Handbook of Clinical Neurology, Vol.

110 (3rd series)

Neurological Rehabilitation
M.P. Barnes and D.C. Good, Editors
# 2013 Elsevier B.V. All rights reserved

Chapter 35

Traumatic spinal cord injury

HEINRICH BINDER*
Department of Neurology, Otto Wagner Hospital, Vienna, Austria

INTRODUCTION in considerable additional disability. If one considers

The after-effects of traumatic spinal cord injury (SCI) are
clearly significant and catastrophic. Ostensibly, what the
observer sees is the paralysis. For those affected, it can also
mean pain, incontinence and a host of other hidden dis-
abilities. Medical consequences of SCI are not confined to
the spinal cord; many other organs are involved, resulting
in a variety of additional problems. It must not be forgot-
ten that SCI has emotional, psychological, social, and eco-
nomic consequences that affect not only the person with
the injury but also their partner, family, and friends.
EPIDEMIOLOGY
One of the first international epidemiological studies on
SCI was carried out by Blumer and Quine (1995), who
estimated the incidence to be between 13 and 33 cases
per million per year and the prevalence to be 110 to 1120
per million population. The incidence of SCI is at its highest
among adolescents and young adults, with half of all cases
falling into the 1630-year age group (DeVivo et al., 1980;
Stover and Fine, 1986). Certainly some of the most com-
mon causes of SCI could be reduced by introducing pre-
ventative measures (US Department of Justice, 1995;
Simon et al., 2001). The life expectancy of patients with
SCI has increased in the course of the last few decades.
In 1983 the average life expectancy of patients aged be-
tween 25 and 34 years was 33 years. In 1997 it had increased
to almost 38 years (McColl et al., 1997). Wyndaele and
Wyndaele (2006) found that the incidence of SCI lies
between 10.4 and 83 per million population per year. Only
a few publications report on its prevalence, and are
restricted to the USA, Australia, and Scandinavia. It has
been estimated that 40
60% of people who have a SCI
also suffer a closed head injury; in one study up to
74.2% of patients had a closed head injury (Davidoff
et al., 1985, 1988a,b; Tolonen et al., 2007). This results
that patients with mild TBI are still complaining of
considerable problems even after 1 year, one can
easily appreciate the poor outcome in those with associated
brain injury (Thornhill et al., 2000; Macciocchi et al., 2004).
MANAGEMENT
Rehabilitation should start in the intensive care unit and
any delay will have negative effects on the patients out-
come and will prolong the period of rehabilitation
(Scivoletto et al., 2005).
The acute traumatic SCI should be treated in a center
for trauma patients with experience in SCI. If this is not
possible, then one should try to transfer the patient as
soon as possible to such an institution. Whilst the modus
operandi for stabilizing the vertebral column is no longer
an issue, because it reduces length of stay and pulmo-
nary complications among other things, a consensus
on decompression of the spinal cord has not been
achieved (Schinkel and Anastasiadis, 2008). Fehlings
and coworkers believe that decompresion during the
first 24 hours, especially in patients with an incomplete
transverse lesion of the cord, improves the outcome. If it
is not performed early, then it makes no real difference
whether an operation takes place after 48 hours or later
(Fehlings and Perrin, 2005). In any case, fast mobiliza-
tion must be the primary goal.
ASSESSMENT
The most practical classification of SCI is the American
Spinal Injury Association (ASIA) system, which defines
the level of the injury and complements the modified clas-
sification according to Frankel (Ditunno, 1992; Ditunno
et al., 1994; Maynard et al., 1997) (Fig. 35.1, Table 35.1).

ohe
Otto
*Correspondence to: H. Binder, M.D., Professor of Neurology, Head of Neurological Department, SMZ Baumgartner H
Wagner Spital, Baumgartner Hohe 1, A-1145 Wien, Austria, E-mail: heinrich.binder@wienkav.at
412 H. BINDER

Fig. 35.1. American Spinal Injury Association standard neurological classification of spinal cord injury.

Table 35 1 internationally used. This method is a widely recom-

ASIA impairment scale
mended supplement for incomplete as well as complete
SCI together with the ASIA protocol (Itzkovich et al.,
ASIA Impairment Scale 2007; Wirth et al., 2008).
A complete No sensory and motor function Recording and documentation of autonomic disor-
within and below S4S5 ders following SCI are regrettably very often either for-
B incomplete Only sensory function below and gotten or neglected. Alexander and coworkers of an
inclusive S4S5
international working group submitted, in 2009, a stan-
C incomplete Motor function below lesion partially
dard for the documentation of autonomic disorders
preserved, more than 50% of core
muscles MRC grade <3 (Alexander et al., 2009) based on the International SCI
D incomplete As C but at least 50% of core muscles Data Sets (Biering-Sorensen et al., 2006; DeVivo et al.,
MRC grade  3 2006) in an abbreviated version of the aforementioned
E normal scales.
SCI usually refers to the functional interruption of
the neural tracts between supraspinal centers and the
As a supplementary assessment, the Functional Inde- spinal cord below the lesion; it rarely involves complete
pendence Measure (FIM) is also regarded as valuable, severance of the spinal cord. Incomplete SCI includes
although not developed especially for SCI a broad spectrum of infralesional residual functions
(Ottenbacher et al., 1996; Middleton et al., 1998, 2006; from minimal sacral function to nearly normal function.
Meiners et al., 2004). Five typical syndromes are recognized: central
The Spinal Cord Independence Measure (SCIM) in its cord syndrome, Brown
Sequard syndrome, anterior
present revised version (Catz et al., 1997, 2001) is an cord syndrome, conus medullaris syndrome, and cauda
alternative specially developed for SCI and is also equina syndrome (Table 35.2).
 TRAUMATIC SPINAL CORD INJURY 413
Table 35 2 During the postacute phase of rehabilitation, MRI is used
The five typical syndromes of SCI to inform the clinician about worsening of symptoms and
signs. In a very high percentage of cases (43%) a syrinx is
Central cord syndrome Exclusively after cervical found. Less frequently, extended atrophy (26%) or mye-
spinal cord injury, more lomalacia (21%) can be found. When one discusses the
impairment of motor possibilities of causal connections, one has to keep in
power in the upper than in
mind that the vast majority of patients in a stable clinical
the lower extremities with
state also show various pathological MRI findings (Potter
varying degrees of
sensory loss and sacral and Saifuddin, 2003).
sparing
BrownSequard syndrome Ipsilateral spastic paresis, PROGNOSIS
loss of proprioceptive
sensation with sensory It is important to have an early prognosis in order to
ataxia and contralateral prepare for rehabilitation without delay. Factors such
loss of pain and as the level of the lesion, whether the lesion is complete
temperature sensations or incomplete, and the grade of the initial paresis are
Anterior cord syndrome Flaccid paralysis at level of very important for prognosis (Ditunno et al., 2002).
lesion and spastic paresis
The greatest improvement can be expected within the
below, loss of bowel and
bladder function,
first 36 months with all types of SCI, although an im-
proprioceptive sensations provement of motor functions and the clinical level of
spared lesion is still possible in 20% of cases even after a couple
Conus medullaris Saddle distribution of of years. Apart from the level of the lesion, important
syndrome bilateral symmetrical indicators for improvement are the muscular strength
dissociation of sensation, present after 72 hours and the pinprick sensitivity around
not marked symmetrical and below the lesion.
motor loss, urinary and Nearly all patients with complete tetraplegia follow-
faecal incontinence, ing a cervical lesion improve over the course of 1 year
erection and ejaculation by one segment. In 3040% of cases, muscles improve
impaired
in strength from 0/5 to 3/5. Improvement of more than
Cauda equina syndrome Saddle complete sensory
two segments is rarely seen. Only 10% of the muscles
loss may be
asymmetrical marked with an initial strength of 0/5 later attain the level 3/5.
sometimes asymmetrical Between 4% and 10% of those with an initially complete
distal weakness, muscular lesion improve in about 30 days from ASIA impairment
atrophy, level A to B. After 1 year a further 5.6% improve and
Sphincter disturbance, after 5 more years a further 2.1% improve. Patients with
sexual functions less incomplete tetraplegia have twice as much chance of
impaired motor recovery of the upper extremities but a very
variable chance as far as the legs are concerned. In cases
of complete paraplegia the prognosis is better the lower
the level of the lesion. Fifteen percent of patients with a
Electrophysiological methods are increasingly used in lesion between T9 and T11 and 55% with a lesion below
order to obtain objective data to judge SCIs, especially in T12 improve muscular strength in their legs, mainly
the posttraumatic phase, for example the Hoffmann re- proximally. In the event of incomplete paraplegia,
flex or evoked potentials motor as well as sensory. 80% of patients will regain strength of at least 3/5 after
Their value in predetermination is not that different 1 year in the muscles of the hip region and the extensors
from a clinical assessment, but they can be used as an in the knee (Kirshblum et al., 2007).
additional tool (Xie and Boakye, 2008).
In the very early phase, radiological techniques are im-
portant. Magnetic resonance imaging (MRI) has proved
POSTTRAUMATIC SYRINGOMYELIA
to be the standard method to localize damage and assess The interval between SCI and the appearance of the
the severity of the damage and thereby arrive at a progno- symptoms of syringomyelia is between a few months
sis (Tewari et al., 2005; Boldin et al., 2006). Computed to- and up to 34 years (El Masri(y) and Biyani, 1996). The
mography (CT) and plain radiography are used in defining incidence of posttraumatic syringomyelia lies between
the bony anatomy of spine (Lammertse et al., 2007). 0.3% and 3.4%. Using MRI, in nearly 51% of the cases
414 H. BINDER
confirmation can be obtained of spinal cysts following an
SCI. In very rare cases surgical intervention is necessary.
A syringomyelia is called such only when the cyst extends
over at least two segments (Umbach and Heilpom, 1988).
It appears nearly twice as often with a complete as with an
incomplete SCI and is much more common in thoracic
and lumbothoracic lesions. Its pathogenesis is not yet clear
(Dworkin and Staas, 1985; Williams, 1990a). One should
consider the diagnosis of syringomyelia when the patient
has an ascending lesion. If pain occurs, or hyperhydrosis,
or spasticity, these symptoms will usually become
worse with coughing or laughing, etc. (Stanworth,
1982). Improvement is obtainable in 85% of cases through
drainage and shunting (Bilello et al., 2003).
SPINAL SHOCK
During the phase of acute SCI, especially after cervical
cord lesions, there is often a neurogenic as well as a spi-
nal shock. The first is defined as hypotension, followed
by hypoperfusion of the spinal cord, whilst spinal shock
usually implies sensory loss and motor paralysis and, in
the very beginning, a loss of spinal reflex activity below
the lesion (Hall, 1850). The latter will recover in distinct
phases: (1) areflexia/hyporeflexia; (2) initial reflex re-
turn; (3) early hyperreflexia; and (4) late hyperreflexia
(Ditunno et al., 2004).
The early phase of spinal shock is dominated by an
uninhibited vagal parasympathetic drive. This may lead
to bradycardia, which can be aggravated by stimulation,
for instance through deep tracheal suction, and can even
lead to cardiac arrest (Bilello et al., 2003). Some patients
also have orthostatic hypotension; therefore early mobi-
lization in this phase is often problematic. Orthostatic hy-
potension may in cases of biomechanical stability lead to
worsening of an incomplete transverse lesion of the cord
(El Masri(y), 1993). In addition, early mobilization in
patients with complete cervical or upper thoracic trans-
verse lesion of the cord will often impair their vital
capacity (Cameron et al., 1995). The decrease in oxygen
saturation together with orthostatic hypotension can be a
hindrance to the process of rehabilitation. Conservative
methods of treatment consist of laying the patient in bed
and only elevating with the help of a tilt table, the use of
compression stockings, abdominal binders, and other
similar devices. Salt tablets and adrenergic agonists
can also be administered. With the return of spinal
reflexes, an autonomic dysreflexia (Krassioukov et al.,
2003) may also develop.
AUTONOMIC DYSREFLEXIA
Autonomic dysreflexia (AD) appears as a reaction to a
stimulus below the lesion and can lead to an uninhibited
sympathetic activity, as a result of lack of modulation
from higher cerebral centers. During the first year, about
92% of patients with SCI show primary signs of AD
(Teasell et al., 2000).
Typical triggers for AD are overdistended bladder,
detrusor-sphincter dyssynergia, kidney and bladder
stones, infections of the urogenital tract, bowel impac-
tion, pressure ulcers, menstrual cramps, and muscular
cramps. The first steps in helping the patient must be to
sit them upright, open tight-fitting clothes, and then treat
with antihypertensives. The cause of the event should be
etablished and eradicated. It should be kept in mind that
any autonomic dysreflexia can eventually increase blood
pressure. For example, complete SCIs above T6 showed in
the course of a routine bowel program an increase of sys-
tolic pressure of 20% in all cases, and up to 40% in about
70% of cases (Kirshblum et al., 2002).
BLADDER
A detrusor areflexia exists during the phase of spinal
shock. Therefore, in the early days, a urethral indwelling
catheter is normally required, which bears the risk of bac-
teriuria, with all its complications. In about 8% of cases, a
transient bacteremia (Sullivan et al., 1973) can appear
immediately after insertion. At 4 weeks after insertion,
bacteriuria is found in about 15%. Therefore the indwelling
catheter should be removed after about 2 weeks and chan-
ged to clean intermittent catherization (CIC) or, if possi-
ble, clean intermittent self-catherization (CISC), thereby
reducing the frequency of infections of the urinary tract
(Dewire et al., 1992). Forty percent of patients given an
indwelling urinary catheter who then died were found to
have pyelonephritis on autopsy (Warren, 1987). Alterna-
tively, a self-contained voiding using either penile sheets
or pads can be carried out. When, after 6
8 weeks, the
activity of the detrusor sets in again, a triggered voiding,
for instance with suprapubic tapping, may be possible.
Nowadays, use of the Crede maneuveris not advised
because of worsening of the vesico-uretheral reflex, nor
the Valsalva maneuver, because of the risk of triggering
autonomic dysreflexia. When the urethral catheter cannot
be removed, patients should move on to a suprapubic
catheter. In the next 36 months it is advisable to
perform a baseline investigation of the urinary tract
with regular frequency
volume charts, ultrasonography
of kidneys and bladder, creatinine clearance, and
video-urodynamics and optional renography (DMSA or
MAG 3) (Abrams et al., 2008).
In the long term there are usually several options: con-
tinence, reflex voiding, CIC/CISC, and indwelling cath-
eter or urostomy. Combination therapy with drugs such
as botulinum toxin is possible, as are invasive therapies
such as dorsal rhizotomy and sacral anterior root stimu-
lation or augmented cystoplasty.
 TRAUMATIC SPINAL CORD INJURY
It is interesting to note that the number of patients
with suprapubic tapping has halved over the years
(57% versus 31%) whilst the use of CIC and CISC has tri-
pled (13% versus 39%) (Hansen et al., 2004). Neverthe-
less, nearly 50% of patients with SCI sustained more
than 10 years previously report some kind of inconti-
nence between once a day and once a week (Hansen
et al., 2009). Patki and coworkers report that 47% of their
patients, who were initially without any problems, dete-
riorated over the years so that they eventually had to use
a urinary catheter. On the other hand, 25% of patients
with CSIC eventually did not need a catheter (Patki
et al., 2006). It is essential to have check-ups performed
by SCI and/or urology specialists.
BOWEL
Nearly all patients with SCI are confronted with neuro-
genic bowel with constipation and incontinence. It is an
emotionally depressing disorder which can lead to social
withdrawal, and so the management of bowel function
should start as early as possible (Consortium for Spinal
Cord Medicine, 2007). The approach with neurogenic
bowel largely depends on whether the upper or lower
motor neuron is damaged.
For upper motor neuron lesions, the bowel program is
ideally implemented three times a day (Consortium for
Spinal Cord Medicine, 1998); it consists of digital stim-
ulation, high fiber intake, oral medication, and rectal
evacuation. A lesion of lower motor neurons leads to in-
continence because of reduced sphincter tone.It should
be checked several times a day and stools removed man-
ually if necessary.
DYSPHAGIA
Up to 30% of patients with tetraplegia suffer from dys-
phagia at the end of acute therapy and at the beginning of
rehabilitation. This mainly concerns cervical SCIs with or
without surgical intervention (Smith-Hammond et al.,
2004). Therefore it is advisable in the initial phase to
insert a nasogastric tube in order to decrease the risk
of aspiration until another form of enteral nutrition
can be found. In the longer term percutaneous endo-
scopic gastrostomy (PEG) feeding is a safer option for
those with continuing dysphagia.
DEEP VEIN THROMBOSIS
Deep vein thrombosis (DVT) is at its highest risk during
the first 3 months (Bendinelli and Balogh, 2008). The
risk factors for DVT are the combination of hyper-
coagulability, stasis, and venous inner wall injury (Aito
et al., 2002). The incidence is greater than 50%. The
commonest site is the calf (Nicolaides et al., 1971) and
415
spread of DVT proximally only occurs in 20% of cases;
these proximal DVTs cause embolism of the lung in
8
10% of cases (Chiou-Tan et al., 2003; Geerts et al.,
2004). The clinical diagnosis of DVT is not an easy one.
The following tests are recommended: for screening and
especially in the proximal region, the very sensitive venous
ultrasonography; the more nonspecific D-dimer assay;
and for confirmation, if necessary, invasive venography.
A 2009 meta-analysis recommends as prophylaxis for
DVT low-molecular-weight heparin and a higher ad-
justed dose of unfractionated heparin together with ex-
ternal pneumatic compression. In high-risk patients one
should consider vena cava filtration, and with acute DVT
enoxaparin is recommended (Teasell et al., 2009).
PAIN
Pain can develop as a result of injuries to musculoskel-
etal structures, like bones, ligaments, muscles, interver-
tebral disks, and facet joints. Normally this pain,
activated by the local nociceptors, is confined to the area
of the lesion, although sometimes it can spread. Over-
stress, for instance in the region of the shoulder and
arms, can cause chronic musculoskeletal pain (Van
Drongelen et al., 2006). The overworked upper extrem-
ity syndrome has been known for a long time and is
found in up to 51% of cases. In 43% it can even disturb
sleep (Nicholas et al., 1979). Pain in hands and wrists fre-
quently appears in patients who over many years have
had to use crutches or wheelchairs (Blankstein et al.,
1985). In 68% of paraplegics, pain can be found some-
where in the region of the upper extremities and 30%
complain of shoulder pain during transfer (Gellman
et al., 1988). In paraplegics compression neuropathies
can develop in the upper extremities.
Visceral pain comes from visceral structures and their
irritations, such as, for instance, infections of the urinary
system and dysfunction of the bowel. A conclusion can-
not be drawn about abdominal pain from the level of the
lesion (Finnerup et al., 2008).
With SCI we find two kinds of neuropathic pain: (1)
segmental pain in the dermatome of the lesion and up
to three segments below (Widerstrom-Noga et al.,
2008); and (2) more diffuse pain below the lesion and/
or the three segments underneath, which can eventually
appear months or years afterwards and has been given
various names
central pain, phantom pain, deafferen-
tiation pain (Siddall et al., 2003). It is a permanent pain,
varies according to the patients mood, and is not depen-
dent upon position or movement. This pain can be trig-
gered by sudden noise or infections of the urinary tract,
constipation, etc. Regrettably, one cannot, by describing
the character of this pain, distinguish between neuro-
pathic and musculoskeletal pain (Putzke et al., 2002).
416 H. BINDER
Neuropathic pain at the height of the lesion or below can
be accompanied by allodynia or by hyperpathia in the
affected dermatomes.
Treatment consists of education, transcutaneous
electrical stimulation, tricyclic antidepressants, anticon-
vulsants, relaxation training, intrathecal medication, and
epidural stimulation; eventually destructive surgical in-
tervention may be needed (Friedman and Nashold, 1986).
SPASTICITY
After easing of the spinal shock, spinal spasticity usually
occurs, and sometimes can be so serious that it causes
significant complications. Great experience in this field
is necessary when treating patients in order to avoid life-
long problems. In patients with chronic SCI lasting lon-
ger than 1 year, 6578% show signs of spasticity
(Maynard et al., 1990; Sk old et al., 1999).
The most frequently used methods to define spastic-
ity with SCI are the Ashworth (AS) and modified
Ashworth Scales (MAS) (Ashworth, 1964; Bohannon
and Smith, 1987; Platz et al., 2005). A number of factors
need to be either kept constant or avoided when using
these scales in order to control and compare all later ex-
aminations: time of day, kind and duration of activity be-
fore the check-up, surrounding temperature, emotional
status, presence of infections, for instance of the urinary
tract, pain, tiredness, drugs, clothing, and position of the
body under examination. The person carrying out the
check-up should be experienced.The scales normally cor-
relate very well with self-judgment according to visual
analog scales (VAS) (Van Drongelen et al., 2006).
Biomechanical methods to define spasticity are still
widely described and mainly concern the major joints
with one-dimensional movement ability, but, so far,
these methods have not found a clear place in clinical
practice (Wood et al., 2005).
Electrophysiological methods to measure spasticity
also play only a minor role. They are useful for establish-
ing the threshold value of the stretch reflex together with
biomechanical techniques for defining the relation of
latency, speed, and turning movement of the reflex-
triggered reaction (Chou et al., 2005; Kim et al., 2005;
van der Salm et al., 2005).
Spasticity is a multilayered problem with many facets
and is therefore difficult to measure. It is not enough to
measure only the activity of muscles, especially when
spasticity affects activities of daily life. One must ques-
tion the patients activity in general, emotion, cognition,
effects of relationships, their profession, and economic
matters. By doing so one finds that the view of the af-
fected person can vary greatly from that of the inter-
viewer (Kleinman, 1980). One must accept that the
experiences of the patient are important for the
appropriate treatment and also that various patients feel
differently about their spasticity (Kleinman, 1988).
Many patients prefer partial control to a total suppres-
sion of their spasticity. The desire for alternatives that
can restore control over the body and so improve the in-
terplay between spasticity and daily life should be under-
stood and acted upon accordingly (Mahoney et al.,
2007).
Spasticity has a negative effect on quality of life (Levi
et al., 1995; Van Drongelen et al., 2006). Apart from the
impairment in caring for oneself and in walking, spastic-
ity can evoke pain, fatigue, and sleep disorder. Spasticity
also induces muscular contraction and pressure ulcers. It
has a negative effect on the necessary nursing proce-
dures (Parziale et al., 1993; Burchiel and Hsu, 2001;
Sheean, 2002; Ward, 2003; Van Drongelen et al.,
2006). Although spasticity has negative effects on the
quality of life, under certain circumstances it can also
have positive effects. It can provide stability in sitting
and standing, can help with some ADLs and transfers,
can slow down muscular atrophy, avoid osteoporosis,
improve venous circulation and therefore prevent
DVT in the legs. These positive effects should be consid-
ered when deciding upon management (Parziale et al.,
1993; St George, 1993).
There is no general recommendation regarding the
treatment of spasticity. Commonly, one starts with the
conservative methods of physiotherapy and oral phar-
macological interventions, followed by injections, then
drugs intrathecally administered, and, finally, surgical
methods (Kirshblum, 1999). In SCI spasticity is not so
much locally as diffusely spread, thus preference should
be given to regional or systemic methods of therapy
(Gracies et al., 1997).
UPPER EXTREMITIES
With a complete SCI below C6, some hand functions
and all wrist functions are still present, whilst with a
lesion at the level of C6 all functions of the hand have
disappeared and only wrist extension together with ra-
dial deviation remains (van Tuijl et al., 2002). No hand
function at all is possible with a lesion above C6. With
incomplete lesions, several kinds of function may be
possible. At least 61% of all cervical SCIs are function-
ally incomplete (National Spinal Cord Injury Statistical
Center, 2004).
Regarding the outcome, one can orientate oneself
according to the arm and hand function, according
to muscle strength, neurological level, and motor score
(Ditunno et al., 2000, 2005; Kirshblum et al., 2004;
Beekhuizen, 2005), or according to the arm hand skilled
performance (Spooren et al., 2006, 2008), which is bet-
ter when operating in the ADL range. Herein one
 TRAUMATIC SPINAL CORD INJURY
distinguishes between a basal task of grasping and reach-
ing and a more complex task of dressing oneself and eat-
ing. Only a few measuring devices are available for this
(van Tuijl et al., 2002), such as the Functional Indepen-
dence Measure, the Spinal Cord Independence Measure,
and the Modified Barthel Index (Wirth et al., 2008).
Recently tests of basic and complex function have
appeared, like the Van Lieshout Test and the grasp
and release test (Harvey et al., 2001; Mulcahey et al.,
2004; Post et al., 2006), which are also very good for doc-
umenting change (Ditunno et al., 2005) and can be used
to optimize therapy (Spooren et al., 2008).
Patients with incomplete lesions profit most from in-
tensive rehabilitation. A modest improvement in master-
ing hand and arm functions can mean a great
improvement in mastering ADL and therefore lead to
an improvement in the quality of life (Snoek et al.,
2004; Ginis and Hicks, 2005). Repetitive activity-based
training and somatosensory stimulation (prolonged
peripheral nerve electrical stimulation at submotor
threshold intensity) have proved useful to regain skills
(Beekhuizen, 2005; Dromerick et al., 2006; Daly and
Ruff, 2007). Much experience is already available in
the field of hand surgery (Murray et al., 2006; Snoek
et al., 2008), functional electrical stimulation (Popovic
et al., 2002; Giuffrida and Crago, 2005), neuroprosth-
eses (Inmann and Haugland, 2004; Rupp and Gerner,
2007), and orthoses (Paternostro Sluga and Stieger,
2004), but all of these work more in the line of compen-
sation and do not necessarily lead to an improvement in
skills. Because of this, they should be carried out in com-
bination with repetitive sensorimotor training (Spooren
et al., 2009).
LOCOMOTION
One of the highest goals of all patients with SCI is the
improvement or restoration of locomotion. There exist
a number of strategies to improve locomotion like tread-
mill training with and without body weight support,
robotic-assisted gait training, and functional electrical
stimulation. At the moment there is no proof that one
strategy is superior to another, either in respect of effi-
ciency or regarding safety or acceptability (Dobkin,
2006; Mehrholz et al., 2008).
RESPIRATION
All tetraplegics and all patients with a high lesion of the
thoracic cord have a fall-out of the intercostal muscles
and therefore a decrease in their respiratory volume, be-
cause they breathe only with the help of the diaphragm.
One should limit the time the patient has to be on the res-
pirator as much as possible, with the exception of course
417
of those patients who, because of the loss of diaphragm
respiration, have to be constantly ventilated.
The kind and extent of respiratory dysfunction is
mainly dependent on the level of lesion, complete or in-
complete, and also on the interval since the trauma
(Brown et al., 2006). A high lesion normally causes a
much greater denervation of expiratory as well as inspi-
ratory muscles, so that patients with cervical and upper
thoracic lesions show a greater impairment of inspiration
and expiration. A complete loss happens only with le-
sions above C3 and demands an immediate and continual
artificial respiration. If the lesion lies between C3 and
C5, the result is a respiratory insufficiency. In lesions
below the cervical cord diaphragm auxiliary respiratory
muscles are not affected, but because of the loss of in-
tercostal muscles and other trunk muscles, which gener-
ate the expansion of the thorax together with a deeper
moving of the diaphragm, ventilation is nevertheless
greatly impaired. In contrast, through the deeper move-
ment of the diaphragm, the thorax can be pressed in-
wards and therefore respiratory capacity is again
reduced. Also the paralyzed expiratory muscles do not
support respiration under stress and therefore again re-
duce respiratory reserve. Inspiratory capacity and expi-
ratory reserve volume are reduced. They are even further
reduced in patients with a high cervical lesion than with a
lower thoracic or lumbar lesion (Baydur et al., 2001).
Forced expiratory volume in 1 second (FEV1) and forced
vital capacity (FVC) are reduced after SCI with a high le-
sion, especially tetraplegia, because of the reduced inspi-
ratory muscle power (Baydur et al., 2001). The
impairment of FEV1 and FVC is less with an incomplete
lesion, but smoking and a longer-lasting SCI are associ-
ated with a greater reduction in FEV1.
Coughing has an important protective function
against infections of the respiratory tract. This capacity
is impaired in most SCIs, caused by a weakening of the
abdominal muscles. One must also take into consider-
ation the role of the respiratory system in its effect upon
language and torso stability, especially with high lesions.
Pre-existent diseases, smoking, and old age can worsen
these problems (Urdaneta and Layon, 2003).
In about two-thirds of patients with dyspnea the cause
is an inspiratory paresis, the intensity of which increases
with the level of the lesion. Improvement in respiratory
muscle power and persistence can improve coughing and
the maximal exercise ventilation and so reduce dyspnea.
The inspiratory muscles similar to the muscles of the
extremities can be trained with diverse devices which
can improve resistive or threshold inspiratory load
(Geddes et al., 2005; Sheel et al., 2008).
Pulmonary complications are the most frequent
causes of death in the first year posttrauma. The fre-
quency lies between 65% and 84% respectively for
418 H. BINDER
thoracic and high cervical lesions. The problem lies
mainly in the paralysis of the abdominal muscles, which
are needed to cough the secretions. Manual techniques
for the support of coughing (quad cough, abdominal
thrust, costophrenic technique) are more effective
than suction, because the latter mainly reaches into the
right major bronchus and eventually through vagal
stimulation worsens bradycardia. Especially in patients
with borderline lung function, positioning on the back
is important as in this position the pressure of the abdom-
inal organs on the diaphragm makes expiration easier.
Patients with high quadriplegia can be trained in glos-
sopharyngeal breathing (Warren, 2002). It is important to
constantly control lung function in patients with SCI. Also
regular vaccinations against influenza or pneumococcus
should be considered for patients with quadriplegia
(Darouiche et al., 1993; Goldstein and Hammond, 2003).
PHYSICAL FITNESS
Fitness is defined as the efficiency of the cardio-
respiratory and musculoskeletal systems to obtain and
retain a certain level of activity (Haisma et al., 2007).
Physical fitness is a health indicator and as such is
important for quality of life (Cress and Meyer, 2003).
Pareses and autonomic disorders obviously reduce
physical fitness (Hjeltnes and Jansen, 1990; Stewart
et al., 2000; Teasell et al., 2000; Haisma et al., 2006a).
Patients with SCI find themselves in a downward spiral
of reduced fitness and the complications arising from
this (Manns et al., 2005). The level of fitness is princi-
pally dependent on age, sex, and level of lesion
factors
that cannot be influenced, but it can be affected by fac-
tors such as bed rest, spasticity, contractures, and other
diverse complications (Capelli et al., 2006; Haisma et al.,
2006b; Lechner et al., 2006). Physical fitness should be
encouraged as much as possible.
FATIGUE
In more than 50% of patients with chronic SCI, fatigue is
reported, which considerably decreases activity and,
thus, quality of life. There is no consensus about the im-
portance of age, time following the injury, and complete/
incomplete SCI (McColl et al., 2003; Barat et al., 2006;
Jensen et al., 2007).
Principally, one has to distinguish between physiolog-
ical and psychological factors of fatigue (Barat et al.,
2006; Fawkes-Kirby et al., 2008). Physiological factors
develop from the weakening of muscles and also phys-
iological deconditioning. However, one should never
overlook affective and cognitive problems, concerning
mood, attentiveness, concentration, and memory
(Jensen et al., 2007; Hammell et al., 2009).
CONTRACTURES
Range of motion (ROM) exercises should be introduced
as soon as possible. For instance, if shoulder ROM is
neglected in the early phase, there is a much greater risk
of developing shoulder pain later in the course of reha-
bilitation. Splints and orthoses for hands and feet should
be applied as early as possible in order to maintain joint
range.
The main goal before any therapy starts is the avoidance
of contracture development, which occurs mainly in shoul-
der, hip, and knee joints. Muscular imbalance, lack of exer-
cise in the joint, and abnormal posture because of spasticity
are predisposing factors (Farmer and James, 2001).
Passive stretching, good posture in bed, and incremen-
tally adjustable as well as dynamic orthoses are the general
provisions for prevention and therapy (Williams, 1990b;
Bonutti et al., 1994; Gelinas et al., 2000; Bromwich
et al., 2002; Harvey et al., 2002). Further possible arrange-
ments are functional electrical stimulation and injections
with botulinum toxin. Attention must be given to the
position of the fingers in patients with tetraplegia, other-
wise the goal of primitive grasping with one functioning
hand may never be reached.
MUSCULAR ATROPHY
Immobilization and inactivity generate not only osteo-
porosis but also muscular atrophy (Garland et al., 1992;
Castro et al., 1999; Shields, 2002). Just 6 weeks postinjury
a distinct and progressive reduction in the mass of muscle
below the lesion starts. After 24 weeks the average reduc-
tion in quadriceps, hamstrings, and adductor muscle, gas-
trocnemius and soleus muscle is 16%, 14%, 16%, 24%, and
12% respectively (Giangregorio and McCartney, 2006).
Dietetic plans should be set up accordingly. If the
input of energy is not adapted to the energy that is used
up, the body starts to store fat (Sedlock and Laventure,
1990). Functional cycle ergometry when performed a
couple of times a week leads to a considerable increase
in muscle mass along with a reduction of fat (Skold et al.,
2002). Regular weight-supported treadmill training also
has a positive effect on the increase in muscle mass
in relationship to fiber types (Stewart et al., 2004;
Giangregorio et al., 2005; Forest et al., 2008). Unfortu-
nately, functional electrical stimulation does not appear
to have such a positive effect on bone
although more
frequent exercise seems to improve the bone density, it is
not yet possible to regain the lost microstructure of bone
(Robling et al., 2002).
HETEROTOPIC OSSIFICATION
Depending largely on the type of examination, hetero-
topic ossification can be found in 1056% of patients
 TRAUMATIC SPINAL CORD INJURY
after SCI (Venier and Ditunno, 1971). The most frequent
sites are the hip joints, followed by knee, and less often
the shoulder and elbow. Ossification usually appears in
the region of the paralysis with spastic as well as flaccid
paralysis, complete or incomplete. It is normally discov-
ered 14 months after the injury, but has appeared as
early as 19 days and even a couple of years after injury
(Hardy and Dickson, 1963). The problem with hetero-
topic ossification is the reduction in mobility of the joint,
which in extreme cases may lead to complete ankylosis.
Following heterotopic ossification, peripheral entrap-
ment syndromes may appear (Brooke et al., 1991). Het-
erotopic ossification may also lead to pressure sores as a
secondary complication, if they are located directly un-
derneath the skin, or can cause a pathological posture of
the body when sitting (Damanski, 1961).
Early symptoms are swelling and locally warmness,
eventually pyrexia. Alkaline phosphatase levels (Freed
et al., 1982) are greatly increased in the active phase
(Garland et al., 1983), and give a direct image of the
ossification process. On average their values begin to in-
crease about 7 weeks before the first clinical symptoms
appear and reach their highest value about 3 weeks after
the first clinical symptoms. In the course the next
5 months the values return to normal levels. Diagnosis
can be supplemented by three-phase bone scanning, a
very sensitive but nonspecific technique, which neverthe-
less can, in combination with the clinical symptoms,
support the likelihood of the diagnosis.
So far there exists no safe prevention against periarti-
cular ossification. Prophylactically, one can only advise
either a reduction in risk factors such as venous thrombo-
sis, pressure ulcers, urinary tract infection, and spasticity,
or a regular careful passive ROM program and the use of
diphosphonates (Stover et al., 1976). How long the latter
should be taken is so far unclear. When heterotopic ossi-
fication leads to a restriction of ROM, an operation may
become unavoidable.
OSTEOPOROSIS
Following SCI an increase in absorption and at the same
time a reduction in new bone formation below the lesion
starts very soon (Dauty et al., 2000; Mamoun et al., 2005,
2006). This predisposes to hypercalcemia, hypercalciuria,
renal calculi, osteoporosis, and fractures (Lazo et al.,
2001). The loss in bone substance approaches 4% in the
trabecular zone and reaches its peak values after 3
5
months until after 2 years a steady state is reached.
Hypercalcemia is actually very rare, but if it occurs then
its effects are lethargy, headache, irritability, or mental
disorder together with cramps, even coma. Polyuria and
polydipsia may also appear, as well as gastrointestinal
419
symptoms such as nausea and vomiting (Carroll and
Schade, 2003).
PRESSURE ULCERS
Patients with SCI are at risk of developing pressure sores,
which are ulcers that spread far into the soft tissue under-
neath the skin. This is due to a loss of sensitivity and also
autonomic dysregulation and spinal shock. Seventeen per-
cent of nonambulatory SCI patients have, after 5 years, a
pressure ulcer at least once every 2 years, while 9% have
an ulcer at least once a year and 4% constantly (Krause
and Broderick, 2004). Many need surgical intervention
with long-term hospitalization, expensive wound dress-
ing, and, last but not least, a considerable decrease in life
quality and life expectancy. The frequency of relapses can
be as high as 60%. The risk factors lie in the medical man-
agement, especially the operative techniques, compliance,
control of the comorbidities, and adequate postoperative
care (Langemo et al., 2000; Cardenas et al., 2004; Charli-
fue et al., 2004; Sorensen et al., 2004); however,
demographic factors also play an important role, such
as age, unemployment, nursing home, and socioeconomic
factors (Krause and Broderick, 2004).
From the very beginning it is important that the pa-
tients position in bed, as soon as the vertebral column
has been stabilized, is changed every 2 hours in order
to relieve the points at risk of pressure ulcers
(Consortium for Spinal Cord Medicine, 2000). Above
all, it seems that by reducing risks and modifying life-
style, the rate of relapse can be reduced through inten-
sive education that is tailored to the individual (Rintala
et al., 2008). Pressure ulcers should be entirely
preventable.
SEXUALITY
Anatomy and physiology of sexual disorders following
SCI have been well studied (Burns et al., 2001; Benevento
and Sipski, 2002; DeForge et al., 2005). The type and
degree of sexual disorder following SCI depends on
the grade and level of the lesion (Biering-Sorensen and
Sonksen, 2001; Sipski et al., 2001). Females in particular
complain of problems when having sexual intercourse
and have difficulties in reaching an orgasm
(Linsenmeyer, 2000). With men the main problem is
an erection, which either fails or is of insufficient inten-
sity and duration.
After SCI, men as well as women complain of a
decrease in libido and decrease in frequency of sexual
activity. Psychological problems include difficulty with
body image, self-consciousness, and social elements like
gender, age, and culture (Sipski and Alexander, 1993).
420 H. BINDER
More than 80% of SCI patients complain of sexual
problems and believe that an improvement in their sexual
function would greatly improve their quality of life
(National Spinal Cord Injury Statistical Center, 2005).
The greatest problem experienced by far is that of inti-
macy (57.7%) as opposed to fertility (1%) (Anderson
et al., 2007). The most frequent problems during sexual
activity are tingling sensations (35.3%) and spasms
(35%), pain (10.8%), headache (8.7%), and shortness of
breath (8.7%).
Not surprisingly there exists a group of patients
(17.5%) for whom bladder and/or bowel incontinence
are a great hindrance to sexual activity, with some cases
of autonomic dysreflexia (31.8%) (Anderson et al., 2007).
A particular problem for men is infertility. Infertility
is the result of ejaculatory dysfunction and abnormal
quality and quantity of sperm, in the sense of reduced
agility and survival time (asthenozoospermia) which ap-
pears after 2 weeks and is generally seen as being mul-
tifactorial (Patki et al., 2008).
There are a number of therapies currently available to
improve erectile dysfunction such as behavioral inter-
ventions, topical and intraurethral agents, intracaver-
nous (penile) injections, vacuum tumescence devices,
phosphodiesterase inhibitors, penile implants, and sacral
stimulation (Kolettis et al., 2002; DeForge et al., 2006).
The use of penile vibratory stimulation or electroejacu-
lation to obtain sperm for artificial insemination of a
partner has become routine (Deforge et al., 2004).
AFFECTIVE DISORDERS
Affective disorders can very often be found in patients
with SCI (Bombardier et al., 2004). They are connected
with higher functional dependency, more secondary
complications, and poor social integration. In the first
months after the trauma 20
45% of patients with SCI
show symptoms of depressive disorder. Drug addiction
and suicide might arise. The suicide rate among patients
with SCI, mainly those suffering from paraplegia, is 2 to
6 times higher than in the general population. Apart from
pharmacological and psychological intervention, reha-
bilitation staff and family can help these patients get
through the critical phase and regain some quality of life
(Kalpakjian et al., 2009).
QUALITY OF LIFE
Quality of life (QOL) is a construction of health-related
quality of life (HRQOL) and well-being (Dijkers, 1999,
2003). HRQOL is based on the definition of health by
the World Health Organization: a state of complete
physical, mental and social well-being and not merely
the absence of disease and infirmity (World Health
Organization, 1958). Well-being is based on three compo-
nents: positive and negative affects which correlate with
the mood and life satisfaction as subjective evaluation
of the good or satisfactory character of a persons life as
a whole (Diener et al., 1985). Health is not part of QOL
but a predictor. QOL can finally be defined as happiness,
global or subjective well-being (Fuhrer, 1994).
The only HRQOL-specific questionnaire comes from
Lundqvist (Lundqvist et al., 1997) and combines generic
with SCI-specific questions like dependency, pain, and
sexuality. In the field of well-being Dieners Satisfaction
With Life Scale (Diener et al., 1985) is used very
frequently.
In a number of studies the QOL compared with the
severity of SCI is much better than expected. Scores
for pain, general health, and physical dimensions are
lower than those of the average population, but scores
for mental health, vitality, and role limitation are compa-
rable. The domains in which QOL is most impaired are
self-care ability, especially in tetraplegics, vocational sit-
uation, and sexual activity (LeDuc and LePage, 2002;
Kreuter et al., 2005).
The severity of the primary impairment has only a
small influence on well-being. Of importance are the
time since the trauma and personal factors like person-
ality, disease cognitions and coping behavior, social
support, and perceived environmental accessibility. Sec-
ondary problems like pressure sores, urinary tract infec-
tions, and spasticity are felt more as mental and social
impairments than physical (Post et al., 1999; Whiteneck
et al., 2004).
To summarize, participation in society is an essential
factor in patients perception of overall well-being. The
main initial goal of rehabilitation is a decrease in disabil-
ity but later every effort should be made to maximize the
patients reintegration into society.
REFERENCES
Abrams P, Agarwal M, Drake M et al. (2008). A proposed
guideline for the urological management of patients with
spinal cord injury. BJU Int 101: 989994.
Aito S, Pieri A, DAndrea M et al. (2002). Primary prevention
of deep venous thrombosis and pulmonary embolism in
acute spinal cord injured patients. Spinal Cord 40: 300303.
Alexander MS, Biering-Sorensen F, Bodner D et al. (2009). In-
ternational standards to document remaining autonomic
function after spinal cord injury. Spinal Cord 47: 3643.
Anderson KD, Borisoff JF, Johnson RD et al. (2007). The im-
pact of spinal cord injury on sexual function: concerns of
the general population. Spinal Cord 45: 328337.
Ashworth B (1964). Preliminary trial of carisoprodol in mul-
tiple sclerosis. Practitioner 192: 540542.
Barat M, Dehail P, de Souze M (2006). Fatigue after spinal
cord injury. Ann Readapt Med Phys 49: 365369.
 TRAUMATIC SPINAL CORD INJURY
Baydur A, Adkins RH, Milic-Emili J (2001). Lung mechanics
in individuals with spinal cord injury: effects of injury level
and posture. J Appl Physiol 90: 405411.
Beekhuizen KS (2005). New perspectives on improving upper
extremity function after spinal cord injury. J Neurol Phys
Ther 29: 157162.
Bendinelli C, Balogh Z (2008). Postinjury thromboprophy-
laxis. Curr Opin Crit Care 14: 673678.
Benevento BT, Sipski ML (2002). Neurogenic bladder, neuro-
genic bowel, and sexual dysfunction in people with spinal
cord injury. Phys Ther 82: 601612.
Biering-Sorensen F, Sonksen J (2001). Sexual function in spi-
nal cord lesioned men. Spinal Cord 39: 455470.
Biering-Sorensen F, Charlifue S, DeVivo M et al. (2006).
International spinal cord injury data sets. Spinal Cord 44:
530534.
Bilello JF, Davis JW, Cunningham MA et al. (2003). Cervical
spinal cord injury and the need for cardiovascular interven-
tion. Arch Surg 138: 11271129.
Blankstein A, Shmuel R, Weingarter I et al. (1985). Hand prob-
lems due to prolonged use of crutches and wheelchairs.
Orthop Rev 14: 735740.
Blumer CE, Quine S (1995). Prevalence of spinal cord injury:
an international comparison. Neuroepidemiology 14:
258268.
Bohannon RW, Smith MB (1987). Interrater reliability of a
modified Ashworth Scale of muscle spasticity. Phys Ther
67: 206207.
Boldin C, Raith J, Frankhauser F et al. (2006). Predicting neu-
rological recovery in cervical spinal cord injury with post-
operative MR imaging. Spine 31: 554559.
Bombardier CH, Richards JS, Krause JS et al. (2004). Symp-
toms of major depression in people with spinal cord injury:
implications for screening. Arch Phys Med Rehabil 85:
17491756.
Bonutti PM, Windau JE, Ables BA et al. (1994). Static pro-
gressive stretch to reestablish elbow range of motion. Clin
Orthop Relat Dis 303: 128134.
Bromwich W, Farmer SE, Forward M et al. (2002). Mechan-
ically applied stretch in the treatment of contractures pre-
liminary results. Physiotherapy 88: 55.
Brooke MM, Heard DL, de Larteur BJ et al. (1991). Hetero-
topic ossification and peripheral nerve entrapment: early
diagnosis and excision. Arch Phys Med Rehabil 72:
425429.
Brown R, DiMarco AF, Hoit JD et al. (2006). Respiratory dys-
function and management in spinal cord injury. Respir Care
51: 853868; discussion 869870.
Burchiel KJ, Hsu FP (2001). Pain and spasticity after spinal
cord injury: mechanisms and treatment. Spine 26:
S146S160.
Burns AS, Rivas DA, Ditunno JD (2001). The management of
neurogenic bladder and sexual dysfunction after spinal
cord injury. Spine 26: S129S136.
Cameron GS, Scott JW, Jousse AT et al. (1995). Diaphrag-
matic respiration in the quadraplegic patient and the
effect of position on his vital capacity. Ann Surg 141:
451456.
421
Capelli C, Antonutto G, Kenfack MA et al. (2006). Factors de-
termining the time course of O2(max) decay during bed-
rest: implications for VO2(max) limitation. Eur J Appl
Physiol 98: 152160.
Cardenas DD, Hoffman JM, Kirshblum S et al. (2004).
Etiology and incidence of rehospitalization after traumatic
spinal cord injury: a multicenter analysis. Arch Phys Med
Rehabil 85: 17571763.
Carroll MF, Schade DS (2003). A practical approach to hyper-
calcemia. Am Fam Physician 67: 19591966.
Castro MJ, Apple DF, Jr. et al. (1999). Influence of complete
spinal cord injury on skeletal muscle within 6 mo of injury.
J Appl Physiol 86: 350358.
Catz A, Itzkovich M, Agranov E et al. (1997). SCIM spinal
cord independence measure: a new disability scale
for patients with spinal cord lesions. Spinal Cord 35:
850856.
Catz A, Itzkovich M, Steinberg F et al. (2001). The Catz-
Itzkovich SCIM: a revised version of the Spinal Cord Inde-
pendence Measure. Disabil Rehabil 23: 263268.
Charlifue S, Lammertse DP, Adkins RH (2004). Aging
with spinal cord injury: changes in selected health
indices and life satisfaction. Arch Phys Med Rehabil 85:
18481853.
Chiou-Tan FY, Garza H, Chan KT et al. (2003). Comparison of
dalteparin and enoxaparin for deep venous thrombosis
prophylaxis in patients with spinal cord injury. Am J Phys
Med Rehabil 82: 678685.
Chou SW, Abraham LD, Huang IS et al. (2005). Starting po-
sition and stretching velocity effects on the reflex threshold
angle of stretch reflex in the soleus muscle of normal and
spastic subjects. J Formos Med Assoc 104: 493501.
Consortium for Spinal Cord Medicine (1998). Neurogenic
Bowel Management in Adults with Spinal Cord Injury.
Paralyzed Veterans of America, Washington, DC.
Consortium for Spinal Cord Medicine (2000). Pressure
Ulcer Prevention and Treatment Following Spinal Cord
Injury: A Clinical Practice Guideline for Health Profes-
sionals. Paralyzed Veterans of America, Washington, DC.
Consortium for Spinal Cord Medicine (2007). Early Acute
Management in Adults with Spinal Cord Injury: A Clinical
Practice Guideline for Health-care Providers. Paralyzed
Veterans of America, Washington, DC.
Cress ME, Meyer M (2003). Maximal voluntary and functional
performance levels needed for independence in adults aged
65 to 97 years. Phys Ther 83: 3748.
Daly JJ, Ruff RL (2007). Construction of efficacious gait and
upper limb functional interventions based on brain plastic-
ity evidence and model-based measures for stroke patients.
Scientific World Journal 7: 20312045.
Damanski M (1961). Heterotopic ossification in paraplegia.
J Bone Joint Surg Br 43: 286299.
Darouiche RO, Groover J, Rowland J et al. (1993). Pneumo-
coccal vaccination for patients with spinal cord injury.
Arch Phys Med Rehabil 74: 13541357.
Dauty M, Perrouin Verbe B, Maugars Y et al. (2000). Suprale-
sional and sublesional bone mineral density in spinal cord
injured patients. Bone 27: 305309.
422 H. BINDER
Davidoff G, Morris J, Roth E et al. (1985). Closed head injury
in spinal cord injured patients: retrospective study of loss of
consciousness and post-traumatic amnesia. Arch Phys Med
Rehabil 66: 4143.
Davidoff G, Thomas P, Johnson M et al. (1988a). Closed head
injury in acute traumatic spinal cord injury: incidence and
risk factors. Arch Phys Med Rehabil 69: 869872.
Davidoff G, Doljanac R, Berent S et al. (1988b). Galveston
Orientation and Amnesia Test: its utility in the determina-
tion of closed head injury in acute spinal cord injury
patients. Arch Phys Med Rehabil 69: 432434.
DeForge D, Blackmer J, Moher D et al. (2004). Sexuality and
reproductive health following spinal cord injury. Evid Rep
Technol Assess (Summ) 109: 18.
DeForge D, Blackmer J, Garritty C et al. (2005). Fertility fol-
lowing spinal cord injury: a systematic review. Spinal Cord
43: 693703.
DeForge D, Blackmer J, Garritty C et al. (2006). Male erectile
dysfunction following spinal cord injury: a systematic
review. Spinal Cord 44: 465473.
DeVivo MJ, Fine PR, Maetz HM et al. (1980). Prevalence of
spinal cord injury: reestimation employing life table
techniques. Arch Neurol 37: 707708.
DeVivo M, Biering-Sorensen F, Charlifue S et al. (2006). In-
ternational spinal cord injury core data set. Spinal Cord 44:
535540.
Dewire DM, Owens RS, Anderson GA et al. (1992). A compar-
ison of the urological complications associated with long-
term management of quadriplegics with and without
chronic indwelling catheters. J Urol 147: 10691071.
Diener E, Emmons RA, Larsen RJ et al. (1985). The satisfac-
tion with life scale. J Pers Assess 49: 7175.
Dijkers M (1999). Measuring quality of life: methodological
issues. Am J Phys Med Rehabil 78: 286300.
Dijkers M (2003). Individualization in quality of life measure-
ment: instruments and approaches. Arch Phys Med Rehabil
84: S3S14.
Ditunno JF (1992). Functional assessment in CNS trauma. J
Neurotrauma 9: S301S305.
Ditunno JF, Young W, Donovan WH et al. (1994). The Interna-
tional Standards Booklet for Neurological and Functional
Classification of Spinal Cord Injury. Paraplegia 32: 7080.
Ditunno JF, Jr., Cohen ME, Hauck WW et al. (2000). Recovery
of upper-extremity strength in complete and incomplete
tetraplegia: a multicenter study. Arch Phys Med Rehabil
81: 389393.
Ditunno JF, Flanders A, Kirshblum SC et al. (2002). Predicting
outcome in traumatic SCI. In: S Kirshblum, DI Campagnolo,
JA DeLIsa (Eds.), Spinal Cord Medicine. Lippincott
Williams & Wilkins, Philadelphia, pp. 108122.
Ditunno JF, Little JW, Tessler A et al. (2004). Spinal shock
revisited: a four-phase model. Spinal Cord 42: 383395.
Ditunno JF, Burns AS, Marino RJ (2005). Neurological and
functional capacity outcome measures: essential to spinal
cord injury clinical trials. J Rehabil Res Dev 42: 3542.
Dobkin BH (2006). Short-distance walking speed and timed
walking distance: redundant measures for clinical trials?
Neurology 66: 584586.
Dromerick AW, Lum PS, Hidler J (2006). Activity-based ther-
apies. NeuroRx 3: 428438.
Dworkin GE, Staas WE, Jr. (1985). Post-traumatic syringomy-
elia. Arch Phys Med Rehabil 66: 329331.
El Masri(y) WS (1993). Physiological instability of the spinal
cord following injury. Paraplegia 31: 273275.
El Masri(y) WS, Biyani A (1996). Incidence, management,
and outcome of post-traumatic syringomyelia. In memory
of Mr Bernard Williams. J Neurol Neurosurg Psychiatry
60: 141146.
Farmer SE, James M (2001). Contractures in orthopaedic and
neurological conditions: a review of causes and treatment.
Disabil Rehabil 23: 549558.
Fawkes-Kirby TM, Wheeler MA, Anton HA et al. (2008).
Clinical correlates of fatigue in spinal cord injury. Spinal
Cord 46: 2125.
Fehlings MG, Perrin RG (2005). The role and timing of early
decompression for cervical spinal injury: update with
a review of the recent clinical evidence. Injury 36:
B13B26.
Finnerup NB, Faaborg P, Krogh K et al. (2008). Abdominal pain
in long-term spinal cord injury. Spinal Cord 46: 198203.
Forest GF, Sisto SA, Barbeau H et al. (2008). Neuromotor and
musculoskeletal responses to locomotor training for an in-
dividual with chronic motor complete AIS-B spinal cord
injury. J Spinal Cord Med 31: 509521.
Freed JH, Hahn H, Menter R et al. (1982). The use of
three-phase bone scan in the early diagnosis of heterotopic
ossification and in the evaluation of Didronel therapy.
Paraplegia 13: 208216.
Friedman AH, Nashold BS, Jr. (1986). DREZ lesions for relief
of pain related to spinal cord injury. J Neurosurg 65:
465469.
Fuhrer M (1994). Subjective well-being: implications for med-
ical rehabilitation outcomes and models of disablement.
Am J Phys Med Rehabil 73: 358364.
Garland DE, Betzabe A, Venos KG et al. (1983). Diphospho-
nate treatment for heterotopic ossification in spinal cord in-
jury patients. Clin Orthop 176: 197200.
Garland DE, Stewart CA, Adkins RH et al. (1992). Osteoporo-
sis after spinal cord injury. J Orthop Res 10: 371378.
Geddes EL, Reid WD, Crowe J et al. (2005). Inspiratory mus-
cle training in adults with chronic obstructive pulmonary
disease: a systematic review. Respir Med 99: 14401458.
Geerts WH, Pineo GF, Heit JA et al. (2004). Prevention of
venous thromboembolism: the Seventh ACCP Conference
on Antithrombotic and Thrombolytic Therapy. Chest 126:
338S400S.
Gelinas JJ, Faber KJ, Patterson SD et al. (2000). The effective-
ness of turnbuckle splinting for elbow contracture. J Bone
Joint Surg Br 82B: 7478.
Gellman J, Sie I, Waters RL (1988). Late complications of the
weight-bearing upper extremity in the paraplegic patient.
Clin Orthop 233: 132135.
Giangregorio L, McCartney N (2006). Bone loss and muscle
atrophy in spinal cord injury: epidemiology, fracture pre-
diction, and rehabilitation strategies. J Spinal Cord Med
29: 489500.
 TRAUMATIC SPINAL CORD INJURY
Giangregorio LM, Hicks AL, Webber CE et al. (2005). Body
weight supported treadmill training in acute spinal cord in-
jury: impact on muscle and bone. Spinal Cord 43: 649657.
Ginis KA, Hicks AL (2005). Exercise research issues in the
spinal cord injured population. Exerc Sport Sci Rev 33:
4953.
Giuffrida JP, Crago PE (2005). Functional restoration of elbow
extension after spinal-cord injury using a neural network-
based synergistic FES controller. IEEE Trans Neural Syst
Rehabil Eng 13: 147152.
Goldstein B, Hammond MC (2003). The importance of influ-
enza vaccinations in persons with spinal cord injury and
disease. J Spinal Cord Med 26: 219220.
Gracies JM, Nance P, Elovic E et al. (1997). Traditional phar-
macological treatments for spasticity. Part II: General and
regional treatments. Muscle Nerve Suppl 6: S92S120.
Haisma JA, van der Woude LH, Stam HJ et al. (2006a). Phys-
ical capacity in wheelchair-dependent persons with a spinal
cord injury: a critical review of the literature. Spinal Cord
44: 642652.
Haisma JA, Bussmann JB, Stam HJ et al. (2006b). Changes in
physical capacity during and after inpatient rehabilitation
in subjects with a spinal cord injury. Arch Phys Med Reha-
bil 87: 741748.
Haisma JA, Bussmann JBJ, Stam HJ (2007). Physical fitness in
people with a spinal cord injury: the association with com-
plications and duration of rehabilitation. Clin Rehabil 21:
932940.
Hall M (1850). Synopsis of the diastaltic nervous system: or
the system of the spinal marrow, and its reflex arcs; as
the nervous agent in all the functions of ingestion and of
egestion in the animal oeconomy. Mallett J., London.
Hammell KW, Miller WC, Forwell SJ et al. (2009). Fatigue
and spinal cord injury: a qualitative analysis. Spinal Cord
47: 4449.
Hansen RB, Biering-Sorensen F, Kristensen JK (2004). Blad-
der emptying over a period of 1045 years after a traumatic
spinal cord injury. Spinal Cord 42: 631637.
Hansen RB, Biering-Sorensen F, Kristensen JK (2009).
Urinary incontinence in spinal cord injured individuals
1045 years after injury. Spinal Cord 17.
Hardy S, Dickson J (1963). Pathologic ossification in trau-
matic paraplegia. J Bone Joint Surg 45: 7687.
Harvey LA, Batty J, Jones R et al. (2001). Hand function of C6
and C7 tetraplegics 116 years following injury. Spinal
Cord 39: 3743.
Harvey LA, Crosbie J, Herbert RD (2002). Does regular stretch
produce lasting increases in joint range of motion? A sys-
temic review. Physiother Res Int 7: 113.
Hjeltnes N, Jansen T (1990). Physical endurance capacity,
functional status and medical complications in spinal cord
injured subjects with long-standing lesions. Paraplegia 28:
428432.
Inmann A, Haugland M (2004). Functional evaluation of nat-
ural sensory feedback incorporated in a hand grasp neuro-
prosthesis. Med Eng Phys 26: 439447.
Itzkovich M, Gelernter I, Biering-Sorensen F et al. (2007). The
Spinal Cord Independence Measure (SCIM) version III:
423
reliability and validity in a multi-center international study.
Disabil Rehabil 29: 19261933.
Jensen MP, Kuehn CM, Amtmann D et al. (2007). Symptom
burden in persons with spinal cord injury. Arch Phys
Med Rehabil 88: 638645.
Kalpakjian CZ, Bombardier CH, Schomer K et al. (2009).
Measuring depression in persons with spinal cord injury:
a systematic review. J Spinal Cord Med 32: 624.
Kim DY, Park CI, Chon JS et al. (2005). Biomechanical
assessment with electromyography of poststroke ankle
plantar flexor spasticity. Yonsei Med J 46: 546554.
Kirshblum S (1999). Treatment alternatives for spinal
cord injury related spasticity. J Spinal Cord Med 22:
199217.
Kirshblum SC, House JG, OConnor KC (2002). Silent auto-
nomic dysreflexia during a routine bowel program in per-
sons with traumatic spinal cord injury: a preliminary study.
Arch Phys Med Rehabil 83: 17741776.
Kirshblum S, Millis S, McKinley W et al. (2004). Late neuro-
logic recovery after traumatic spinal cord injury. Arch Phys
Med Rehabil 85: 18111817.
Kirshblum SC, Priebe MM, Ho CH et al. (2007). Spinal cord
injury medicine. 3. Rehabilitation phase after acute spinal
cord injury. Arch Phys Med Rehabil 88: S62S70.
Kleinman A (1980). Patients and Healers in the Context of
Culture. University of California Press, Berkeley.
Kleinman A (1988). The Illness Narratives. Basic Books, New
York.
Kolettis PN, Lambert MC, Hammond KR et al. (2002). Fertil-
ity outcomes after electroejaculation in men with spinal
cord injury. Fertil Steril 78: 429431.
Krassioukov AV, Furlan JC, Fehlings MG (2003). Autonomic
dysreflexia in acute spinal cord injury: an underrecognized
clinical entity. J Neurotrauma 20: 707716.
Krause JS, Broderick L (2004). Patterns of recurrent pressure
ulcers after spinal cord injury: identification of risk and
protective factors 5 or more years after onset. Arch Phys
Med Rehabil 85: 12571264.
Kreuter M, Siosteen A, Erkholm B et al. (2005). Health and
quality of life of persons with spinal cord lesions in Austra-
lia and Sweden. Spinal Cord 43: 123129.
Lammertse D, Dungan D, Dreisbach J et al. (2007). Neuroim-
aging in traumatic spinal cord injury: an evidence-based
review for clinical practice and research. J Spinal Cord
Med 30: 205214.
Langemo DK, Melland H, Hanson D et al. (2000). The lived
experience of having a pressure ulcer: a qualitative
analysis. Adv Skin Wound Care 13: 225235.
Lazo MG, Shirazi P, Sam M et al. (2001). Osteoporosis and
risk of fracture in men with spinal cord injury. Spinal Cord
39: 208214.
Lechner HE, Frotzler A, Eser P (2006). Relationship between
self- and clinically rated spasticity in spinal cord injury.
Arch Phys Med Rehabil 87: 1519.
LeDuc B, LePage Y (2002). Health-related quality of life after
spinal cord injury. Disabil Rehabil 24: 196204.
Levi R, Hultling C, Seiger A (1995). The Stockholm Spinal
Cord Injury Study: 2. Associations between clinical patient
424 H. BINDER
characteristics and post-acute medical problems. Paraple-
gia 33: 585594.
Linsenmeyer TA (2000). Sexual function and infertility fol-
lowing spinal cord injury. Phys Med Rehabil Clin N Am
11: 141156.
Lundqvist C, Siosteen A, Sullevan L et al. (1997). Spinal cord
injuries: as shortened measure of function and mood.
Spinal Cord 35: 1721.
Macciocchi SN, Bowman B, Coker J et al. (2004). Effect of co-
morbid traumatic brain injury on functional outcome of
persons with spinal cord injuries. Am J Phys Med Rehabil
83: 2226.
Mahoney JS, Engebretson JC, Cook KF et al. (2007). Spastic-
ity experience domains in persons with spinal cord injury.
Arch Phys Med Rehabil 88: 287294.
Mamoun L, Couret I, Mariano-Goulart D et al. (2005).
Changes in osteoprotegerin/RANKL system, bone mineral
density and bone biochemical markers in patients with re-
cent spinal cord injury. Calcif Tissue Int 76: 404411.
Mamoun L, Fattal C, Micallef JP et al. (2006). Bone loss in
spinal cord injured patients: from physiopathology to ther-
apy. Spinal Cord 44: 203210.
Manns PJ, McCubbin JA, Williams DP (2005). Fitness, in-
flammation, and the metabolic syndrome in men with para-
plegia. Arch Phys Med Rehabil 86: 11761181.
Maynard FM, Karunas RS, Waring (1990). Epidemiology of
spasticity following traumatic spinal cord injury. Arch
Phys Med Rehabil 71: 566569.
McColl MA, Walker J, Stirling P et al. (1997). Expectations of
life and health among spinal cord injured adults. Spinal
Cord 35: 818828.
McColl MA, Arnold R, Charlifue S et al. (2003). Aging, spinal
cord injury, and quality of life: structural relationships.
Arch Phys Med Rehabil 84: 11371144.
Mehrholz J, Kugler J, Pohl M (2008). Locomotor training for
walking after spinal cord injury. Cochrane Database Syst
Rev 2: CD006676.
Meiners T, Bohm V, Schl uter E (2004). Analysis of FIM data
collected during hospital treatment of patients with acute
spinal cord injury. Rehabilitation 43: 129136.
Middleton J, Truman G, Geraghty T (1998). Neurological
level effect on the discharge functional status of spinal cord
injured persons after rehabilitation. Arch Phys Med Reha-
bil 79: 14281432.
Middleton JW, Harvey LA, Batty J et al. (2006). Five addi-
tional mobility and locomotor items to improve responsive-
ness of the FIM in wheelchair-dependent individuals with
spinal cord injury. Spinal Cord 44: 495504.
Mulcahey MJ, Smith BT, Betz RR (2004). Psychometric rigor
of the Grasp and Release Test for measuring functional lim-
itation of persons with tetraplegia: a preliminary analysis. J
Spinal Cord Med 27: 4146.
Murray WM, Hentz VR, Friden J et al. (2006). Variability in
surgical technique for brachioradialis tendon transfer: evi-
dence and implications. J Bone Joint Surg Am 88:
20092016.
National Spinal Cord Injury Statistical Center (2005). Annual
Report for the Model Spinal Cord Injury Care Systems.
University of Alabama, Birmingham, AL.
National Spinal Cord Injury Statistical Center, Birmingham
Alabama (2004). Spinal cord injury: facts and figures at
a glance. J Spinal Cord Med 27: 2.
Nicholas P, Norman P, Ennis J (1979). Wheelchair users
shoulder. Scand J Rehabil Med 11: 2932.
Nicolaides AN, Kakkar VV, Field ES et al. (1971). The origin
of deep vein thrombosis: a venographic study. Br J Radiol
44: 653663.
Ottenbacher KJ, Hsu Y, Granger CV et al. (1996). The reliabil-
ity of the Functional Independence Measure: a quantitative
review. Arch Phys Med Rehabil 77: 12261232.
Parziale JR, Akelman E, Herz DA (1993). Spasticity:
pathophysiology and management. Orthopedics 16: 801811.
Paternostro-Sluga T, Stieger M (2004). Hand splints in rehabil-
itation. Crit Rev Phys Rehabil Med 16: 233256.
Patki P, Woodhouse J, Hamid R et al. (2006). Lower urinary
tract dysfunction in ambulatory patients with incomplete
spinal cord injury. J Urol 175: 17841787.
Patki P, Woodhouse J, Hamid R et al. (2008). Effects of spinal
cord injury on semen parameters. J Spinal Cord Med 31:
2732.
Platz T, Eickhof C, Nuyens G et al. (2005). Clinical scales for
the assessment of spasticity, associated phenomena, and
function: a systematic review of the literature. Disabil
Rehabil 27: 718.
Popovic MR, Popovic DB, Keller T (2002). Neuroprostheses
for grasping. Neurol Res 24: 443452.
Post M, Ros W, Schrijvers A (1999). Impact of social support
on health status and life satisfaction in people with a spinal
cord injury. Psychology and Health 14: 679695.
Post MWM, Van Lieshout G, Seelen HAM et al. (2006).
Measurement properties of the short version of the van
Lieshout Test (VLT-SF). Spinal Cord 44: 763771.
Potter K, Saifuddin A (2003). MRI of chronic spinal cord in-
jury. Br J Radiol 76: 347352.
Putzke JD, Richards JS, Hicken BL et al. (2002). Pain
classification following spinal cord injury: the utility of
verbal descriptors. Spinal Cord 40: 118127.
Rintala DH, Garber SL, Friedman JD et al. (2008). Preventing
recurrent pressure ulcers in veterans with spinal cord
injury: impact of a structured education and follow-up
intervention. Arch Phys Med Rehabil 89: 14291441.
Robling AG, Hinant FM, Burr DB et al. (2002). Shorter, more
frequent mechanical loading sessions enhance bone mass.
Med Sci Sports Exerc 34: 196202.
Rupp R, Gerner HJ (2007). Neuroprosthetics of the upper
extremity clinical application in spinal cord injury and
challenges for the future. Acta Neurochir Suppl 97: 419426.
Schinkel C, Anastasiadis AP (2008). The timing of spinal
stabilization in polytrauma and in patients with spinal cord
injury. Curr Opin Crit Care 14: 685689.
Scivoletto G, Morgagni B, Molinari M (2005). Early versus
delayed inpatient spinal cord injury rehabilitation: an Ital-
ian study. Arch Phys Med Rehabil 86: 512516.
Sedlock DA, Laventure SJ (1990). Body composition and rest-
ing energy expenditure in long term spinal cord injury.
Paraplegia 28: 448454.
Sheean G (2002). The pathophysiology of spasticity. Eur J
Neurol 9: 39.
 TRAUMATIC SPINAL CORD INJURY
Sheel AW, Reid WD, Townson AF (2008). Effects of exercise
training and inspiratory muscle training in spinal cord in-
jury: a systematic review. J Spinal Cord Med 31: 500508.
Shields RK (2002). Muscular, skeletal, and neural adaptations fol-
lowing spinal cord injury. J Orthop Sports Phys Ther 32: 6574.
Siddall PJ, McClelland JM, Rutkowski SB et al. (2003). A lon-
gitudinal study of the prevalence and characteristics of pain
in the first 5 years following spinal cord injury. Pain 103:
249257.
Simon T, Mercy J, Perkins C (2001). Injuries from violent
crime, 199298. Bureau of Justice Statistics, US Depart-
ment of Justice, and Centers for Disease Control and Pre-
vention, US Department of Health and Human Services,
Washington, DC.
Sipski ML, Alexander CJ (1993). Sexual activities, response
and satisfaction in women pre- and post-spinal cord injury.
Arch Phys Med Rehabil 74: 10251029.
Sipski ML, Alexander CJ, Rosen R (2001). Sexual arousal and
orgasm in women: effects of spinal cord injury. Ann Neurol
49: 3544.
old C, Levi R, Seiger A (1999). Spasticity after traumatic
Sk
spinal cord injury: nature, severity, and location. Arch Phys
Med Rehabil 80: 15481557.
Skold C, Lonn L, Harms-Ringdahl K et al. (2002). Effects of
functional electrical stimulation training for six months on
body composition and spasticity in motor complete tetraple-
gic spinal cord-injured individuals. J Rehabil Med 34: 2532.
Smith-Hammond CA, New KC, Pietrobon R et al. (2004). Pro-
spective analysis of incidence and risk factors of dysphagia in
spine surgery patients: comparison of anterior cervical, pos-
terior cervical, and lumbar procedures. Spine 29: 14411446.
Snoek GJ, Ijzerman MJ, Hermens HJ et al. (2004). Survey of
the needs of patients with spinal cord injury: impact and
priority for improvement in hand function in tetraplegics.
Spinal Cord 42: 526532.
Snoek GJ, van Til JA, Krabbe PF et al. (2008). Decision for
reconstructive interventions of the upper limb in individ-
uals with tetraplegia: the effect of treatment characteristics.
Spinal Cord 46: 228233.
Sorensen JL, Jorgensen B, Gottrup F (2004). Surgical treat-
ment of pressure ulcers. Am J Surg 188: 4251.
Spooren AI, Janssen-Potten YJ, Post MW et al. (2006). Mea-
suring change in arm hand skilled performance in persons
with a cervical spinal cord injury: responsiveness of the
Van Lieshout Test. Spinal Cord 44: 772779.
Spooren AIF, Janssen-Potten YJM, Snoek GJ et al. (2008). Re-
habilitation outcome of upper extremity skilled perfor-
mance in persons with cervical spinal cord injuries. J
Rehabil Med 40: 637644.
Spooren AI, Janssen-Potten YJ, Kerckhofs E et al. (2009). Out-
come of motor training programmes on arm and hand func-
tioning in patients with cervical spinal cord injury
according to different levels of the ICF: a systematic re-
view. J Rehabil Med 41: 497505.
Stanworth PA (1982). The significance of hyperhidrosis in pa-
tients with post-traumatic syringomyelia. Paraplegia 20:
282287.
Stewart MW, Melton-Rogers SL, Morrison S et al. (2000). The
measurement properties of fitness measures and health
425
status for persons with spinal cord injuries. Arch Phys
Med Rehabil 81: 394400.
Stewart BG, Tarnopolsky MA, Hicks AL et al. (2004). Tread-
mill training-induced adaptations in muscle phenotype in
persons with incomplete spinal cord injury. Muscle Nerve
30: 6168.
St George CL (1993). Spasticity. Mechanisms and nursing
care. Nurs Clin North Am 28: 819827.
Stover SL, Fine PR (Eds.) (1986). Spinal Cord Injury: The
Facts and Figures. University of Alabama at Birmingham,
Birmingham, AL.
Stover SL, Hahn HR, Miller JM et al. (1976). Disodium etidro-
nate in the prevention of heterotopic ossification following
spinal cord injury (preliminary report). Paraplegia 14: 146156.
Sullivan NM, Sutter VL, Mims MM et al. (1973). Clinical as-
pects of bacteremia after manipulation of the genitourinary
tract. J Infect Dis 127: 4955.
Teasell R, Arnold J, Krassioukov A (2000). Cardiovascular
consequences of loss of supraspinal control of the sympa-
thetic nervous system after spinal cord injury. Arch Phys
Med Rehabil 81: 506516.
Teasell RW, Hsieh JT, Aubut JL et al. (2009). Venous throm-
boembolism after spinal cord injury. Arch Phys Med Reha-
bil 90: 232234.
Tewari M, Gifti D, Singh P et al. (2005). Diagnosis and prog-
nostication of adult spinal cord injury without radiographic
abnormality using magnetic resonance imaging: analysis of
40 patients. Surg Neurol 63: 204209.
Thornhill S, Teasdale GM, Murray GD et al. (2000). Disability
in young people and adults one year after head injury: pro-
spective cohort study. BMJ 320: 16311635.
Tolonen A, Turkka J, Salonen O et al. (2007). Traumatic brain
injury is under-diagnosed in patients with spinal cord in-
jury. J Rehabil Med 39: 622626.
Umbach I, Heilpom A (1988). Evaluation of post-traumatic
cervical syringomyelia: case report. Paraplegia 26: 5661.
Urdaneta F, Layon AJ (2003). Respiratory complications
in patients with traumatic cervical spine injuries: case
report and review of the literature. J Clin Anesth 15: 398405.
US Department of Justice, (1995). The nations two crime
measures. US Department of Justice, Washington, DC.
http://www.ojp.usdoj.gov/bjs/pub/pdf/ntcm.pdf.
van der Salm A, Veltink PH, Hermens HJ et al. (2005). Devel-
opment of a new method for objective assessment of spas-
ticity using full range passive movements. Arch Phys Med
Rehabil 86: 19911997.
Van Drongelen S, De Groot S, Veeger HE et al. (2006). Upper
extremity musculoskeletal pain during and after rehabilita-
tion in wheelchair-using persons with a spinal cord injury.
Spinal Cord 44: 152159.
van Tuijl JH, Janssen-Potten YJ, Seelen HA (2002). Evalua-
tion of upper extremity motor function tests in tetraplegics.
Spinal Cord 40: 5164.
Venier LH, Ditunno JF, Jr. (1971). Heterotopic ossification in
the paraplegic patient. Arch Phys Med Rehabil 52: 475479.
Ward AB (2003). Long-term modification of spasticity.
J Rehabil Med 41: 6065.
Warren JW (1987). Catheter-associated urinary tract infec-
tions. Infect Dis Clin North Am 1: 823854.
426 H. BINDER
Warren VC (2002). Glossopharyngeal and neck accessory
muscle breathing in a young adult with C2 complete
tetraplegia resulting in ventilator dependency. Phys Ther
82: 590600.
Whiteneck G, Harrison-Felix C, Mellick D et al. (2004).
Quantifying environmental factors: a measure of physical,
attitudinal, service, productivity, and policy barriers. Arch
Phys Med Rehabil 85: 13241335.
Widerstrom-Noga E, Biering-Srensen F, Bryce T et al.
(2008). The International Spinal Cord Injury Pain Basic
Data Set. Spinal Cord 46: 818823.
Williams B (1990a). Post-traumatic syringomyelia, an update.
Paraplegia 28: 296313.
Williams PE (1990b). Use of intermittent stretch in the preven-
tion of serial sarcomere loss in immobilised muscle. Ann
Rheum Dis 49: 316317.
Wirth B, van Hedel HJ, Kometer B et al. (2008). Changes in
activity after a complete spinal cord injury as measured
by the Spinal Cord Independence Measure II (SCIM II).
Neurorehabil Neural Repair 22: 145153.
Wood DE, Burridge JH, van Wijck FM et al. (2005). Biome-
chanical approaches applied to the lower and upper limb for
the measurement of spasticity: a systematic review of the
literature. Disabil Rehabil 27: 1932.
World Health Organization (1958). The First Ten Years of the
World Health Organization. World Health Organization,
Geneva.
Wyndaele M, Wyndaele J-J (2006). Incidence, prevalence
and epidemiology of spinal cord injury: what learns a
worldwide literature survey? Spinal Cord 44: 523529.
Xie J, Boakye M (2008). Electrophysiological outcomes after
spinal cord injury. Neurosurg Focus 25: E11.