Spinal Cord Injury and Paralysis

Ovid: Spine

Editors: Bono, Christopher M.; Garfin, Steven R.
Title: Spine, 1st Edition
> Table of Contents > Section II – Trauma > 6 – Spinal Cord Injury and Paralysis

Spinal Cord Injury and Paralysis
Robert F. Heary
Artem Y. Vaynman
Approximately 10,000 spinal cord injury (SCI) patients
present to emergency departments annually in the United States. The
immediate mortality of a complete cervical SCI is close to 50%. For
survivors who make it to a hospital, the mortality is much lower (4% to
16%). The causes of SCI are divided according to age and gender. Of SCI
patients, 80% to 85% are male, and 15% to 20% are female; at least 50%
of patients are between 20 and 50 years old. The cervical spinal cord
is the most common level of injury (50% to 60%). Thoracic,
thoracolumbar, and lumbosacral spine regions represent 15% each in
multiple series.
Fracture-dislocations and burst fractures are the most
common mechanisms, constituting 70% of injuries that result in SCI.
Compression fractures and isolated dislocations make up 10% and 5%,
respectively. Since the advancements of magnetic resonance imaging
(MRI) technology and the ready availability of MRI in most trauma
centers, spinal cord injury without radiologic abnormality (SCIWORA)
has become nearly obsolete. When imaged with MRI, SCIWORA shows signal
changes in T2-weighted sagittal and axial sequences. The prognosis for
patients with SCIWORA is good with cervical collar immobilization.
Spinal cord injury without radiologic evidence of trauma (SCIWORET)
also has been reviewed. High-resolution computed tomography (CT) and
MRI usually show cervical spondylosis or congenital anomalies that
predispose patients with minimal trauma to have profound deficits.
SCI is more common in patients with multiorgan injuries.
A definite relationship exists between head injury and SCI, which makes
an accurate physical exam more difficult and may lead to the diagnosis
of SCI being delayed. Spinal shock resulting from SCI complicates the
recognition and treatment of intraabdominal and chest injuries.
Neurologic recovery of patients with SCI in the presence of multitrauma
is reduced because of multiple factors that are discussed later.
The initial trauma to the spinal cord tissue can destroy
a certain number of cells directly. It also sets in motion a
multifactorial process that causes more cell death and damage.
Disruption of the normal blood flow creates ischemia in the gray matter
of the cord by either mechanical obstruction of feeding arteries or
vasospasm of arterioles. This ischemia usually occurs within 2 to 3
hours after injury. Although the white matter blood supply may not
diminish, vasospasm can affect the ascending and descending tracts as
arterioles pass through the gray matter to reach these tracts.
Vasoconstriction can increase progressively over the first 24 hours,
and it is affected greatly by the release of histamine, prostaglandins,
serotonin, and neurotransmitters such as norepinephrine. Thrombosis of
injured arteries contributes to ischemia, which is tolerated poorly by
central nervous system tissue, initiating a cascade of ion derangement,
inflammation, and apoptotic cell death.
Injured cells release proinflammatory substances that
attract neutrophils to the area within 24 to 48 hours; this causes an
expansion of the damage in the rostral and the caudal directions. In 48
hours, macrophages and microglial cells migrate to the site and release
reactive oxygen radicals that cause damage to the surrounding healthy
tissue. Cellular membrane breakdown ensues with resultant ionic
imbalance and nucleolysis. As the energy supply necessary for
restoration of membrane potential is depleted, potassium ions move out
of the cell, and sodium ions move into the cell. Additionally, calcium
is released from storage granules, and it activates enzymes in the
proteolytic pathway that destroy the cytoskeletons of cell bodies and
axons. All of these events lead to demyelination and necrotic cell
The intrinsic suicide mechanism of cells, also known as apoptosis,
is initiated by the release of excitatory neurotransmitters, such as
glutamate, and by an increase in calcium concentration. Heat-shock
proteins are synthesized and released. This release causes activation
of a lytic cascade that results in apoptotic death of the
oligodendrocytes. Because oligodendrocytes are responsible for the
maintenance of myelinated pathways, demyelination of the ascending and
descending tracts of the spinal cord, which were not injured by the
initial trauma, causes further loss of function. All these events start
4 to 6 hours after SCI and can continue for 3 weeks.
At present, available scientific data suggest that acute


SCI is a complex phenomenon. Many interrelated events can lead to
progressive, reversible and irreversible damage to spinal cord tissue.
The primary damage, which occurs at the time of the SCI, is not
correctable. Evidence from multiple investigators suggests, however,
that inflammation and ionic disturbances initiate vicious cycles
damaging tissue that was not injured by the initial trauma. This
so-called secondary injury has been the focus of much research because
this phase of the SCI cascade is potentially modifiable with effective
treatments. Complex regeneration patterns also are being studied;
however, further work is required before any definitive conclusions
about the prevention of secondary injury or stimulation of regeneration
can be made.

At present, the American Spinal Injury Association
(ASIA) scale, endorsed by the International Medical Society of
Paraplegia (IMSOP) and published in 1992 in the International Standards for Neurological and Functional Classification of Spinal Cord Injury,
is recommended for use by all physicians treating patients with acute
SCIs. This system attempted to detail more accurately patients with
incomplete neurologic deficits. Specifically, in the ASIA system,
preserved sensation at the S4-5 level now is required for an incomplete
classification to be made. A scoring method to describe sensation also
has been added, with 0 = none, 1 = impaired, and 2 = intact. The
previously used term quadriplegia has been replaced by tetraplegia. Another change is replacement of the term zone of injury with zone of partial preservation,
which is defined as the number of levels below the neurologic level of
injury that remain partially innervated. The motor exam consists of
testing 10 bilateral muscle groups with assigned neurologic level of
innervation and tabulating a score. All these data are entered into an
ASIA card that can be used for statistical analysis.
Certain signs and symptoms, even in unconscious patients, can lead to a higher suspicion of SCI. Examples include the following:
  • Flaccid paralysis
  • Hemodynamic instability with bradycardia
  • Priapism
  • Lack of response to painful stimuli in the arms and legs
  • Paradoxical respiration
Spinal shock occurs most frequently in cervical SCIs. It
has a wide range of duration, but sensory and somatic motor symptoms
usually resolve in 4 to 6 hours, whereas autonomic symptoms can persist
for days or weeks.
Although complete SCI presents as a distinct entity,
incomplete SCI has several well-described symptomatic patterns.
Recognition of these patterns can help in determining the patient’s
Cervicomedullary Syndrome
The cervicomedullary syndrome includes injuries from the lower medulla to the C4 region. It presents with the following:
  • Respiratory difficulty
  • Spinal shock
  • Tetraplegia with the arms weaker than the legs
  • Sensory level at C1-4
  • Facial sensory loss (damage to the ascending tract of the spinal trigeminal nerve)
Examination of the face is important because the more
lateral the facial sensory loss, the lower the lesion is. The prognosis
is variable. The presence of significant motor deficits or spinal shock
or both worsens the prognosis.
Central Cord Syndrome
The presentation of the central cervical cord syndrome
varies in its severity; the major diagnostic criteria include the
  • Tetraparesis with arms, and in particular hands, weaker than legs
  • Variable sensory loss that does not involve the face
Many patients with central cord syndrome show fast
recovery and can be observed to plateau in 24 hours. This scenario
occurs most commonly in elderly patients, with preexisting narrow
spinal canals, who sustain an injury with an extension mechanism.
Anterior Cord Syndrome
The anterior cord syndrome is due to a space-occupying
lesion anterior to the cord, such as a disc, fragments of fractured
vertebrae, or a hematoma. The presentation includes the following:
  • Complete paralysis
  • Preservation of vibration and touch sensations
In less severe cases, some motor function can be
preserved through the lateral corticospinal pathways. Flexion
mechanisms are the most common etiology, and the prognosis for
neurologic recovery with these injuries is usually poor.
Posterior Cord Syndrome
A distinct, although rare, entity, posterior cord
syndrome is due to damage to the posterior tissue with some sparing of
anterior cord.
  • Tetraparesis is due to disruption of the lateral corticospinal tracts.
  • Sensory loss is profound with the exception of pain and temperature.
Brown-Séquard Syndrome
Brown-Séquard syndrome, initially described in patients
with complete hemisection of the spinal cord, presents with the

  • Ipsilateral paralysis
  • Ipsilateral vibration and touch sensory loss
  • Contralateral pain and temperature loss
Brown-Séquard syndrome also has been observed in
combination with other types of incomplete injury, when different
spinal levels are affected to varying degrees. It can present acutely
or develop gradually over several days. Anal sphincter function can be
preserved or recovered. This injury is seen most frequently in
penetrating stab wounds.
Conus Medullaris Syndrome
Compression or burst fractures of T12 or L1 can result
in a loss of function involving only the sacral segments of the spinal
cord, which are located in the conus medullaris. Paraparesis, loss of
bowel and bladder function, and sensory loss in legs with perianal
sparing can be observed. In severe injuries, progression to the
development of a neurogenic bladder is inevitable.
Cauda Equina Syndrome
Although it is included in the ASIA/IMSOP scale, cauda
equina injury is strictly a peripheral nerve injury and carries a
higher rate of recovery. It presents with varying degrees of motor and
sensory loss, “saddle anesthesia,” and bowel/bladder dysfunction. The
better prognosis is believed to be due to the higher resistance of
lower motor neurons to injury.
Other Syndromes
Several well-described syndromes of SCI have variable
degrees of functional loss and are transient in nature. “Burning hands
syndrome” is seen most commonly among athletes and presents with
paresthesias and dysesthesias of the hands, which usually disappear
within several hours. It is thought to be due to a hyperextension
injury. Spinal cord concussion also is common and presents with sudden
onset of weakness and numbness with rapid improvement. This condition
is associated frequently with congenitally narrowed spinal canals in
athletes. The exact pathophysiology is unknown, but cellular-ionic and
vascular mechanisms have been proposed.
SCI also can be observed in patients with cardiogenic
shock or any other condition leading to prolonged hypotension. States
of low blood flow or occlusion of major feeding arteries, such as
vertebral arteries and radicular branches from the aorta, can lead to
hypoperfusion of the spinal cord tissue and ischemia, resulting in
spinal cord infarction. Infarction can occur even in the absence of
cerebral ischemia and can be diagnosed by MRI.
Emergency Department Evaluation and Treatment
As previously mentioned, acute SCI is diagnosed most
accurately in the presence of a high index of suspicion. Most often,
either an abnormal physical exam or a history of symptoms and a
mechanism of injury suggesting SCI are the clues to a correct
diagnosis. All patients presenting to a hospital emergency department
after a motor vehicle accident, fall, sports injury, multitrauma, or
head injury and patients who are under influence of drugs, alcohol, or
medication should be worked up for an acute SCI. If possible, a
detailed motor exam of all groups of the upper and lower extremities
should be completed. Additionally, a sensory exam of all dermatomes,
including S4-5, should be performed. Deep tendon reflexes, rectal tone,
and respiratory function should be evaluated at the same time. If a
physical exam is unobtainable for medical or any other reasons, the
spine should be assumed to be unstable. As such, the cervical spine
should be immobilized with a rigid collar, and the rest of the spine
should be immobilized with logroll precautions. Either plain
anteroposterior and lateral radiographs of the cervical spine or a
dedicated CT scan of the cervical spine with coronal and sagittal
reconstructions should be obtained. If any destabilizing injury to the
cervical spine is documented, and the physical exam is still
unavailable, cervical traction with Gardner-Wells tongs should be
considered. Data from animal studies support early decompression and
realignment of the cervical spine, even in the absence of spinal canal
compromise. We believe that relief of venous congestion and improvement
of spinal cord blood flow may be obtained with cervical traction, and
this may result in an improved outcome.
Any patient with an apparent SCI should undergo MRI of
the cervical spine to rule out a traumatic disc herniation or a
ligamentous injury or both. It is not advisable to manipulate the spine
or get flexion/extension radiographs before the absence of such an
injury has been documented. Because many patients with SCI present with
other trauma and depressed mental status and cannot be examined
reliably at the time of presentation, there is a risk of increased
compression of the spinal cord during such manipulation. Specifically,
flexion/extension radiographs should be avoided in patients with
odontoid fractures, patients who are obtunded, and patients with
central cord syndrome injuries because the motion can lead to an
irreversible neurologic worsening.
Controversy exists over the timing of imaging studies in
SCI patients. In our institution, patients who have spinal injuries who
either are neurologically intact or have an incomplete neurologic
deficit have MRI before any traction or surgery. In patients with a
complete neurologic deficit and plain film evidence of bilateral facet
subluxations, immediate traction with reduction is performed before any
additional imaging studies. Although there is the theoretical risk of a
herniated disc worsening the scenario, the time saved with these early
reductions seems justified. Immediately after the emergent reduction,
the patient is taken for advanced imaging studies.
Medical Treatment of Spinal Cord Injury Patients
Since the 1990s, the medical treatment of SCI patients
has received heightened attention. It now is apparent that allowing
patients with acute cervical SCIs to remain hypotensive


bradycardic for the initial hours after injury is not ideal. The
immediate treatment of acute SCI patients involves support with
intravenous fluid administration and early use of vasopressors to
combat hypotension. The goal is to get the mean arterial blood pressure
to greater than 85 mm Hg immediately and keep it above this level for a
minimum of 7 days. Likewise, it is essential to ensure the adequacy of
oxygenation on initial evaluation and to supply supplemental oxygen, as
necessary, to ensure that adequately oxygenated blood is perfusing the
injured spinal cord.

Our practice, and that supported by the American
Association of Neurological Surgeons/Congress of Neurological Surgeons
Joint Section on Disorders of the Spine and Peripheral Nerves in the
2002 position statement, has been to maintain patients with cervical
SCIs in an intensive care unit for a minimum of 7 days after the
injury. Liberal use of vasopressors and judicious use of intravenous
fluids to keep the mean arterial blood pressure greater than 85 mm Hg
have proved to be rewarding in our institution. As in many aspects of
the treatment of acute SCI, well-documented studies proving that this
approach is optimal have not been completed.
Pharmacologic Treatments
Many different pharmacologic agents have been used in
the treatment of SCI patients. Although many experimental drugs have
been tested, none has gained uniform acceptance. Based on existing
basic science theories, three medications have undergone formal
clinical testing in multicenter, prospective study formats. These
pharmacologic agents include:
  • Methylprednisolone
  • Ganglioside GM1
  • Naloxone
One theory has been aimed at the prevention of oxidative
phosphorylation as a method of treating SCI. This is the rationale
behind the use of high-dose methylprednisolone in the treatment of
SCIs. In the National Acute Spinal Cord Injury Study—Part II (NASCIS
2), published in 1990, a statistically significant benefit was found in
SCI patients treated with high-dose methylprednisolone (30 mg/kg body
weight bolus over 15 minutes, followed by a 45-minute delay, then 5.4
mg/kg/h for 23 hours) compared with patients treated with placebo. Used
in this dosage regimen, methylprednisolone does not act by its
glucocorticoid mechanism; rather, it functions as an antioxidant. It
generally is held that the impact of methylprednisolone occurs in the
gray matter of the spinal cord.
Criticisms of the NASCIS 2 study have centered on two
main points. First, the benefits achieved were not of much functional
benefit to the patients and may reflect merely a more rapid return of
nerve root, rather than spinal cord, function. Second, in this high
dose, methylprednisolone has side effects, including increased
bleeding, increased infections, and detrimental effects on spinal
fusions. None of these side effects were determined to have statistical
significance in the NASCIS 2 study; however, with the questionable
neurologic benefits achieved, the use of high-dose methylprednisolone
has not been embraced uniformly by spine surgeons. Additionally, in
1997, the NASCIS 3 protocol was published, which involved a minor
alteration in the duration of methylprednisolone dosing.
There has been significant controversy over the use of
methylprednisolone as recommended by NASCIS 2. A retrospective analysis
of the raw data obtained in the NASCIS 2 study has shown that many
confounding factors were omitted—accurate documentation of medical and
surgical treatments at different centers, functional outcome, and
medical complications. It has become clear that although steroids
decrease inflammatory reaction within the injured spinal cord, the
protocol recommended by NASCIS 2 does not offer a conclusive benefit
over the risks of infection, bleeding, effects on subsequent fusions,
pulmonary and endocrine complications, and difficulty with
administration (there has been a national shortage of
methylprednisolone). At present, our recommendations are as follows:
There is no proven benefit that favors the administration of
methylprednisolone for acute SCI, and because the risk-to-benefit ratio
is not in favor of its use, we do not administer this drug routinely to
SCI patients.
Further work is under way to develop drugs that would
inhibit more specifically oxidative phosphorylation (antioxidants)
without having the side effects of glucocorticoid agents. In a position
statement of the American Association of Neurological Surgeons/Congress
of Neurological Surgeons Joint Section of Disorders of the Spine and
Peripheral Nerves published in 2002, the physician treating SCI
patients is advised that methylprednisolone is an option that may be
used in treatment with the understanding that the risks of this
treatment outweigh its benefits.
An additional theory involves the use of GM1
ganglioside. This agent is believed to exert its action at the white
matter level in the spinal cord. A preliminary report published in 1991
was a cause for optimism with good results being reported on a few
patients in a single center. A follow-up, multicenter, controlled study
performed at 28 institutions failed to show benefit with the use of GM1 ganglioside at 26-week or 52-week outcome analyses. As such, enthusiasm for this agent has waned.
One theory has emerged that attempts to explain the role
of opiate receptors and opiate antagonists in SCIs. According to
observations by different authors, naloxone, which is a µ-subtype
antagonist, has a neuroprotective action. This action seems to be dose
dependent and has such a multifactorial, multilayered activity that
more studies are necessary to evaluate fully the possibility of
naloxone use in treating acute SCI. In the doses used in the NASCIS 2
study, naloxone did not show a statistically significant beneficial
effect in the treatment of acute SCIs.
Selection of Surgical Candidates and Timing of Surgery
A large body of literature exists concerning the timing
of surgery and candidate selection in the setting of an acute SCI.
Until more recently, the prevailing opinion among spine surgeons was
not to operate early after an injury, with “early” being defined as
within 3 weeks. High morbidity and mortality from early intervention
were documented in


studies. With advances in neurocritical care and neuroanesthesia,
however, early surgical intervention after injury has become safer. It
also is intuitive that the sooner the spinal cord and nerve roots are
decompressed, the greater the potential is for recovery of function. In
recent years, the definitions of “early” and “late” intervention have
changed. We define “early surgery” as being done within 24 hours after
injury and “delayed surgery” as being done after 24 hours. Although the
NASCIS 2 study was not designed to evaluate the timing of surgery, an
analysis of the raw data from this study did show an improved outcome
from early surgical treatment. This outcome is equally true for most
complete and incomplete injury syndromes, with the exclusion of central
cord syndrome, in which injury usually is due to hyperextension with
preexisting stenosis. In central cord syndrome patients, initial
immobilization, with observation, and surgery at a later time is a
common approach. Early intervention has other benefits in the cases of
incomplete injuries. When the spine is stabilized, intensive physical
therapy can be initiated so that other systemic complications of SCI
can be reduced.

Other criteria used to select patients for early
surgical intervention include associated systemic injuries and the
general medical condition of the patient. Acute SCI, as previously
mentioned, is associated with multiorgan trauma, plus SCI itself can
cause systemic shock with hypotension, respiratory deterioration with
pulmonary edema, and an increased risk for infection. When surgical
decompression or stabilization of the spine is delayed, medical
treatment of an acute SCI patient becomes essential in maximizing the
neurologic outcome. At present, there is no consensus as to the timing
of surgery for patients with SCI resulting from blunt trauma.
Author: Please verify drug doses.
AP, Levy ML. Pathogenesis and pharmacological strategies for mitigating
secondary damage in acute spinal cord injury. Neurosurgery
EC, Larson SJ. Functional recovery after decompressive spine operation
for cervical spine fractures. Neurosurgery 1987;20:742-746.
CH, Fehlings MG. Review of the secondary injury theory of acute spinal
cord trauma with emphasis on vascular mechanisms. J Neurosurg

This website uses cookies to improve your experience. We'll assume you're ok with this, but you can opt-out if you wish. Accept Read More