Traumatic Spinal REVIEW ARTICLE


Cord Injury C O NT I N U U M A U D I O
I NT E RV I E W A V A I L AB L E
O NL I N E
By Alejandro A. Rabinstein, MD, FAAN

S U P P L E M E N T A L D I G I T AL
CONTENT (SDC)
ABSTRACT A V AI L A B L E O N L I N E

PURPOSE OF REVIEW: This article provides an update on the acute and subacute
management and prognostication of patients with traumatic spinal cord
injury.

RECENT FINDINGS: Immobilization of the spine and spine clearance should be

individualized depending on the ability to perform a reliable neurologic
examination, the presence of neck pain, and the imaging findings. Early
surgery (within 24 hours) to achieve definitive cord decompression and
spine stabilization may be beneficial. Ensuring adequate oxygenation and
perfusion and avoiding secondary systemic complications remain the goals
of the critical care of these patients. No neuroprotective treatment has
been shown to improve outcomes. In fact, the use of high-dose
methylprednisolone is now generally discouraged because of its major
systemic adverse effects. Survivors of severe cervical traumatic spinal
cord injury typically sustain substantial long-term functional impairment.
Advances in our understanding of neuroregenerative strategies, especially
stem cell transplantation, can offer the future hope of functional
improvement to the many patients currently living with the consequences
of traumatic spinal cord injury. Yet, at present, these therapies remain
strictly investigational. CITE AS:
CONTINUUM (MINNEAP MINN)
2018;24(2, SPINAL CORD DISORDERS):
SUMMARY: The treatment of traumatic spinal cord injury remains supportive, 551–566.

and prognosis is still poor for patients who are severely affected. While
Address correspondence to
much remains to be learned about how to optimize the acute management Dr Alejandro A. Rabinstein, Mayo
of these patients, future efforts would be most useful if focused on Clinic, Department of Neurology,
injury prevention and the development of effective neuroregenerative W8B, 200 1st St SW, Rochester,
MN 55905, rabinstein.
therapies. alejandro@mayo.edu.

RELATIONSHIP DISCLOSURE:
Dr Rabinstein has received
research/grant support from
INTRODUCTION DJO Global, Inc and receives

T
raumatic spinal cord injury is a serious and complex condition that publishing royalties from Elsevier,
Oxford University Press, and
requires a multidisciplinary approach. Neurologists, neurosurgeons,
UpToDate, Inc.
emergency physicians, intensivists, and rehabilitation specialists must
collaborate to optimize the management of these patients in the UNLABELED USE OF
PRODUCTS/INVESTIGATIONAL
acute, subacute, and chronic phases. Neurologists can be crucial for USE DISCLOSURE:
refined evaluation of the degree of clinical deficits, diagnosis and management of Dr Rabinstein reports no
acute and chronic complications, and estimation of prognosis. This article disclosure.

provides an updated review on traumatic spinal cord injury with a focus on © 2018 American Academy
what a neurologist should know about the condition. of Neurology.

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TRAUMATIC SPINAL CORD INJURY

EPIDEMIOLOGY
The annual incidence of traumatic spinal cord injury in the United States has been
recently estimated at 54 cases per million population, representing approximately
17,000 new cases of traumatic spinal cord injury each year.1 Between 243,000 and
347,000 persons with traumatic spinal cord injury are currently living in the
United States. Many of these people are young, which causes staggering costs in
terms of loss of productivity. Although the average age of patients with traumatic
spinal cord injury has increased over the past few decades from 29 years in the 1970s
to 42 years at present, many patients are still younger than 30 years of age at the
time of the injury.1 Furthermore, some of the most severe cases of traumatic spinal
cord injury occur in this very young segment of the population.
Motor vehicle accidents remain the most common cause of traumatic spinal
cord injury (38%), especially among the young.1 Other frequent causes include
falls (particularly in the elderly; 31%), gunshot wounds and other forms of
violence (14%), and sports or other recreational activities (9%). Traumatic spinal
cord injury occurs predominantly in men (80%) and is overrepresented among
non-Hispanic blacks. Most injuries affect the cervical spinal cord, and an injury is
typically considered high cervical when it involves the cord above the C5 level. At
the time of discharge from the acute hospitalization, the most frequent degree of
injury is incomplete quadriplegia (45%), followed by incomplete paraplegia
(22%), complete paraplegia (20%), and complete quadriplegia (13%).1,2 Recent
trends indicate a growing proportion of incomplete injuries due to falls.2,3
Average expenses during the first year after the injury for a patient with high
quadriplegia can exceed $1 million. Lifetime expenses among young patients
with severe high-cervical traumatic spinal cord injury can top $4.5 million, even
without including indirect costs (eg, losses in wages, fringe benefits, and
productivity) and may average more than $70,000 per year.1

PATHOPHYSIOLOGY
The main mechanisms of primary injury to the spinal cord are direct impact with
persistent or transient compression, vertebral fracture and displacement, and cord
laceration or transection. Multiple classification systems have been proposed to
categorize cervical spine injuries, depending on the morphology of the bone damage,
disruption of the ligaments and intervertebral disks, and degree of neurologic
impairment.4 Flexion injuries can produce wedge fractures, vertebral subluxations,
and facet dislocations. Extension injuries can cause fractures of the posterior column
of the spine; less severe extension can provoke transient spinal cord compression in
patients with cervical spondylosis. Axial load injury can result in burst fractures of
cervical or thoracic vertebrae. Lacerations and transections are less frequent and occur
as a consequence of penetrating injuries. All these primary injuries are the direct
consequences of mechanical forces at the time of the injury (and over the following
hours in case of persistent compression) and are mostly not amenable to treatment.
The therapeutic focus in traumatic spinal cord injury is the avoidance and
correction of secondary injuries. Among them, early hypoxia and hypoperfusion
are currently the most correctable. However, animal models have elucidated
multiple mechanisms of secondary injury, including reperfusion, acute
inflammation, local swelling from intracellular and extracellular edema,
impaired vasomotor function, blood–spinal cord barrier disruption,
microhemorrhages, microthrombosis, excitotoxicity, mitochondrial damage,
lipid peroxidation, free radical formation, excessive intracellular calcium, and

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activation of apoptotic signals.5 The cord swelling resulting from these acute KEY POINTS
secondary insults tends to peak after 3 to 6 days and subsides slowly over the
● Motor vehicle accidents
ensuing weeks. This acute phase appears to be followed by a progressive remain the most common
neurodegeneration mediated by persistent inflammation and characterized by cause of traumatic spinal
extensive microglial and astroglial activation.6 cord injury (38%), especially
among the young.
EVALUATION
● Most traumatic spinal
Physical examination in the field and upon arrival to the emergency department as cord injuries affect the
well as emergency spine imaging and immediate neck immobilization by the first cervical spinal cord, and an
responders are indispensable for any patient with suspected acute injury to the spine. injury is typically considered
high cervical when it
involves the cord above the
Clinical Assessment C5 level.
Early recognition of traumatic spinal cord injury in the field is crucial to avoid
additional cord damage during transportation. However, the early evaluation of ● The main mechanisms of
any patient with traumatic spinal cord injury should include a careful exclusion primary injury to the spinal
cord are direct impact with
of other serious injuries, such as to the head, chest, abdomen, and pelvis. In fact, cord compression, vertebral
traumatic brain injury is present in one-fourth to one-half of patients with fracture/dislocation,
traumatic spinal cord injury.7 and cord laceration
Patients with high-cervical traumatic spinal cord injury always present with or transection.
respiratory failure because of loss of diaphragmatic function. However, lower
● The therapeutic focus in
cervical and some upper thoracic injuries can also precipitate ventilatory failure traumatic spinal cord injury
either at presentation or later during the acute phase. These patients exhibit a is the avoidance and
typical breathing pattern known as quad breathing, manifested by inward motion correction of secondary
of the chest and outward motion of the abdomen with each inspiratory effort injuries, especially hypoxia
and hypoperfusion.
(the opposite of the paradoxical breathing pattern of patients with diaphragmatic
weakness) resulting from preserved diaphragmatic contraction and absent ● Cord swelling after
innervation of chest and abdominal muscles. trauma tends to peak
Cervical and upper thoracic injuries can cause refractory hypotension and after 3 to 6 days and
subsides slowly over the
bradycardia due to neurogenic shock (ie, loss of sympathetic outflow with ensuing weeks.
unopposed vagal activity). The severity of the neurologic impairment can
initially be exaggerated by spinal shock, a transient severe dysfunction of the ● Patients with
spinal cord that develops within the first hours after the injury and can last for high-cervical traumatic
spinal cord injury always
days or even a few weeks, typically manifesting with areflexic flaccid paralysis
present with respiratory
and anesthesia below the level of the lesion. These two phenomena can coexist failure because of loss of
but represent different consequences of traumatic spinal cord injury, and the two diaphragmatic function.
terms should not be used interchangeably.
A detailed neurologic examination is necessary to determine the level of the ● Cervical and upper
thoracic injuries can cause
injury and the severity of the neurologic impairment. The American Spinal Injury refractory hypotension
Association (ASIA) international standards are recommended as the preferred and bradycardia due to
tool to standardize the neurologic examination and classify the severity of the neurogenic shock.
injury.8 The complete examination worksheet can be freely accessed online and
● The severity of the
is included in this issue (SDC APPENDIX, links.lww.com/CONT/A245).9 The
neurologic impairment in
neurologic level of the injury is defined as the most caudal segment of the spinal traumatic spinal cord injury
cord with antigravity muscle strength (3/5 or better) and intact sensation (to light can initially be exaggerated
touch and pinprick) provided motor and sensory function are normal rostral by a temporary spinal shock.
to this level. In addition, motor and sensory levels should be determined on
each side of the body. Impairment is considered incomplete if some function is
preserved below the neurologic level of injury. Examination should include careful
evaluation to determine if any sacral function is spared, which can be manifested
by voluntary anal contraction, preserved tactile sensation in S4-S5 dermatomes,

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TRAUMATIC SPINAL CORD INJURY
KEY POINTS
● The American Spinal
Injury Association
international standards are
recommended as the
preferred tool to standardize
the neurologic examination
and classify the severity of
traumatic spinal cord injury.
● The American Spinal
Injury Association grade of
impairment has strong
prognostic implications for
traumatic spinal cord injury.
● The central cord syndrome
is characterized by loss of
cervical motor function with
relative sparing of strength
in the legs.
● The need for radiologic
assessment of the spine
after trauma depends on the
mental condition of the
patient, the presence of
neck or back pain, and the
ability to perform a reliable
physical examination.
● High-quality CT scan is
the initial preferred imaging
modality after traumatic
spinal cord injury. MRI within
the first 48 hours can help
exclude ligamentous injury.
● MRI can reliably show the
extent of cord compression
and signs of cord injury.
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or sensation to deep anal pressure. These assessments allow the stratification of
patients into five grades of neurologic impairment according to the ASIA Impairment
Scale.10 The ASIA grade of impairment has strong prognostic implications.11
When evaluating the degree of neurologic impairment, it is necessary to
keep in mind that patients may initially appear worse because of spinal shock or
worsen after presentation because of swelling. Thus, for prognostication
purposes, it is advisable to use the ASIA impairment grade determined at the
end of the initial hospitalization or at the beginning of the rehabilitation phase.
Certain specific syndromes that can be seen in patients with traumatic spinal
cord injury deserve recognition. The central cord syndrome is caused by cord
contusion from buckling of the ligamentum flavum during neck hyperextension.
It is characterized by loss of cervical motor function with relative sparing of
strength in the legs because the motor fibers going to the arms are located more
medially within the descending corticospinal tracts. Patients with central cord
syndrome may also experience a suspended sensory loss in cervicothoracic
dermatomes. The Brown-Séquard syndrome is produced by hemisection of the
cord resulting in ipsilateral loss of proprioception and motor function and
contralateral loss of pain and temperature sensation. Complete cord transection,
anterior cord syndrome (more common with spinal cord infarction), posterior
cord syndrome (more common with infectious, metabolic, vascular, or
inflammatory causes or compression from an epidural mass), and conus or cauda
equina syndromes (more common with compression or infections) can also
occur after trauma but much less frequently.
Radiologic Assessment
The need for radiologic assessment of the spine after trauma depends on the
mental condition of the patient, the presence of neck or back pain, and the ability
to perform a reliable physical examination.12 Evidence-based recommendations
to guide the decision of when and how to image the cervical spine after trauma
have been proposed by the Joint Section on Spine and Peripheral Nerves of
the American Association of Neurological Surgeons and the Congress of
Neurological Surgeons, as outlined in TABLE 8-1.8
The additional value of MRI in patients with no evidence of structural damage
on high-quality CT remains controversial. MRI (including short tau inversion
recovery [STIR] sequences) can detect ligamentous injury that could explain
persistent pain and put the patient at risk for subluxation after mobilization of
the neck is allowed.13 However, ligamentous injury is best appreciated within
48 hours of the trauma and may not necessarily imply spinal instability, limiting
its value to guide discontinuation of the cervical collar.8
MRI can reliably show the extent of cord compression and signs of cord injury
(edema, hemisection, transection, hemorrhage, and, with less sensitivity,
ischemia) (FIGURE 8-1).13 These findings may help guide surgical decisions and
have prognostic implications.14 In the subacute and chronic phases, MRI can also
help explain rare cases of delayed decline caused by a syrinx or progressive
ascending myelomalacia.13 Newer MRI modalities, such as diffusion tensor
imaging, magnetic resonance spectroscopy, and functional MRI (fMRI) are being
investigated as techniques that could refine the ability to assess the integrity of
the cord at various stages after trauma.15
Some patients may have clinical signs and symptoms of spinal cord
dysfunction without any evidence of structural damage on CT. These cases of
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spinal cord injury without radiologic abnormalities (SCIWORA) are more
common in children16 but can also be seen in adults.17 However, SCIWORA is
diagnosed based on the absence of abnormalities on x-rays and CT scan only.
MRI of the region of suspected injury or the entire spine is recommended in these
cases because it often (but not always) shows intraneural or extraneural
abnormalities. In these cases, prolonged immobilization (for 12 weeks) is
recommended, and spinal stability should be confirmed with delayed
flexion/extension x-rays before immobilization is discontinued.8

Recommendations for Cervical Spine Imaging and Cervical Immobilization TABLE 8-1
After Traumaa

Level of
Clinical Situation Recommendation Recommendation

Patient is alert and not intoxicated, is Cervical spine imaging is not recommended, and Level I
asymptomatic (no neck pain or tenderness), cervical immobilization can be discontinued
has normal neurologic examination, does not
have associated injuries that detract from his or
her general evaluation, and is able to complete
a functional range of motion examination

Patient is alert and symptomatic High-quality CT of the cervical spine is Level I

recommended
If high-quality CT is not available, a three-view
(anteroposterior, lateral, and odontoid views)
cervical spine x-ray series is recommended, but it
should be supplemented with CT if it becomes
available
If CT or three-view cervical spine series is normal, Level III
cervical immobilization should be continued until
one of the following conditions is met:
Patient becomes asymptomatic
Normal and adequate dynamic flexion and
extension x-raysb
Normal MRI within 48 hours of the injury
It is safe according to the treating physician

Patient is not alert or cannot be reliably High-quality CT of the entire spine (three-view Level I
evaluated cervical series and x-rays of lower spine if CT not
available followed by CT if it becomes available)
Discontinuation of cervical immobilization as Level III
stated for alert and symptomatic patients

CT = computed tomography; MRI = magnetic resonance imaging.

a
Data from Walters BC, et al, Neurosurgery.8
b
Lateral flexion-extension cervical x-rays must be performed under controlled conditions to ensure that the movement of the neck does not
exceed the point of worsening symptoms, and they must include the C7-T1 disk space.

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TRAUMATIC SPINAL CORD INJURY

FIGURE 8-1
MRI of a young patient with lower cervical traumatic spinal cord injury with C5-C6 fracture
and dislocation with associated traumatic disk herniation and severe spinal cord
compression. Intramedullary signal change is seen on the sagittal T2-weighted image with
fat saturation (A) and more prominently appreciated on the sagittal short tau inversion
recovery (STIR) image (B). An axial T2-weighted image shows severe anterior compression
of the cord at the level of maximal displacement of the spinal elements (C) and extensive
intramedullary changes one level below (D).

TREATMENT
The therapeutic tenets of traumatic spinal cord injury include immobilizing the
spine; ensuring adequate ventilation, oxygenation, and perfusion; and
determining whether the patient needs surgical decompression.

Initial Stabilization and Medical Management

Providing adequate oxygenation is a major priority during the initial stabilization
phase after major trauma. When spinal injury is suspected, it is recommended
that the spine be immediately immobilized (with the sole exception of patients

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with penetrating trauma, in whom any delay in resuscitation can be fatal),8 KEY POINTS
although the level of evidence supporting this widely accepted recommendation
● When spinal injury is
is not very strong.18 This is particularly important for patients with traumatic suspected, it is recommended
spinal cord injury who need tracheal intubation, because displacement of cervical that the spine be
spine elements can occur during this procedure. Consequently, patients with immediately immobilized.
suspected cervical traumatic spinal cord injury should have their necks manually
● Patients with suspected
stabilized in-line during tracheal intubation. Immobilization measures should traumatic spinal cord injury
include a rigid cervical collar, transportation on a rigid spine board, and should be transported to a
logrolling of the patient. When at all possible, patients with suspected traumatic specialized acute traumatic
spinal cord injury should be transported to a specialized acute traumatic spinal spinal cord injury treatment
center.
cord injury treatment center.8,19 Clearance of the cervical spine should then
proceed according to the recommendations outlined in TABLE 8-1. It is useful to ● The optimal timing of
remember that while immobilization of the spine can prevent serious secondary surgery for traumatic spinal
spinal cord damage in patients with spinal instability, its use is not devoid of cord injury has not been
conclusively established,
potential risks. Pain, pressure sores, airway compromise, increased risk of but prospective cohort
aspiration, and limitation of upper chest wall expansion can all be consequences studies suggest that
of cervical spine immobilization, particularly if prolonged. early intervention may
Avoiding hypoperfusion from systemic hypotension is also crucial. Patients be preferable.
with traumatic spinal cord injury can develop neurogenic shock with bradycardia
● Respiratory failure may
and reduced myocardial contractility due to loss of sympathetic innervation. occur at presentation or
Thus, a sympathetic agent with positive chronotropic and inotropic effects (such develop over the subsequent
as norepinephrine or epinephrine) is preferred to sustain the blood pressure. 5 days.
Also, other causes of shock that can occur after major trauma should be excluded,
● The duration of mechanical
such as active bleeding, pericardial tamponade, and tension pneumothorax. ventilation is typically
prolonged in patients with
Surgical Indications and Timing cervical traumatic spinal cord
The goals of spine surgery are decompression of neural elements with correction injury, but liberation from the
ventilator is possible in the
of deformities of the spinal canal, reduction of vertebral fractures, and fixation great majority of cases.
and fusion to ensure long-term spinal stability. Rapid closed reduction (to restore
spine alignment) is recommended for fracture and dislocation injuries until
the patient is taken to surgery.8
The optimal timing of surgery has not been conclusively established.
Prospective cohort studies favor early intervention.20 The largest among these
studies, the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS),
evaluated 313 patients and showed that those who underwent decompressive
surgery within 24 hours of the injury (mean 14.2 hours) were twice as likely to
have a two-grade improvement on the ASIA Impairment Scale at 6 months as
compared to patients undergoing surgery later (mean 48.3 hours).21 The Surgical
Treatment for Spinal Cord Injury study (SCI-POEM), another prospective
cohort study, is currently evaluating if surgery within 12 hours can be
beneficial.22 No randomized controlled trials have been conducted to address this
clinical question.

Critical Care
The critical care of patients with traumatic spinal cord injury is multifaceted and
demanding, but the respiratory and cardiovascular systems require the most
attention, particularly in the hyperacute phase.

RESPIRATORY MANAGEMENT. Respiratory failure after trauma can occur acutely

from injury to the brain, brainstem, or cervical spinal cord; secondary to

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TRAUMATIC SPINAL CORD INJURY

aspiration; or because of airway obstruction. The diaphragm is innervated by the

C3-C5 roots and is the primary inspiratory muscle. Thus, complete injuries above
C3 inevitably cause acute ventilator failure in the field (CASE 8-1). When the
high-cervical cord lesion is partial or the level of injury is at C3 through C5,
ventilation can sometimes be maintained by accessory inspiratory muscles:
external intercostals (T1 through T11), sternocleidomastoids (cranial nerve XI),
trapezii (cranial nerve XI), and scalenes (C3 through C8). Although expiration
is normally driven by passive elastic recoil of the thoracic wall, patients with
severe trauma often depend on active expiration that requires the contraction
of the internal intercostal muscles (T1 through T11) and abdominal muscles
(T7 through L2). These anatomic considerations can help predict which
patients with traumatic spinal cord injury will be at higher risk of developing
respiratory failure and how likely they will be to remain dependent on
artificial ventilation. The development of respiratory failure is directly related to
the severity of the traumatic spinal cord injury as assessed by the ASIA
Impairment Scale.23
Patients with traumatic spinal cord injury who do not require immediate
mechanical ventilatory assistance often need it within the following 5 days.
Respiratory muscle fatigue, progressive atelectasis, accumulation of secretions

CASE 8-1 A 29-year-old woman with a history of type 1 diabetes mellitus and juvenile
rheumatoid arthritis was an unrestrained passenger when the car she
was riding in crashed and rolled over. She was found unconscious and
apneic by the paramedics who arrived promptly at the scene. She was
immediately intubated with manual in-line stabilization of the neck
and then transferred to a specialized trauma center with her spine
immobilized. On arrival to the emergency department, she was
hypotensive despite having received boluses of fluids, and she was also
bradycardic. Her hemodynamic parameters improved substantially after
initiation of a norepinephrine infusion. Her trauma survey was negative for
injuries to the head or elsewhere.
Examination showed flaccid quadriplegia with areflexia and complete
anesthesia below the neck. CT of her neck revealed fracture/dislocation at
the C2-C3 level with severe cord compression (FIGURE 8-2A). She underwent
closed reduction and was admitted to the neuroscience intensive care unit.
Her norepinephrine was adjusted to maintain a mean arterial pressure of
85 mm Hg to 90 mm Hg. Sixteen hours after the injury, she had surgical fusion
from C2 to C4. MRI of the cervical spine showed improvement of the cord
compression after the reduction but demonstrated extensive signs of cord
damage (FIGURES 8-2B and 8-2C). Except for atelectasis and pneumonia, her
intensive care unit course was uneventful. Her norepinephrine was weaned off
on day 7. She underwent tracheostomy and percutaneous gastrostomy on
day 8. As her spinal shock resolved, she regained some sensation below
the level of the injury and developed increased muscle tone in the
shoulders and upper chest. After slow weaning of the ventilator
assistance, she was liberated from the ventilator on day 42.

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and mucous plugging due to ineffective cough, aspiration pneumonia,
pulmonary edema and pleural effusions after fluid resuscitation, and the direct
consequences of chest trauma may all contribute to respiratory failure.
Depending on the main causes, the respiratory failure may be hypoxemic,
hypercapnic, or—most commonly—mixed. When mechanical ventilation is
deemed necessary, intubation should not be delayed. Noninvasive ventilation has
a very limited role in the acute care of patients with traumatic spinal cord injury.
The duration of mechanical ventilation is typically prolonged in patients with
cervical traumatic spinal cord injury, but liberation from the ventilator is possible
in the great majority of cases.24 The duration of ventilator dependence depends
on the evolution of the neurologic deficits and whether major pulmonary
complications occur. As thoracic muscles go from flaccid to spastic, improvement
in chest wall stability may facilitate weaning. Yet, tracheostomy is often needed
in patients with poor ASIA motor scores.25 The optimal timing of tracheostomy is
not well defined. Patients with complete C1 to C3 cord injuries can sometimes
be liberated from the ventilator by means of diaphragmatic pacing.26

CARDIOVASCULAR MANAGEMENT. Aggressive treatment of hypotension during

the acute phase after the injury is associated with better outcomes in patients

FIGURE 8-2
Imaging of the patient in CASE 8-1. A, Sagittal reformatted CT shows a C2-C3 fracture with
severe dislocation compromising the spinal canal. After closed reduction, T2-weighted MRI
(B) and short tau inversion recovery (STIR) (C) show frank improvement of the dislocation
with some residual cord compression and clear evidence of spinal cord injury seen on the
T2-weighted image (B), but is better visualized on the STIR image (C).

This case illustrates the typical course of a young patient with severe upper COMMENT
cervical traumatic spinal cord injury causing respiratory failure and
neurogenic shock. Her cord compression was appropriately treated with
closed reduction followed by surgical decompression and fusion. The initial
examination was confounded by spinal shock, and her deficits improved
after this resolved, allowing for gradual liberation from the ventilator.

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TRAUMATIC SPINAL CORD INJURY
KEY POINTS
● Current guidelines
recommend maintaining a
mean arterial pressure
between 85 mm Hg and
90 mm Hg during the first
week after the injury,
although the evidence
supporting this
recommendation is weak.
● Patients with traumatic
spinal cord injury may have
multiple other complications
during their acute
hospitalization, but they
are mostly preventable.
● No evidence currently
supports the use of any
pharmacologic or
nonpharmacologic
interventions for
neuroprotection in patients
with traumatic spinal
cord injury.
● Administration of
high-dose steroids can
produce major adverse
effects in patients with
traumatic spinal cord injury
and is not advisable.
● Rigorous clinical trials are
necessary to determine if
therapeutic hypothermia
can improve neurologic
outcomes in patients with
severe traumatic spinal
cord injury.
● The goals of rehabilitation
efforts for patients with
traumatic spinal cord injury
should be individualized to
achieve the patient’s fullest
physical, emotional, social,
vocational, and functional
recovery.
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with traumatic spinal cord injury.27 Current guidelines recommend maintaining
a mean arterial pressure between 85 mm Hg and 90 mm Hg during the first week
after the injury, although this recommendation is based on weak quality of
evidence.28 A recent study has shown that maintaining a spinal cord perfusion
pressure (ie, the difference between mean arterial pressure and CSF pressure
measured with an intrathecal catheter) above 50 mm Hg is associated with better
functional outcomes.29 Achieving this mean arterial pressure goal very often
demands the use of vasopressors. Using agents with a1-adrenergic receptor and
b1-adrenergic receptor agonistic effects is advisable to correct the bradycardia
that accompanies hypotension from neurogenic shock. The risks of vasopressors
should be carefully considered in each case, taking into consideration potential
deleterious consequences in other organs (including the brain in patients with
concomitant head injury).
OTHER ASPECTS OF CRITICAL CARE. Patients with traumatic spinal cord injury
may have multiple other complications during their acute hospitalization, but
they are mostly preventable (TABLE 8-2).30,31 Care in specialized units with
intensivists, nurses, and physiatrists experienced in the management of patients
with traumatic spinal cord injury can minimize these risks. Neurologists can
contribute to the recognition and treatment of some of these complications, such
as autonomic alterations, dysphagia, spasticity, pain, sphincter dysfunction, and
mood disorders. Neurologists are also essential for the management of patients
with associated traumatic brain injury.
NEUROPROTECTION. No evidence currently supports the use of any
pharmacologic or nonpharmacologic interventions for neuroprotection in
patients with traumatic spinal cord injury. High-dose methylprednisolone was
tested in the National Acute Spinal Cord Injury Study (NASCIS) trials.32,33 These
trials showed higher rates of pneumonia, sepsis, acute respiratory distress
syndrome, gastrointestinal hemorrhage, and death among patients treated with
corticosteroids. An association with modest improvement in motor outcome
was only observed on a post hoc analysis restricted to patients treated within
8 hours of the injury.34 Another randomized clinical trial that included a group
of patients treated with methylprednisolone found no benefit in neurologic
outcomes at 1 year.35 Current guidelines do not recommend the use of
corticosteroids for traumatic spinal cord injury.8
Therapeutic hypothermia has shown promising results in translational studies
using local epidural or systemic cooling.36,37 However, no solid data exist to
support its use in clinical practice. The Hypothermia Following Acute Spinal
Cord Injury study, a prospective observational study with a planned size of
100 patients, is currently being conducted (NCT01739010),38 but no randomized
studies are under way. Various pharmacologic agents are also being investigated
as possible neuroprotectants in traumatic spinal cord injury. They include
riluzole, minocycline, and fibroblast growth factor.5
REHABILITATION
The rehabilitation of patients with traumatic spinal cord injury starts in the
intensive care unit, and the neurologic and systemic complications observed
during the acute and rehabilitation phases frequently overlap. The goals of
rehabilitation efforts should be individualized to achieve the patient’s fullest
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Main Complications After Traumatic Spinal Cord Injury TABLE 8-2

Complication Prevention and Management

In the field
Spinal shock Preservation of adequate oxygenation and perfusion
Neurogenic shock Fluids and vasopressors
Respiratory failure Mechanical ventilation
In the hospital
Refractory shock Clarify mechanism(s), fluids and vasopressors
Respiratory failure Aggressive respiratory therapy, mechanical ventilation
Dysphagia Video swallowing, nasogastric tube/percutaneous gastrostomy
Infections Identify source, antibiotics
Venous thromboembolism Intermittent pneumatic compression, low-molecular-weight heparin, inferior vena
cava filter in some cases
Stress gastroduodenal ulcers Consider histamine 2 receptor blocker or proton pump inhibitor

In the rehabilitation unit (and beyond)

Autonomic dysreflexia Identify and avoid triggers
Orthostatic hypotension Compressive hoses, abdominal binder, midodrine (conservative dosing)
Pressure sores Meticulous surveillance of pressure spots, frequent mobilization, special bed when
available
Leg edema Leg elevation, compressive hose
Spasticity Physical therapy, baclofen, botulinum toxin injections
Chronic pain Physical therapy, analgesics and medications for neuropathic pain as pertinent
Temperature dysregulation Maintain stable room temperature
(“quad fever”)
Urinary retention Intermittent bladder catheterization
Constipation Cathartics
Obesity Caloric restriction
Heterotopic ossification Anti-inflammatory medications, bisphosphonates, local radiation
Renal stones (hypercalciuria) Hydration, monitoring and treatment of hypercalciuria
Sexual dysfunction Adjustment strategies
Depression and anxiety Psychotherapy, antidepressants as pertinent
Sleep disorders Sleep hygiene, control of pain and spasticity, melatonin, continuous positive airway
pressure if sleep breathing disorder with obstruction

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TRAUMATIC SPINAL CORD INJURY
KEY POINTS
● Autonomic dysreflexia is
a common delayed
complication in patients
with spinal cord injuries
above the T6 level and can
provoke sudden severe
hypertension.
● The American Spinal
Injury Association Impairment
Scale grade, the level of
injury, and the appearance
of the cord on the MRI are
the main prognostic
indicators after traumatic
spinal cord injury.
● Mortality is highest within
the first 6 to 12 months
after a traumatic spinal cord
injury, but it remains higher
for patients with traumatic
spinal cord injury than in the
general population even
years later.
562
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
physical, emotional, social, vocational, and functional recovery. Establishing
realistic goals and a feasible long-term plan to meet them is a crucial first step.
These goals will depend on the level and severity of injury, the age of the patient,
and the presence of comorbidities.
Mobilization, bowel and bladder training, and respiratory care can start before
transfer to the rehabilitation unit. Physical and occupational therapists will work
with the patients on range of motion and strengthening exercises but also will
help manage edema in the extremities, recommend orthotic devices to provide
support and prevent contractures, and train patients on the use of devices to
assist their function (eg, different forms of functional electrical stimulation,
electric wheelchairs, robotic systems for locomotor retraining, emerging
brain-controlled neuroprostheses). Education of patients and families lies at the
core of this work.
Some of the most frequent complications during this phase are listed
in TABLE 8-2. Among them, autonomic dysreflexia can be particularly
problematic. Autonomic dysreflexia may occur in over half of patients with
cervical or high thoracic cord injuries (T6 or higher) and is especially common
among patients with complete lesions; however, the degree of symptoms is
highly variable, and in a sizable proportion of cases the diagnosis can only be
made with certainty by using information from specific autonomic testing
(such as urodynamic studies).39 Manifestations of autonomic dysreflexia may
emerge shortly after resolution of the initial spinal shock or, more often,
weeks or even months later (CASE 8-2). They result from unopposed
sympathetic discharge triggered by an intense stimulus below the level of the
lesion.39 Signs and symptoms include sudden hypertension, tachycardia or
reflex bradycardia, and severe headache. Patients may also have flushing,
sweating, and increased secretions above the level the lesion because of
compensatory increase in the parasympathetic tone. Meanwhile, below the
lesion, patients can exhibit piloerection and signs of vasoconstriction (pale, cool
limbs) from excessive sympathetic innervation. The main triggers of autonomic
dysreflexia include bladder distension, detrusor sphincter dyssynergia, fecal
impaction, and pressure sores. Identification and elimination of the precipitating
factor are the most effective treatment interventions. Hypertension can be very
severe and require specific treatment. Patients should be placed in an upright
sitting position, and, if medications are needed, short-acting direct vasodilators
(such as hydralazine) are preferred. Vasoactive medications should be dosed
conservatively because patients can react excessively to them, resulting in
sudden hypotension.
PROGNOSIS
The ASIA Impairment Scale grade, the level of injury, and the appearance of
the cord on MRI are the main prognostic indicators after traumatic spinal cord
injury.11,14,41–43 The Spinal Cord Independence Measure is the most recommended
tool to categorize the functional outcome and monitor the evolution of these
patients.8 This linear scale ranges from 0 to 100 and comprises sections on self-care
activities, respiratory function, bladder and bowel management, and mobility.44,45
However, many other disability scales with different characteristics and
relative advantages are also available.46
Mortality is highest within the first 6 to 12 months after the injury. The main
causes of death are respiratory failure, pulmonary embolism, cardiovascular
APRIL 2018
 A 20-year-old man sustained a C5-C6 fracture dislocation with cord CASE 8-2
compression (FIGURE 8-3A) after a high-speed collision as an unrestrained
driver. He was admitted to a specialized trauma center where traction
reestablished spine realignment (FIGURE 8-3B). One day later, his spine
was stabilized with a C5 through T1 anterior fusion. He had persistent
deficits consistent with American Spinal Injury Association (ASIA)
Impairment Scale grade A at the C6 level. His acute course in the intensive
care unit included neurogenic shock treated with norepinephrine, sepsis
from pneumonia that resolved on antibiotics, and a deep venous
thrombosis in his leg that was managed with a combination of
anticoagulation with low-
molecular-weight heparin and
a retrievable inferior vena
cava filter.
Ten days after the accident,
he was transferred to the acute
rehabilitation unit. There he
started to have sudden
episodes of severe headache
associated with facial flushing
and severe hypertension. These
episodes were precipitated
by bladder or abdominal
distension. Typically, the
hypertension could be
controlled by having the FIGURE 8-3
patient sit upright, but Imaging of the patient in CASE 8-2. A,
occasionally it required Reformatted sagittal neck CT reveals a C5-C6
fracture-dislocation with complete distortion of
administration of a direct
the spinal canal that caused transection of the
vasodilator. Adjustments to the cord at that level. B, Sagittal T2-weighted
bladder and bowel program MRI obtained after closed reduction of the spine
progressively led to near demonstrates the extensive cord damage that had
resolution of these episodes. resulted from its originally severe compression.

This patient with a lower cervical cord injury had developed classic COMMENT
manifestations of autonomic dysreflexia. This complication is triggered by
stimulation below the level of the cord lesion (which the patient may not
feel because of anesthesia) that results in an exaggerated sympathetic
response that, in turn, provokes a compensatory increase of vagal
transmission. As a result, patients can develop signs and symptoms of
excessive parasympathetic tone above the cord lesion and excessive
sympathetic tone below the cord lesion. Sudden and sometimes extreme
hypertension is the most dangerous manifestation of this autonomic disorder.

CONTINUUMJOURNAL.COM 563

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TRAUMATIC SPINAL CORD INJURY

KEY POINT
● Neuroregenerative
strategies, especially stem
cell transplantation, are
promising but currently are
strictly investigational.
diseases, and sepsis.47 Early mortality is greater in older patients, those with high
cervical lesions, and those with the most severe neurologic deficits.11,48 Overall,
the adjusted mortality of patients with traumatic spinal cord injury is up to 3
times higher than in the general population.42 Unfortunately, the life expectancy
of patients with traumatic spinal cord injury has not improved over the past
few decades.1
It is estimated that only 12% of patients with traumatic spinal cord injury are
employed 1 year after the injury.1 This proportion increases over time, primarily
among young patients, but remains low nonetheless. Rehospitalizations are very
common (about 30% of patients in any given year). The main causes include
urinary infections, pressure sores, and a variety of other diagnoses.1

NEUROREGENERATION
The search for effective neuroregenerative strategies is undoubtedly the most
active area of research in the field of spinal cord injury. These strategies offer the
possibility of improvement in patients with chronic cord injury. Inhibitors of the
rho-associated protein kinase pathway (Rho/ROCK pathway) and enzymes that
degrade chondroitin sulfate proteoglycans are only some of the pharmacologic
strategies under investigation.5 However, cell-based therapies capture the most
attention. Transplantation of embryonic stem cells, induced pluripotent stem
cells, neural stem cells, mesenchymal stem cells, oligodendrocyte precursor cells,
Schwann cells, and olfactory ensheathing cells is the focus of acute research by
various teams across the world.5,49 At present, all these therapies remain
strictly investigational.

CONCLUSION
Trauma to the spinal cord remains a very serious condition with limited effective
therapies. Early and delayed mortality rates are still high, and survivors sustain
major functional impairments. Undoubtedly, injury prevention will always be
the most efficacious strategy to diminish the societal impact of this condition.
Once the injury has occurred, immediate attention to the prevention of hypoxia
and hypoperfusion and transportation to a center with experience in the
management of patients with traumatic spinal cord injury should be the
priorities. Currently, no proven strategies exist for neuroprotection, but
preservation of adequate oxygenation and perfusion and prevention of systemic
complications can improve outcomes. Advances in our understanding of the
molecular mechanisms preventing cord restoration after the trauma and a
growing knowledge of cell lines capable of facilitating cord healing have opened
windows for the development of neuroregenerative strategies. Collaborative
research and adequate funding may allow the discovery of an effective treatment
for patients with chronic spinal cord injuries in the future.

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