vertebrae in such a way
that there is not initial damage or subsequent irritation to
the spinal cord or nerve roots and, in addition, there is no
development of incapacitating deformity or pain caused by
structural changes.” A commonly accepted model for tho-
racolumbar stability, which is also often used in the middle
and lower cervical spine, was developed by Denis.36 The
CHAPTER 49 Spinal Cord Injury 1101
Posterior Middle Anterior
FIGURE 49-9 The three-column concept of spinal anatomy. (Redrawn from
Ferguson RL, Allen BL Jr: A mechanistic classification of thoracolumbar spine
fractures, Clin Orthop 189:77-88, 1984, with permission.)
model divides the spine into three columns: anterior,
middle, and posterior (Figure 49-9). The anterior column
is composed of the anterior longitudinal ligament, the
anterior portion of the vertebral body, and the anterior
portion of the annulus fibrosis or disk. The middle column
is composed of the posterior portion of the vertebral body,
the posterior portion of the annulus fibrosis, and the pos-
terior longitudinal ligament. The posterior column is com-
posed of the pedicles, facet joints, laminae, supraspinous
ligament, interspinous ligament, facet joint capsule, and
ligamentum flavum. When the integrity of the middle and
either the anterior or the posterior column is affected, the
spine is likely to be unstable.36 The columns can be com-
promised by either fracture or ligamentous disruption.
Gunshot wounds, because of the nature of the injury, can
affect more than one column and the spine can still remain
stable. It should also be noted that SCI can occur without
obvious radiographic findings.
Fractures or dislocations in the thoracic and lumbar
spine most commonly involve the T12 and the L1 verte-
brae, respectively. Common mechanisms include
compression-flexion, distraction-flexion, translation, and
torsion-flexion. Axial loading of a flexed spine can cause
several different patterns of injury depending on the vector
of force. There might be only compression of the anterior
column leading to a compression fracture or, with a greater
compressive force, compression of the anterior column
with distraction of the posterior elements. If the vector of
force causes the axis of rotation to be anterior to the ver-
tebral body, a Chance-type distraction can occur with dis-
traction of all three columns, through the bony vertebra
alone (Figure 49-10), through the ligamentous structures
alone, or through a combination of bony and ligamentous
structures. In addition, there can be compression of all
three columns with retropulsion of the middle column
into the spinal canal. The latter often causes SCI. Transla-
tion of adjacent vertebrae, as occurs, for example, when a
person falls from a height and strikes part of the torso on
an immovable object, is the injury pattern most likely to
cause SCI. If there is translation more than 25% of the
width of a vertebra, ligamentous structures in all three
columns are probably disrupted. Compression and rota-
tion of the anterior column, and distraction and rotation
1102 SECTION 4 Issues in Specific Diagnoses
FIGURE 49-10 A Chance fracture. (Redrawn from Schultz RJ: The language of
fractures, Baltimore, 1990, Williams & Wilkins, with permission of Williams &
Wilkins.)
of the posterior column, cause a torsion-flexion injury
where the facets and the anterior longitudinal ligament are
usually disrupted, and SCI is likely.
Lap belt injuries in motor vehicle collisions occur most
often in children weighing less than 60 lb who are wearing
a regular lap belt above the pelvic rim.116 A clinical triad of
abdominal wall bruising, intraabdominal injuries, and SCI
at or close to the thoracolumbar junction is often seen in
these children.116
Fractures or dislocations in the cervical spine are usually
caused by excessive forceful flexion, extension, or axial
loading. An abrupt deceleration, commonly seen in motor
vehicle crashes, causes a person’s head to be propelled
forward on a relatively immobilized torso, leading to a
flexion-type injury. Abrupt acceleration causes the oppo-
site, an extension-type injury. Axial loading is also a
common comechanism to flexion or extension injuries in
the cervical spine, such as occurs when a diver’s head strikes
the bottom of a pool. Knowledge of the mechanism of
injury is important for recognizing injuries that might not
be seen easily on imaging. For example, flexion injuries can
cause disruption of the ligaments in the posterior column
that might not be apparent on plain radiographs.
Craniovertebral junction injuries (i.e., atlantooccipital
or atlantoaxial) are relatively common in children but not
adults. Often they result in immediate death and the SCI
can go undetected.
A Jefferson fracture, originally described by Sir Geoffrey
Jefferson, is a burst fracture of the atlas (C1 vertebra). This
is caused by axial compression, which can occur, for
example, when a football player spears another player with
his helmet (Figure 49-11).
A hangman’s fracture is a traumatic spondylolisthesis of
the axis (C2 vertebra). It is caused by bilateral fractures
through the pars interarticularis of the axis that result from
hyperextension and axial compression, as can occur in an
abrupt deceleration when a person’s forehead strikes the
windshield. A fracture of the odontoid process of the axis
can be caused by hyperflexion, hyperextension, or excessive
lateral bending. The traditional classification of odontoid
fractures includes three types. Type 1 is a fracture through
the tip of the odontoid, type 2 is a fracture through the
FIGURE 49-11 A Jefferson fracture. A comminuted fracture of the ring of
C1. (Redrawn from Schultz RJ: The language of fractures, Baltimore, 1990, Williams
& Wilkins, with permission of Williams & Wilkins.)
base of the odontoid, and type 3 is a fracture that extends
from the base of the odontoid into the axis proper.
Hyperflexion of the subaxial cervical spine (C3-C7) can
cause an anterior subluxation, a simple compression frac-
ture, bilateral facet dislocations, a flexion teardrop fracture,
or a clay-shoveler’s fracture. A flexion teardrop fracture is
characterized by retropulsion of the larger portion of a
vertebral body into the spinal canal, detached from an
anterior fragment (teardrop); it is associated with posterior
facet and ligamentous disruption (Figure 49-12). Flexion
teardrop fractures are often associated with an anterior
cord syndrome, if not a complete SCI. A clay shoveler’s
fracture is an avulsion fracture of the spinous process of
C6, C7, or T1. It is not typically associated with neurologic
injury. Hyperflexion with rotation often causes a unilateral
facet dislocation.
Hyperextension of the subaxial cervical spine typically
distracts the anterior column of the spine and compresses
the posterior column. Anterior distraction often disrupts
the anterior longitudinal ligament, the intervertebral disk,
and the posterior longitudinal ligament, whereas posterior
compression causes the ligamentum flavum to buckle into
the spinal canal. If the spinal cord is pinched between the
vertebral body and the ligamentum flavum and/or hyper-
trophied facet joints, a central cord syndrome often devel-
ops. This syndrome, occurring only with cervical spinal

FIGURE 49-12 A flexion teardrop fracture. The spinal cord is compressed
by the posteroinferior aspect of the vertebrae. (Redrawn from Schultz RJ: The
language of fractures, Baltimore, 1990, Williams & Wilkins, with permission of
Williams & Wilkins.)
cord lesions, is characterized by sacral sensory sparing and
greater weakness in the upper limbs as compared with the
lower limbs. A hyperextension teardrop fracture is charac-
terized by an avulsion of the anterior inferior aspect of the
vertebral body above the hyperextension injury by the
anterior longitudinal ligament, without retropulsion of a
vertebral body into the spinal canal. Compression of the
posterior column during excessive forceful hyperextension
can also result in lamina fractures.
Finally, and not uncommonly, significant axial loading
of the subaxial cervical spine causes a burst fracture,
whereby an intervertebral disk implodes through the supe-
rior end plate of the vertebral body below, causing this
vertebral body to burst into multiple fragments. These frac-
tures usually include at least two columns, are generally
unstable, and are often associated with SCI.
Classification of Spinal Cord Injury
The diagnosis of SCI can be made promptly by performing
a neurologic examination. The International Standards for
Neurologic Classification of Spinal Cord Injury (ISNCSCI)
provides a procedure for classifying an SCI.68 Comprehen-
sive online e-learning modules are available through the
American Spinal Injury Association (ASIA) website. The
examination, which is safe to perform soon after SCI, even
in people with an unstable spine, is performed with the
injured individual in the supine position. Subsequent
examinations are always performed in the same position.
The procedure includes a systematic evaluation of all the
dermatomes and extremity myotomes. Because SCI usually
affects the spinal cord at a discrete site, determining the
last intact sensory and motor level can reliably and accu-
rately determine an NLI. A complete injury is defined
within the ISNCSCI as an injury in which there is the lack
of any sensory or motor function in the lowest sacral
segment; this includes pressure sensation within the anus,
CHAPTER 49 Spinal Cord Injury 1103
sensation at the anal mucocutaneous junction, or a volun-
tary contraction of the external anal sphincter. An incom-
plete injury is defined as an injury in which there is at least
partial sensory or motor function in the lowest sacral
segment.
The sensory portion of the neurologic examination
includes the testing of a key point for absent, impaired, or
normal sensation in each of the 28 dermatomes on each
side of the body for both light touch and pinprick. Pinprick
sensation is elicited with a disposable safety pin, whereas
touch sensation is elicited by a wisp of cotton or a fingertip.
For an inability to distinguish between pinprick and touch,
sensation should be graded as absent for pinprick sensa-
tion. The motor portion of the neurologic examination
includes the testing of a key muscle function for strength
on a 6-point scale for each of 10 myotomes on each side
of the body, as well as testing for contraction of the external
anal sphincter. Detailed descriptions and demonstrations
for testing each specific sensory point and key muscle
group are demonstrated on the ASIA Learning Center
website (lms3.learnshare.com).
The testing of every key muscle should begin in the
grade 3 testing position. If the muscle is shown to have
greater than antigravity strength (grade 3), then the muscle
should be tested in the grades 4 and 5 testing positions.
Conversely, if the muscle is shown to have less than anti-
gravity strength when tested in the grade 3 testing position,
the muscle should be tested in the grade 2 testing position.
If the muscle is shown to not even have grade 2 strength,
then the grade 1 testing position is used. Before testing
muscle strength for a particular key muscle, the range of
motion (ROM) for the joint that particular muscle crosses
should be tested. Knowing this available ROM is a neces-
sary condition for accurately grading the strength.
The NLI is defined as the most caudal segment of the
spinal cord with normal sensation and motor function
bilaterally. For the ISNCSCI, key muscles have been chosen
that primarily have innervation by two roots, with each
successive key muscle overlapping the muscle above in
either the cervical or the lumbar region, by a single root
innervation. By ISNCSCI definition, if a key muscle has a
motor strength grade of 5/5, it is innervated by two intact
nerve segments. If a key muscle has a motor strength grade
of 3/5 or 4/5 (and the key muscle above has a motor
strength grade of 5/5), it is innervated by at least one intact
nerve segment, the segment for which that key muscle
is named. If a key muscle has a motor strength grade of
2/5 or less, neither of its nerve segments is intact. For the
cervical segments, because the innervation of the elbow
flexors is C5 and C6, the wrist extensors is C6 and C7, and
the elbow extensors is C7 and C8, the ISNCSCI-named
segmental innervations are C5, C6, and C7, respectively.
If the elbow flexors are graded as 5/5, the wrist extensors
as 4/5, and the elbow extensors as 2/5, it is assumed that
the C5 and C6 myotomes are fully innervated, but the
C7 myotome is partially innervated only. For myotomes
where there are no designated key muscles to test, motor
function is assumed to be normal where sensory function
is normal.
The ISNCSCI also includes a scale of impairment called
the ASIA Impairment Scale (AIS), which classifies an SCI
into five categories of severity, labeled A through E, based
1104 SECTION 4 Issues in Specific Diagnoses
on the degree of motor and sensory loss. An SCI that
results in the absence of any sensory or motor function in
the sacral segments S4-S5 would have an AIS category of A
and be designated as complete. For an SCI where sensation
is preserved in the sacral segments S4-S5, but there is no
motor function caudal to three segments below the NLI,
the AIS is B. For an SCI where sensation is preserved in the
sacral segments S4-S5, but more than half the key muscles
below the NLI have a muscle grade less than 3/5, the AIS
is C. For an SCI where sensation is preserved in the sacral
segments S4-S5, but at least half the key muscles below the
NLI have a muscle grade greater than or equal to 3/5,
the AIS is D. When sensory and motor function is normal,
the AIS is E. AIS categories B through E designate incom-
plete injuries.
There are certain issues that need to be taken into con-
sideration when conducting an examination on children.
There is a learning module on the ASIA Learning Center
website (lms3.learnshare.com) specifically addressing
these concerns.
Nontraumatic Spinal Cord Injury
Nontraumatic SCI can be caused by a variety of diseases,
including neoplastic, infectious, inflammatory, vascular,
degenerative (spondylotic), congenital, and toxic-
metabolic disorders. People affected by nontraumatic SCI
are clinically very different from those with traumatic inju-
ries. Those with nontraumatic SCI generally have less
severe injuries, and almost always have incomplete inju-
ries that are associated with a far better prognosis for neu-
rologic improvement than complete injuries. Also, unlike
people with traumatic SCI, people with nontraumatic SCI
are significantly more likely to have paraplegia than
tetraplegia.82
Neoplastic Causes of Spinal Cord Injury
Tumors associated with SCI can arise from either the neural
elements in the spinal canal, such as the spinal cord or
spinal nerves, or the structures comprising the spinal
column, most commonly the vertebral bodies. Tumors
arising from the spine (extradural tumors) are much more
common than those arising from neural elements (intra-
dural tumors).
Classification of Spinal Tumors
The most common method of classifying tumors relates to
the anatomic location of tumor involvement. Spinal
tumors are extradural when they arise from structures
outside the dura, most commonly the vertebral body. A
less likely origin is from the structures of the posterior
bony arch or the soft tissues outside the dura. Most tumors
metastatic to the spine are extradural, making up more
than half of all spinal tumors.73 The most common primary
sites of metastatic tumors to the spine are lung, breast,
prostate, and kidney.59 The mechanisms of metastasis
include direct extension of tumor from adjacent tissues,
and hematogenous spread through the Batson vertebral
venous plexus, a valveless venous system draining the tho-
racic, abdominal, and pelvic viscera. Primary spine tumors
that are present in the extradural region make up less than
1% of all spinal tumors. These include multiple myeloma,
osteogenic sarcoma, vertebral hemangioma, chondrosar-
coma, and chordoma.59
Tumors arising within the intradural space include
those that are intramedullary (i.e., tumors arising from the
parenchyma of the spinal cord) and those that are intra-
dural but extramedullary. Intramedullary tumors are
usually primary tumors, most commonly ependymomas
and astrocytomas, which together make up 75% of all
intramedullary tumors.59 Ependymomas tend to be well
encapsulated and regularly shaped in contrast to astrocy-
tomas, which tend to be irregularly shaped with multiple
extensions into the cord parenchyma. Most intradural
extramedullary tumors are both benign and primary, and
include meningiomas and nerve sheath tumors such as
schwannomas and neurofibromas.59 Those metastatic
tumors that are seen can arise either by hematogenous
spread or as “drop metastases,” lesions that directly extend
from the CSF in association with malignant brain tumors
such as medulloblastomas.73
Clinical Presentation of Spinal Tumors
Pain is the most common presenting symptom of a spinal
tumor. Pain associated with spinal tumors is often worse
in the supine position, in contrast to the pain associated
with degenerative spondylosis, which is usually worse in
the upright position. If the tumor involves only skeletal
structures, the pain is usually axial. If the tumor involves
nerve roots, it occurs typically in a radicular distribution.
If the tumor involves the spinal cord, the pain can present
as at-level or below-level spinal cord pain. Constitutional
symptoms such as night sweats, fevers, unexplained weight
loss, and anorexia can also suggest spinal tumor.
Acute spinal cord compression is associated with rapid
neurologic decline, and constitutes a medical emergency
because it can rapidly progress to paraplegia or tetraplegia.
When signs and symptoms of acute spinal cord compres-
sion related to neoplastic involvement of the spine are
present, most patients will have substantial radiographic
abnormalities. The syndrome of acute spinal cord com-
pression, when related to spinal tumors, most often results
from the invasion of spinal structures by extradural
metastases.
Management of Spinal Cord Compression by Tumor
Acute spinal cord compression is managed with corticoste-
roids, radiation, and surgical intervention. Corticosteroids,
typically dexamethasone, are administered to reduce
tumor-related inflammatory changes and prostaglandin
production.59 Radiation therapy is often used in cases of
spinal cord compression resulting from soft tissue
encroachment. It can be used alone in the setting of spinal
stability or in combination with surgery. Radiation therapy
is less often used for the treatment of intradural or intra-
medullary tumors, unless such tumors are deemed unre-
sectable or when surgical resection is incomplete.59
Radiosensitive tumors involving the spine include lym-
phomas, small cell lung cancer, and multiple myeloma,
whereas less radiosensitive tumors include breast, prostate,
non–small cell lung, and renal cell cancers.59 Complica-
tions of radiation directed to the spine include radiation

myelopathy and radiation plexopathy. In the setting of
acute spinal cord compression, the immediate goal of sur-
gical treatment is decompression of the cord to preserve or
improve neurologic function.
For most intramedullary and intradural extramedullary
tumors, surgical treatment is the most effective. Ependy-
momas, because of their encapsulated nature, often can be
completely resected with good preservation of neurologic
function. In contrast, because astrocytomas are irregular
and invasive without a clear plane for resection, the goal
of surgery is a subtotal resection of clearly abnormal tissue.
Intradural extramedullary meningiomas arise from the
dura and are resected along with the involved dura after
being accessed through a laminectomy. Nerve sheath
tumors can be entirely intradural or, in the case of the
neurofibroma, can have extradural extension through an
enlarged neural foramen. In neurofibromatosis type 2,
extensive intradural involvement throughout much of the
spinal cord can be present. In such cases, tumor debulking
rather than complete resection is usually the surgical goal.
Infectious and Inflammatory Causes of Spinal
Cord Injury
Bacterial Infection
Bacteria can invade a vertebral body either hematogenously
or by direct extension from a contiguous focus of infection,
causing vertebral osteomyelitis. People at increased risk for
bacterial vertebral osteomyelitis include those who use
intravenous drugs; immunosuppressed individuals; people
with diabetes; or people with renal disease who are receiv-
ing dialysis. Children are relatively susceptible to bacterial
diskitis alone, probably because of a relatively robust
blood supply to the intervertebral disk. The bacteria most
commonly implicated in vertebral osteomyelitis is Staphy-
lococcus aureus, which accounts for more than half of all
infections.53 Although infection can be seen in any portion
of the spine, the lumbar spine is the most common area.
Spine pain is by far the most common symptom of verte-
bral osteomyelitis, seen in greater than 90% of people
affected.53 Other symptoms can include fever or a neuro-
logic deficit related to spinal cord compression from ver-
tebral body collapse, or the presence of an epidural abscess.
Laboratory markers of inflammation, such as the erythro-
cyte sedimentation rate and C-reactive protein, are very
frequently found to be elevated with active infection. Isola-
tion of the etiologic pathogen is vital to treatment success.
This can be accomplished by recovery of the organism in
blood cultures or through cultures of tissue obtained from
the spine, either by needle or open biopsy. Treatment of
vertebral osteomyelitis involves intravenous antibiotic
administration for at least 4 weeks. Surgical treatment is
indicated when appropriate antibiotics have been ineffec-
tive, when there is spinal cord or nerve root compression
causing a neurologic deficit, or when there is spinal insta-
bility or spinal deformity.
Tuberculosis of the spine, also known as Pott disease,
results from hematogenous spread of the bacterium Myco-
bacterium tuberculosis to the spine, typically from a pulmo-
nary focus. Spinal tuberculosis is treated with at least two
and as many as four antituberculous agents for a 6- to
12-month duration.
CHAPTER 49 Spinal Cord Injury 1105
Human Immunodeficiency Virus and Human
T-Lymphotropic Virus Infection
People with human immunodeficiency virus (HIV) infec-
tion are susceptible to spinal cord disease, which can occur
as vacuolar myelopathy, as primary HIV myelitis, or as a
result of opportunistic infections of the spinal cord. Vacu-
olar myelopathy clinically presents as incomplete spastic
paraplegia with loss of proprioception and vibration sense.
Human T-lymphotropic virus type 1 (HTLV-1) is another
retrovirus that causes a progressive chronic myelopathy.
The clinical condition is a slowly progressive spastic para-
plegia, which is referred to as both tropical spastic parapa-
resis and HTLV-1–associated myelopathy. The virus is
transmitted through blood, sexual contacts, and from
mother to child in breast milk. It occurs in the Caribbean,
southern Japan, central and south Africa, and regions of
South America.53
Transverse Myelitis
Myelitis is a neurologic disorder of the spinal cord (myelop-
athy) that is caused by inflammation. The term “transverse”
was first added to “myelitis” in the case report of an acute
inflammatory myelopathy complicating a pneumonia,107
in which “transverse” in this case referred to the clinical
finding of a bandlike horizontal area of altered sensation
at the dermatomal level of the lesion within the cord.
When a person has a rapidly evolving myelopathy with
no history of trauma or physical or radiographic evidence
of a structural lesion, the differential diagnosis should
include potential causes of myelitis such as systemic lupus
erythematosus, Sjögren syndrome, multiple sclerosis, neu-
romyelitis optica, neurosarcoid, paraneoplastic syndromes,
nutritional deficiencies, vascular insufficiency, decompres-
sion sickness, and infection. Myelitis can progress over the
course of several hours or over a few weeks. Even when
infection is thought to be a cause, causative organisms are
rarely if ever isolated. Although transverse myelitis can
occur in any region of the spinal cord, the thoracic region
is most common. In people with transverse myelitis, mag-
netic resonance imaging (MRI) scanning often shows
spinal cord swelling, with a region of increased signal on
T2-weighted images that correlates with the NLI.
Acute treatment of myelitis is aimed at halting the
inflammatory process. The standard treatment is the
administration of high-dose intravenous (IV) methylpred-
nisolone at 1000 mg daily for 3 to 7 days. If the response
is suboptimal, then plasma exchange is recommended to
remove any humoral factors that may be contributing to
the pathologic process. Lastly, if there is still no improve-
ment with plasma exchange, IV immunoglobulin, cyclo-
phosphamide, rituximab, or azathioprine, the latter two
for neuromyelitis optica, may be of benefit.120
Vascular Causes of Spinal Cord Injury
Ischemia of the spinal cord, although less common than
ischemia of the brain, is a well-known cause of SCI. It is
most commonly associated with the anterior cord syn-
drome and can occur as a result of systemic or local spinal
cord hypoperfusion, embolization, or rarely thrombosis.
Ischemia can also result from the presence of a type I spinal
1106 SECTION 4 Issues in Specific Diagnoses

arteriovenous malformation (AVM). This is a dural arterio-
venous fistula that arises when a single dural arterial feeder,
either spontaneously or after trauma, develops a fistula to
the spinal venous circulation. This fistula causes venous
congestion and hypertension, which results in hypoperfu-
sion of the spinal cord. Symptoms caused by type I AVMs
are usually of gradual onset, with a progressive course,
although there can be stepwise episodes of deterioration
interspersed with periods of clinical stability. Sensory
symptoms are the most common initial presenting symp-
toms, but weakness and sphincter disturbances are often
present by the time the diagnosis has been made.65
Outcomes of Traumatic Spinal
Cord Injury
It is not uncommon for clinicians involved in the care of
a person who has experienced a traumatic SCI to be asked
the following questions: “Will I walk again?” “Will I regain
Neurologic Recovery and Ambulation
A combination of age (<65 years versus ≥65 years), the
motor score of the stronger quadriceps femoris muscle, the
motor score of the stronger gastrocsoleus muscle, and light
touch sensation at the L3 and S1 dermatomes show excel-
lent discrimination in distinguishing people who will be
able to walk and those who will not be able to walk at 1
year (Figure 49-13, Table 49-2).113
Functional Recovery
Prognostication of functional outcome depends on the
physical examination findings, familiarity with the pub-
lished functional outcomes of people with SCI of different
NLI, and an ability to integrate into a prognosis a host of
100
90

Probability of walking independently (%)

use of my hands?” “Will I regain control of my bowel and 80
bladder?” These questions prove the importance of prog-
70
nosticating neurologic and functional outcomes as early as
possible after an SCI, to allow development of a specific 60
treatment plan and to allow psychological adjustment to
begin. Prognostication of neurologic outcome depends on 50
the physical examination findings, especially as defined by
the ISNCSCI. With regard to outcomes, older people gener- 40
ally do less well than younger people, reaching lower levels
30
of independence in walking and self-care.
20
Neurologic Recovery in Complete Tetraplegia
10
After traumatic cervical SCI, 20% to 30% of people classi-
fied as AIS A convert to AIS B or better by 1 year. This has 0
–10 –5 0 5 10 15 20 25 30 35 40
been consistent across several independent large database
analyses.78,103 Within the Model Systems Database, for Prediction rule score
those initially AIS A, 8% convert to AIS C, whereas 7% FIGURE 49-13 Probability of walking independently 1 year after injury based
convert to AIS D. For those initially AIS B, 30% become on prediction rule score. (From van Middendorp JJ, Hosman AJ, Donders AR,
AIS C and 37% become AIS D. For those initially AIS C, et al: A clinical prediction rule for ambulation outcomes after traumatic spinal
cord injury: a longitudinal cohort study, Lancet 377:1004-1010, 2011.)
over 80% convert to AIS D or E.
Of those who convert from AIS A to AIS B or greater, up
to two thirds convert by 1 month with the remainder con- Table 49-2 Clinical Prediction Rule Variables
verting within 3 months; it is rare to convert after that. Range of Weighted Minimum Maximum
The change in upper extremity motor score (UEMS) Test Scores Coefficient Score Score
over the first year postinjury, which can be calculated by Age ≥65 0-1 −10 −10 0
adding all the muscle grades for the key muscles in the years
upper extremities (for a total 50 points), for people with Motor 0-5 2 0 10
C4-C7 AIS A tetraplegia averages 10 points.78,103 The motor score L3*
level stays the same or worsens in 35% of people, improves
Motor 0-5 2 0 10
one level in 42%, improves two levels in 14%, and improves score S1*
more than two levels in 9%. A motor zone of partial pres-
Light touch 0-2 5 0 10
ervation of more than two segments is associated with a score L3*
gain of more than two levels. The chance of functional
recovery of a muscle two levels below the motor level of Light touch 0-2 5 0 10
score S1*
injury, when the first muscle below the motor level is grade
0, is exceedingly rare. The typical pattern of neurologic Total −10 40
improvement with regard to gains in motor score is char- From van Middendorp JJ, Hosman AJ, Donders AR, et al: A clinical prediction rule for
acterized by the greatest changes within the first 3 months, ambulation outcomes after traumatic spinal cord injury: a longitudinal cohort study, Lancet
377:1004-1010, 2011.
lesser changes over the next 3 months, with even lesser *Only the best score of each motor score or light touch score (i.e., right or left)
changes thereafter with plateauing by 1 year. should be applied for the prediction rule.

other factors. These factors include, but are not limited to,
preexisting medical conditions, concomitant injuries, sec-
ondary complications, cognitive impairments, age, body
habitus, availability of financial resources and insurance
coverage, psychological factors, social factors, and cultural
factors. The information in Table 49-3 is modified from
the Outcomes Following Traumatic Spinal Cord Injury clinical
practice guideline, which was first published by the Para-
lyzed Veterans of America in 1999.122 The expected out-
comes are stratified by NLI and described for several
different domains. They reflect the level of independence
that can be expected of an average individual with a motor
complete SCI under optimal circumstances 1 year after
injury.
Acute Phase of Injury
Prehospital Care
The first 24 hours after trauma are the deadliest. In this
period, primary and secondary injuries to the central
nervous system are the leading cause of death. The first step
in the treatment of a person with a suspected spinal injury
is ensuring an adequate airway, breathing, and circulation.
Patients with cervical cord injuries are at high risk for
respiratory failure and must be monitored closely for the
need for ventilatory support. Even if intubation is not
needed urgently, arterial blood gas and vital capacity (VC)
measurements are useful tools in identifying delayed respi-
ratory muscle fatigue. When intubation is necessary, it
must be done carefully in the setting of suspected or con-
firmed cervical spine trauma to avoid secondary cord
injury. The standard technique for urgent intubation in this
setting is rapid sequence induction with cricoid pressure
and manual inline stabilization.30 Alternatively, awake
fiberoptic intubation is an appropriate alternative, and
may be the preferred technique, in a cooperative patient.
All people with suspected acute SCI should have their
spines immobilized. People with altered mental status,
evidence of intoxication, suspected limb fracture or dis-
tracting injury, focal neurologic deficit, and spine pain or
tenderness should also be suspected of having a traumatic
SCI. The entire spine should be immobilized in a neutral
supine position regardless of the position the individual
was found in after the accident. This is best accomplished
with the use of a combination of a rigid cervical collar with
supportive blocks on a backboard that has straps to secure
the body. On the spine board, an occipital pad for an adult
or an occipital recess for a child younger than 6 years can
be used to compensate for the different sizes of the head
relative to the body in people of different age groups.
Once on the spine board, the individual is transported
to a trauma center where the initial goals are to establish
hemodynamic stability, to prevent hypoxemia and aspira-
tion of stomach contents, and to maintain spinal immo-
bilization until definitive management is accomplished.
Maintenance of adequate blood pressure is critical because
hypotension and shock are extremely deleterious to the
injured spinal cord. A target mean arterial blood pressure
of 85 mm Hg for a minimum of 7 days has been associated
with favorable outcomes. Although neurogenic shock is
CHAPTER 49 Spinal Cord Injury 1107
associated with cervical and high thoracic injuries, it is
important to evaluate the patient fully for other causes of
shock including hemorrhage, pneumothorax, myocardial
infarction, cardiac tamponade, sepsis from intraabdominal
injury, or even acute adrenal insufficiency in patients with
concomitant brain injury. Neurogenic shock is a result of
sympathetic denervation and is characterized by hypoten-
sion and bradycardia in the setting of flaccid paralysis.
Bradycardia results from unopposed parasympathetic
input to the heart, but can also be stimulated by endotra-
cheal suctioning. Neurogenic shock is treated with restora-
tion of intravascular volume and vasopressor agents. The
ideal vasopressor agents have both alpha-adrenergic and
beta-adrenergic actions to counter the loss of sympathetic
tone and provide chronotropic support to the heart.30 Atro-
pine is helpful to rapidly reverse the bradycardia. A tem-
porary or permanent cardiac pacemaker insertion is rarely
necessary. Hemorrhagic shock is treated by controlling
bleeding and vigorous fluid resuscitation. Core tempera-
ture should be monitored because people with cervical or
high thoracic injuries can become relatively poikilothermic
because of autonomic nervous system disruption. Place-
ment of a nasogastric tube in the acute period is important
to prevent emesis and aspiration of gastric contents, and
an indwelling bladder catheter ensures adequate bladder
drainage in a situation where urinary retention is the rule.
Early contact between the receiving trauma center and a
specialized SCI center should be established, with arrange-
ments made for transfer to the spinal injury center once
medical stability has been secured.
Once stabilized medically, a thorough evaluation of
neurologic status and spinal stability is performed. The
neurologic status is determined using the ISNCSCI. Serial
examinations should be performed to detect neurologic
deterioration or improvement, particularly in the first 3
days after injury and after manipulation such as transport,
closed reduction, or surgical treatment. Spinal stability is
assessed for the entire spine, not just the clinically likely
area of injury, because there is an approximately 20%
chance of finding noncontiguous spine fractures. Com-
puted tomography (CT) imaging of the entire spine is
recommended because of the lack of sensitivity of plain
film protocols, particularly in the craniocervical region and
at the cervicothoracic junction. MRI evaluation is essential
for evaluating nonbony tissues, including the spinal cord,
nerve roots, ligaments, and intervertebral disks, and should
be performed to evaluate the area of a known or suspected
SCI. MRI evaluation is particularly important for identifica-
tion of spinal pathology in people with a neurologic deficit
not identified by CT and for those people who are uncon-
scious or obtunded.
Specific to children, SCIWORA has been reported in up
to 20% of children with SCI, whereas in those with frac-
tures, multiple noncontiguous fractures are seen in one
third of children with SCI.13
Surgical Management
In the specific case of dislocation of the cervical spine,
rapid closed reduction of the spine using skeletal traction
remains a valid treatment option. Closed reduction of a
Text continued on p. 1112
1108 SECTION 4 Issues in Specific Diagnoses

Table 49-3 Expected Functional Outcomes by Neurologic Level of Injury

C1-C4 C5
Domain
Domain Description Expected Outcome Equipment Expected Outcome Equipment
Respiratory Ability to breathe Ventilator or Ventilator(s) (C1-C3) Low endurance and vital
with or without diaphragm/phrenic Suction equipment capacity secondary to
mechanical pacer dependent (C1-C3) paralysis of intercostal
assistance and (C1-C3) Back-up generator muscles; may require
clear secretions Inability to clear (C1-C3) assist to clear
secretions Nebulizer secretions

Bowel Management of Total assist for digital Padded reclining Total assist including Padded reclining
elimination and stimulation, insertion commode chair with insertion of commode chair
perineal hygiene of minienema or head support minienema or
suppository, and Roll-in shower suppository and
perineal hygiene digital stimulation

Bladder Management of Total assist for Foley catheter or Total assist for inserting Foley or external
elimination and inserting indwelling external catheters indwelling catheter catheters
perineal hygiene catheter Urine drainage bags (transurethral or Urine drainage bags
(transurethral or suprapubic) or
suprapubic) or applying an external
applying an external catheter to penis
catheter to penis

Bed mobility Rolling, scooting, Total assist but Fully electric hospital Some assist but Fully electric hospital bed
and bridging, supine independent in bed with available independent in with Trendelenburg
positioning to sit direction of care Trendelenburg direction of care and feature and side rails
position and side rails controlling bed with accessible remote
Pressure relieving control
mattress Pressure relieving
mattress
Transfers Total assist but Transfer board Total assist but Transfer board
independent in Power or mechanical lift independent in Power or mechanical lift
direction of with sling direction of transfers with sling
transfers
 CHAPTER 49 Spinal Cord Injury 1109

C6-C7 C8 T1-T12 L1-S5

Expected Expected Expected Expected
Outcome Equipment Outcome Equipment Outcome Equipment Outcome Equipment
Low endurance Low endurance Low endurance Normal
and vital and vital and vital
capacity capacity capacity
secondary to secondary to secondary to
paralysis of paralysis of paralysis of
intercostal intercostal intercostal
muscles; may muscles; may muscles for
require assist require assist higher level
to clear to clear lesions
secretions in secretions in
setting of setting of
respiratory respiratory
infection infection
Some to total Padded commode Independent Padded Independent Padded Independent Padded toilet
assist for setup chair digital commode digital commode digital seat
and perineal Suppository stimulation, chair stimulation, chair stimulation,
hygiene inserter suppository or suppository or suppository or
Independent Digital bowel minienema minienema minienema
suppository stimulator insertion, and insertion, and insertion, and
insertion with Mirror perineal perineal perineal
suppository hygiene hygiene hygiene
inserter
Independent
rectal
stimulation
with digital
bowel
stimulator
Total assist for Bimanual catheter Independent Straight Independent Straight Independent Straight
inserting inserter intermittent catheters intermittent catheters intermittent catheters
indwelling Foley, straight, or catheterization catheterization catheterization
catheter external
(transurethral catheters
or suprapubic) Urine drainage
or applying an bags
external
catheter to
penis
Independent
self-
catheterization
through a
continent
urinary
diversion
(Mitrofanoff
procedure)
with an
abdominal
stoma for
woman or
penis for men
with
equipment
Some assist Full electric Independent Full to king Independent Full to king Independent Full to king
hospital bed standard bed standard bed standard bed
side rails or full Pressure Pressure
to king standard relieving relieving
bed mattress mattress
Pressure relieving overlay overlay
mattress overlay
Level: Some assist Transfer board Independent with Transfer board Independent with Transfer board Independent
to independent or without or without
Uneven: Some to transfer board transfer board
total assist
Continued on following page
1110 SECTION 4 Issues in Specific Diagnoses

Table 49-3 Expected Functional Outcomes by Neurologic Level of Injury (Continued)

C1-C4 C5
Domain
Domain Description Expected Outcome Equipment Expected Outcome Equipment
Wheelchair Power: Independent Power: Power recline Power: Independent Power: Power recline
propulsion Manual: Total assist for and/or tilt wheelchair Manual: Independent to and/or tilt wheelchair
and pressure propulsion and with postural support some assist indoors with arm drive control
reliefs pressure reliefs and head, chin, or on noncarpeted level Manual: Ultralightweight
breath control surfaces and some to rigid or folding frame
Manual: Manual recline total assist outdoors with handrim
and/or tilt wheelchair for propulsion; some modifications and
Pressure-relieving assist for pressure postural support
wheelchair cushion reliefs Pressure-relieving
wheelchair cushion

Standing and For exercise, Not indicated Standing: Total assist Hydraulic standing frame
ambulation psychological Ambulation: Not
benefit, or for indicated
functional
activities

Eating, dressing, Total assist Bathing: Handheld Eating: Independent with Eating: Wrist splint with
and bathing shower, padded equipment after total universal cuff, bent
reclining commode assist for setup fork or spoon, nonslip
chair with head including cutting food mat, plate guard, and
support, and roll-in Dressing and bathing: possibly a mobile arm
shower Total assist support
Bathing: Handheld
shower, padded
reclining commode
chair with head
support, and roll-in
shower

Communication Keyboard use, Total assist to Mouth stick Independent to some Adaptive devices as
handwriting, and independent after Voice-activated devices assist after setup with needed for page
telephone use setup with or infrared head equipment turning, writing, and
equipment control devices for button pushing
computer and Voice-activated devices
environmental control Bluetooth
Inline speaking valve for
ventilator tubing
Transportation Driving, attendant- Total assist Attendant-operated van Independent with highly Highly specialized
operated (e.g., lift, tie-downs) specialized equipment; modified van with lift
vehicle, and or accessible public some assist with
public transportation accessible public
transportation transportation; total
assist for attendant-
operated vehicle
 CHAPTER 49 Spinal Cord Injury 1111

C6-C7 C8 T1-T12 L1-S5

Expected Expected Expected Expected
Outcome Equipment Outcome Equipment Outcome Equipment Outcome Equipment
Power: Power: Power Manual: Ultralightweight Manual: Ultralightweight Manual: Ultralightweight
Independent recline and/or Independent rigid or Independent all rigid or Independent rigid or
with standard tilt wheelchair all surfaces folding frame surfaces folding frame all surfaces folding frame
arm drive on with arm drive Pressure- Pressure- Pressure-
all surfaces control or relieving relieving relieving
Manual: power-assist wheelchair wheelchair wheelchair
Independent wheelchair cushion cushion cushion
indoors and Manual:
some assist Ultralightweight
outdoors for rigid or folding
propulsion; frame with
independent handrim
for pressure modifications
reliefs and postural
support
Pressure-relieving
wheelchair
cushion
Standing: Total Hydraulic standing Standing: Some Standing frame Standing: Standing frame Standing: Standing frame
assist frame assist to Independent Knee-ankle- Independent KAFO or
Ambulation: Not independent Ambulation: For foot orthosis Ambulation: ankle-foot
indicated Ambulation: Not exercise only (KAFO) Functional if orthosis
indicated Walker or only one Forearm
forearm KAFO needed crutches or
crutches cane as
indicated
Eating: Eating: Adaptive Eating: Dressing: Independent Independent
Independent devices as Independent Adaptive
with or indicated (e.g., Dressing and devices as
without wrist splint with bathing: Some indicated
equipment, utensil holder assist to (e.g., button;
except cutting, or universal cuff, independent hook; loops
which is total adapted utensils, with adaptive on zippers,
assist nonslip mat, equipment pants; socks,
Dressing and plate guard) Velcro on
bathing: Dressing: Adaptive shoes)
Independent devices as Bathing: Padded
upper body; indicated (e.g., tub transfer
some to total button; hook; bench or
assist for loops on commode
lower body zippers, pants; chair, wash
socks, Velcro on mitt, and
shoes) handheld
Bathing: Padded shower
tub transfer
bench or
commode chair,
wash mitt, and
handheld
shower
Independent with Adaptive devices Independent Adaptive Independent Independent
or without as needed for devices as
equipment page turning, indicated
writing, and
button pushing
Bluetooth

Independent Modified van with Independent car Car with hand Independent car Car with hand Independent car Car with hand
driving from lift, sensitized if independent controls Independent controls controls
wheelchair hand controls, with transfer Modified van driving Modified van depending on
and tie-downs and wheelchair with lift and modified van with lift and degree of
for wheelchair loading/ hand from captain’s hand lower
unloading controls seat controls extremity
Independent function
driving
modified van
from captain’s
seat
1112 SECTION 4 Issues in Specific Diagnoses
cervical dislocation is performed by applying a series of
increasing distracting forces through the long axis of the
body by means of a two-point attachment to the skull with
a tong device. The tong device is attached to a rope that
passes through a pulley and is attached to a weight. When
the obstruction to normal alignment is overcome with the
applied distraction force, and the spine is realigned (e.g.,
a jumped facet), the distracting forces are reduced again.
Use of tongs for traction in children has been associated
with dural leaks and halo fixators are generally used
instead, with increased number of pins (8 to 10 as com-
pared with 4 for adults) and lower halo pin torques than
are used for adults.13 Surgery is performed after closed
reduction to reestablish spinal stability.
Operative treatment of acute spinal injury is generally
performed either to stabilize an unstable spine or to
decompress compressed neural elements, for example,
spinal cord or nerve roots. The best available studies indi-
cate that there is better neurologic recovery, decreased
acute care and total hospital lengths of stay, and fewer
medical complications when surgery is performed early
(<24 hours after injury) as compared with later on.49,83
If a traumatic SCI is not associated with spinal cord
compression or spinal instability, surgery might not be
indicated. For example, this could apply in the case of a
person with preexisting cervical spinal stenosis who falls
and sustains a central cord injury where there is no frac-
ture, subluxation, disk herniation, or spinal cord compres-
sion. A cervical collar might be all that is indicated. Use of
a spinal orthoses as the mainstay of management is also
feasible for bony fractures, such as a compression fracture
affecting only the anterior column of the spine without
spinal cord compression.
Most practitioners of SCI medicine are in agreement
that people with incomplete injuries and spinal cord com-
pression are best served by performing a decompressive
procedure to maximize the potential for neurologic recov-
ery. Decompression of the spinal cord in the setting of a
neurologically complete injury has been more controver-
sial. It is well established that decompression of the cord
in a complete injury is not usually associated with a change
from complete to incomplete status. Therefore, the role of
surgery in neurologically complete lesions is to provide
early stability and rapid involvement of the injured person
in rehabilitation, potentially minimizing the occurrence of
medical complications in the early phase of the postinjury
period. Decompression of the cord in complete injuries
might also reduce the incidence of posttraumatic cystic
myelopathy.
The surgical approach to the spine is determined based
on the mechanism of injury, the location of spinal cord
compression, and the surgeon’s experience and expertise
with the various surgical techniques. An anterior surgical
approach provides the most direct decompression of the
spinal cord when the compression of the cord is caused by
retropulsion of bone fragments or disk material into the
spinal canal. Anterior column reconstruction and restora-
tion of spinal stability can often be accomplished with just
an anterior approach. There are, however, significant poten-
tial complications of an anterior approach. In the cervical
region, surgical injury to the recurrent laryngeal nerve can
cause problems with speech and swallowing, whereas
injury to the pharynx or esophagus can lead to mediasti-
nitis or fistula formation to the trachea or skin. Because
the anterior approach to the thoracic and upper lumbar
spine requires entry into the chest or retroperitoneum,
there is a risk for respiratory complications and vascular
injuries in addition to infectious complications. Moreover,
several regions of the spine are inaccessible to repair via an
anterior approach, including the occipitocervical region,
the upper thoracic spine, and the lower lumbar spine. A
posterior approach is technically easier and less fraught
with complications, although decompression of the spinal
cord might be indirect.
In addition to the use of stabilizing hardware, which
may include combinations of plates, screws, cages, and
rods, the spine surgeon uses bone grafts to ensure future
spinal stability, because stabilization using instrumenta-
tion alone can fail over time, leading to instability and
deformity. Bone used for spinal fusion can be autograft,
obtained directly from the injured individual, or allograft,
obtained from a bone “bank.” Potential sites for autolo-
gous bone harvest include the iliac crest, the fractured
spine itself, or a fibula. Spinal orthoses are commonly used
to immobilize the spine after spinal fusion surgery, to
facilitate bone fusion. In most cases, orthoses are worn for
6 to 12 weeks postoperatively to allow for radiographically
evident spinal fusion.
Penetrating injuries to the spinal cord are overwhelm-
ingly caused by gunshot wounds. Stab wounds as a cause
of SCI are relatively rare. Surgical management for such
injuries is only rarely indicated. As a rule, neither of these
mechanisms of injury cause spinal instability. Removal of
bullets or bullet fragments is typically performed only if
their presence in the spinal canal is associated with pro-
gressive neurologic deterioration.
Chemical and Cellular Treatment of Acute
Spinal Cord Injury
Because motor and sensory recovery after traumatic SCI is
often poor, there has been an intense interest in finding an
effective treatment for SCI. A number of clinical trials have
investigated or are currently investigating potential chemi-
cal and cellular treatments for acute traumatic SCI, includ-
ing methylprednisolone, GM1 ganglioside, gacyclidine,
tirilazad, naloxone, bone marrow-derived and umbilical
cord blood mesenchymal stem cells, olfactory ensheathing
cells, and autologous activated macrophages. None of
these treatments have been definitively demonstrated to
improve neurologic outcomes.
Of the treatments investigated, only high-dose methyl-
prednisolone sodium succinate has been regularly admin-
istered, and even considered the standard of care; however,
it is no longer recommended as a standard treatment
because of a lack of documented effectiveness in people.30
Rehabilitation Phase of Injury
Interdisciplinary Team
Rehabilitation goals after SCI include maximizing physical
independence, becoming independent in direction of care,

and preventing secondary complications. An interdisci-
plinary team approach is the model that has historically
been used in the rehabilitation treatment of people with
SCI to achieve these goals. The team is optimally led by a
physician who has obtained subspecialty board certifica-
tion in SCI medicine and has undergone formal training
in the interdisciplinary team approach. Other members of
the team typically include the person with SCI, family
members, physical therapists, occupational therapists,
nurses, aides, dieticians, psychologists, recreation thera-
pists, vocational therapists, and social workers or case
managers. Other consultant physicians, respiratory thera-
pists, speech pathologists, clinician educators, orthotists,
and driving instructors can also be members of the team,
depending on the specific injury and rehabilitation goals.
In the acute hospital setting, staff members who are not
fully familiar with treating people with SCI need to be
educated about the potential secondary complications of
SCI and how to prevent them. The patient and family
members need to be educated about the nature of an SCI
and the patient’s prognosis and the uncertainty of such.
Transfer to a specialized SCI rehabilitation unit should also
be facilitated, because patients treated in a specialized SCI
center have increased overall survival rates, decreased com-
plication rates for pressure ulcers and other problems, a
decreased length of hospital stay, greater functional gains
during rehabilitation, a greater likelihood of home dis-
charge, and lower rehospitalization rates.11,39 Physical and
occupational therapists in the acute hospital should facili-
tate prevention of secondary complications such as con-
tractures, pressure ulcers, and disuse atrophy. This is done
through maintenance of joint ROM, splinting, positioning,
and selective muscle strengthening. ROM of all joints is
performed and taught by the therapists to people with SCI
and their caregivers as soon as it is medically safe to do so.
Performance of an adequate daily stretching program can
prevent joint contractures. Splinting of joints, with either
an off-the-shelf or a custom splint fabricated by an occu-
pational therapist, is also often used to provide a pro-
longed stretch, to facilitate a functional joint position, and
to prevent skin breakdown.
The inpatient rehabilitation setting is the cornerstone of
the rehabilitation process for people with SCI, and seems
to be essential for attaining the above-mentioned broad
goals of SCI rehabilitation, and to allow discharge from
the hospital to the least restrictive possible setting, ideally
to home. As the length of acute rehabilitation hospitaliza-
tion decreases, many of the tasks described later are refined
or even learned in an outpatient, subacute nursing facility
or home setting. The rehabilitation process in all of its set-
tings should empower individuals with SCI to know more
than anyone else about their own bodies and to provide
the resources to find solutions to all the problems that they
might encounter in their daily activities and life.
The person with SCI and their family members are
essential members of the team. If the person with SCI does
not participate in the SCI rehabilitation program, it is not
likely to be of much benefit. Rehabilitation nurses, in addi-
tion to performing their standard nursing duties, provide
education on prevention and treatment of secondary com-
plications, in addition to training in bowel and bladder
management. Psychologists help to reduce depression and
CHAPTER 49 Spinal Cord Injury 1113
anxiety, as well as facilitate adjustment to a catastrophic
and life-altering injury, by supporting people with SCI
(and their families) through the grieving process. This is
achieved by providing individual psychotherapy, cognitive-
behavioral techniques to enhance adaptive coping, and
group psychotherapy to provide additional support and
information sharing. Social workers or case managers help
individuals with SCI, their families, or their caregivers to
obtain needed available resources, benefits, and services.
They facilitate the transition from an inpatient rehabilita-
tion unit to the home or another facility, and provide
family support. Other physician consultants are typically
involved at various points in the rehabilitation process,
especially if secondary complications develop. Speech
therapists evaluate and treat the swallowing and commu-
nicating problems that are common in individuals with
tracheotomies, high cervical neurologic levels of injury,
and anterior approach cervical spinal surgeries. They com-
monly perform bedside swallowing evaluations and par-
ticipate in modified barium swallow tests.
Physical Skill Training
Physical and occupational therapists train people with SCI
in mobility, self-care skills, and other activities of daily
living (ADL). Achieving adequate joint ROM and strength,
necessary to perform these skills, is facilitated through
ROM exercises, fabrication and use of appropriate ortho-
ses, and resistance exercises. Individuals whose injuries
prevent them from being independent without assistance
also need to be educated on how to direct caregivers to
provide the assistance they need. The person with SCI
should be able to instruct caregivers on how to deliver the
needed care in a safe and efficient manner. This is impor-
tant to prevent injury both to the person with the SCI and
to the caregivers.
Training in activities that are performed on a therapy
mat is commonly begun as soon as a patient is able to
tolerate being out of bed. These activities, which are often
composed of separately performed parts of a more complex
functional skill, are typically sequenced from the easiest to
the most difficult. In progressing through these graduated
skills, people with SCI, who are often able to do little
for themselves initially, move to a level of stability within
a specific training posture. Finally, they are able to move
in a safe and effective manner to complete functional
tasks.98 When the tasks are mastered on the mat, they are
performed in other more real-life environments, such as
in bed.
Mat activities include rolling, prone on elbows position-
ing, prone on hands positioning, supine on elbows posi-
tioning, long sitting, short sitting, quadruped positioning,
and transfer training. In first learning to roll on a mat,
individuals with SCI rhythmically move the clasped out-
stretched arms side to side while lying flat on the back, and
then forcefully throw the outstretched arms to the side to
which they are rolling. Rolling can be facilitated by starting
a roll from a semi–side-lying position, with a pillow under
one side of the back or with crossed legs. Assuming a
supine-on-elbows position is a task that can later facilitate
going from a supine to a long sitting position. It can
also help strengthen shoulder extensor and adductor
1114 SECTION 4 Issues in Specific Diagnoses
musculature. This position can be achieved in several steps
by individuals with SCI. First, they place their hands under
their hips; next, they flex their elbows; and finally, they
shift their weight from side to side to maneuver their
elbows underneath their upper body. When a person with
SCI first starts to sit on a mat, balance exercises are prac-
ticed, either in a long sitting position with the legs extended
on the mat or in a short sitting position with the knees
bent at a 90-degree angle and resting on the ground. Sitting
push-ups are also learned, because these facilitate moving
about the mat and transfers.
Transfer training for a person with a complete paraple-
gia or lower tetraplegia is usually first taught with a sliding
board. For a transfer into or out of a manual wheelchair,
the wheelchair is positioned at an angle of 30 to 45 degrees
from a parallel position to the mat, with the front of the
seat nearest the mat. This allows clearance of the rear
wheels by the buttocks during the transfer. For a transfer
into or out of a power wheelchair, the wheelchair is posi-
tioned parallel to the mat, because the high wheels that
are present on a manual wheelchair are not in the way on
a power chair. Next, the individual scoots forward in the
chair, removes the armrest, inserts the sliding board deep
under the leg closest to the mat, and then rocks the head
and shoulders away from the mat while simultaneously
pushing up and toward the mat with the arm furthest from
the mat. This causes the buttocks to move onto the sliding
board. The rocking and pushing is repeated until the indi-
vidual is safely on the mat, at which time the sliding board
is removed. Leg rests might need to be removed for the
transfer. A popover transfer is similar, except that a sliding
board is not used. In addition to these techniques, several
other different types of transfer techniques are used by
people with varying levels of neurologic function. These
FIGURE 49-14 The swing-through gait pattern used by a person with complete paraplegia with long leg braces. (Redrawn from Schmitz TJ: Traumatic spinal cord
injury. In O’Sullivan SB, Schmitz TJ, editors: Physical rehabilitation: assessment and treatment, Philadelphia, 2001, FA Davis, with permission of FA Davis.)
include the dependent lift transfer, mechanical lift transfer,
stand-pivot transfer, sit-pivot transfer, and floor-to-chair
transfer. The mechanical lift transfer uses a mechanical
device attached to a sling. The dependent lift transfer and
the mechanical lift transfer are used mainly for individuals
who are unable to physically assist in the transfers. The
stand-pivot and sit-pivot transfers require weight bearing
on the lower limbs, and are useful only if a person has
significant lower extremity extensor tone or adequate lower
extremity strength to briefly squat or stand. The floor-to-
chair transfer is important for anyone who falls out of the
wheelchair or otherwise ends up on the floor, and needs
to get back into the chair or another higher surface. Stand-
ing can be initiated on a standing frame, a tilt table, or with
an exoskeletal device. Standing seems to help lessen bone
loss after an acute injury, improve physical self-concept,
and improve self-reported health.15
Standing should be implemented only with caution in
individuals with chronic SCI, because of osteoporosis.
Individuals with osteoporosis have a risk for fracture even
without weight bearing. Although ambulation is an
expressed goal of most people who have experienced an
SCI, recovery of ambulation is variable. For people with
incomplete motor SCI, gait training can be facilitated by
body weight support (BWS), although BWS training has
not been shown to be superior to conventional gait train-
ing for ambulation.43 For people with complete thoracic
level injuries who wish to undergo ambulation training,
orthoses that stabilize the knees and ankles are required.
A swing-through gait pattern (Figure 49-14) is taught in
several steps similar to the mat activities described earlier.
This begins in the parallel bars and includes going from sit
to stand, balancing with extended hips, push-ups in the
standing position, turning while standing, recovery from a

flexed hip position, advancement of the lower extremities
with hip hiking, performance of a step-to gait, and finally
a swing-through gait pattern. After the swing-to or swing-
through gait pattern is mastered in the parallel bars, it is
performed with a walker or crutches.
The use of exoskeletons for ambulation for people who
have some truncal stability and the use of their arms to
allow the use of upper extremity assistive devices, such as
a walker or forearm crutches, is beginning to be used in
clinical settings in the United States and around the world.
These devices can allow upright walking in people who do
not have adequate lower extremity strength to allow
walking with or without conventional bracing with only
minimal to moderate energy expenditure.
Wheelchair Skills
Physical and occupational therapists not only train people
with SCI in wheelchair mobility but also help select the
proper seating systems to ensure proper sitting position.
Wheelchair users are taught to manage or to direct the
management of all wheelchair components, including the
brakes, armrests, footrests, wheels, and seat cushion. They
are taught how to fold or break down the chair so it can
be placed properly in a vehicle. They are taught wheelchair
propulsion, first indoors over level surfaces, then outdoors
over uneven terrain. Proper body mechanics are taught to
achieve efficient wheelchair propulsion patterns, including
an ideal propulsive stroke and an ideal recovery stroke. An
ideal propulsive stroke is one that occurs at a steady speed
that maximizes the handrim “contact” or “push” angle
(angle along the arc of the pushrim) while keeping stroke
frequency and forces to a minimum. Although self-selected
wheelchair propulsion patterns are often not the most effi-
cient ones, experienced wheelchair users often significantly
improve propulsion biomechanics from early to late during
extended propulsion. Individually selected wheelchair pro-
pulsion patterns are often influenced by poor wheelchair
sitting positions. Of several propulsion patterns that have
been described, differing primarily in their recovery phase,
a semicircular wheelchair propulsion pattern has been
shown to be the most efficient and least stressful on the
shoulders and nerves crossing the wrist.18 Another basic
wheelchair mobility skill is performance of a wheelie, in
which the individual in the wheelchair balances on the rear
two wheels. This is an important skill that needs to be
mastered, to become independent in curb and single-step
climbing in a wheelchair.
Spinal Cord Injury Education
During the early phases of SCI, most patients and their
families have little knowledge or understanding of the
injury; its multiple consequences; the myriad of interven-
tional and management options, community resources,
and equipment needs; and the prognosis for life, health,
and function. They are often overwhelmed by the gravity
of the situation and unable to adjust to a changed lifestyle
and self-image. A comprehensive education program is an
essential part of any SCI rehabilitation program and, if
properly designed, helps the person with SCI and the
family members not only to gain knowledge but also to
CHAPTER 49 Spinal Cord Injury 1115
emotionally adjust and prepare for a successful commu-
nity reintegration. Although some of the learning occurs
in formal education classes, group discussions, reading
specific educational materials published by various SCI
organizations, or extracting information on the Internet,
one-on-one instruction by health care professionals is the
most helpful in addressing individual needs and concerns.
With proper education and the ability to access appropri-
ate information readily, the person with SCI becomes best
able to manage successfully the various impairments and
ensure the highest possible function and quality of life.
The curriculum of a structured SCI education program
should be as broad as possible and include the anatomy,
physiology, and classification of SCI, as well as the various
medical consequences of SCI, psychosocial adjustments
that need to be made, the effect of SCI on sexual health
and fertility, assistive technology available for people with
SCI, nutritional needs with SCI, available community
resources, and ongoing research to improve neurologic
function.
Home and Environmental Modifications
It has long been recognized that helping a person with SCI
regain mobility by the use of a wheelchair is of little use if
the architecture at home and elsewhere is such that the
individual is unable to enter or exit buildings or move
about freely inside. Without accessible environments at
home, school, work, and in the community, the dignity,
self-sufficiency, and quality of life are severely jeopardized.
The Specially Adapted Housing Act of 1948 provided grant
assistance to veterans with service-connected disability to
obtain special wheelchair-accessible housing. In 1990,
the Americans with Disabilities Act (ADA) expanded the
rights of people with disabilities, including prohibiting
discrimination against them. It also required removal of
architectural barriers in facilities owned by organizations
that receive federal funding. This was intended to give
people with disabilities equal access to all organizational
facilities.
The ADA does not demand removal of architectural bar-
riers in private homes, most of which remain inaccessible
for wheelchair users. A home evaluation is best performed
before a new wheelchair user returns home. This begins
with a review of the floor plan, followed by a home visit,
recommendations for architectural changes, and contract-
ing with architects and builders. The main home areas of
concern include the main entrance, bathroom, bedroom,
and kitchen. The home must also have an exit that the
person with SCI can use in an emergency.
Driver Training
Being able to drive an automobile enhances the mobility
and quality of life for people with SCI. Most people with
SCI can drive an automobile with the proper adaptive
equipment and training. Only people with C1-C4 neuro-
logic levels and those with other severe impairments are
unable to drive. People with paraplegia can usually drive
with basic hand controls for acceleration and braking, and
most are capable of transferring between the driver’s seat
and the wheelchair independently, and of loading the
1116 SECTION 4 Issues in Specific Diagnoses
chair into the car. People with tetraplegia usually choose
to drive a modified van with a wheelchair lift or a ramp,
and varying degrees of modification of the control
mechanisms.
Some people with C5 tetraplegia are able to drive, but
usually not within 1 year of injury. Most such individuals
use a power wheelchair for mobility and are not able to
transfer to and from the wheelchair and the car. They
require a van with power door openers, automatic lift or
ramp, and extensive modifications of the control mecha-
nisms. Occasionally, they require a multiaccess driving
system in which the steering, accelerator, and brake are
operated by a single control lever.
Driving skills of people with C6 tetraplegia vary consid-
erably, but most are able to turn the steering wheel. Many
are not capable of operating regular hand control mecha-
nisms, and require powered or electronic hand controls for
braking and acceleration. Most people with C7-C8 tetra-
plegia have enough upper limb strength to operate a stan-
dard steering wheel with a terminal device. The terminal
device compensates for their poor handgrip, examples
include a knob, cuff, tri-pin, or special grip.
Over the years, major advances in assistive driving tech-
nology have made it possible for more people with dis-
ability to safely operate a vehicle. The primary controllers
of a vehicle, such as steering and braking, can even be
concentrated in a complete system that can be operated
with only one hand, through a tri-pin or joystick terminal
device. This can incorporate the secondary controllers, for
example, the gear shift, turn signals, hazard warning lights,
horn, dimmers, cruise control, washer, wipers, radio, air
conditioner, heater, defroster, doors, lift, and steering tilt.
All drivers must use seat belts, but those with reduced
trunk control must also use safety belts to secure trunk
stability, such as shoulder, chest, or lap belts.
All people with disability wanting to drive should
undergo a driving evaluation by a specialist, usually an
occupational therapist certified by the Association of Driver
Educators for the Disabled (ADED). The ADED website
can help to locate certified driving evaluators in the United
States and Canada. A predriving evaluation includes an
assessment of the person’s medical and driving history, as
well as functional capabilities. Interactive driving simula-
tors can present the users with diverse challenges in a safe
environment, and can provide objective measurement of
driving behaviors. Ultimately, however, an actual on-the-
road driving evaluation is essential. Selection of the proper
vehicle and appropriate modifications to fit the user’s
ability can involve input from various members of the
rehabilitation team. After the vehicle has been modified,
the driving educator ensures that all the equipment is
appropriate and that the driver is able to use the controls.
Behind-the-wheel training by the driving educator can be
a lengthy process for people with high-level tetraplegia,
because of the complexity of the equipment and the
impairment of the learner. The high cost of vehicles and
modifications, and the complexity of training, are the most
common reasons some people with high-level tetraplegia
(C5-C6) choose not to drive. Finally, it should be noted
that people with physical disability do not have worse
safety records than other drivers.
Vocational Training
Not only do people who have SCI and are employed report
higher levels of psychological adjustment, satisfaction with
life, independence, and general health than those who are
unemployed, but their risk of mortality is lower.71 Never-
theless, approximately only 25% of all individuals with
SCI are employed. Among people listed in the National
SCI database, approximately 63% were employed at the
time of their SCI, 19% were students, and 17% were unem-
ployed. The relatively high number of unemployed people
at the time of injury is recognized as a factor negatively
affecting postinjury employment.70
Predictors of employment after SCI include being
employed before SCI, having a less physically demanding
occupation before SCI, being younger at the time of SCI,
having a less severe SCI, having lived more years with SCI,
having more education before SCI, being motivated to
work, and being white.70 Education has been found to be
the factor most strongly associated with postinjury employ-
ment. Only 5% of people in the National SCI database
with less than 12 years of education were found to be
employed, but with each successive educational milestone
completed, employment numbers improved, reaching a
high of 70% employment of people with doctoral degrees.
In general, by postinjury year 10, one third of people with
paraplegia and a quarter of those with tetraplegia are
employed.
Vocational rehabilitation is concerned with supporting
efforts by a person with a disability to return to and main-
tain employment. Rehabilitation counselors, who facilitate
this process, usually have master’s degrees in rehabilitation
counseling and optimally are accredited by the Council on
Rehabilitation Education. Vocational rehabilitation typi-
cally begins with an evaluation of the person’s functional
limitations, barriers to employment, transferable skills,
career interests, and previous achievement. The assessment
might also include an assessment of performance during
simulated or actual work. Assessment might be followed
by counseling and support with regard to educational or
vocational reentry, job accommodation, and supported
employment. Educational or vocational reentry is often
facilitated by a rehabilitation counselor who can liaise with
employers, because most employers have little experience
interacting with people with disability and can have diffi-
culty imagining how a person with an SCI could perform
a specific job. Job accommodation, or the modification of
a job to make it accessible to a person with SCI, might
involve modification of the job site, use of adaptive equip-
ment, or job policy changes. Modifications of the job site
can range from the simple, such as adjustment of desk
height to accommodate a wheelchair, to the complex, such
as redesign of an assembly line. Adaptive equipment can
include tools with special handles or sit-stand worksta-
tions. Job policy changes can include reassignment of
physical tasks or changes in the number and length of
workday breaks. Supported employment refers to the need
by the individual with SCI for additional assistance in the
workplace, ranging from a need for a full-time personal
care assistant to the occasional need for manipulation of
work materials.

Several legislative initiatives have been implemented
with a goal of promoting employment of people with dis-
abilities. The Rehabilitation Act of 1973 provides federal
funding for vocational rehabilitation programs in each
state. The ADA attempts to prevent discrimination in
employment against qualified individuals who are able to
perform essential functions of a job with or without accom-
modation.1 Workers’ compensation programs in most
states provide a vocational rehabilitation program for
workers who are injured at work, including retraining of
those who cannot return to a previous or similar job.
Reconstructive Surgery of the Upper Limbs
Tenodesis refers to the surgical attachment of a tendon to
a bone. In contrast, tenodesis action refers to the passive
tightening of a tendon when stretched by the movement
over a proximal joint over which it crosses, causing a move-
ment of a distal joint. A passive tenodesis hand is one in
which there is no volitional control of intrinsic or extrinsic
hand muscles or the wrist extensors. Opening and closing
of the hand can only occur with passive tenodesis action
through forearm pronation and supination, respectively.
An active tenodesis hand is one in which there is the addi-
tion of active wrist extension that allows for passive move-
ment of the fingers into a grasp dependent on tenodesis
action; relaxation of the wrist extension allows for release.
Grasp attributable to tenodesis action is usually more
effective in a hand that has developed tightness of para-
lyzed muscles to achieve a functional grasp position. It can
be accentuated through the reconstructive surgical proce-
dure described later. An active extrinsic hand is one with
voluntary control of wrist extensors and extrinsic finger
flexors that can allow some grasp with or without tenodesis
action, whereas an active extrinsic-intrinsic hand is one in
which there is volitional control of both the intrinsic and
extrinsic hand musculature. Arthrodesis refers to joint
fusion whereby the joint cartilage is removed from either
side of the joint, and the exposed bony ends are opposed
and allowed to fuse. Tendon transfer refers to the detach-
ment of a tendon of an expendable innervated muscle
from one of its attachments, and reattachment of the
innervated muscle and tendon to another tendon that
lacks an innervated muscle but whose regained function is
sought.
Functional upper limb surgical reconstruction has his-
torically been delayed for 1 year postinjury to allow for
neurologic recovery in targeted muscles. Muscles are chosen
for transfer if they have a strength grade of 4 or 5, because
one grade of muscle strength is usually lost with the trans-
fer. Transferred muscles with a strength grade of less than
3 generally do not improve function. Muscles should not
be chosen for transfer if their loss would result in a func-
tional decline. After a tendon transfer procedure, the
tendon constructs are typically immobilized for several
weeks in a nonstretched position, followed by gradual
mobilization, strengthening, and reeducation. Functional
electrical stimulation (FES) is often used to facilitate neu-
romuscular reeducation. Common tendon transfers and
tenodesis procedures are shown in Table 49-4 stratified to
ISNCSCI motor levels and the more specific International
CHAPTER 49 Spinal Cord Injury 1117
Classification for Surgery of the Hand in Tetraplegia
(ICSHT) motor groups.80
Functional improvements achieved after a deltoid or
biceps to triceps transfer primarily occur through an
increased ability to stabilize the arm and reach overhead.
Improvements can be seen in feeding, grooming, pressure
relief performance, and writing. Functional improvements
after a brachioradialis (BR) to extensor carpi radialis brevis
transfer can include an increased ability to pick up objects,
feed, groom, write, and type. Functional improvements
after a BR to flexor pollicis longus (FPL) transfer can
include an increased ability to pick up a pen and write,
more efficient grooming, and less dependence on a wrist-
hand orthosis for grasp. The combination of BR to FPL and
extensor carpi radialis longus to flexor digitorum profun-
dus (FDP) tendon transfers has been shown to lead to
improved key pinch, grasp strength, and subjective ADL
performance. Functional improvements after the combina-
tion of BR to FPL and pronator teres to FDP tendon trans-
fers have been noted in manual wheelchair propulsion,
lower limb dressing, opening of jars, and the transferring
of objects with the reconstructed hands.
Functional Electrical Stimulation for
Therapeutic Exercise
Sedentary lifestyle and impaired autonomic function in
people with SCI lead to many degenerative physiologic
changes that can affect their health and wellness. Muscle
bulk, strength, endurance, and bone density are lost in the
paralyzed limbs; cardiovascular fitness, VC, and lean body
mass are reduced; and certain endocrine functions are
altered. FES-induced leg exercise, achieved most commonly
on cycle ergometers but also with rowing, poling, stepping,
and other repetitive exercise machines, in people with SCI
has been shown to improve cardiorespiratory fitness, lower
extremity circulation, exercise capacity; increase muscle
size; decrease pain; and alter bone mineral density (BMD).32
During arm exercise with concurrent FES cycling or FES
rowing, oxygen uptake is higher than arm or leg exercise
alone. This increase in oxygen uptake is not associated with
an increase in perceived exertion.
FES is not effective in stimulating muscles paralyzed by
LMN damage (i.e., damage affecting the anterior horn cells,
motor nerve roots, or both), but such damage usually
occurs at the level of the SCI lesion. FES is usually a rela-
tively safe intervention, but its application in the presence
of cardiac pacemakers or implanted defibrillators is best
avoided. Caution is also warranted in the presence of
various heart conditions (especially dysrhythmia and con-
gestive heart failure) and during pregnancy.
Body Weight Support Ambulation Training on
a Treadmill
Specific intensive walking training of people with incom-
plete SCI significantly improves walking capabilities. Such
training consists of upright walking on a treadmill, with
partial BWS provided by a suspending harness, with a ther-
apist guiding and setting the limbs. BWS training has been
shown to be effective in improving ambulatory function
1118 SECTION 4 Issues in Specific Diagnoses

Table 49-4 International Classification for Surgery of the Hand in Tetraplegia, International Standards for Neurologic Classification of Spinal
Cord Injury, and Possible Tendon Transfers
ICSHT ISNCSCI Motor Innervated Muscles, Muscle Function after
Group Level Grade 4 or 5 Muscle Function Transfer Possible Transfer
0 C5 (if grade 3 BR ≤ grade 3 Flexion/supination of
elbow flexion) elbow
1 C5 BR Flexion/supination of Deltoid to TR or biceps Elbow extension*, wrist
elbow to TR*, BR to ECRB** extension**
2 C6 Group 1, ECRL Radially deviated FPL to volar radius Passive thumb flexion
wrist extension (Moberg procedure)*, (lateral pinch)*, Active
BR to FPL** thumb flexion**
3 C6 Group 2, ECRB Wrist extension BR to FPL*, ECRL to Active thumb flexion*,
FDP** active finger flexion**
4 C6 Group 3, PT Wrist pronation BR or PT to FPL*, ECRL Active thumb flexion*,
to FDP**, EPL and EDC active finger flexion**,
to dorsum of the wrist passive thumb and
(extensor tenodesis)*** finger extension***
5 C7 Group 4, FCR Wrist flexion BR to FPL*, ECRL or PT Active thumb* and finger
to FDP**, extensor flexion**, passive thumb
tenodesis*** and finger extension***
6 C7 Group 5, EDC Finger extension BR to FPL*, ECRL or PT Active thumb* and finger
to FDP** flexion**
7 C7 Group 6, EPL Thumb extension BR to FPL*, ECRL or PT Active thumb* and finger
to FDP** flexion**
8 C8 Group 7, finger flexors Finger flexion
9 C8 Lacks hand intrinsics only Finger flexion, strong
From McDowell CL, Moberg E, House JH: Second International Conference on Surgical Rehabilitation of the Upper Limb in Traumatic Quadriplegia, J Hand Surg Am 11:604-608, 1986;
McDowell CL, Moberg EA, Smith AG: International Conference on Surgical Rehabilitation of the Upper Limb in Tetraplegia, J Hand Surg Am 4:387-390, 1979; Waters RL, Muccitelli LM:
Tendon transfers to improve function of patients with tetraplegia. In Kirshblum S, Campagnolo DI, DeLisa JA, eds: Spinal cord medicine, Philadelphia, 2002, Lippincott Williams & Wilkins.
NOTE: The asterisks in each row are meant only to relate a particular transfer to a particular muscle function after transfer, all within a specific row. For example, the deltoid to TR or
biceps to TR transfer would allow for elbow extension after the transfer procedure is performed.
BR, Brachioradialis; ECRB, extensor carpi radialis brevis; ECRL, extensor carpi radialis longus; EDC, extensor digitorum communis; EPL, extensor pollicis longus; FCR, flexor carpi radialis;
FDP, flexor digitorum profundus; FPL, flexor pollicis longus; ICSHT, International Classification for Surgery of the Hand in Tetraplegia; ISNCSCI, International Standards for Neurologic
Classification of Spinal Cord Injury; PT, pronator teres; TR, triceps.

after SCI, although not more effective than equivalent over-
ground mobility training.43
Epidural Spinal Cord Stimulation
Epidural subthreshold motor stimulation (using a com-
mercially available epidural stimulator as is used for the
treatment of pain) in conjunction with voluntary motor
training and standing or stepping in people with chronic
motor complete paraplegia has shown effectiveness in pro-
moting volitional motor recovery in some people.2
Chronic Phase of Injury
Adjustment to Disability
SCI is a catastrophic event with a profound effect on the
injured person as well as on family members. Different
personal, interpersonal, and cultural factors ultimately
determine how successfully an individual with SCI will
adjust or adapt to the disability. Successful adjustment is
thought to have occurred when the disability is no longer
the dominant concern in the person’s life. Such adjustment
is highly individually variable and has been estimated by
some to occur over 2 to 5 years, whereas others propose
that adjustment is a lifelong process. Adjustment has been
considered by many to consist of sequential psychological
reactions according to stage theories, beginning with denial
and followed by anger, bargaining, depression, and finally
acceptance or adjustment. Although such sequential reac-
tions are often seen in people with SCI, they tend to be
highly individualized with some people never seeming to
pass though some of the stages and others being stuck in
one stage forever.
Despite an overwhelming sense of loss initially after
SCI, most people eventually learn to cope emotionally and
conform to their premorbid personality styles of interact-
ing with the environment. A number of psychological
problems, however, primarily depression and anxiety, can
interfere with adjustment and quality of life. These prob-
lems can lead to substance abuse, divorce, dependency,
self-neglect, and even suicide.
The prevalence of major depression in people with SCI
at any one time is approximately 20% of whom 15% have
suicidal ideation.60 The natural history seems to be that for
those evaluated at 5 years postinjury, 50% have chronic
depression, whereas the other 50% have depression that
was not present at 1 year postinjury. Declining health,
worsening pain, and cessation of unhealthy alcohol use are
risk factors for developing major depression when one was
not depressed earlier. Other risk factors for depression are
similar to those in able-bodied individuals, especially a
family history of depression. Factors specific to the SCI,
such as the presence of complete neurologic injury, poor
self-perceived health, functional impairments, and medical

comorbidities, increase the likelihood of developing
depression. Because major depression is treatable and not
intrinsic to experiencing an SCI any more than other pre-
ventable secondary complications, all people with SCI
should be screened for depression and treatment with psy-
chotherapy, and psychopharmacotherapy should be initi-
ated if indicated. Most people with SCI and depression
currently do not receive guideline-level treatments for
depression.48
Quality of Life
Quality of life is a concept that is difficult to define but
that can be described as a determination of the individual’s
satisfaction with life, for example, whether or not the indi-
vidual is able to do the things he or she personally wants
to do. Compared with nondisabled people, people with
SCI tend to report decreased well-being and a poorer state
of health, and score lower on physical, emotional, and
social health domains of life.41 A metaanalysis has shown
no relationship between the neurologic level, the com-
pleteness of SCI, and the subjective quality of life. Some
factors are thought to affect quality of life positively, such
as mobility and ADL independence, emotional support,
good overall health, self-esteem, absence of depression,
physical and social activities and integration, being married
and employed, having completed more years of education,
and living at home. In general, dissatisfaction with life after
SCI seems more related to social disadvantages than to
physical limitations.
Recovery-Enhancing Therapies
Most patients with SCI, even those with neurologically
complete lesions, experience some degree of spontaneous
neurologic recovery. This occurs as a result of resolution of
the acute pathology, with recovery of nerve roots and
spinal cord at the level of the lesion.
Despite major efforts to find effective treatments to
enhance neurologic recovery during chronic SCI, no reports
of scientifically conducted clinical trials exist that show
effectiveness for any specific pharmacologic agents.
Late Neurologic Decline
New motor or sensory deficits are reported to develop in
approximately 20% to 30% of people with chronic SCI.74
Most common is entrapment of a peripheral nerve, espe-
cially of the median nerve at the carpal tunnel, or of the
ulnar nerve at the elbow. Further damage of the spinal cord
can be caused by posttraumatic syringomyelia (PTS), also
called posttraumatic cystic myelopathy, by tethering or by
compression of the cord.
Although it is common to find MRI evidence of a cyst
within the spinal cord at the level of the injury, only 5%
of all people with SCI develop PTS. It becomes a problem
when the cyst expands longitudinally and damages the
cord, causing clinical symptoms such as pain, sensory loss,
weakness, altered muscle tone, and a variety of autonomic
symptoms.74 The exact cause of PTS is unknown, but it
might be related to obstruction of the normal flow of CSF
because of scarring or canal narrowing. This leads to
CHAPTER 49 Spinal Cord Injury 1119
abnormal increases in CSF pressure during coughing and
straining, ultimately causing a longitudinal dissection of
the cord.74
The diagnosis of PTS is confirmed by MRI or CT myelo-
gram with delayed images. The clinical symptoms of PTS
and their progression vary greatly. If no neurologic decline
is noted on regular follow-up examinations, the treatment
can be symptomatic. Activity restrictions are usually advis-
able, especially avoiding strenuous exercise that could raise
venous and CSF pressure. When continuous neurologic
decline or intractable pain is associated with PTS, surgical
treatment is usually indicated to reduce the size of the
syrinx or to prevent its expansion. Surgical approaches
include placement of a shunt in the syrinx to drain the
fluid into the peritoneal, pleural, or subarachnoid spaces;
marsupialization of the syrinx; and duraplasty.74 When
treatment is successful, strength might increase, and pain
and spasticity might diminish.
Tethering of the spinal cord as a result of meningeal or
arachnoid scar formations can occur after SCI and prevent
normal rostrocaudal sliding of the cord within the spinal
canal on motion. Tethering of the cord in the cervical spine
can generate enough cord traction with flexion of the neck
to cause cord or brainstem displacement and neurologic
symptoms, such as weakness, sensory deficits, and pain. If
this occurs, surgical untethering should be considered.
Late compression of the spinal cord or nerve roots can
occur for multiple reasons and cause neurologic decline.
Common causes include progressive spondylosis, spinal
stenosis, intervertebral disk herniations, and posttraumatic
changes. Proper imaging studies are needed for diagnosis.
Surgical intervention can be needed if there is a rapid neu-
rologic loss or severe, intractable pain.
Secondary Conditions
Pulmonary System
Pulmonary complications, including atelectasis, pneumo-
nia, respiratory failure, pleural complications, and PE, are
the leading causes of death for people with SCI in all years
after SCI.88 They accounted for 37% of all deaths during
the first year after SCI, and 21% of the deaths beyond the
first year, in a large sample from the Model SCI Care
Systems and Shriner’s Hospitals.40
The incidence of ventilatory failure following acute tet-
raplegia is as high as 74% with up to 95% of patients with
injury level above C5 with AIS A status requiring mechani-
cal ventilation at least temporarily.30
There are several reasons why children with SCI have a
higher mortality and risk of complications resulting from
pulmonary issues as compared with adults, including
increased restrictive lung disease as a result of the ubiquity
of scoliosis, impaired respiratory development in infants
and young children, and the increased risk of sleep-
disordered breathing in infants and young children with
cervical injuries.101
Anatomy and Mechanics of the Pulmonary System
SCI can lead to alterations in lung, chest wall, and airway
mechanics. The degree of respiratory dysfunction after SCI
1120 SECTION 4 Issues in Specific Diagnoses

Vagus(X)
Muscles of breathing
tents into the diaphragm, allowing a more efficient dia-
Accessory (XI) phragmatic resting position.
Sternomastoid
C1 Airway hyperreactivity seen in people with SCI is respon-
Trapezius
C2 High tetra
C3
sive to inhaled bronchodilators and is thought to be caused
Diaphragm C4 by unopposed cholinergic tone.97
C5 People with a neurologic level of C2 or above with a
Scalenes
C6 Low tetra Pectoralis major complete SCI usually have no diaphragmatic function and
C7 require mechanical ventilation or diaphragmatic or phrenic
C8 Expiratory
muscles pacing. People with a complete C3 SCI have severe dia-
T1
T2
phragmatic weakness and commonly require mechanical
T3 High para ventilation, at least temporarily. People with a complete
T4 Lateral internal
C4 SCI also often have severe diaphragmatic weakness and
Lateral external T5 intercostals can also require mechanical ventilation, at least temporar-
intercostals T6 ily. People with a complete C5-C8 SCI are usually able to
T7 maintain independent breathing, but because of the loss
T8 Low para
T9
of innervation to the intercostal and abdominal muscles,
Rectus abdominis
T10 External obliques
they remain at high risk for pulmonary complications. This
Inspiratory risk for pulmonary complications is also present for those
T11 Internal obliques
muscles
T12 Transverse abdominus with complete thoracic-level SCI, although to a lesser
L1 degree depending on the segmental extent of the loss of
L2 innervation.
L3
L4 Management of Pulmonary Complications
FIGURE 49-15 Diagram showing levels of innervation of the inspiratory and Atelectasis is the most common respiratory complication
expiratory muscles. (From Schilero GJ, Spungen AM, Bauman WA, et al: Pulmo-
nary function and spinal cord injury, Respir Physiol Neurobiol 166:129-141, 2009.) in people with SCI and can predispose to pneumonia,
pleural effusion, and empyema. Pneumonia commonly
occurs in areas of atelectasis. Pleural effusions often develop
in close proximity to areas of atelectasis. It is thought that
is strongly correlated to the NLI and degree of motor the areas of lung that collapse pull the parietal pleural away
impairment. The pulmonary function profile of people from the visceral pleura, leaving an empty space that con-
with chronic tetraplegia and high paraplegia reveals sequently then fills with a fluid, causing an effusion. Treat-
decreased lung volumes and decreased thoracic wall com- ment of atelectasis includes lung expansion, secretion
pliance as a result of the restriction caused by respiratory mobilization, and secretion clearance. If an individual is
muscle weakness, as well as airway hyperreactivity. Specifi- receiving mechanical ventilation, a gradual increase in
cally, spirometric and lung volume studies in people with tidal volumes (TVs) to a target of greater than 20 mL/kg of
tetraplegia and high levels of paraplegia demonstrate a ideal body weight (IBW) has been shown to be effective in
significant reduction of VC, total lung capacity (TLC), expi- decreasing atelectasis as compared with maintaining the
ratory reserve volume (ERV), and inspiratory capacity (IC), TV at less than 20 mL/kg IBW.30 Intermittent positive-
along with a significant increase in residual volume (RV) pressure breathing, bilevel positive airway pressure, or con-
and little or no change in functional residual capacity tinuous positive airway pressure (CPAP) devices can all be
(FRC)97 The diaphragm, innervated by anterior horn cells used with or without tracheostomy tubes to help with lung
located in the C3-C5 segments, is the major primary muscle expansion and to prevent or treat atelectasis. Secretion
of inspiration (Figure 49-15). The sternocleidomastoid mobilization techniques include postural drainage and
and trapezius muscles, innervated by the spinal accessory chest percussion or vibration. Postural drainage uses gravity
nerve and the C2-C4 and C1-C4 roots, respectively, are to assist in drainage of accumulated secretion from specific
accessory muscles of inspiration and can be necessary to lung areas. Chest percussion, optimally performed in con-
allow adequate ventilation in people with higher level SCI. junction with postural drainage, can be performed with a
Use of a simple bedside spirometer to measure VC can give cupped hand, with a mechanical vibrator, by donning a
a quantitative measure of respiratory muscle strength, vibrating vest, or by lying in a vibrating bed. Secretion
equivalent to doing a manual muscle test of an extremity clearance techniques include suctioning, manually assis-
muscle. Inspiratory resistive training and aerobic exercise tive cough, use of a mechanical insufflator-exsufflator, and
training at a high level (70% to 80% of maximal heart rate) bronchoscopy. The insufflator-exsufflator supplies a posi-
in people with tetraplegia has been shown to improve the tive pressure to the airway, followed immediately by a
strength and endurance of a weak diaphragm and improve negative pressure, either through the mouth or a tracheos-
lung function. tomy tube. This rapid pressure change induces a high expi-
The VC of people with tetraplegia or high paraplegia is ratory flow rate similar to a cough. It is less traumatic than
posturally dependent, being up to 15% lower in the upright suctioning. Bronchoscopy is usually reserved for persistent
position than in the supine position. In the sitting position atelectasis or lung collapse.
in people with paralyzed abdominal muscles, the effect of Medications are useful adjuncts in treating and prevent-
gravity on the abdominal contents leads to an increased ing atelectasis. Bronchodilators reduce airway hyperreactiv-
RV. Use of an abdominal binder in the sitting position ity and inflammation that contribute to atelectasis
helps to reverse this effect by pressing the abdominal con- formation and sputum production, and stimulate the
 CHAPTER 49 Spinal Cord Injury 1121

secretion of surfactant. Use of a beta-2-adenergic medica-

tion has been shown to improve expiratory pressures,
which can lead to a more effective cough. Mucolytics can
be given orally, such as guaifenesin, or via a nebulizer, such
as acetylcysteine. Adequate hydration thins pulmonary
secretions.
Indications for initiation of mechanical ventilation
include physical signs of respiratory distress (cyanosis,
accessory muscle use, tachypnea, tachycardia, diaphoresis,
altered mental status, hypotension, hypertension), hyper-
carbia (partial pressure of carbon dioxide in arterial blood
[PaCO2] >50 mm Hg), hypoxia (partial pressure of oxygen
in arterial blood [PaO2] <50 mm Hg) unresponsive to
oxygen therapy, a falling VC (<15 mL/kg IBW), and/or an
inability to handle secretions. If intubation is expected to Air movement
last more than 5 days, a tracheostomy should be through vocal
performed. cords
The mode of mechanical ventilation used convention-
ally in a rehabilitation setting has been assist-control or Unidirectional
controlled mandatory ventilation during rest. Weaning valve
then occurs as progressive ventilator-free breathing (PVFB),
starting with a trial of as little as 2 minutes per day with
the individual completely disconnected from the ventila-
tor. Oxygen is given via a tracheostomy mask or T piece.
The time away from the ventilator is gradually increased in
duration, in single or multiple trials per day, depending on
the length of each trial, as tolerated. It should be borne in
mind that after lengthy mechanical ventilation, the dia-
phragm muscle becomes atrophied and deconditioned,
requiring a lengthy period of reconditioning before FIGURE 49-16 Functioning of a Passy-Muir tracheostomy speaking valve.
ventilator-free breathing is achieved. PVFB is also useful for (Redrawn from Manzano JL, Lubillo S, Henriquez D, et al: Verbal communication
people who are not expected to fully wean, giving them of ventilator dependent patients, Crit Care Med 21:512-517, 1993, with
some confidence and endurance to remain off the ventila- permission.)
tor for a short period if an unforeseen problem occurs with
their ventilator setup.
A further advantage of the use of the assist-control or phrenic nerves in the chest or neck through a thoracotomy.
the controlled mandatory ventilation modes of ventilation A phrenic nerve pacing system includes a radiocontrolled
for people with a tracheostomy, in contrast to other modes, implanted stimulator under the skin and an external
is that it allows the individual to speak if the cuff on the control unit and battery. Stimulation is started 2 weeks
tracheostomy tube is partially or wholly deflated. When postoperatively, and reconditioning of the diaphragm can
the cuff is deflated, air expired from the lungs can escape take 2 to 3 months. Diaphragm pacing differs in that the
around the tracheostomy tube and balloon up through the electrodes are implanted directly into the diaphragm via a
larynx to allow voicing. To compensate for the loss of such less invasive laparoscopic approach, eliminating the risk
air around the tracheostomy tube and not entering the for phrenic nerve injury. In the diaphragmatic pacing
lungs, the set TV should be increased. Many individuals are system, electrode wires protrude through the skin and are
able to vocalize while using a mechanical ventilator in this attached to an external battery-powered stimulator unit.
manner, timing their speech to coincide with exhalation. Stimulation can be begun immediately after implantation,
In addition, a one-way air-flow valve can be put in line and reconditioning can also take several months, although
with the ventilator tubing, such as a Passy-Muir valve. This it has been accomplished in as early as 1 week.
maximizes the air flow through the larynx by not allowing
Sleep Disorders
air to escape through the tracheostomy into the ventilator
tubing (Figure 49-16). These one-way valves must be used Obstructive sleep apnea (OSA) is characterized by a repeti-
only with a tracheostomy tube that has a deflated cuff or tive collapse of the upper airway during sleep. This can
no cuff at all. Such valves can be attached to the tracheos- cause fragmentation of sleep, loss of the restorative func-
tomy tube alone to also allow voice during the ventilator- tion of sleep, and increased sympathetic nervous system
free weaning periods. activity. It results in excessive sleepiness, systemic and pul-
Phrenic nerve and direct diaphragm pacing can each monary hypertension, and an increased risk for developing
stimulate the diaphragm to allow nonmechanical ventila- stroke or myocardial infarction. The prevalence of OSA in
tion in people without spontaneous diaphragm motor individuals with tetraplegia is thought to be as high as 50%
function. Both techniques require intact phrenic nerves. to 60%, depending on the diagnostic method.55 This is in
Phrenic nerve pacing is the more invasive of the two tech- contrast to a prevalence of 4% to 9% in the general popula-
niques, with electrical stimulating cuffs placed around the tion without SCI. Identified factors associated with sleep
1122 SECTION 4 Issues in Specific Diagnoses
apnea after SCI include daytime sleepiness, obesity, supine
positioning, higher neurologic level of injury, and use of
antispasticity medication.55 CPAP, a highly effective treat-
ment that prevents narrowing and closure of the upper
airway, is the treatment of choice. Unfortunately, even
in those without SCI, long-term compliance with CPAP
is low.
Vascular System
People with SCI are prone to stasis of the venous circula-
tion, hypercoagulability of the blood, and intimal vascular
injuries. These risk factors for development of venous
thromboembolism (VTE) are known as a Virchow triad.
Stasis is a direct result of the loss of the muscle-pumping
action of the lower limbs and peripheral vasodilatation.
Hypercoagulability is caused by release of procoagulant
factors after injury, whereas intimal injury can occur from
trauma.
Deep venous thrombosis (DVT), one type of VTE along
with PE, develops in approximately 50% to 75% of those
with SCI who do not receive VTE prophylaxis.57,86 The risk
for DVT is greatest between days 7 and 10 after injury.57,86
Because most people with SCI who develop DVT do not
have clinical signs or symptoms, such as swelling, warmth,
or pain, it is common practice to screen people with SCI
with a duplex ultrasound during the period of high risk.
Identified risk factors for DVT include motor complete
injuries and injuries at the thoracic level and below;
however, the incidence of PE has not been found to be
related to the level or extent of injury.
PE and the postphlebitic syndrome are not uncommon
sequelae of DVT. PE is the cause of death for approximately
10% of individuals who have SCI.40,92 Most of these deaths
are thought to occur within the first year.40 The most
common symptoms of PE include dyspnea and chest pain,
although many cases are clinically silent with a significant
number exhibiting no clinical features of a DVT. PE without
associated DVT may be even more common than PE associ-
ated with DVT in people with associated chest trauma,
when it is thought that the pulmonary thrombosis devel-
ops de novo rather than having traveled from the periph-
ery, as has been traditionally thought.112
Because of the high incidence of DVT and potential fatal
outcome of a PE, VTE prophylaxis is the standard of care.
Several large trials comparing subcutaneously adminis-
tered low-molecular–weight heparin (LMWH) and fixed-
dose unfractionated heparin have shown LMWH to be
more effective in preventing both DVT and PE after SCI.109
Guidelines recommend that pharmacologic prophylaxis
should continue for 8 to 12 weeks postinjury with the
addition of distal lower extremity pneumatic compression
garments during the first 2 weeks after injury.109
The treatment regimen for DVT or PE typically involves
therapeutic anticoagulation unless contradicted. Treatment
is generally continued for 6 months after DVT is diagnosed
to prevent progression and recurrence of thrombosis. If
there is recurrence, then indefinite anticoagulation is rec-
ommended. Inferior vena cava (IVC) filters are indicated
for people who have failed anticoagulant prophylaxis with
the development of DVT or PE despite adequate anticoagu-
lation, or who have a thromboembolus within the IVC or
iliac veins. They are also indicated in those who have a
contraindication to anticoagulation or who have a compli-
cation of anticoagulation such as hemorrhage or thrombo-
cytopenia. Removable IVC filters should almost always be
used, and they should be removed generally within 8 to
12 weeks if no thromboembolism has developed.
Children with SCI seem to be at lesser risk than adoles-
cents with SCI, although the literature is sparse. In one
large review, the incidence of VTE in a pediatric population
with SCI was less than 5%.110
Cardiovascular and Autonomic System
Cardiovascular Disease
People with SCI are at increased risk for cardiovascular
disease (CVD). People with SCI, both those with paraple-
gia and tetraplegia, have a high prevalence of asymptom-
atic coronary artery disease as detected by thallium stress
testing.8,9
The cardiometabolic syndrome consists of several core
risk factors for CVD including abdominal obesity, hyper-
triglyceridemia, low plasma high-density lipoprotein cho-
lesterol (HDL-C), hypertension, and fasting hyperglycemia.
A combination of three or more of which confers the same
health risk as known coronary artery disease.87
Approximately one third of adults with SCI are obese
and more than half of children with spina bifida, as an
example, have body mass index values greater than the
95th percentile.64 More than one third of people with SCI
have a low HDL level. Impaired glucose tolerance and
reduced lean body mass are also significantly more preva-
lent in people with SCI than those without SCI. These
metabolic abnormalities are thought to be directly related
to poor physical fitness and lack of adequate aerobic exer-
cise after SCI.
Fitness and Exercise
Upper extremity moderate or greater intensity exercise pro-
grams that are performed consistently have been shown to
decrease insulin resistance, raise HDL-C levels, and increase
lean body mass in people with SCI.87 Participation in a
regular, vigorous exercise or wheelchair sports program can
improve health status, and also challenge individuals with
SCI to overcome physical obstacles and to achieve greater
functional independence.56 Wheelchair sports can also
improve psychosocial outcomes by reducing stigmatiza-
tion, stereotyping, and discrimination by promoting accep-
tance of those with disabilities as fully functioning
members of society.56 Sports participation by wheelchair
users has been associated with fewer physician visits per
year, fewer rehospitalizations, and fewer medical complica-
tions over time.105 Common organized wheelchair sports
include basketball, tennis, table tennis, swimming, soft-
ball, snow skiing, sled hockey, track and road racing, rugby
for those with tetraplegia (quad rugby), air rifle and pistol,
archery, fencing, billiards, and bowling. These wheelchair
sports require that individuals be classified, based on a
medical history, muscle test, and a functional evaluation,
to allow people with different levels of disability to compete
fairly.58 Wheelchair rugby, for example, was developed in
the 1970s as an alternative to wheelchair basketball,
because most people with cervical neurologic levels of

injury either lacked the capacity to play basketball or spent
most of the time on the bench. It is a mixture of wheelchair
basketball, ice hockey, and football played on a basketball
court with goal lines on either end. A goal is scored when
a player in possession of the (volley)ball crosses the oppos-
ing goal line. A player in possession of the ball must pass
or bounce the ball within 10 seconds.58 All of these sports
can also be performed noncompetitively. The International
Paralympic Committee organizes the Summer and Winter
Paralympic Games, and serves as the International Federa-
tion for nine sports, for which it supervises and coordi-
nates the World Championships and other competitions.
More information can be found on the official website of
the Paralympic Movement (www.paralympic.org).
Autonomic Dysfunction
The autonomic nervous system is under supraspinal
control, and therefore its function is disturbed by SCI. The
autonomic nervous system normally controls visceral func-
tions and maintains internal homeostasis through its nerve
supply to smooth muscles, cardiac muscle, and glands. The
parasympathetic system has a cranial and sacral outflow
from the central nervous system and modulates “at rest”
functions such as digestion, gastrointestinal motility,
reduction of heart rate, breathing, and blood pressure. The
sympathetic system has T1-L2 outflow, which is activated
in stressful situations to raise heart rate and blood pressure,
and to cause vasoconstriction to certain organs. Both the
sympathetic and parasympathetic systems consist of pre-
ganglionic and postganglionic efferent nerve fibers that
regulate visceral function through autonomic reflexes elic-
ited by efferent nerves. After SCI, autonomic reflex function
is generally retained, but in those with high-level SCI, this
is without supraspinal control. Some clinical conditions
related to autonomic dysfunction are discussed in this
section, whereas others are discussed elsewhere in this
chapter. More information including online training on
the International Autonomic Standards for the Classifica-
tion of SCI can be found on the ASIA Learning Center
website (lms3.learnshare.com).
Orthostatic Hypotension. Immediately after SCI, there is
a complete loss of sympathetic tone, resulting in neuro-
genic (“spinal”) shock with hypotension, bradycardia, and
hypothermia. The hypotension occurs as a result of sys-
temic loss of vascular resistance, accumulation of blood
within the venous system, reduced venous return to the
heart, and decreased cardiac output. Over the course of
time, the sympathetic reflex activity returns, with normal-
ization of blood pressure. Supraspinal control continues
to be absent in those individuals with high-level and neu-
rologically complete SCI, however, and they continue to
be prone to orthostatic hypotension. This is defined as a
reduction in blood pressure when body position changes
from supine to upright. The symptoms associated with
orthostatic hypotension include lightheadedness, dizzi-
ness, pallor, and syncope.
Management of orthostatic hypotension includes appli-
cation of elastic stockings and abdominal binders, ade-
quate hydration, gradually progressive daily head-up tilt,
and at times, administration of salt tablets, midodrine, or
fludrocortisone.
CHAPTER 49 Spinal Cord Injury 1123
Bradycardia. Bradycardia occurs in people with neuro-
logically complete high-level SCI immediately after injury,
because of the unopposed parasympathetic effect. During
the first month, over one third of those with cervical injury
have sinus bradycardia with episodes of heart rate less than
50 beats per minute, whereas over 60% have episodes of
heart rate less than 60 beats per minute.7 People with cervi-
cal SCI also experience sinus node arrest (up to 30%),
supraventricular arrhythmias (up to 40%), and rarely
cardiac arrest during this first month post-SCI. Cardiac
arrests are most common in those with high-level SCI,
C1-C2 AIS A. As the neurogenic shock resolves and sym-
pathetic tone returns, usually over several weeks, heart rate
returns to near normal. Bradycardia can still occur with
vagal stimulation thereafter, such as during tracheal suc-
tioning. Bradycardia is less common during the chronic
phase of SCI, except during episodes of intense vagal stim-
ulation, such as during episodes of autonomic dysreflexia
(AD), as discussed later.
Bradycardia during acute SCI requires close monitoring,
but usually no specific treatment is required unless the
bradycardia is extreme (<40 beats per minute) or is associ-
ated with sinus block. Intravenous atropine might have to
be administered prophylactically before tracheal suction-
ing and other activities associated with vagal stimulation.
Persistent, severe bradycardia or other arrhythmia can
require insertion of a temporary or permanent demand
pacemaker.
Autonomic Dysreflexia. AD is a syndrome and clinical
emergency that affects people with SCI usually at the T6
level or above, which is characterized by the acute elevation
of arterial blood pressure and bradycardia, although tachy-
cardia may also occur. The hypertension can be profound
and can result in intracerebral hemorrhage, status epilep-
ticus, myocardial ischemia, and even death.117 AD is trig-
gered by a noxious stimulus below the injury level, which
elicits a sudden reflex sympathetic activity, uninhibited by
supraspinal centers, resulting in profound vasoconstriction
and other autonomic responses. The symptoms of AD are
somewhat variable but include a pounding headache; sys-
tolic and diastolic hypertension; profuse sweating and
cutaneous vasodilatation with flushing of the face, neck,
and shoulders; nasal congestion; pupillary dilatation; and
bradycardia.
The noxious stimulus responsible for AD frequently
stems from the sacral dermatomes, most often from a dis-
tended bladder. Other causes include fecal impaction,
pathology of the bladder and rectum, ingrown toenails,
labor and delivery, surgical procedures, orgasm, and a
variety of other conditions. It more commonly occurs in
people with complete injuries (>90%) than in those with
incomplete injuries (approximately 25%) and is more
likely to occur in the chronic phase of injury.69 The T6 level
of injury is the characteristic defining level, for which
people with a lower level seem much less likely to experi-
ence AD; this is attributed to the preservation of the
splanchnic outflow innervation with levels below T6.
Treatment of acute AD must be prompt and efficient to
prevent a potential morbidity and mortality. Recognition
of symptoms and identification of the precipitating stimu-
lus are paramount. The individual should be sat up,
1124 SECTION 4 Issues in Specific Diagnoses
constrictive clothing and garments should be loosened, the
blood pressure monitored every 2 to 5 minutes, and evacu-
ation of the bladder done promptly to ensure continuous
drainage of urine. If symptoms are not relieved by these
measures, fecal impaction should be suspected and, if
present, resolved. Local anesthetic agents should be used
during any manipulations of the urinary tract or rectum.
If hypertension is present, fast-acting antihypertensive
agents should be administered, preferably with something
that can be removed if it causes hypotension, such as a
topical nitrate.
Occasionally, people experience recurrent symptoms
of AD with or without an identifiable stimulus, a condi-
tion that requires chronic pharmacologic therapy typically
with alpha-adrenoceptor antagonists, alpha- and beta-
adrenoceptor antagonists, or the centrally acting alpha-2-
adrenoceptor agonist clonidine.
Thermal Regulation. Thermal regulation is impaired in
people with SCI, especially in those with complete lesions,
because of loss of supraspinal control. Body tempera-
ture is controlled physiologically primarily by the hypo-
thalamus and secondarily by personal behavior, to increase
or decrease heat loss. Heat and cold signals are normally
carried by afferent nerves to the hypothalamus, where
they are integrated and thermal regulation is conse-
quently mediated by inhibition or activation of the
sympathetic nervous system. With an increase in core
temperature, sympathetic inhibition occurs with vaso­
dilatation and sweating. A decrease in core temperature
causes sympathetic stimulus, with vasoconstriction, and
shivering. With high-level and neurologically complete
SCI, the afferent and efferent pathways are interrupted. As
a result, vasomotor control and the ability to shiver and
sweat are lost. People with SCI therefore tend to have a
higher body temperature in warm environments and a
lower temperature in cold environments. This is termed
poikilothermia.
Most of the time, people with SCI maintain relative
thermal stability. However, proper heating and cooling of
the environment is needed to ensure continuous thermal
stability, especially for those with high-level SCI. Appropri-
ate clothing should be worn, strenuous exercise in a hot
environment avoided, and cool moist compresses applied
when body temperature rises.
Calcium Metabolism and Osteoporosis
An imbalance between bone formation and bone resorp-
tion occurs after SCI. The potential adverse clinical effects
of this imbalance are fractures related to osteoporosis,
hypercalcemia, and renal calculi resulting from hypercalci-
uria. Markers of bone resorption, including N- and
C-telopeptide cross-links of type 1 collagen, become mark-
edly elevated soon after injury and peak 2 to 4 months
after SCI, whereas serum osteocalcin, a marker of bone
formation, only modestly increases during the first 6
months after SCI, without correlation to the resorption
markers.75 During this time of prominent bone resorption,
the release of calcium and phosphorus from bone tissue
into the blood causes a significant decrease in parathyroid
hormone (PTH).
The decreased PTH levels in individuals is thought to
act in the kidney to decrease calcium resorption and to
inhibit 1,25(OH)2D synthesis, the active form of vitamin
D, which indirectly results in a decrease in intestinal
calcium absorption; both mechanisms minimizing the
possibility that the skeletal calcium loss will lead to
hypercalcemia.
However, in adolescent boys, who seem to have espe-
cially high bone turnover, within the first 3 to 4 months
after SCI, hypercalcemia is not uncommon, perhaps indi-
cating that the protective mechanisms noted earlier are
overwhelmed.79 Symptoms of hypercalcemia include
abdominal pain, nausea, vomiting, malaise, polyuria,
polydipsia, and dehydration. Management of hypercalce-
mia includes hydration with saline infusion, administra-
tion of diuretics, and bisphosphonates. Additional risk
factors for hypercalcemia include motor complete injury,
tetraplegia, dehydration, and prolonged immobilization.
A low calcium intake is not typically effective for lowering
elevated serum or urinary calcium concentrations, and
restrictions of dietary calcium and vitamin D intake are not
recommended.
PTH levels generally return to normal by 1 year postin-
jury126 and development of secondary hyperparathyroid-
ism can even sometimes occur, which can lead to ongoing
bone resorption and osteoporosis. People with chronic SCI
are often vitamin D-deficient because of inadequate nutri-
tional intake or reduced sunlight exposure. Supplementa-
tion with calcium and vitamin D (which can improve
calcium resorption), particularly in the chronic phase
when a hypercalcemic status is not present, can be effective
in minimizing bone loss.
The degree of lower limb BMD after SCI has been cor-
related with fracture risk.125 BMD is typically progressively
greater as measured from proximal to distal sites in the
lower limbs below the level of injury.52
A number of physical interventions have been studied
in the hope of preventing and treating the loss of BMD.
Individuals with SCI who perform passive weight-bearing
standing with the aid of a standing device might have
better-preserved BMD in their lower limbs than those
who do not stand,15 whereas FES cycle ergometry has
been shown to provide modest reductions in the rate of
bone loss.15
Several bisphosphonate antiresorptive therapies have
been shown to be effective in either maintaining lower
extremity BMD after acute SCI or improving low BMD.75
Vitamin D supplementation in and of itself has also been
shown to protect against bone loss after SCI.10
Gastrointestinal System
Gastrointestinal Complications
Although impaired evacuation of the colon is the most
profound and universal change that a person with SCI will
probably encounter with regard to the gastrointestinal
system, several other gastrointestinal complications can be
experienced. In the acute phase of a cervical SCI, dysphagia
is not uncommon. Factors contributing to dysphagia
include immobilization of the cervical spine by an orthosis,
soft tissue swelling or nerve trauma after anterior cervical
spine surgery, and limitation of laryngeal elevation by a

tracheostomy tube.67 In the acute phase of injury, especially
within the first several weeks after injury, the incidence of
gastric erosions, gastric and duodenal ulcers, and perfora-
tion is increased.104 It is standard practice to administer
gastrointestinal ulcer prophylaxis with histamine-2 recep-
tor antagonists or proton pump inhibitors during this time,
and usually for 3 months postinjury.
Gallbladder disease and pancreatitis can also have an
increased incidence in people with high paraplegia or tet-
raplegia, because of decreased sympathetic stimulation to
these organs. People with tetraplegia also have slower
gastric emptying than people with low paraplegia. Ady-
namic ileus commonly occurs within the first 1 to 2 days
postinjury, but usually resolves within 2 to 3 days with
bowel rest. The mechanism is attributed to the loss of
sympathetic and parasympathetic tone during spinal shock.
An acute abdomen is also not uncommon early in the
postinjury period, occurring in up to 5% of individuals.6
In people with a complete high paraplegia or tetraple-
gia, symptoms of any abdominal pathology are likely to
be vague and poorly localized. Referred patterns of pain
can occur instead of the typical localized abdominal pain
that might be present in a person with a low paraplegia or
no SCI who has the same abdominal pathology. Symp-
toms of AD, anorexia, altered bowel patterns, nausea, or
vomiting can be present, any of which can be the most
prominent symptom. Given the frequent atypical presenta-
tion of abdominal pathology in these individuals, it is not
unreasonable to have a high level of suspicion for abdomi-
nal pathology, and a low threshold for ordering laboratory
tests or abdominal imaging to confirm the presence or
absence of disease.
Bowel Management
The parasympathetic innervation to the portion of bowel
extending from the esophagus to the splenic flexure of
the colon, which modulates peristalsis, is provided by
the vagus nerve. The parasympathetic innervation to the
descending colon and rectum is provided by the pelvic
nerve, which exits from the spinal cord at segments S2-S4.
The somatic pudendal nerve, also originating from seg-
ments S2-S4, innervates the external anal sphincter and
pelvic floor musculature.
An SCI that damages segments above the sacral seg-
ments produces a reflexic or UMN bowel in which defeca-
tion cannot be initiated by voluntary relaxation of the
external anal sphincter, although there can be reflex-
mediated colonic peristalsis. In contrast, an SCI that
includes destruction of the S2-S4 anterior horn cells or
cauda equina produces an areflexic or LMN bowel in which
there is no reflex-mediated colonic peristalsis. There is only
slow stool propulsion coordinated by the intrinsically
innervated myenteric plexus. The anal sphincter of an LMN
bowel is typically atonic and prone to leakage of stool.
A bowel program is a treatment plan for managing a
neurogenic bowel, with the goal of allowing effective and
efficient colonic evacuation while preventing incontinence
and constipation. A bowel program should be scheduled
at the same time of day, usually every day in the beginning.
The program should be scheduled later on at least once
every 2 days to avoid chronic colorectal overdistention. The
scheduling of a bowel routine after a meal can take
CHAPTER 49 Spinal Cord Injury 1125
advantage of the gastrocolic response. Although a person
with SCI should learn how to perform a bowel routine in
bed and on a commode chair, regular performance of the
routine sitting up on a commode is preferred to allow
gravity to facilitate complete emptying. A diet high in fiber
can help produce a bulky, formed stool and promote con-
tinence. Medications can also be used, such as stool soften-
ers to modulate stool consistency, and stimulant and
hyperosmolar laxatives to improve bowel motility. Miniene-
mas and suppositories can be used to trigger colonic reflex
evacuation in people with a UMN bowel. Stimulant and
hyperosmolar laxatives, if used, are usually taken 8 to 12
hours before the evacuation portion of a bowel routine.
Two mechanical methods are used to evacuate the
rectum: digital stimulation and digital evacuation. Digital
stimulation is dependent on the preservation of sacral
reflex arcs, and is typically effective only for people with a
UMN bowel. Digital stimulation is performed by inserting
a gloved, lubricated finger into the rectum and slowly rotat-
ing the finger in a circular movement until relaxation of
the bowel wall is felt, flatus passes, or stool passes.28 This
typically occurs within 1 minute. Digital stimulation is
repeated every 10 minutes until there is cessation of stool
flow, palpable internal sphincter closure, or the absence of
stool results from the last two digital stimulations. In con-
trast, digital evacuation is not dependent on the preserva-
tion of sacral reflex arcs and is typically performed by a
person with an LMN bowel. Digital evacuation is per-
formed by inserting a gloved, lubricated finger into the
rectum to break up or hook stool and pull it out. Abdomi-
nal wall massage, starting in the right lower quadrant and
progressing along the course of colon, is a useful adjunct
for attempting to move stool along the colon.
If an effective bowel routine cannot be achieved with
the above techniques, pulsed water irrigation has been
shown to be effective in some people in decreasing the
time it takes to complete a bowel routine and reducing the
incidence of bowel accidents and constipation. With this
technique, a rectal catheter with an inflatable balloon is
inserted into the rectum to allow pulsed warm water to
facilitate colonic peristalsis and stool evacuation. Finally,
placement of a colostomy has also been shown to be effec-
tive in eliminating bowel accidents, dramatically decreas-
ing the time it takes to perform bowel care, and decreasing
the amount of assistance needed to perform bowel care.
Colostomies are especially useful if incontinence of stool
is interfering with wound healing.
Children with SCI should begin management of a neu-
rogenic bowel as they would toilet training.85 Young chil-
dren with lower level injuries can be placed on a toilet after
each meal (to take advantage of the gastrocolic reflex) and
encouraged to push to evacuate. These regular toileting
times should last no more than 15 minutes. This procedure
is generally most successful in children with LMN-type
bowels. For those children with UMN-type bowels the use
of suppositories or small volume enemas with or without
digital stimulation is often necessary. One particularly
effective reversible surgical procedure, called the antegrade
continence enema (ACE) procedure, entails attaching the
distal end of the appendix (or other fabricated bowel
conduit if the appendix has been removed) to the abdomi-
nal wall to create an appendicostomy. This procedure can
1126 SECTION 4 Issues in Specific Diagnoses
be effective in allowing a child (or adult) who otherwise
was having difficulty with a conventional routine to achieve
continence. With an ACE, enemas are administrated
through the abdominal wall stoma into the cecum allow-
ing stool and to be propelled throughout the colon from
the most proximal section of colon down through its entire
length and out of the anus.
Genitourinary System
Physiology of the Bladder
The parasympathetic innervation to the bladder, which
modulates contraction of the urinary bladder with opening
of the bladder neck to allow voiding, is provided by the
pelvic splanchnic nerves, which exit from the spinal cord
at segments S2-S4. The sympathetic innervation to the
bladder and bladder neck or internal urethral sphincter,
which modulates relaxation of the body of the bladder and
narrowing of the bladder neck to inhibit voiding, is pro-
vided by the hypogastric nerves, which exit from the spinal
cord at segments T11-L2. The somatic pudendal nerve, also
originating from segments S2-S4, innervates the external
urinary sphincter.
SCI that damages segments above the sacral segments
produces a reflexic or UMN bladder in which urination
cannot be initiated by voluntary relaxation of the external
urinary sphincter, although reflex voiding can occur. In
contrast, an SCI that includes destruction of the S2-S4
anterior horn cells or cauda equina produces an areflexic
or LMN bladder in which there is no reflex voiding. The
external urinary sphincter of an LMN bladder is typically
atonic and prone to leakage of urine. Because central coor-
dination of normal voiding is thought to occur at the level
of the pons, in a person with a UMN bladder resulting
from SCI, coordination of contraction (or relaxation) of
the bladder with relaxation (or contraction) of the external
urinary sphincter is lost. This leads to a pattern of simul-
taneous reflex contractile activity called detrusor-sphincter
dyssynergia, which often results in elevated bladder
pressures.
Management of Neurogenic Bladder
The goal of management of a neurogenic bladder is to
achieve a socially acceptable method of bladder emptying,
while avoiding complications such as infections, hydrone-
phrosis with renal failure, urinary tract stones, and AD.
During the immediate postinjury period an indwelling
catheter is placed within the bladder, because virtually all
people with SCI have urinary retention. Other bladder
management options are explored later on, depending on
the person’s gender, level and completeness of injury, and
other comorbidities.
Intermittent bladder catheterization (IC) is generally
accepted as the best option, other than regaining normal
voiding, for the long-term bladder management of people
who can perform IC themselves. This is because of the
physiologic advantage of allowing for regular bladder
filling and emptying, the social acceptability of not needing
a drainage appliance, and fewer complications than with
other methods. IC is usually performed several times daily
with a target catheterized volume of 500 mL each time, for
a total fluid intake of approximately 2000 mL/day. IC
often needs to be combined with anticholinergic medica-
tions in people who have a UMN bladder, to inhibit
voiding between catheterizations. To improve bladder
capacity and permit successful IC when anticholinergic
medication is unable to provide adequate bladder relax-
ation, or when the side effects of anticholinergics are intol-
erable, injections of the neurotoxin botulinum toxin have
been shown to be effective; however, they must be repeated
on a regular basis.66,84 A more permanent solution, aug-
mentation cystoplasty, a procedure that involves harvesting
a portion of intestine and attaching the portion of intestine
to the native bladder to create a high-capacity but low-
pressure reservoir, has also been shown to be effective.24
Reflex voiding is another viable option for men with
UMN bladder in whom bladder pressures are generated
that are greater than the outlet pressures of the sphincters
to allow spontaneous voiding. A condom catheter is
applied to the penis and connected via tubing to a leg
bag or bedside bag. Reflex voiding can sometimes be
triggered by suprapubic tapping. The completeness of
voiding can be determined by measurement of a postvoid
residual urine volume. High RVs predispose to urinary
tract infection (UTI) and bladder stone formation. Fur-
thermore, reflex voiding is often associated with elevated
voiding pressures, which can predispose to vesicoureteral
reflux, hydronephrosis, and eventual renal failure. It is
critically important for reflex voiders to undergo regular
imaging with a renal ultrasound to identify reflux or
hydronephrosis.
Urodynamic testing is a procedure in which pressure
sensors attached to a catheter are inserted through the
urinary sphincter into the bladder and the bladder is then
slowly filled with water. It can theoretically be useful in
estimating relative risk of upper tract deterioration in
people who reflex void and others by quantitatively docu-
menting the duration and pattern of detrusor pressures
during bladder filling. When accompanying urination, the
symptoms and signs of AD typically indicate there is high-
pressure (within detrusor) voiding occurring. alpha-
Adrenergic receptor antagonist medications, such as
prazosin, terazosin, doxazosin, tamsulosin, or alfuzosin,
are often effective in decreasing bladder outlet resistance
and secondarily decreasing bladder pressures and postvoid
RVs.95 Historically, two transurethral surgical procedures
have been performed to decrease bladder outlet resistance.
One is the nondestructive placement of a tubular wire
mesh stent at the level of the external sphincter. The second
is a transurethral external sphincterotomy, performed
either with a scalpel or a laser. Botulinum toxin has also
been shown to be effective when injected into the sphinc-
ter to improve bladder emptying.33 Reflex voiding, however,
is a poor option for women with SCI, because an accept-
able external collecting device for women does not exist at
present.
Long-term bladder drainage with an indwelling catheter
is a reasonable option for people with tetraplegia who are
unable to perform IC, or men who are unable to effectively
maintain an external catheter on their penis. Use of an
indwelling catheter inserted through the urethra is associ-
ated with UTI, bladder stone formation, epididymitis, pros-
tatitis, hypospadias, and bladder cancer.119 Placement of a
suprapubic cystostomy tube in people requiring long-term

indwelling catheters can avoid some of these complica-
tions, such as prostatitis, epididymitis, and hypospadias.
Although UTI is clearly a common complication, con-
troversy exists concerning exactly what constitutes a UTI in
people with SCI. Symptoms of fever, spontaneous voiding
between catheterizations, hematuria, AD, and increased
spasticity, when associated with cloudy or foul-smelling
urine and other nonspecific symptoms, such as malaise or
vague abdominal discomfort, strongly suggest the presence
of UTI and the need for treatment. Although the presence
of pyuria can increase the suspicion that a UTI is present,
it is unclear whether the presence of pyuria and bacteriuria
should lead to the use of antibiotics if the person is other-
wise asymptomatic. Bacteriuria is virtually omnipresent in
people with neurogenic bladders, and certainly seems to
occur in any person who uses IC, an external collecting
device, or an indwelling catheter. Frequent treatment of
asymptomatic bacteriuria can lead to bacterial resistance.
Nevertheless, simple UTIs can be complicated by the devel-
opment of pyelonephritis, epididymitis, orchitis, prostatic
abscesses, and urosepsis. Over the course of time, recurrent
UTIs can lead to renal scarring, secondary decreased renal
function, and the development of urinary tract stones.
In children, neurogenic bladder training should begin
at the same time as toilet training would ordinarily begin.
Self-intermittent catheterization usually is successful only
in those whose developmental age is older than 5 years.
Because continence is a social expectation for children in
school, children should be encouraged to become inde-
pendent in bladder management as soon as they are able
to prevent social isolation, which can result from teasing
by peers if bladder accidents occur.85
Sexuality and Fertility
The ability to have psychogenic erections for men and
psychogenic vaginal vasocongestion and lubrication for
women is mediated by the sympathetic and parasympa-
thetic nervous systems and directly related to the degree of
light touch and pinprick sensory preservation within the
T11-L2 dermatomes.102 The ability to have reflex erections
for men and reflex vaginal vasocongestion and lubrication
for women is mediated by the parasympathetic nervous
system and related to sacral reflex preservation. If a hyper-
active BC reflex is present, reflex erections and lubrication
are usually possible, although the quality of arousal might
differ from preinjury levels. If there is a hypoactive BC
reflex with some preservation of sensation within the S4-S5
dermatomes, reflex erections and lubrication are usually
possible. However, if the BC reflex is absent and there is
no sensation within the S4-S5 dermatomes, the ability to
have reflex erections and lubrication is lost, and the ability
to generate erections and lubrication psychogenically is
related to T11-L2 sensory preservation.
The neurologic control of orgasm has not been well
delineated. It is generally believed to be a spinal-level reflex
response that can be inhibited or excited by the brain. If
on physical examination the BC and anocutaneous reflex
are absent and there is no sensation at S4-S5, attainment
of orgasm is unlikely. Approximately 40% of men and
women with SCI report orgasm; however, achieving orgasm
is known to take longer after SCI.
CHAPTER 49 Spinal Cord Injury 1127
Effective treatments for male erectile dysfunction, not
ejaculatory dysfunction, resulting from SCI include (1)
oral medications, (2) vacuum tumescence devices, (3)
intracavernous (penile) injections, and (4) penile implants.
Oral type 5 phosphodiesterase inhibitors such as sildenafil,
vardenafil, and tadalafil have been found to be effective in
65% to 75% of individuals in randomized clinical trials,
and are now first-line therapies for erectile dysfunction
after SCI.34 Vacuum tumescence devices are effective in
producing an adequate erection in more than 50% of indi-
viduals, although oral medications have consistently been
preferred by users when the methods have been compared
directly in studies. Because penile necrosis has been
reported if the constricting ring is left in place for too long,
the ring should not be left in place for more than 30
minutes. Intracavernous injections with papaverine, phen-
tolamine, or prostaglandin E1 used alone or in combina-
tion, as one has not been shown to be more effective than
the others, have a 90% reported satisfactory erectile
response rate in pooled cases series.34 Reported complica-
tions of injections include priapism (more often with
phentolamine and papaverine), penile scarring after
repeated use, local swelling, and pain at the injection site.
Penile implants are very effective but have been shown to
consistently have a serious complication rate of 10%,
including erosion through the skin and infection.34 If the
implanted prosthesis is removed after a serious complica-
tion occurs, the penile tissue is invariably damaged, and
the other methods of erectile dysfunction treatment are not
effective.
Treatment of infertility in men with SCI is initially
focused on producing an ejaculate, because only 10% to
20% of men are able to ejaculate naturally after SCI. Inter-
ventions including manual or partner masturbation, penile
vibratory stimulation, and electroejaculation can lead to
success in ejaculation in 95% of individuals.35 Penile vibra-
tory stimulation is the application of a vibrating disk to
the frenulum and glans penis to activate the ejaculatory
reflex. This can be performed alone or in concert with
electroejaculation, whereby an electrical probe is placed in
contact with the rectal wall near the prostate gland and
seminal vesicles, and up to 15 to 35 stimulations are
administered at progressively increasing voltages. After
either procedure, the bladder can be catheterized to harvest
any retrograde ejaculation.
Semen quality deteriorates significantly within the first
2 weeks after SCI.76 This deterioration has been character-
ized by reduced numbers of spermatozoa, decreased sperm
motility, and the presence of inhibitory factors within the
seminal fluid. Given these barriers, pregnancy rates are
approximately 50% in partners of men with SCI using
assisted ejaculation or advanced fertility treatments such as
testicular biopsy or aspiration, in vitro fertilization, or
intracytoplasmic sperm injection.35
Women with SCI are not thought to have decreased
fertility, although this has not been closely evaluated. Most
women experience temporary amenorrhea postinjury that
lasts for an average of 4 months.62 Pregnancy can alter
the ability of a woman with SCI to transfer, perform pres-
sure reliefs, and propel a wheelchair. The introduction of
sliding boards and motorized wheelchairs can be helpful
during a pregnancy. Because of the enlarging abdomen,
1128 SECTION 4 Issues in Specific Diagnoses
self-catheterization can become difficult, necessitating use
of an indwelling catheter. Respiratory function can be com-
promised during pregnancy, especially in women with tet-
raplegia. The onset of labor can be accompanied by
significantly increased spasticity. Labor might not be per-
ceived by women with injury levels above T10. Uterine
contractions during labor have been associated with AD in
women with injury levels above T6, and this needs to be
differentiated from the blood pressure elevations seen in
preeclampsia.21 AD associated with labor, however, can be
treated or prevented with epidural anesthesia.
Pressure Ulcers
A pressure ulcer is a localized injury to the skin and/or
underlying tissue usually over a bony prominence resulting
from direct pressure, where the force vector is perpendicu-
lar to the tissue contact area, or shear, where force vector
is tangential to the tissue contact area.16 This applied pres-
sure, if prolonged and of greater magnitude than the sup-
plying capillary and lymphatic vessel tolerance to remain
patent, can result in occluded blood and interstitial fluid
flow, ischemia, and ultimately tissue necrosis.
In addition to pressure itself, numerous secondary risk
factors are associated with the development of pressure
ulcers. These risk factors can be divided into demographic,
SCI-related, comorbid medical, nutritional, psychological,
social, and support surface–related categories. Pressure
ulcer risk increases both with time since injury and chrono-
logic age, especially in those older than 50 years of age.26
With regard to the SCI itself, urinary and bowel inconti-
nence or severe spasticity leading to shear and poor posi-
tioning are also risk factors. Diabetes mellitus, smoking,
respiratory disease, and hypotension all confer increased
risk.26,114 Biochemical markers of nutrition associated with
pressure ulcers include a low prealbumin, albumin, hemo-
globin and hematocrit, and total lymphocyte count.51
Depression can be associated with inactivity, self-neglect,
and poor medical adherence to recommendations with
regard to skin care, all of which can lead pressure ulcers.
Support surfaces for both bed and wheelchair if worn out
or are improperly selected also increase risk for pressure
ulcer development.
A quarter of those hospitalized in the acute hospital or
rehabilitation units of the SCI Model Systems develop at
least one pressure ulcer.25 At 1, 5, 10, and 20 years postin-
jury, the prevalence has been reported as 15%, 20%, 23%,
and 29%, respectively.124 During acute rehabilitation, pres-
sure ulcers are seen in the following distribution: sacrum,
39%; calcaneus, 13%; ischium, 8%; occiput, 6%; and
scapula, 5%.25 This contrasts with the distribution seen 2
years after injury: ischium, 31%; trochanter, 26%; sacrum,
18%; calcaneus, 5%; and malleolus, 4%.124 The higher dis-
tribution of ulcers in the sacrum and calcaneus in the acute
group is probably because of the increased time spent
supine in bed soon after injury, as opposed to more time
sitting in a wheelchair later.
Assessment of Pressure Ulcers
An assessment of a pressure ulcer should include a nota-
tion of location, stage of wound, size, characteristics of the
ulcer cavity, and characteristics of the surrounding skin.
Table 49-5 outlines a six-category/stage classification of
pressure ulcers refined by the National Pressure Ulcer Advi-
sory Committee.16
A determination of the potential causes of the break-
down should be made. The location of the wound is often
very helpful in determining the underlying mechanism
responsible for causing the increased pressure that has led
to wound development. For example, a sacral ulcer in a
person who does not get out of bed might suggest unre-
lieved direct pressure from the mattress. A sacral or coc-
cygeal ulcer in a person who is sitting with these areas in
contact with the rear portion of the seat might suggest
shear over the sacrum and coccyx from sitting. In this latter
example, relieving pressure only when in bed and ignoring
the poor positioning when in the chair will not allow the
ulcer to heal, even with appropriate wound care dressings.
A sacral ulcer that recurs after a person sits on a commode
might suggest unrelieved pressure created by the edge of
the cutout of the seat of a commode chair.
Treatment of Pressure Ulcers
Pressure ulcer healing comprises a sequence of loosely
linked components that include inflammation, matrix syn-
thesis and deposition, angiogenesis, fibroplasia, epitheli-
alization, contraction, and remodeling. Growth factors are
important determinants of this sequence. Different catego-
ries/stages of wounds require different components to
heal. Category/Stage II ulcers might need only epitheliali-
zation, whereas a category/stage III or IV ulcer can require
matrix synthesis and deposition, angiogenesis, fibroplasia,
and contraction.
Pressure ulcers can acquire necrotic tissue. Necrotic
tissue releases endotoxins that inhibit fibroblast and kera-
tinocyte migration. It is also an excellent growth medium
for bacteria. The bacteria produce enzymes and proteases
that degrade fibrin and growth factors, leading to impaired
healing. Removal of necrotic tissue can be done by a
number of different methods of débridement, including
autolysis and chemical, sharp, and mechanical débride-
ment. Autolysis is promoted when a moisture-retentive
barrier is applied over a superficial ulcer, allowing endog-
enous enzymes to degrade the necrotic tissue. Chemical
débridement refers to the application of commercially
available enzymes that selectively degrade necrotic tissues.
Sharp débridement refers to excision of necrotic tissue or
scar with a sharp instrument. Mechanical débridement can
be performed with application of wet-to-dry dressings.
Dressings are topical products used for protection of a
pressure ulcer from contamination and trauma, applica-
tion of medication, débridement of necrotic tissue, and to
provide an environment in which tissue hydration levels
and the viability of the wound tissue are maintained by
something other than the skin. The wound dressing can be
viewed as the substitute skin. The major dressing categories
include transparent films, hydrocolloids, hydrogels, foams,
alginates, and gauze dressings. Transparent films are adhe-
sive, nonabsorptive, semipermeable membranes, whereas
hydrocolloids are adhesive wafers with water-absorbing
particles that have a minimal to moderate absorptive
capacity. Both allow autolytic débridement and are indi-
cated for use in the treatment of partial-thickness wounds.
 CHAPTER 49 Spinal Cord Injury 1129

Table 49-5 National Pressure Ulcer Advisory Panel Category/Staging System, 2007 Revision
Pressure Ulcer
Categories/Stages Description
Suspected deep tissue injury Purple or maroon localized area of discolored intact skin or blood-filled blister resulting from damage of underlying
soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy,
warmer, or cooler as compared with adjacent tissue. Deep tissue injury may be difficult to detect in individuals
with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve
and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal
treatment.
Category/Stage I Intact skin with nonblanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin
may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft,
warmer, or cooler as compared with adjacent tissue. Category/Stage I damage may be difficult to detect in
individuals with dark skin tones.
Category/Stage II Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May
also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without
slough or bruising.* This category/stage should not be used to describe skin tears, tape burns, perineal dermatitis,
maceration, or excoriation.
Category/Stage III Full-thickness tissue loss. Subcutaneous fat may be visible, but bone, tendon, or muscle is not exposed. Slough may
be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a
category/stage III pressure ulcer varies by anatomic location. The bridge of the nose, ear, occiput, and malleolus
do not have subcutaneous tissue and category/stage III ulcers can be shallow. In contrast, areas of significant
adiposity can develop extremely deep stage III pressure ulcers. Bone/tendon is not visible or directly palpable.
Category/Stage IV Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of
the wound bed. Often include undermining and tunneling. The depth of a category/stage IV pressure ulcer varies
by anatomic location. The bridge of the nose, ear, occiput, and malleolus do not have subcutaneous tissue and
these ulcers can be shallow. Category/Stage IV ulcers can extend into muscle and/or supporting structures (e.g.,
fascia, tendon, or joint capsule) making osteomyelitis possible. Exposed bone/tendon is visible or directly palpable.
Unstageable/Unclassified Full-thickness tissue loss in which the base of the ulcer is covered by slough (yellow, tan, gray, green, or brown)
and/or eschar (tan, brown, or black) in the wound bed. Until enough slough and/or eschar is removed to expose
the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact
without erythema or fluctuance) eschar on the heels serves as “the body’s natural (biological) cover” and should
not be removed.
From Black J, Baharestani MM, Cuddigan J, et al: National Pressure Ulcer Advisory Panel’s updated pressure ulcer staging system, Adv Skin Wound Care 20:269-274, 2007.
*Bruising indicates suspected deep tissue injury.

Foams are nonadherent, hydrophobic, or hydrophilic
materials with minimal to moderate absorptive capacity.
Hydrogels are water-based or glycerin-based gels with
minimal to moderate absorptive capacity. Alginates are
soft, absorbent, nonwoven, seaweed-derived dressings that
have a cottonlike appearance, with a moderate to heavy
absorptive capacity. Foams, hydrogels, and alginates all fill
dead space within an ulcer crater, require a secondary
dressing, and are appropriate for both partial-thickness
and full-thickness wounds.
Other adjunctive therapies that have shown benefit in
randomized controlled studies and case series have
included electrical stimulation for which there is the most
evidence and negative pressure wound therapy.3,61 However,
negative pressure wound therapy is not without risk includ-
ing bleeding and infection.
Adequate nutrition is essential to heal a pressure ulcer.
Caloric requirements are increased for a person with SCI
who has a pressure ulcer. An estimate of the difference in
basal energy expenditure between people with SCI who
have severe pressure ulcers and those who do not have
pressure ulcers is approximately 5 kcal/kg of body weight/
day.51 Because protein requirements are increased for a
person with an SCI and pressure ulcers, recommendations
for increased protein requirements range from 1.25 to 2 g
protein/kg of body weight/day, with the higher require-
ments suggested for those with ulcers of greater severity.51
Pressure redistribution support surfaces and proper
positioning in them can help prevent pressure ulcers from
developing, and help to heal them if they occur. Pressure
redistribution support mattresses are typically designed to
either be active with powered alternating pressure cham-
bers or reactive with high or low air loss through a single
or multiple connected porous chambers. Less effective
options for pressure redistribution in bed include the use
of active or reactive mattress overlays. Because few indi-
viduals with SCI are not at risk for developing pressure
ulcers, some type of pressure redistribution support surface
should be routinely prescribed. For those with pressure
ulcers, a history of pressure ulcers, or multiple risk factors
for the development of pressure ulcers, an active or reactive
pressure redistribution mattress is indicated. It has been
traditionally thought that people with SCI and poor sensa-
tion need to be repositioned onto a different support
surface every 2 hours, whether or not a pressure redistribut-
ing mattress is used. One standard turning position, which
redistributes pressure from both the sacrum and the greater
trochanters, requires a 30-degree angled, side-lying posi-
tion, with pillows behind the back and between the knees.
Another standard turning position is the prone position,
with pillows placed under the thorax, pelvis, thighs, and
shins relieving all bony prominences.
Pressure-relieving cushions designed for wheelchairs
should be used to prevent pressure ulcers over the ischial
tuberosities, greater trochanters, and sacrum/coccyx in
those who sit in a position where these bony prominences
bear weight. Cushions can be composed of air, foam, gel,
or some combination of these. It is also essential when
1130 SECTION 4 Issues in Specific Diagnoses
sitting that pressure relief techniques be performed approx-
imately every 15 to 30 minutes for a duration of 2 minutes.29
Effective manual pressure relief techniques include a
forward-lean in the chair (perhaps the most effective), a
side-to-side lean, or a push-up. Moreover, individualized
wheelchair seating systems that tilt and/or recline or allow
standing should be prescribed to all people who are unable
to effectively perform these manual pressure relief tech-
niques on their own; powered seating systems are recom-
mended if their living environment is accessible. Category/
Stage III and IV ulcers might not heal in a timely manner,
depending on their location and size, and operative repair
to close the defect is often indicated. Individuals who
cannot tolerate surgery for medical reasons, who have a
short life expectancy, or who are unlikely to protect the
area of operative repair are poor candidates for operative
repair. Successful operative repairs typically include exci-
sion of the ulcer, the surrounding scar, and the underlying
necrotic or infected bone. The coverage is typically a
regional pedicle flap that includes muscle and its blood
supply. Postoperatively, a person should be positioned off
the surgical site for several weeks to allow healing. During
this healing period, use of an alternating air mattress or
high air loss (air fluidized) bed is recommended.
Pain
Approximately 80% of people with SCI report chronic
pain, and approximately one half report chronic, severe
pain that interferes with activity and affects quality of life.23
Many different types of pain are experienced by people
with SCI. The International Spinal Cord Injury Pain Clas-
sification organizes pains commonly seen after SCI hierar-
chically into three tiers (Table 49-6).20 Within this first tier,
nociceptive pain is defined as pain arising from activation
of peripheral nerve endings or sensory receptors that are
capable of transducing and encoding noxious stimuli,
whereas neuropathic pain is defined as pain that arises as
Table 49-6 International Spinal Cord Injury Pain (ISCIP) Classification
Tier 1: Pain Type Tier 2: Pain Subtype
□ Nociceptive pain □ Musculoskeletal pain
□ Visceral pain
□ Other nociceptive pain
□ Neuropathic pain □ At level SCI pain
□ Below level SCI pain
□ Other neuropathic pain
□ Other pain
□ Unknown pain
From Bryce TN, Biering-Sorensen F, Finnerup NB, et al: International Spinal Cord Injury Pain Classification: part I. Background and description, Spinal Cord 50:413-417, 2012.
a direct consequence of a lesion or disease affecting the
somatosensory system. Other pain as defined within the
first tier is pain that occurs when there is no identifiable
noxious stimulus or detectable damage to the nervous
system responsible for the pain.
Musculoskeletal Pain
Musculoskeletal (nociceptive) pain refers to pain occurring
in a region where there generally is at least some preserved
sensation and the pain is thought to be arising from noci-
ceptors within musculoskeletal structures (muscles,
tendons, ligaments, joints, bones). It might occur at any
location where there are musculoskeletal structures, includ-
ing areas below the NLI.
The enormous demands placed on the upper limbs of
individuals with SCI during their daily activities, work, and
sports lead to a high incidence of overuse injuries and
musculoskeletal pain. Overuse injuries are caused by repet-
itive motions and recurrent microtrauma, which can be
aggravated by more major acute injury. The treatment of
overuse injuries in the upper limbs depends on the specific
etiology, but can be divided into overlapping phases:
• Control of inflammation and pain with protection,
rest, ice application, compression, elevation, and
nonsteroidal antiinflammatory drugs (NSAIDs).
• Mobilization to regain joint ROM.
• Strengthening exercises once 80% to 85% of painless
ROM is achieved.
• Functional restoration.
The goal is to achieve the previous level of function
while preventing recurrence.
Shoulder pain is the most common and incapacitating
upper limb overuse injury and can be caused by bicipital
tendonitis, rotator cuff impingement syndrome, subacro-
mial bursitis, capsulitis, and osteoarthritis. The prevalence
of shoulder pain in people with SCI, either paraplegia or
tetraplegia, is approximately 50%.45 The etiology of shoul-
der pain after tetraplegia, in contrast to shoulder pain after
Tier 3: Primary Pain Source and/or Pathologic Condition (write or type in)
□ ____________________
e.g., glenohumeral arthritis, lateral epicondylitis, comminuted femur fracture,
quadratus lumborum muscle spasm
□ ____________________
e.g., myocardial infarction, abdominal pain due to bowel impaction, cholecystitis
□ ____________________
e.g., migraine headache, surgical skin incision
□ ____________________
e.g., spinal cord compression, nerve root compression, cauda equina compression
□ ____________________
e.g., spinal cord ischemia, spinal cord compression
□ ____________________
e.g., carpal tunnel syndrome, trigeminal neuralgia, diabetic polyneuropathy
□ ____________________
e.g., fibromyalgia, complex regional pain syndrome type I, interstitial cystitis, irritable
bowel syndrome
□ ____________________

paraplegia, more often includes pain that stems from
shoulder instability, resulting from weakness of the muscles
that stabilize the shoulder joint, as well as capsulitis and
contracture caused by a lack of passive or active ROM and
underlying spasticity.
Specific treatment (and prevention) strategies for shoul-
der pain originating from the rotator cuff in people with
SCI should include strengthening, stretching, optimizing
posture, and avoidance of activities that promote impinge-
ment. Strengthening of the dynamic shoulder stabilizers
should occur in a balanced manner. A program should
emphasize strengthening the posterior shoulder muscles,
including the external rotators, the posterior scapular
muscles (rhomboids and trapezius), and the adductors.
Wheelchair use promotes strengthening of the antagonists
to these muscles (i.e., the anterior shoulder musculature).19
Stretching of the dynamic shoulder stabilizers, especially
the anterior shoulder muscles, is also necessary to achieve
a balanced shoulder. This is because these muscles often
become hypertrophied and contracted through constant
use during wheelchair propulsion and transfer activities. In
one controlled study of wheelchair users, an intervention
consisting of a 6-month exercise protocol (two exercises
for stretching anterior shoulder musculature and three
exercises for strengthening posterior shoulder muscula-
ture) was effective in decreasing the shoulder pain that
interfered with functional activities.31 Elbow pain in people
with paraplegia is also fairly common and is often caused
by lateral or medial epicondylitis.
Visceral Pain
Visceral (nociceptive) pain refers to pain usually located in
the thorax, abdomen, or pelvis that is believed to be pri-
marily generated in visceral structures.20 This category
includes abdominal pain caused by fecal impaction, bowel
obstruction, bowel infarction, bowel perforation, cholecys-
titis, choledocholithiasis, pancreatitis, appendicitis, splenic
rupture, bladder perforation, pyelonephritis, or superior
mesenteric syndrome.
The presence of visceral pain is suggested by evidence
of visceral pathology on imaging or other testing that is
consistent with the pain presentation. Although the pain
is characteristically vague and poorly localized, tenderness
of the offending visceral structures on palpation of the
abdomen might be elicited, depending on the level and
completeness of injury. Visceral pain can be associated
with symptoms of AD, anorexia, altered bowel patterns
(e.g., constipation), nausea, or vomiting, any of which can
be more prominent than the pain itself. “Cramping,”
“dull,” and “tender” are common pain descriptors of vis-
ceral pain, and a relationship to food intake is often
present.
Other (Nociceptive) Pain
AD headache pain can be severe and usually is described
as “pounding.” It is most common in a person with an NLI
at or above T6. AD headache is associated with an elevated
blood pressure, and often with diaphoresis, piloerection,
cutaneous vasodilatation above the level of injury, brady-
cardia or tachycardia, nasal stuffiness, conjunctival conges-
tion, and mydriasis. AD is usually triggered by a noxious
stimulus caudal to the NLI, usually related to the bowel or
CHAPTER 49 Spinal Cord Injury 1131
bladder (e.g., bowel impaction or UTI). Treatment of AD
headache is discussed earlier in the Cardiovascular and
Autonomic System section.
Neuropathic Pain
At-Level Spinal Cord Injury (Neuropathic) Pain.
At-level SCI (neuropathic) pain refers to neuropathic pain
perceived in a segmental pattern anywhere within the der-
matome representing the NLI and/or within the three der-
matomes below this level and not in any lower dermatomes.
A necessary condition for classifying a pain as at-level SCI
pain is that a lesion or disease must affect the spinal cord
or nerve roots, and the pain is believed to arise as a result
of this damage. The pain can be unilateral or bilateral.
Neuropathic pain occurring in this distribution that cannot
be attributed to spinal cord or nerve root damage should
be classified as other (neuropathic).
The presence of at-level SCI pain is suggested by allo-
dynia or hyperalgesia within the pain distribution and by
the following pain descriptors: hot-burning, tingling,
pricking, sharp, shooting, squeezing, painful cold, electric
shocklike, and numb.20 It is often difficult to distinguish
between the two subcategories of at-level SCI pain, spinal
cord pain and radicular pain, because both are typically
involved in any traumatic SCI. Radicular pain is generally,
although not always, unilateral and radiating in a derma-
tomal pattern. At-level radicular pain is usually paroxys-
mal, whereas at-level spinal cord pain is typically constant.
When at-level SCI pain is associated with spinal instability
in which spinal movement exacerbates the pain, it is pre-
sumably more likely to be radicular pain.
Syringomyelia often presents initially with at-level
spinal cord pain, either on coughing or spontaneously. The
character of pain caused by syringomyelia is typically
burning or dull aching, although it can be sharp, electrical,
or stabbing, and can be localized either unilaterally or
bilaterally.
Below-Level Spinal Cord Injury (Neuropathic) Pain.
Below-level SCI (neuropathic) pain or below-level spinal
cord pain refers to neuropathic pain that is perceived more
than three dermatomes below the dermatome representing
the NLI. It might or might not be perceived within the
dermatome representing the NLI and the three derma-
tomes below the NLI. A necessary condition for classifying
a pain as below-level SCI pain is that a lesion or disease
must affect the spinal cord and that the pain is thought to
arise as a result of this damage. Neuropathic pain occurring
in this distribution that cannot be attributed to the spinal
cord damage should be classified as other (neuropathic).
The presence of below-level spinal cord pain is sug-
gested by the same pain descriptors mentioned for at-level
SCI pain.20 Allodynia or hyperalgesia can be present within
the pain distribution for people with incomplete injuries.
The distribution of below-level spinal cord pain is gener-
ally not dermatomal but regional, enveloping large areas
such as the anal region, the bladder, the genitals, the legs,
or commonly the entire body below the NLI. It is usually
continuous in presence, although the intensity of the pain
can fluctuate in response to a number of factors, including
psychological stress, anxiety, fatigue, smoking, noxious
stimuli below the level of injury, and weather changes.
1132 SECTION 4 Issues in Specific Diagnoses
Treatment of At-Level and Below-Level Spinal Cord
Injury (Neuropathic) Pain. Treatments of neuropathic
pain after SCI have historically not been shown to be par-
ticularly effective. However, a few oral pharmacologic
agents, namely pregabalin, gabapentin, tramadol, and
amitriptyline, have shown effectiveness for some in ran-
domized controlled trials for the treatment of neuropathic
pain after SCI.50 Also, although there are not many data
specific to the treatment of pain after SCI for other inter-
ventions, other medications are commonly prescribed,
including the selective serotonin and norepinephrine reup-
take inhibitors, opioids (oral, transdermal, and intrathe-
cal), and neurotoxins (intrathecal ziconotide). Modalities
including desensitization techniques for evoked pain,
massage, and especially exercise can also be beneficial.
Psychological interventions including education, cognitive-
behavioral therapy, relaxation, and especially hypnosis63
can allow people to manage this pain over the long term
and to minimize its impact on their lives. Neurointerven-
tional techniques such as surgical nerve root decompres-
sion and transforaminal epidural steroid injections for
radicular pain, and dorsal root entry zone microcoagula-
tion for spinal cord pain, can also be considered.27,47
Other (Neuropathic) Pain. Compressive neuropathy
pain occurs in a specific peripheral nerve distribution distal
to the root level and is attributed to compression of a
specific peripheral nerve or plexus of nerves. Symptoms
most often include either spontaneous or evoked numb-
ness or tingling in a specific peripheral nerve distribution.
This category includes median, ulnar, radial, and axillary
neuropathies in people with paraplegia. The signs and
symptoms of carpal tunnel syndrome (i.e., numbness or
tingling of thumb, index, or middle fingers; abnormal sen-
sation on testing; or numbness or tingling with provocative
tests) are common in people with paraplegia. This syn-
drome is thought to result from a combination of repeti-
tive trauma, as occurs with propulsion of manual
wheelchairs, and ischemia from repetitive marked increases
in carpal canal pressures, as occurs with push-up pressure
reliefs or transfers from one seating surface to another.54 A
higher risk for developing pain has been shown in those
who are overweight or use improper wheelchair propul-
sion biomechanics.17
Strategies of treatment and prevention of a compressive
neuropathy at the wrist include avoidance of weight-
bearing on a flexed or extended wrist by substituting a
handgrip for the flat placement of either hand on a surface
whenever possible. Other strategies include weight loss,
provision of the lightest possible wheelchair that meets the
needs of the individual, use of power and power-assist
wheelchairs, and instruction and training in an efficient
wheelchair propulsion pattern.94 This typically is a pattern
that minimizes the forcefulness and frequency with which
the wrist strikes the wheel (i.e., long and smooth arm
strokes). Side-to-side or forward-lean pressure relief tech-
niques should also be substituted for push-up pressure
relief techniques.
Spasticity
Spasticity is a syndrome of different components, includ-
ing a velocity-dependent increased resistance to passive
motion, involuntary muscle contractions or spasms, and
hyperreflexia. The involuntary muscle contractions result
from different muscles acting synergistically, typically in a
specific flexion or extension pattern. Although spasticity
can cause difficulty with mobility, positioning, and
comfort, and might even predispose to skin breakdown, it
can also be helpful for ambulating and performing ADL.
An example is allowing individuals to bridge their buttocks
to allow them to pull their trousers over their buttocks. The
decision of whether to treat spasticity, and how to do so,
should be based on an evaluation that has identified all
the activities and other medical issues that are helped or
hindered by one or more of the components of spasticity.
Activities that need to be evaluated, at least through self-
report and perhaps by observation, include bladder man-
agement, sexual functioning, sleep, dressing, bathing,
positioning, wheelchair mobility, and ambulation. Medical
issues that need to be evaluated include the presence of
pressure ulcers and pain, because spasticity can predispose
to both and can be the underlying factor behind the devel-
opment of these secondary conditions. Determining the
specific patterns of involuntary muscle contraction is also
important because nonsystemic treatments of spasticity
depend on the specific pattern. For example, an intramus-
cular injection of alcohol or botulinum toxin needs to be
targeted to a specific offending muscle to be effective.
Because the different components of spasticity often do
not correlate with each other, different assessment tools
that address the different components should also be per-
formed during any evaluation. Common assessment tools
include 5-point ordinal scales for grading resistance to
passive movement, such as the Ashworth Scale and a modi-
fied form of this scale, and ordinal ranking scales that rate
the frequency of significant involuntary muscle contrac-
tions per unit time.
Treatment of Spasticity
Stretching of spastic muscles is the mainstay of treatment
of spasticity for virtually all people with SCI. Steady static
stretching, to the limits of the ROM of a joint, has been
shown to result in a reduction of reflex activity that can last
for several hours after the exercise. ROM exercises should
be performed regularly on all affected joints by members
of the rehabilitation team, support staff, or family members,
after instruction in proper technique. Proper positioning,
in bed or in wheelchairs, can effectively control increased
muscle tone, as well as provide a prolonged static stretch
to spastic muscles. An example of this is sleeping in a
prone position to provide a sustained stretch of hip and
knee flexors. The increased tone in the trunk encountered
while sitting in a wheelchair can be improved by slightly
tilting the seat or by adding a wedge. The use of positioning
orthoses or serial casts can improve spasticity by placing
the affected muscle in a position of sustained stretch. An
example of this is using a padded ankle-foot orthosis or
cast to maintain a spastic ankle plantar flexor in the neutral
position. Passive standing on a standing frame or tilt table
can also provide a significant stretch to the hip, knee, and
ankle plantar flexors.
Many pharmacologic options are available for the treat-
ment of spasticity. Many practitioners consider oral
baclofen to be the first-line pharmacologic treatment for
spinal spasticity. Baclofen is a structural analog of

gamma-aminobutyric acid (GABA), the main inhibitory
transmitter of the spinal cord, and binds to GABAB recep-
tors. Starting doses are typically 5 to 10 mg given 2 to 4
times per day, with gradual increases as clinically indicated.
Although the maximum recommended dose is 80 mg/day,
significantly larger doses have been both well tolerated and
effective. Adverse effects of baclofen include fatigue and
dizziness, and seizures can occur with abrupt withdrawal.
Diazepam and other benzodiazepines bind to the GABAA
receptor. Benzodiazepines can cause physical dependence,
as well as lethargy and diminished concentration. If used
clinically, it can be difficult to wean people off these agents,
and weaning should be very gradual. Tizanidine hydro-
chloride is a central alpha-2-adrenergic agonist that has
been shown to be effective in treating spasticity after SCI.
Adverse effects of tizanidine include sedation and liver
function abnormalities.
When only a few specific muscles are affected by prob-
lematic spasticity, targeted injections of these muscles with
a neurotoxin (e.g., botulinum toxin) or an alcohol (e.g.,
benzyl alcohol [phenol] or ethyl alcohol) can be carried
out. These injections work by weakening these muscles and
can be very effective in reducing the problem spasticity.77
Targeting specific peripheral nerves with an alcohol can
provide similar effectiveness. Botulinum toxin injected
into a muscle binds to receptor sites on the presynaptic
nerve terminal in the neuromuscular junction, inhibiting
the release of acetylcholine and preventing neuromuscular
transmission. Alcohols injected perineurally or directly
into muscles destroy nerve axons and muscle in a nonselec-
tive manner. Needle electrical stimulation to localize motor
points or peripheral nerves, or electromyography to iden-
tify motor end plates, can improve the effectiveness of the
injections. The clinical effect obtained by local injection of
neurotoxin or alcohols depends on several factors, includ-
ing the dose administered, the size of the muscle injected,
and the severity of spasticity of the targeted muscle. The
clinical effect of a botulinum toxin injection can be noted
within 2 to 3 days and persist for 3 to 6 months, whereas
the clinical effect of an alcohol injection is more variable,
with reported effectiveness persisting from 1 month to
several years. Local destruction of tissue by injection of an
alcohol can be painful in people with preserved sensation,
and paresthesias can be induced by destruction of a sensory
nerve. Botulinum toxin does not typically cause pain. Alco-
hols, however, are significantly less costly than botulinum
toxins. Injections seem to be most effective when com-
bined with an effective stretching program of the affected
muscles.
The administration of baclofen intrathecally is the most
effective treatment for severe, generalized spasticity in
people with SCI.81 Baclofen can be delivered intrathecally
through a catheter that extends from the intrathecal space
out through the dura and spine, and through a subcutane-
ous tunnel to a battery-driven infusion pump located in a
subcutaneous pocket in the abdomen. The entire system is
implanted, and there are no external components. Dosage
adjustments are made by radiotelemetry using a handheld
computer. Pump reservoir refills are performed percutane-
ously. Several different modes of drug delivery are avail-
able, including one that allows different rates of baclofen
infusion at different times of the day. Candidates for place-
ment of an intrathecal pump include those people whose
CHAPTER 49 Spinal Cord Injury 1133
spasticity is uncontrolled by pharmacologic and noninva-
sive treatments, and who are reliable enough to consis-
tently undergo regular pump refills. To confirm efficacy
and appropriateness before a pump is implanted, the can-
didate usually receives an intrathecal bolus test dose of
baclofen delivered via lumbar puncture. If the test dose is
deemed successful and a pump is implanted, the intrathe-
cal baclofen dose is gradually titrated until the desired
benefit is obtained. Effective maintenance dosage ranges
are fairly variable among individuals. An expected decrease
in spasticity with intrathecal baclofen as measured by Ash-
worth scores is a reduction from 3 to 4 at baseline to 1 to
2 when the dose is optimally titrated.81
Musculoskeletal Conditions
A variety of musculoskeletal conditions can affect people
with SCI and cause pain and reduce functional ability.
Most of these conditions are preventable, but when they
occur successful management can be very difficult.
Contractures
A contracture is a common finding in the paralyzed limbs
of people with SCI. A contracture refers to a fixed stiffness
of a soft tissue that limits joint motion in a particular
direction. Joint contractures can prevent achievement of
full functional capacity, inhibit hygiene, lead to abnormal
positioning with resultant pain or pressure ulcer develop-
ment, and prevent use of a joint in the future should
motor recovery occur in a delayed manner. The primary
cause of contracture is prolonged joint immobilization,
but secondary factors include edema, muscle imbalance,
spasticity, and local trauma. Certain joints seem more
prone to develop contractures than others. Upper limb
contractures develop primarily in people with tetraplegia
and can interfere significantly with performance of self-
care functions. At the shoulder, contractures limiting
adduction and internal rotation are very common. These
contractures can limit transfer ability, grooming, dressing,
and positioning in the prone position. Elbow flexion con-
tracture often develops in people with C5 tetraplegia
because of muscle imbalance, and interferes with the
ability to transfer, the ability to propel a wheelchair,
feeding, and grooming. Flexion contracture at the wrist
and fingers can also interfere with performance of self-care
activities, although contractures of the finger flexors in
people with C6 tetraplegia can permit a grasp through the
tenodesis action. In the lower limbs, flexion contractures
of the hips and knees interfere with proper bed position-
ing, transferring, and dressing, and increase the risk for
developing pressure ulcers. Adduction contractures of the
hips hinder perineal care. All of these contractures, as well
as plantar flexion contracture of the ankles, interfere with
comfortable standing and ambulation.
Contractures are best prevented by proper positioning
in bed, by performing passive ROM and stretching exer-
cises of all joints at least daily, and sometimes by use of
prophylactic static splints. Additional preventive measures
include effective management of spasticity and edema.
Edema should be managed by elevation, massage, and
compression garments. Once a contracture is present,
aggressive ROM exercises should be started, which often
require pretreatment with pain medications. In addition,
1134 SECTION 4 Issues in Specific Diagnoses
static and dynamic splints are used to maintain the maxi-
mally corrected position. Serial casting with adequately
padded splints can be applied. Spasticity can be treated
with medications administered orally or intrathecally, or
by performing nerve blocks. Surgical interventions are
occasionally required, such as tenotomies and tendon-
lengthening procedures.
Fractures
Major trauma can result in a fracture of any bone, but in
people with SCI, fractures in the paralyzed lower limbs
without major trauma are of particular concern. Significant
osteoporosis develops in the lower limbs during the first
few months after SCI, which makes the bones brittle and
prone to fractures. Osteoporotic fractures are both associ-
ated with increased risk for hospitalization and mortality
in older individuals with SCI.22 Fracture incidence has been
shown for men with complete paraplegia to increase with
time after SCI, from 1% within the first year to approxi-
mately 5% per year after 20 years.125 Most fractures are
caused by a fall during transfer activities, followed in fre-
quency by fractures caused by ROM exercises and those
without known cause. The most common site of fracture
is the supracondylar region of the femur. The diagnosis of
a fracture in an anesthetic limb can be a challenge. Most
patients complain of a recent onset of unilateral leg swell-
ing, not feeling well, and having a low-grade fever. On
examination, a swelling and a bruise might be present. If
the fracture is severe, a deformity or crepitus can be present.
Traditional fracture management is indicated for people
with SCI who are ambulatory. Treatment of fractures in
people with SCI who are nonambulatory is usually non-
operative for nondisplaced or minimally displaced lower
limb fractures. The goal of treatment is to preserve prefrac-
ture function, avoid complications, and secure proper
healing and alignment. Because most people with SCI are
sedentary and not ambulatory, some shortening and angu-
lation at the fracture site is acceptable. However, rotational
deformity should be avoided because it would prevent
proper foot placement on the wheelchair’s footrest. Despite
the osteoporosis in the paralyzed limb, bone healing
usually occurs readily, often with exuberant callus forma-
tion. Most fractures are treated with a soft, well-padded
splint or brace that keeps the limb in extension. The anes-
thetic skin should be inspected frequently. Circumferential
casting and external fixation are associated with a high risk
and complication rate in this population and are best
avoided. For displaced fractures, however, surgical fixation
is often indicated.
Osteoporotic extremity fractures occur in approximately
15% of children and adolescents with SCI, a rate higher
than in adults. Prevention is challenging because of the
risk-taking activities of children and adolescents. Weight
bearing, adequate nutrition, and sunlight exposure (for
vitamin D) should be encouraged in children as in adults.
Heterotopic Ossification
Heterotopic ossification (HO) is true bone in extraskeletal
ectopic sites (Figure 49-17). For unknown reasons, plu-
ripotent mesenchymal cells in soft tissues differentiate into
osteoblasts and other cell lines involved with bone forma-
tion.93 These cells produce an extracellular osteoid matrix,
FIGURE 49-17 Heterotopic ossification of the hip.
which is then calcified through the deposition of hydroxy-
apatite and remodeled by the coupled actions of osteo-
blasts and osteoclasts into well-organized bone over several
months.93
HO has been reported to occur in 20% to 30% of people
with SCI, with approximately 10% of those with HO devel-
oping restriction of joint ROM sufficient to significantly
interfere with mobility and self-care.106 Most commonly,
HO develops within 4 months of SCI, and incidence rates
decline thereafter.108 HO most often develops around the
hips (90%), but other locations where it can appear include
the knees, shoulders, and elbows.
HO usually presents clinically as a warm local swelling
adjacent to a joint. This is followed by a more generalized
edema of the affected paralyzed limb. Low-grade fever can
be present and, in time, joint mobility can be reduced. The
differential diagnosis at this early stage includes DVT, infec-
tion, trauma, and impending pressure ulcer.
The serum alkaline phosphatase level during the acute
stage is elevated, and a bone scan or MRI of the area is
positive.108 Plain films show normal findings because of yet
insufficient local deposition of calcium. As the HO matures,
it becomes more visible on plain films, but the serum
alkaline phosphatase level and radioisotope uptake gradu-
ally decrease.
Prophylactic use of NSAIDs to prevent HO has been
shown to be effective, although they are generally not
administered for this purpose given the relatively low inci-
dence of disabling consequences of HO and the potential
adverse effects of treatment with NSAIDs, including the
potential for inhibiting bone healing after fracture.108 If
detected, however, treatment of established HO should
begin promptly and is aimed at halting the process, as well
as maintaining joint ROM and function. Etidronate, a
bisphosphonate, is believed to inhibit the mineralization
of organic osteoid, thereby preventing, when given for up
to 6 months, soft tissue ossification in most of those people
having only bone scintigraphic evidence of HO. Less than
half the people with radiographic evidence of HO, however,
show a response with inhibited soft tissue ossification.4

Radiation therapy for HO is effective, but it is uncom-
monly used because of unknown long-term risks. Gentle
ROM exercises are generally recommended with forceful
stretching discouraged.108 Surgical resection of HO can be
done when joint mobility is severely restricted, when HO
interferes with self-care and sitting in a wheelchair, or both.
It should also be considered when HO contributes to the
development of pressure ulcers or causes compression of
nerves and blood vessels. The goal of surgery is not to
resect the entire HO but to restore joint motion and func-
tional skills. The surgical procedure usually consists of
wedge resection and creation of a pseudarthrosis. The risk
for postoperative recurrence can be reduced by administer-
ing etidronate, antiinflammatory agents, radiation therapy,
and by performing ROM exercises.5
HO has been reported to occur in less than 5% of chil-
dren and adolescents, a significantly lower percentage than
occurs in adults. It usually presents on average after 1 year
postinjury. Bisphosphonates should be used with caution
because there is a risk of developing rickets. Surgery is
indicated if there are significant functional deficits, but
postresection radiation is less commonly used because of
concerns regarding the long-term consequences.
Hip and Spine Deformities in Children
The growing child with SCI can experience a variety of
additional orthopedic problems, the most significant of
which are spine deformity and hip instability. The preva-
lence of scoliosis can be as high as 98%.12 Close observa-
tion with annual spine radiography is essential. The use of
a prophylactic thoracolumbar orthosis is recommended by
many, and almost always when curvatures exceed 20
degrees. Surgical spinal fusion can significantly affect future
functional skills and is therefore best avoided. Surgery can
be necessary, however, for curvatures greater than 40
degrees. Hip instability develops most frequently in chil-
dren injured at an early age, and is usually associated with
muscle imbalance caused by spasticity, or by underdevel-
opment of the femoral head and acetabulum that occurs
because of flaccid hip muscles. Nearly all children injured
younger than 5 years of age and over 80% of those injured
younger than 10 years of age develop hip instability. Unsta-
ble and dislocated hips do not interfere with sitting or
ADLs. However, the high incidence in hip dislocation in
children often leads to pelvic obliquity and secondary pres-
sure ulcers. Treatment is usually directed toward preven-
tion of contractures and creating bone stability by
prophylactic application of a hip abduction orthosis.12
Summary
SCI is a catastrophic event that results in physical disability
and impaired function of various organ systems. Despite
decades of intense research, a cure still does not exist. Great
progress has occurred, however, in the management of SCI
and its associated conditions. Because of advances in clini-
cal practice, people with SCI have increased life expectancy.
Morbidity is also reduced, as reflected in reduced hospital
lengths of stay after SCI and fewer rehospitalizations during
follow-up years. Spasticity can be effectively managed, and
male fertility is now much improved. Application of
CHAPTER 49 Spinal Cord Injury 1135
modern technology has enhanced the function and quality
of life of many people with SCI. The International Stan-
dards for Neurologic Classification of SCI has been adapted
worldwide as the preferred assessment instrument of
people with SCI seeking clinical care, and for those partici-
pating in research studies. This has been supplemented by
the Autonomic Standards for Classification of SCI. In addi-
tion, multiple international SCI data sets (available at
www.iscos.org.uk/international-sci-data-sets) have been
developed to standardize the collection and reporting of a
minimal amount of information necessary to evaluate and
compare results of published studies from around the
world. Clinical practice guidelines such as those that
have been developed by the Consortium of Spinal Cord
Medicine (available at www.pva.org) have also led to
greater conformity and quality of care for people with
SCI. Development of comprehensive multidisciplinary
educational websites such as elearnSCI (accessed through
www.elearnSCI.org), an initiative of the International
Spinal Cord Society, which had been accessed more than
10,000 times within 2 years of its introduction, promises
to further raise the level of knowledge of SCI among clini-
cians throughout the world. People with SCI have estab-
lished influential organizations and peer support networks
that have advanced their rights and made health-related
information widely available. Current wheelchair designs
and seating systems are far superior to older models and,
respectively, permit increased mobility and allow safe
sitting for much longer periods. People with disability also
now use computers, tablets, and smartphones in their daily
lives for recreational, educational, and vocational purposes
with great success.
Advances in clinical care are not a justification for com-
placency. The health and function of people with SCI are
still at risk without proper medical and nursing care, social
support, appropriate equipment, supplies, and medica-
tions. Too many continue to experience problems related
to urinary and bowel dysfunction. Many still have chronic
pain that interferes with their quality of life. We must
increase our understanding of the value of physical exercise
and proper diet to reduce the high prevalence of obesity,
diabetes, and CVD in people with SCI. Ambulation and
complete self-sufficiency are impossible for too many.
Social support is often lacking, and relatively few return to
work. To solve these and other remaining issues that affect
the wellness of people with SCI, private, state, and federal
support of health services is needed to improve the health
care of people with SCI, as well as a better social support
system and a comprehensive disability policy.
The ultimate goal of people with SCI and those who
care for them is to find a cure for this condition, which is
to reverse the neurologic damage of SCI. Until that elusive
goal is reached, people with SCI, their families, their care-
givers, and society at large must work together to eliminate
barriers to health care and ensure their full participation
in all aspects of community life.
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