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Spinal Cord Injury

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51 views16 pages

Spinal Cord Injury

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zwecker4458
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
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Review Article

Spinal Cord Injury


Address correspondence
to Dr Mark A. LiVecchi,
Unity Health System,
89 Genesee Street,
Rochester, NY 14611, Mark A. LiVecchi, DMD, MD, FAAPMR
[email protected].
Relationship Disclosure:
Dr LiVecchi reports no
disclosure. ABSTRACT
Unlabeled Use of A spinal cord injury is a devastating, life-changing neurologic event that challenges
Products/Investigational
Use Disclosure: Dr
patients, families, and caregivers. A myriad of neurologic and medical sequelae occur
LiVecchi reports no subsequent to the original insult. This article discusses epidemiology, primary and
disclosure. secondary injuries, acute therapy, and neuroprotective agents as well as the exciting
Copyright * 2011, areas of spinal cord recovery and regeneration, with an emphasis on cellular trans-
American Academy of
Neurology. All rights plantation. Neurologic neurorehabilitation techniques and equipment are also
reserved. reviewed, with a focus on their relation to increasing the independence and functional
capacity of the patient. The article concludes with the clinical presentation and
management of common spinal cord injury complications.

Continuum Lifelong Learning Neurol 2011;17(3):568–583.

EPIDEMIOLOGY the cord proper. Fractures and disloca-


The incidence of spinal cord injury (SCI) tions are common etiologies. Complete
in the United States is approximately 40 transection of the cord is rare and is
cases per million population per year. noted primarily in instances of pene-
The estimated prevalence is 350,000, trating knife or bullet wounds. SCIs are
with a male-to-female ratio of about 4 to most common in the cervical region
1, according to the National SCI Statis- and at the thoracolumbar junction, with
tical Center Database (www.nscisc.uab. the C5 level being most common.
edu/public_content/nscisc_database. Edema often further compromises cord
aspx). The average age at time of injury function acutely, and it is not uncom-
is 31.7 years, with teenagers and young mon for a level to ascend over the first
adults having the greatest risk. The most 24 hours. Significant damage to the
common etiology is motor vehicle ac- spinal cord produces spinal shock with
cident (34.5%), followed by falls (22%), subsequent flaccid paralysis below the
penetrating injuries such as gunshot level of the lesion. During this period
wounds (17.2%), and sports injuries of spinal shock, the tonic and phasic
(8%). Falls are the most common cause stretch reflexes are reduced or absent,
of SCI in people over 60 years of age. The and the bladder is flaccid. The syn-
most common sports injury is diving. drome is transient and lasts from 24
The American Spinal Injury Associa- hours to 3 months, with 3 weeks being
tion (ASIA) Impairment Scale is used to the average length. The return of the
assist with grading SCIs (Appendix A). bulbocavernosus reflex heralds the end
Grading the injury as complete or in- of the spinal shock period. The inci-
complete has prognostic and therapeu- dence of traumatic paraplegia and tet-
tic implications. raplegia is approximately equivalent, as
is the incidence of complete versus in-
PATHOPHYSIOLOGY complete injuries. Approximately 95%
Most SCIs result in acute cord compres- of patients with initially complete le-
sion and vascular compromise due to sions will have permanent neurologic
displacement of bone and/or disk into impairments. The level of the lesion

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KEY POINT
may change as edema resolves over calcium in the interstitial fluid can disturb h A loss of impulse
several weeks. Patients with incomplete neuronal excitability and synaptic trans- conduction in
lesions often experience considerable mission. Total tissue calcium is increased anatomically intact
neurologic recovery, and improvement in injured spinal segments, becoming tracts is widely
may continue for several years. Con- significantly elevated at 45 minutes post- recognized in both
versely, those with partial SCI often ex- injury and peaking at 8 hours postinjury. animal models and
perience worsening neuropathic pain Elevated calcium levels persist for at least human patients with
and spasticity. Functional abilities are 1 week following injury. Intracellular cal- spinal cord injury. Even
dictated by the level of the lesion per cium accumulation may occur via influx small alterations
the ASIA grading method. The ASIA through either voltage-dependent cal- in the concentration of
certain ions in the
defines the level of injury as the lowest cium channels or the NMDA-receptor
interstitial fluid can
intact segment where the associated channel, along with failure of the calcium
disturb neuronal
key muscle is graded a 3 (antigravity) or adenosine triphosphataseYmediated ex- excitability and
better (Appendix A). Appendix A also trusion and/or release from intracellular ultimately synaptic
summarizes the key muscles and their organelles. Increased calcium levels have transmission.
corresponding innervation levels. also been linked to sequestration and
The initial insults to the spinal cord formation of complexes with organic phos-
cause immediate and irreversible dam- phates. Excess calcium exerts deleterious
age. Additionally, the spinal cord is sub- effects on a variety of cellular functions.
jected to secondary insults mediated The activation of calcium-dependent
by cellular and molecular events in a phospholipases results in breakdown of
cascading fashion.1 Although these cas- cellular membranes and subsequent pro-
cades propagate over days to weeks, duction of arachidonate. The metabolism
experimental SCI models have shown of arachidonate in turn yields throm-
that the most extensive cell death boxanes, leukotrienes, and free rad-
occurs within hours postinjury.2 Sub- icals, all of which contribute to tissue
stances involved in secondary injury injury. Calcium in excess may in fact
include membrane breakdown products serve as the common mechanism of
such as arachidonic acid, leukotrienes, cellular death following a variety of CNS
and thromboxane.3Y5 Excitatory amino insults.
acids, monoamines, neuropeptides, and Extracellular potassium levels are
cations such as calcium also play a role acutely elevated following SCI, with sub-
in the secondary mechanism of injury. sequent chronic depletion. This acute
Localized edema and ischemia are fol- elevation appears to result in partial
lowed by inflammation and ultimately membrane depolarization, contributing
necrosis. This early time period is critical to conduction block along with the afore-
and is currently the subject of studies mentioned calcium aberrations. The
geared toward possible interventions. eventual loss of potassium from the con-
Calcium is of particular interest be- tused spinal cord may be reflective of
cause it plays many vital roles in the re- membrane instability and impending cell
gulation and maintenance of the cellular death. Free radicals propagated during
environment. Calcium is involved in the SCI can damage the phospholipid and
regulation of sodium and potassium con- cholesterol components of biological
ductance during neuronal excitation as membranes. These radicals are formed
well as the modulation of many critical by the reactive iron species supplied by
enzymes. In addition, calcium is inte- hemoglobin during an SCI hemorrhage.
gral to the storage and release of neuro- A marked increase of the excitatory
transmitters at synaptic junctions. Even amino acids glutamate and aspartate also
small alterations in the concentration of occurs early in the postinjury process.

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Spinal Cord Injury

KEY POINTS
h Following traumatic These levels peak in the first few minutes Peripheral cell populations are recruited
spinal cord injury, after trauma. to the site of SCI. Activated microglia and
the first detectable In vitro studies have implicated glu- astroglia are noted. The microglial cells
morphologic tamate receptor activation in delayed become phagocytic when activated and
abnormality in the tissue injury as a result of cell swelling lead to further neuronal degeneration.
tissue is an alteration of and activated proteases, kinases, and Neutrophils are recruited in a similar
the microvasculature in phospholipases, which follow the intra- time frame as the microglia, within hours
the central gray matter. cellular accumulation of both sodium of the spinal cord insult. Lymphocytes
h Clinical trials from and calcium. Studies have also demon- and monocytes are present by day 3 and
animal models suggest strated a role for NMDA receptors in peak in number by day 7. The role of
that only a small secondary tissue injury. In fact, NMDA- the immune response6 to SCI is quite
number (5% to 10%) receptor blockade reduces the extent of complex. Unfortunately, the result of
of surviving axons are histologic damage. !-amino-3-hydroxy- this complicated process is an extension
needed to support 5-methyl-4-isoxazole propionic acid re- of the initial injury zone and the
functional recovery.
ceptors also appear to play a role in production of a nonfunctional scar in
h If the conduction secondary tissue insult. The first detect- the spinal cord. Interestingly, evidence
deficits caused by focal able morphologic abnormality in in- demonstrates that considerable func-
demyelination could jured spinal cord tissue is seen as an tional recovery can be achieved even if
be remediated, other
alteration in the microvasculature of the only 5% to 10% of spinal axons survive
medical interventions
central gray matter. Within minutes, the injury.4 This gives hope that acute
may ultimately become
more effective for
small multifocal petechial hemorrhages interventions that minimize tissue in-
patients with spinal are present at the site of compression jury due to the aforementioned im-
cord injury. and spread in a radial manner through mune and inflammatory processes may
the involved gray matter. This spread have significant potential to assist with
h Studies of blood
flow in the injured
continues into the white matter over functional recovery after SCI.
spinal cord reveal the next few hours. At 4 to 8 hours, Studies of postinjury blood flow in
hypoperfusion of the aneurysmal dilations and arterial rup- the spinal cord have consistently found
gray matter as tures are often seen. Microthrombi are hypoperfusion of the gray matter.7 In-
a consistent frequently noted in capillary-sized ves- terestingly, both hypoperfusion and
pathologic finding. sels within the first 24 hours. As the hyperperfusion of the white matter
centrally located petechiae enlarge, glial have been observed. It remains unclear
reactions and neuronal alterations whether the etiology of this hypoper-
become evident. In the first postinjury fusion is systemic hypotension or a
hour, eosinophilia of nerve cells is loss of autoregulation. This reduction
noted. Subsequently, shrunken neu- of blood flow to the spinal cord results
rons with indistinct nuclei, smudged in a significant reduction of oxygen de-
cytoplasm, absent Nissl bodies, and livery to its tissues.
irregular shapes and hyperchromatiza-
tion are encountered. These necrotic ACUTE THERAPY AND
alterations occur initially in the gray NEUROPROTECTION
matter and then spread into the white In 1990, the Second National Acute
matter by 8 hours. Retraction bulbs Spinal Cord Injury Study (NASCIS-2)
representing severed axon cylinders ap- demonstrated that high doses of
pear and progress in a centrifugal man- methylprednisolone (MP; 30 mg/kg/bolus
ner toward the pial surface of the spinal followed by 5.4 mg/kg/h for 23 hours)
cord over the next several days. The improved motor and sensory neuro-
relatively slower evolution of necrotic logic scores by approximately 20% in
changes in the white matter as com- patients with SCI compared with the
pared to the gray matter is of interest. placebo or naloxone groups.8 MP was

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only effective when administered within within 3 hours of SCI, and initiation of
8 hours postinjury, but it improved re- treatment within the first 3 hours was
covery in patients with both complete determined to be optimal. Additionally,
and incomplete injuries. This recovery tirilizad was as effective as 24-hour
of function occurred over an extended MP treatment. Lastly, the study demon-
period of time, with improvements in strated that if treatment is begun more
the treated group being observed as than 3 hours following SCI, the MP
long as 1 year postinjury. MP appears dosing regimen should be extended to
to interfere with the secondary injury 48 hours. It is worth noting that the
cascade by inhibiting free radical forma- incidence of pneumonia and sepsis sig-
tion and subsequent lipid peroxidation nificantly increased with 48-hour MP
and breakdown.9 Adverse effects of MP dosing. Interestingly, tirilizad showed
were observed during the NASCIS-2. no typical glucocorticoid side effects in
The most common complications were this study. This knowledge may lend
urinary tract infections and pneumo- itself to the use of tirilizad beyond the
nia.8 The incidence of wound infections 48-hour window, when lipid peroxida-
and gastrointestinal hemorrhages was tion reactions may still cause damage to
slightly higher in treated subjects com- an injured spinal cord.
pared with controls but did not reach GM1 ganglioside is a glycolipid com-
statistical significance. Nonetheless, this pound containing sialic acid found in
research confirmed that the neuropro- mammalian cell membranes that plays
tective effects of MP were independent a vital role in neuronal development
of its glucocorticoid properties and ini- and differentiation. A number of stud-
tiated the search for a new class of ies have demonstrated that these gly-
antioxidant drugs lacking the unwanted colipids promote neuronal sprouting,
glucocorticoid side effects. This led to outgrowths, and synaptic transmission
the discovery of 21-aminosteroid com- when exogenously administered after
pounds (lazaroids). Of these, the most experimentally induced SCI. Analysis of
promising in its neuroprotective effects the data from the GM1 SCI study dem-
in experimental models of SCI was onstrated enhanced function in the
tirilizad mesylate.10,11 lower extremities of subjects who re-
The NASCIS-3 incorporated tirilizad, ceived this intervention.12 However,
which is actually a more potent inhibitor interpretation of these data is compli-
of lipid peroxidation than MP. Three cated by the fact that all subjects re-
groups of patients were evaluated. The ceived MP and that the number of
first group (control) was treated with patients in the study was 34, with only
the 24-hour MP dosing regimen shown 16 receiving GM1. The second multi-
to be effective in the NASCIS-2. The center GM1 trial, enrolling hundreds of
second group was also treated with MP, patients, has yet to be published.
with the infusion extended to 48 hours. Recent research suggests that the
The third group was treated with a most reactive oxygen free radical species
single 30 mg/kg IV bolus of MP plus in acute SCI may be peroxynitrite, which
48-hour administration of tirilizad.10 Of is formed by superoxide and nitric oxide
note, this study had no placebo group, radicals combining. Peroxynitrite causes
as it was deemed unethical to withhold diffuse damage to lipids, proteins, and
MP from any patient with SCI. The nucleic acids.13 Prototypical scavengers
study revealed that all three treatment of peroxynitrite include penicillamine
arms produced a comparable degree of and 2,2,6,6-tetramethylpiperidine-1-oxyl,
recovery when treatment was initiated both of which are neuroprotective in cell

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Spinal Cord Injury

KEY POINT
h Demyelination of axons culture and in vivo models of acute CNS formation of a dense glial scar that in-
within the spinal cord injury.14 hibits axonal extension.18,19 It was once
is a consistent Blood pressure management is com- believed that the scar alone was a
component of the plex and should be considered on a dense physical barrier to axonal growth
pathology of spinal case-by-case basis. Based on the amount and development; however, it has re-
cord injury. of cellular damage related to ischemia, cently been discovered that the astro-
a prudent recommendation for mean ar- cytes express key growth inhibitory
terial pressure in the acute phase of SCI molecules that also appear to suppress
is between 80 mm Hg and 100 mm Hg. axonal regeneration irrespective of the
Cellular damage and dysfunction sec- scar’s presence. In addition to astro-
ondary to ischemia ultimately lead to cytes, oligodendrocytes within the in-
a decrease in cellular energy produc- jury region and within myelinated tracts
tion, further compounding the damage beyond the injury zone express sev-
cycle. Future research possibilities may eral inhibitory factors that inhibit ax-
include supplementing patients with onal growth and propagation. Many of
SCI with energy substrates such as crea- these inhibitory molecules are actual
tine phosphate or ribose, which may components of the myelin sheath.20,21
help thwart some of the secondary cel- In fact, axonal sprouting in the adult
lular damage linked to a decrease in CNS is inversely proportional to the
adenosine 5¶-triphosphate production degree of myelination. Pioneering
and maintenance as a result of hypoten- work by Schwab and colleagues, along
sion and ischemia. with later studies, revealed the inhib-
itory nature of these molecules, which
RECOVERY AND REGENERATION include Nogo-A, myelin-associated gly-
The most dramatic effects of SCI are coprotein, and chondroitin sulfate
mediated by the interruption of long proteoglycan.22Y25 This led to the de-
tracts that carry information to and from velopment of functional blocking anti-
the brain and distal regions of the spinal bodies against Nogo-A. Animals treated
cord. As previously mentioned, the with antibodies against Nogo-A exhib-
survival of only a small number of axons ited long-distance axonal regeneration
(5% to 10%) is needed to support func- in the CNS.26 In addition, immunologic
tional recovery.4 In the early 1980s, treatments directed at the myelin
studies by Aguayo demonstrated that sheath resulted in a well-defined region
grafts of peripheral nerves could stim- of complete demyelination that could
ulate the long-distance regeneration of be precisely controlled. Of note, no
amputated central axons in both the axonal damage occurred. Remyelina-
optic nerve and spinal cord.15Y17 These tion was observed to begin approxi-
studies revealed that CNS axons have mately 14 days after the cessation of
the inherent ability to regenerate under the treatment.27Y29
the right conditions and suggest that Cell transplantation in the CNS
the inability of the adult CNS to regen- has been most successful in treating
erate can be attributed to an inhospit- Parkinson disease. A relatively long his-
able CNS environment. This unsupportive tory of research exists on the possible
CNS environment consists of active use of fetal tissue in the treatment of
inhibitors of axonal outgrowth along SCI. Transplanted fetal tissue has been
with a tissue environment lacking essen- shown to survive within the spinal cords
tial neurotrophic molecules. The prolif- of animals with both acute and chronic
eration of reactive astrocytes within and injuries. In addition, the density and
around the SCI site contributes to the extent of host axonal growth of fetal

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KEY POINT
transplant tissue can be enhanced by plantation into adult rats with midthora- h The spinal cord,
the administration of neurotrophic fac- cic spinal cord hemisection injury.48Y50 severed from
tors such as brain-derived neurotrophic The spinal cord, when severed from supraspinal structures,
factor (BDNF)30 or neurotrophin-3 supraspinal structures, is capable of gen- is capable of generating
(NT-3).31Y33 Furthermore, the combi- erating alternating motor activity useful alternating motor
nation of fetal tissue transplantation for locomotion based on spinal cord activity useful for
and growth factor administration has circuitry termed the ‘‘central pattern locomotion based on
been shown to result in the upregulation generator.’’ Thus, when considering spinal cord circuitry
of the inducible transcription factor c- the potential for ambulation in patients termed the ‘‘central
Jun, which is associated with the regen- with SCI, more than the lower extremity pattern generator.’’
eration of axotomized CNS axons.33Y35 motor score (based on muscle strength)
The growth permissiveness of the needs to be considered. Body weightY
peripheral nerve is largely because supported treadmill training (BWSTT)
of the Schwann cells and their basal has been used extensively to induce
lamina.36Y38 Unfortunately, Schwann coordinated stepping and locomotion
cells transplanted into the CNS do not in patients with SCI who have less than
provide for the regeneration of injured the requisite conventional lower ex-
axons. The discovery of the olfactory tremity motor score (strength). In fact,
ensheathing cell (OEC) may provide a ASIA A and ASIA B patients who do not
more growth-permissive axonal envi- have the minimal strength required for
ronment in the CNS.12,39,40 The olfac- conventional ambulation using devices
tory system is unique in that it supports such as the parallel bars are able to
the regeneration of axons from the execute the stepping pattern and loco-
olfactory epithelium into the CNS motion using BWSTT. See Video Seg-
throughout the life of the organism. ment 14 for an example of the use of
This ability has been attributed to the BWSTT in a patient with partial SCI.
OEC.41Y43 These cells also secrete a EMG studies have shown that the level
number of neurotrophic factors such as of excitation and activation of the lower
BDNF, NT-3, and nerve growth factor limbs in patients with SCI during step-
(NGF).31Y33 Recent in vivo studies re- ping using BWSTT exceeds what can be
port a remarkable axonal regeneration achieved by attempting voluntary activa-
and functional recovery following the tion of the same muscles.51Y53 It appears
transplantation of OECs into transec- that the spinal cord can learn to activate
tion injuries of the spinal cord.39 This a greater percentage of motor units
regeneration was correlated with a and/or activate them at a higher fre-
marked improvement of forelimb use quency as a result of step training using
in rats, per Raisman and colleagues.44Y46 BWSTT.54,55 Furthermore, after step
Ramón-Cueto and colleagues also com- training, ambulatory ability often im-
mented on the high degree of axonal proves without any change in the lower
regeneration and its correlation with extremity motor score.56 The drawback
partial recovery of function in adult to this approach is the time, intensity,
rats.45,47 Gene therapy for SCI has been and therapy support often required to
employed using NGF-secreting fibro- produce noticeable functional gains. The
blasts. Regeneration strategies using spinal cord is much more ‘‘plastic’’ than
fibroblasts have mostly involved geneti- once thought. It appears that a high
cally engineered overexpression of neu- level of processing of complex proprio-
rotrophic factors. These NGF-secreting ceptive input occurs in the spinal
fibroblasts have been shown to elicit cord.57 Although fine motor control of
axonal elongation following their trans- the lower extremities is mainly derived

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Spinal Cord Injury

KEY POINTS
h Patients with lesions from the brain, most of the details as- stroke, and cardiac insults may result.
at T6 or higher are sociated with the neural control of stand- The patient must immediately be placed
at risk for autonomic ing and stepping can be processed solely in an upright position and a search for
dysreflexia, a potentially within the spinal cord circuitry. The level the cause must begin expeditiously.
life-threatening medical of motor function that emerges follow- Hypertension may be treated with hydra-
complication of spinal ing SCI is defined and shaped in large lazine, labetalol, or transdermal nitrates.
cord injury. part by use-dependent mechanisms.58Y60 Blood pressure needs close monitoring
h The demineralization The use of BWSTT combined with phar- for several hours after treatment to
of bone is common macologic interventions, such as adrener- watch for aberrations in this sensitive
following spinal cord gic agonists shown to induce locomotion population. Dysreflexia is a major com-
injury and occurs very and coordinated stepping in patients with plication of labor and delivery, and
quickly after the onset SCI, represents an area of great promise spinal epidural anesthesia is the treat-
of paralysis, with up to in the rehabilitation of this population. ment of choice for patients with SCI.
22% of bone stores 4-Aminopyridine (4-AP) blocks fast
affected within a Orthostatic Hypotension
voltage-dependent potassium channels
3-month period.
in nerve membranes, thereby increasing Like autonomic dysreflexia, orthostatic
the excitability of nerve cells or axons by hypotension also affects patients with
delaying the repolarization of the mem- lesions higher than T6. It may be elicited
brane following an action potential. As by tilting the patient above 60 degrees or
of March 2010, 4-AP is available in the by a postprandial state. The lack of sym-
United States in a sustained-release pre- pathetic outflow and the patient’s inabil-
paration known as dalfampridine and is ity to vasoconstrict the splanchnic bed
approved by the US Food and Drug Ad- are ultimately at the root of this problem.
ministration for the treatment of multi- Reflex tachycardia is insufficient to main-
ple sclerosis. Clinical trials with 4-AP in tain cerebral perfusion, and the patient
human subjects with chronic incomplete loses consciousness. Treatment consists
SCI have demonstrated enhancement of placing the patient in the Trendelen-
of voluntary motor unit recruitment, de- burg position in the acute phase, with
creased spasticity, and a temporary im- subsequent preventive measures such as
provement in both motor and sensory compression stockings, abdominal bind-
function below the lesion. It is interesting ers, salt tablets, and adequate fluid main-
that this improved neurologic status tenance. Refractory cases may require
extended beyond the expected pharma- pharmacologic interventions such as flu-
cokinetic time course for 4-AP. drocortisone, ephedrine, or midodrine.

REHABILITATION Bone Demineralization


MANAGEMENT PROBLEMS Bone demineralization is a common
complication of SCI that occurs quickly
Autonomic Dysreflexia after the onset of paralysis. Muscular in-
Patients with SCI with lesions at T6 or activity and a marked decrease in weight
higher are at risk for developing auto- bearing set the stage for an imbalance in
nomic dysreflexia, which is a true medi- the cellular activity of bone. Osteoclastic
cal emergency. Autonomic dysreflexia activity outpaces osteoblastic activity and
occurs when a noxious stimulus below results in a net loss of bone mass. Tra-
the level of the lesion, most commonly becular bone is most affected by this pro-
urologic or gastrointestinal, triggers cess. Symptomatic hypercalcemia may
headache, hypertension, bradycardia, develop, resulting in nausea, vomiting,
diaphoresis, anxiety, and piloerection. or anorexia. The osteopenic bone is
Intracerebral hemorrhage, seizures, susceptible to fractures, which present a

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diagnostic challenge in the absence of flow, decreased nutrition, and inferior
pain. Soft splints, rather than casts or fix- structural collagen. Patients and care-
ators, are the treatment of choice for givers need to be diligent with position-
fractures in the SCI population. Studies changing techniques such as wheelchair
are now underway evaluating the effects pushups and turning every 2 hours. The
of biphosphonate treatments combined absence of certain neurotrophic factors may
with high doses of vitamin D3 and ele- also play a role in pressure ulcer formation.
mental calcium in an attempt to normal- Wheelchairs play a vital role in in-
ize the bone mass in this population. creasing the functional independence
Weight-bearing activities in a standing and mobility of patients with SCI. Tilt-
frame and BWSTT provide some benefits. in-space wheelchairs provide the addi-
tional advantage of offering pressure
Gastrointestinal Issues relief and assisting with orthostatic hy-
Constipation is extremely common after potension management. By tilting the
SCI. To assist with defecation, the physi- chair more than 30 degrees, shear forces
cian may use pharmacologic agents such decrease, spasticity decreases, and pul-
as stool softeners and motility agents monary secretion mobilization and man-
which, along with suppositories, consti- agement is improved. However, in order
tute a bowel program to allow for regu- to truly redistribute the skin pressure,
lated and timed bowel movements. the system must be capable of tilting a
Gastroesophageal bleeding is not un- minimum of 30 degrees, with the ability
common after SCI. Increased gastric acid to tilt 45 degrees considered ideal.
secretion coupled with a decrease in the Wheelchair cushions assist with pressure
sympathetically mediated vasoconstriction relief, aid in truncal and pelvic stability,
may lead to ulceration and hemorrhage. and increase patient comfort. Choice of
The SCI population also has a threefold cushion is determined by the patient’s
increased risk of cholecystitis, which is the needs as well as the cushion’s charac-
most common cause of emergency sur- teristics. For example, a Roho cushion
gery in this population after the acute provides excellent pressure relief; how-
injury phase. Possible etiologies include ever, it is an extremely compliant surface
abnormal gallbladder motility and biliary that may not be stable enough for a
secretions and impaired enterohepatic patient who would be using the cushion
circulation. Pancreatitis is common in the to assist with wheelchair transfers. Ulti-
first month postinjury and appears to be mately, a balance between cushion com-
related to the elevated blood calcium fort and functionality will determine the
levels and concomitant increase in pan- correct cushion choice for each patient.
creatic secretion viscosity.
Syringomyelia (Posttraumatic
Pressure Ulcers Cystic Myelopathy)
Pressure ulcers are common in both Syringomyelia occurs in 0.3% to 3.2%
acute and chronic patients with SCI. In of the SCI population and is the most
fact, they are present in an estimated 30% common cause of progressive myelop-
of these patients at some point during athy in this group (Case 9-1). Lesions
their lifetime. These ulcers are costly and are located around the level of injury and
disabling; however, they are mostly pre- usually progress in a cephalad direction.
ventable by strict adherence to patient A decrease in strength or temperature
positioning and turning schedules. Skin sensation in a previously unaffected mo-
below the lesion level is not only insen- tor or sensory level and neuropathic
sate but also suffers a decrease in blood pain often herald the presence of a
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Spinal Cord Injury

KEY POINT
h Pulmonary function is
abnormal in virtually all
Case 9-1
A 24-year-old man with chronic T2 American Spinal Injury Association B spinal
patients with spinal
cord injury (SCI) presented to the clinic. His initial SCI was 4 years earlier. He
cord injury.
reported that approximately 6 months ago he began to have difficulty
telling the difference between warm and cold objects in his hands. Shortly
thereafter he experienced left- and then right-sided root pain in the T2
distribution. More recently he had noticed increasing spasticity in his legs,
difficulty with transfers, and new onset of weakness in his grip bilaterally.
MRI demonstrated an intramedullary cavity extending from T2 in a
caudal direction including T1, C8, and C7. Neurosurgery was consulted and
a shunt was placed. Despite this surgical intervention, the patient had
no significant return of strength in the intrinsic muscles of his hand. His
T2 root pain and lower extremity spasticity improved. The addition of
gabapentin and an increase in baclofen dose yielded further pain relief.
Comment. This case deals with syringomyelia and is directly related to
SCI management. It also deals with the management of spasticity.

syrinx. MRI is the most accurate diag- to cough and clear their airway. In fact,
nostic technique available. Treatment 67% of all patients with SCI develop
is the surgical placement of a shunt. atelectasis or pneumonia within the first
Repeat imaging may be necessary over 24 days postinjury. Furthermore, pneu-
the span of several months, as symp- monia is the leading cause of death
toms may appear prior to the actual among all patients with SCI over time. A
development of the syrinx. great deal of attention needs to be placed
on preventing pulmonary complications
Pulmonary Complications in this population. Incentive spirometry
Pulmonary function is abnormal in vir- is absolutely essential. Additional inter-
tually all patients with SCI. Those with ventions such as teaching cough-assist
lesions at C4 and above have a paralyzed techniques to caregivers and the use of a
diaphragm and are usually ventilator pneumobelt can also assist with secre-
dependent. For lesions above C4, motor tion management. A pneumobelt is an
neurons of the phrenic nerve may be inflatable device that compresses the
intact, and phrenic nerve pacing may be abdominal wall, assisting with exhalation.
a viable solution for those patients with Also, the diaphragms of patients with SCI
SCI who would otherwise be ventilator are at a mechanical disadvantage when
dependent. Phrenic nerve pacing is the patient is upright. The use of an
done 6 months postinjury to allow the abdominal binder in this position assists
flail chest to develop the necessary in the mechanics of breathing.
rigidity. Patient survival is improved with
pacing. Patients with SCI present with a Neurogenic Bladder
restrictive pattern of lung dysfunction. During the acute period after a spinal
All lung volumes, except for residual cord insult, the patient presents with
volume, are decreased on pulmonary what is termed an areflexic bladder, a
function testing. Patients with lower bladder incapable of generating contrac-
cervical and midthoracic to high tho- tion on its own. An indwelling Foley
racic lesions have paralysis of the catheter is the treatment of choice
abdominal muscles, which increases in- during this time period to safely rid the
trathoracic pressure during exhalation. patient of urine as well as to monitor
As a result, they have a decreased ability fluids, especially during resuscitative

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attempts. Once patients with SCI are out best diagnostic tool for detecting heter-
of spinal shock, approximately 85% will otopic ossification. Treatment is with
manifest what is termed detrusor etridronate 20 mg/kg per day for 2
sphincter dyssynergia. Clinically, this weeks followed by 10 mg/kg per day
presents as small, infrequent voids with for 10 weeks. No surgery is recom-
a significant amount of urine retained mended until the heterotopic bone ma-
as the bladder contracts against an tures, which takes approximately 12 to
already-contracted external urinary 18 months. Of note, heterotopic bone is
sphincter. It is extremely important to highly vascular and presents a significant
keep the retained urinary volume less risk of bleeding during surgical removal.
than 400 mL to 500 mL. Once the vol-
ume gets above 400 mL, vesicourethral Spasticity
reflux may develop, which predisposes Spasticity occurs in 40% to 60% of pa-
the patient to kidney infection and po- tients with SCI. A sudden change in spas-
tential kidney damage. Postvoid bladder ticity may be a diagnostic clue heralding
scanning and intermittent catheteriza- the onset of a pathologic process such
tion programs can be used to keep as a urinary tract infection, fecal impac-
bladder residual volumes less than tion, or pressure ulcer. The first action
400 mL. In addition, pharmacologic should always be a clinical investigation
agents such as alpha-blockers can assist into the possible etiology representing a
with decreasing the external sphincter change in the patient’s tone. Each pa-
tone and promote more efficient urinary tient’s spasticity and tone should be eval-
emptying when the detrusor does con- uated based on functional perspective.
tract. A bladder program is vital to ensure For example, some increase in tone may
acute and long-term urinary and renal actually be considered beneficial and
system integrity in the patient with SCI. functional, decreasing the burden of care
and improving activities of daily living.
Heterotopic Ossification However, if the increased spasticity and
Heterotopic ossification most commonly tone are interfering with patient care
occurs between the first and fourth (eg, perineal hygiene, transferring) or
month following SCI. It is clinically sig- decreasing the patient’s independence,
nificant in an estimated 10% to 20% of the clinician is faced with choosing
patients with SCI and most commonly appropriate treatment options. Physical
affects the following joints, in order of modalities such as passive range-of-
prevalence: hips, knees, shoulders, and motion exercises, the application of cold
elbows. Risk factors for the formation of and warmth, vibration, acupuncture, and
heterotopic ossification include spastic- splinting are important nonpharmaco-
ity, age, pressure ulcer and proximity to logic methods for reducing spasticity and
the joint, the completeness of the SCI, tone for variable durations. Neverthe-
and trauma to the joint area. The clinical less, pharmacologic treatment is often
diagnosis will consist of a localized soft required in the management of spasticity
tissue swelling that may mimic a deep in this population. Baclofen, a ,-amino-
vein thrombosis and require a clinical butyric acid agonist, remains the treat-
workup to rule out venous involvement. ment of choice to decrease spasticity
The joint will have decreased range of in patients with SCI. Unfortunately, bac-
motion and the patient or therapist lofen can produce sedation and the dose
may also note a decrease in the ability must be adjusted in patients with renal
to perform tasks that were previously impairment. In cases of severe spasticity
possible. A triple-phase bone scan is the refractory to oral baclofen, intrathecal
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Spinal Cord Injury

baclofen delivered via an implantable tion of childbearing in the female pop-


pump may be necessary. It should be ulation with SCI. Attainment of orgasm
noted that baclofen delivered intrathecally and sexual satisfaction in women with SCI
is 100 times more potent than its oral have not been adequately studied.
analog. Another systemic agent available SCI also affects male sexuality and
for the treatment of spasticity is tizana- fertility. Psychogenic erections are medi-
dine. An alpha agonist, this agent restores ated through both the sympathetic nerv-
the noradrenergic reduction of tone in ous system via the hypogastric plexus
patients with SCI. Side effects include an- (T11 through L2) and the parasympa-
kle edema, depression, and hypotension. thetic nervous system sacral plexus (S2
For more focal spasticity, botulinum toxin through S4). Conversely, reflexogenic
injections may be used. Because botuli- erections result from sacral stimulation
num toxin is injected in a focal manner, via the parasympathetic nervous system
the possibility of unwanted systemic side (S2 through S4). With stimulation, the
effects is decreased. In cases of severe arteriolar walls within the penis relax,
refractory spasticity affecting perineal which allows the rapid influx of blood.
hygiene or skin integrity, a surgical Distension of the spongy lacunes with
tenotomy of the affected musculature blood causes compression of the venous
such as the adductors may be required. outflow which helps to maintain an erec-
tion. Male orgasm is divided into two
Sexuality phases: emission and ejaculation. The
An SCI can have a significant impact on a emission phase is mediated by the sym-
person’s body image and self-esteem pathetic nervous system (T10 through
because of feelings of loss, particularly L2), while the ejaculatory phase is medi-
with respect to human sexuality issues. ated by the sacral parasympathetic nerv-
Patients with SCI often report that they ous system and the somatic outflow from
receive little to no information or dialog the pelvic nerve and pudenal nerves (S2
regarding sexual functioning or repro- through S4). Males with complete SCIs
ductive issues after their SCI. Several are unable to obtain psychogenic erec-
issues regarding sexual function and tions, but they are able to obtain reflexo-
fertility in both men and women with genic erections via the intact sacral spinal
SCI should be considered. cord (S2 through S4). Interestingly, 92% of
Women with a complete SCI have males with SCI are able to obtain erec-
reflexogenic but not psychogenic vaginal tions. Ejaculation poses more of an
lubrication. Women with an incomplete obstacle to conception. Even when ejacu-
SCI may actually have both psychogenic lation is obtained by natural, electrical, or
and reflexogenic vaginal lubrication. Of vibratory methods, the difficulty with con-
note, the lower vagina is innervated by ception involves the resultant sperm qual-
the pudendal nerve (S2 through S3), ity. Sperm quality, in particular low sperm
while the afferent sensory fibers from motility, is significantly impaired in males
the upper vagina pass via the splanchnic with SCI and is a large contributor to male
nerve of the parasympathetic nervous sys- infertility in this population. Approximately
tem (S2 through S4). Immediately follow- 40% of all males with SCI are ultimately
ing SCI, amenorrhea occurs in 50% to successful in fathering a child with proper
60% of women, and by 6 months post- medical treatment and oversight.
injury 50% of these women resume men-
struating. Once menses returns, a woman Tendon Transfers
with SCI has the ability to have children. The goal of neurorehabilitation is to in-
Premature infants are a known complica- crease the functional ability and quality

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of life for patients with SCI. Tendon for patients with cervical SCI are noted
transfers are surgical techniques that af- in Table 9-1. This table demonstrates
ford patients with tetraplegia the possi- that the increase of just one cervical
bility of increasing their functional level level obtained from a tendon transfer
of independence. Potential outcomes can have profound effects on the

TABLE 9-1 Potential Expected Functional Outcomes for Patients With Complete Cervical
Spinal Cord Injury

Function C3-C4 C5 C6 C7 C8-T1


Feeding May be able Independent Independent Independent Independent
with adapted with equipment with equipment
equipment after set-up
Grooming Dependent Independent with Independent Independent Independent
equipment after with equipment with equipment
set-up
Upper Dependent Requires assistance Independent Independent Independent
Extremity
Dressing
Lower Dependent Dependent Requires May be Independent
Extremity assistance independent
Dressing with equipment
Bathing Dependent Dependent Independent Independent Independent
with equipment
Bed Dependent Requires assistance Independent Independent Independent
Mobility with equipment
Weight Independent Requires assistance Independent Independent Independent
Shifts with power
chair,
dependent in
manual chair
Transfers Dependent Requires assistance Possibly Independent Independent
independent with or without
with transfer board except
board floor transfer
Wheelchair Independent Independent with Independent in Independent Independent
Propulsion with power power chair; short manual chair except curbs
chair, distances in manual with plastic
dependent in chair with lugs or rims on level
manual chair plastic rims on surfaces
level surfaces
Driving Unable Unable Specially Car with hand Car with hand
adapted van controls or controls or
adapted van adapted van
Bowel and Dependent Dependent Independent Independent Independent
Bladder with bowel;
needs assists
with bladder

Reprinted with permission from Kirshblum S, Gonzalez P, Nieves J, et al. Spinal cord injuries (SCI). In: Cuccurullo SJ, ed. Physical medicine and
rehabilitation board review. New York: Demos, 2004.

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Spinal Cord Injury

patient’s independence with activities excellent resources include evidence-


of daily living. Based on the work of based treatment recommendations
Bunnel, it was discovered that tenod- (www.pva.org).
esis could be used to accomplish tip- Survival following SCI has improved
to-tip pinch for patients with tetraple- dramatically, with life expectancies now
gia. Further work by Moberg revealed extending into the sixth and seventh
that the key grip form of opposition decades. As a result, these patients are
between the thumb and the index at risk to develop health conditions
finger was far more valuable to a typically associated with the aging pro-
patient with tetraplegia than the oppo- cess. In addition, continued modifi-
sition pinch described by Bunnel. cation of rehabilitation programs and
Moberg’s goal was for a C5-C6 patient equipment may be necessary as the
to undergo surgical reconstruction to patient with SCI ages. Rehabilitation of
obtain active elbow extension and key patients with SCI focuses on education,
grip for at least one upper extremity. training, and techniques to work around
An international classification of the impairments. The provision of adaptive
upper limb in patients with tetraplegia equipment and environmental modifica-
has since evolved and is based on the tions affords this population increased
remaining useful motor and sensory independence, which is invaluable to
resources available to the patient. Mus- self-esteem and overall quality of life.
cle strength is assessed using the Future scientific advancements in phar-
standard 0 to 5 scale, and the limb is macology, genetics, acute treatment
further classified according to the protocols, and adaptive equipment hold
number of grade 4 to 5 muscles still great promise for patients with SCI.
functioning distal to the elbow. Of Advancements in recent years, such as
note, the timing of the surgical proce- BWSTT and stem cell research, offer
dure is extremely important in this hope that the near future will see ad-
population. The patient should be vances in SCI medicine that not only
neurologically stable for at least 6 delimit the disease process but ultimately
months, with optimal timing being 1 improve the patient’s quality of life.
year postinjury to ensure the muscle’s
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