SPINAL CORD INJURY

There is still no cure for spinal cord injury (SCI). Recovery in the spinal cord is thwarted by
two fundamental obstacles: the inherently weak regenerative ability of central nervous system
(CNS) axons and a powerfully inhibitive—and often deleterious—postinjury milieu of
physical and chemical factors. These factors are intertwined in a so-called secondary
response of tremendous complexity that ironically does more to injure the spinal cord further
than to heal it. Years of research have slowly elucidated the pathophysiologic processes that
follow a traumatic insult to the spinal cord. This chapter reviews the biochemical and
physiologic features of the SCI response and establishes a foundation on which the latest
therapeutic strategies can be understood. The first section discusses the inlammatory cascade
that occurs in the moments after an assault to the spinal cord. The second section reviews
current understanding of the inhibitory extracellular environment that results from the injury
response and that ultimately prevents axonal regeneration. the chapter concludes with a
review of the biochemical processes that can be targeted by candidate therapies.

Pathophysiologic Response to Spinal Cord Injury

The acutely traumatized spinal cord is subjected to multiple physical and chemical mediators
that cause additional (secondary) injury. This concept of secondary injury has been validated
in both animal and clinical studies, and secondary injury mechanisms have been the target of
the bulk of pharmacologic interventions to date. hese processes begin immediately following
the injury and continue for weeks.

Hemorrhage and Circulatory Collapse

Upon injury, the blood–spinal cord barrier is disrupted and intraparenchymal hemorrhage
occurs, the extent of which depends on the force of the initial trauma. Microcirculatory
insuiciency follows. Vascular hypoperfusion due to capillary loss, capillary spasm,
thrombosis, systemic hypotension, and autonomic regulatory interruption lead to cellular
ischemia at the epicenter of cord injury. he neuronal cell bodies in the gray matter are highly
vulnerable to ischemia. The resultant shit in pH renders neuronal cell body and axonal
membranes highly vulnerable to subsequent injury.

Oxidative Damage

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Reperfusion and oxidative stress follow the transient period of hypoperfusion. he introduction
of oxygen to the compromised cell membranes produces a highly toxic environment in which
the membrane lipid fatty acids undergo oxidation. This membrane lipid peroxidation
produces several varieties of free radicals that, in turn, drive even further lipid peroxidation
and free radical production. Some of the free radicals accumulate within the cell and denature
deoxyribonucleic acid, mitochondrial proteins, and eventually bring energy production to a
halt, resulting in irreversible damage and cell death.

Excitotoxicity
Disruption of the neuronal cellular membrane undermines one of the crucial features of
cellular equilibrium—ionic regulation. The destabilized neurons undergo an inlux of sodium
ions that eventually alters cellular pH and leads to cytotoxicity. The ionic balance is
perturbed by, and will cause neuronal destruction via, an additional important mechanism: the
cellular release of the ubiquitous neurotransmitter glutamate changes the extracellular space
into a hostile extracellular milieu. Glutamate activates various cell surface receptors that, in
turn, mediate a large variety of intracellular processes. Excessive glutamate will drive these
processes to the point of fatal overload to the cell. he most studied of the glutamic receptors is
the N-methyl-D-aspartate receptor, which mediates entry of Ca2+ into cellular cytoplasm
from both extracellular and intracellular stores. While calcium in physiologic amounts is the
necessary component for many important enzyme-mediated cellular processes,
pathophysiologic quantities of calcium lead to the persistent activity of destructive enzymes,
including lipoxygenases and phospholipases. These enzymes will target the beleaguered cell
membrane again to generate free radicals from lipid oxidation. he radicals will disrupt
cellular proteins, in particular, those that mediate the ability of mitochondria, the chief source
of cellular energy, to drive oxidative phosphorylation.

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Mitochondrial Collapse and Cytotoxicity
The aforementioned free radical formation and glut of Ca2+ ions abolish mitochondrial
integrity by activating mitochondrial permeability transition pores. The opening of these
pores leads to a massive increase in mitochondrial membrane permeability. he organelle loses
its electrochemical gradient, adenosine triphosphate production ceases, and the outer
membrane swells until it ruptures. he damage is far-reaching. Calcium ions, free radicals, and
cytochrome c, once sequestered within the mitochondria, are now free to escape into the
neuronal cytoplasm where they immediately activate necrosis and apoptosis.

Neuroimmunologic Response
The cells of the immune system are eventually attracted to the neuronal self-destruction. Over
the next hours to weeks, they will lay the foundations for an extracellular environment that
will inhibit axonal regeneration. he irst of these cells to appear at the site of injury are
circulating neutrophils. Once active, neutrophils will secrete cytokines that stimulate
production of phospholipases and cyclooxygenase. The former will consume neural
membranes to produce arachidonic acid, which the latter (cyclooxygenase) uses to produce
prostaglandins and thromboxanes. Prostaglandins (PGE2, PGD2, PGF2α, PGI2) serve (1) to
amplify the inlammatory response by increasing capillary permeability to allow additional
inlammatory cell inlux; (2) to increase neuronal calcium concentration, thus promoting
excitotoxicity; and (3) to activate other inlammatory cells. Thromboxanes promote platelet
aggregation within capillaries and thus worsen local tissue ischemia. Macrophages, local
microglia, and astrocytes eventually appear and begin secreting the two most important

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factors of the cytotoxic inlammatory response: interleukin-1 and tumor necrosis factor α.
Interleukin-1 stimulates the expression of adhesion factors on endothelial cells, which will
allow circulating lymphocytes to penetrate the blood–brain barrier. Tumor necrosis factor α
serves to recruit activated cytotoxic lymphocytes to irst adhere to endothelial cells and then to
the site of injury. he recruited lymphocytes, which target myelin basic protein, are
particularly adept at causing disruption of the all-important myelin sheath—a critical
component of nerve conductivity and axonal regeneration. The epicenter of traumatic injury
thus becomes an inlammatory tangle of necrosis, apoptosis, and demyelination. Over the
coming weeks, the cellular debris will first liquefy into a posttraumatic cyst and then organize
into the notorious astroglial scar, which will inhibit axonal regeneration.

PATHOPHYSIOLOGY OF SPINE INJURIES

Stable and unstable injuries
Spinal injuries carry a double threat: damage to the vertebral column and damage to the
neural tissues. While the full extent of the damage may be apparent from the moment of
injury, there is always the fear that movement may cause or aggravate the neural lesion;
hence the importance of establishing whether the injury is stable or unstable and treating it as
unstable until proven otherwise.
A stable injury is one in which the vertebral components will not be displaced by normal
movements; in a stable injury, if the neural elements are undamaged there is little risk of
them becoming damaged.
An unstable injury is one in which there is a
significant risk of displacement and consequent
damage – or further damage – to the neural tissues.
In assessing spinal stability, three structural
elements must be considered: the posterior
osseoligamentous complex (or posterior column)
consisting of the pedicles, facet joints, posterior
bony arch, interspinous and supraspinous
ligaments; the middle column comprising the
posterior half of the vertebral body, the posterior

27.1 Structural elements of the spine The

part of the intervertebral disc and the posterior
vertical lines show Denis’ classification of the longitudinal ligament; and the anterior column
structural elements of the spine. The three
elements are: the posterior complex, the
middle component and the anterior column.
This concept is particularly useful in
assessing the stability of lumbar injuries. 4
composed of the anterior half of the vertebral body, the anterior part of the intervertebral disc
and the anterior longitudinal ligament (Denis, 1983). All fractures involving the middle
column and at least one other column should be regarded as unstable. Fortunately, only 10
per cent of spinal fractures are unstable and less than 5 per cent are associated with cord
damage.

Mechanism of injury
There are three basic mechanisms of injury: traction (avulsion), direct injury and indirect
injury.
Traction injury In the lumbar spine resisted muscle effort may avulse transverse processes; in
the cervical spine the seventh spinous process can be avulsed (‘clayshoveller’s fracture’).
Direct injury Penetrating injuries to the spine, particularly from firearms and knives, are
becoming increasingly common.
Indirect injury This is the most common cause of significant spinal damage; it occurs most
typically in a fall from a height when the spinal column collapses in its vertical axis, or else
during violent free movements of the neck or trunk. A variety of forces may be applied to the
spine (often simultaneously): axial compression, flexion, lateral compression, flexion-
rotation, shear, flexion-distraction and extension.

Assessment of the Spine-Injured Patient

Initial Evaluation
Patients sustaining blunt trauma should be assumed to have a potential spinal column injury.
During transport, patients are placed on a backboard and immobilized in a hard extraction
collar. he immediate primary care is to evaluate airway, breathing, and cardiovascular
functions, and begin resuscitation. The secondary exam includes visual examination of the
spinal column by log rolling the patient and palpation to determine tenderness, crepitus, and
gaps or step-ofs between spinous processes. Hemorrhage, contusion, and abrasion on the
face, head, or dorsal spine should raise suspicion of spinal injury. The goal of spinal
evaluation is to identify patients who require further imaging and to critically measure
neurologic function.

Clearing the Cervical Spine

The goal of this evaluation is to identify patients who have significant cervical injury after
trauma. Patients can be divided into four categories: asymptomatic, temporarily not

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evaluable, symptomatic, and obtunded. Asymptomatic patients are those who have no pain,
tenderness to palpation, normal cognitive function, and no distracting injuries. Distracting
injuries are other sources of trauma that may decrease or eliminate cervical spine signs or
symptoms. Examples of distracting injuries are fracture-dislocations, long-bone fractures,
burns, shock, chest trauma, and craniofacial trauma.

Asymptomatic Patients
Asymptomatic adult patients can be cleared of cervical spine injury without any radiologic
imaging. he National Emergency X-Radiography Utilization Study (NEXUS) screened
34,068 patients using the criteria and identiied 99.8% of all injuries. Six of the eight missed
cases were trivial fractures and two were signiicant (odontoid fractures) that did not develop a
neurologic injury. he speciicity was low (12.8%), indicating that many patients still required
imaging, which was negative. A simple modification is the Canadian Cervical Spine Rule
(CCR), which adds 45 degrees of pain-free rotation of the head to the examination. Stiell
reported a 100% sensitivity using this method and improved specificity over the NEXUS
method. Both of these protocols are not applicable to children and are less accurate in
geriatric patients.

Temporarily Not Evaluable

These patients are less well deined. However, they could be cleared using the asymptomatic
criteria, but have distractinginjuries or impaired cognitive function, such as intoxication, that
will clear or be corrected within 24 to 48 hours. Initially, they are immobilized in an orthosis,
then later reevaluated based on NEXUS or CCR criteria. If negative at that time, they may be
cleared with further imaging. If clearance is required immediately, then they should be
evaluated as described later for obtunded patients.

Symptomatic Patients
All symptomatic patients following blunt trauma are at high risk for cervical spine injury,
thus require radiologic imaging. Computed tomography (CT) in adults is highly sensitive and
preferred over plain radiography. Magnetic resonance imaging (MRI) is not recommended as
a screening examination due to its cost and high rate of false positives. MRI is indicated in
patients who have unexplained neurologic deicits (such as central cord syndrome), for
patients for whom there is suspected ligamentous injury, in patients with signiicant

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degenerative or postsurgical changes, as well as to aid surgical decision making. A negative
MRI, however, does accurately exclude the presence of a cervical spine injury.

Obtunded Patients
The clearance of obtunded patients remains controversial. Maintaining spine precautions and
cervical immobilization in this patient population is associated with reduced pulmonary
function, increased intracranial pressure, and risk of skin decubitus. hus, timely clearance is
important. Two options are available in obtunded patients: utilize results of CT or include
MRI. Modern helical CT is highly sensitive and rarely have signiicant injuries been reported
following CT.
Most cases are results of misreading by radiologists. MRI, however, has been shown to
identify more injuries than CT and, in some studies, resulted in need for surgical treatment.
Like investigations regarding CT, these studies are small retrospective studies without
adequate statistical power. I recommend that each institution utilize its own protocol and
continue to monitor efectiveness.

Neurologic Examination
A complete neurologic examination is performed, including cognitive function, cranial nerve,
motor sensory function in the extremities, relexes, and pathologic relexes. In addition, in
patients with any neurologic deicits, careful evaluation of perineal function is performed.
Patients’ neurologic function should be reported per American Spinal Injury Association
(ASIA) standards. The ASIA motor score is the summation of motor function of 10 key
muscle groups, five in the upper and five in the lower extremities, bilaterally; each is graded
from 0 to 5. Summation of these scores deines the ASIA motor score and the total ranges
from 0 to 100. Sensory examination of each dermatome is recorded as intact, hypoesthesia, or
absent. Perianal examination is essential, as patients may have only sacral root sparing, which
can dramatically change the prognosis.
Perianal rectal function is determined by digital rectal examination, assessing the initial tone
and asking the patient to perform voluntary rectal contractions. he bulbocavernosus relex and
the anal wink are spinal cord–mediated relexes at the level of the conus medullaris. he anal
wink is obtained by brushing the paraspinal area with a pin and observing for an anal
contraction. he bulbocavernosus relex is best obtained during digital rectal examination by
placing tension on a Foley catheter and observing for a rectal contraction. These reflexes are

7
present in intact patients. Although they are typically absent in acute spinal cord–injured
patients, they may return early (within 7 to 10 days ater spinal cord injury).
Intact perianal function in injuries at the conus medullaris, such as L1 or T12 fractures, or for
cauda equina injuries is a good prognostic sign, as it indicates that the aferent and eferent
neurons and the conus are functional. Deep tendon relexes, including biceps, triceps, patella,
and Achilles, are assessed. In acute spinal cord injuries, the reflexes below the level of injury
are usually absent due to spinal shock, but will return in 10 to 21 days when they will become
hyperrelexic. In addition, pathologic relexes—such as Hofman, Babinski, and clonus—
should be recorded. Priapism, if present, is a sign of acute spinal cord injury.

Spinal Cord Injury Classiication

Spinal cord injuries are classiied at the level and extent of injury. ASIA deines the level as the
lowest segment with at least antigravity (grade _3) motor function. The extent of spinal cord
injuries is how much of the cross-sectional area of the cord is injured. Complete cord injuries
are deined as complete loss of motor and sensory function; incomplete cord injuries have
some retained motor and/or sensory function below the zone of injury. Special attention
needs to be focused in the perineal area, as this may be the only area distinguishing complete
from incomplete injuries. Incomplete cord injuries are important to recognize and have a
much better prognosis.
The anterior cord syndrome represents loss of the anterior two-thirds of the spinal cord,
where there is paralysis of distal motor function and loss of pain and temperature sensation.
These patients have retained dorsal column function, so that they may experience light touch,
proprioception, and vibratory sensation, but no pinprick or motor function.
Central cord syndrome is a common cord injury in which there is loss of gray matter and
central white matter. he white matter tracts are laminated, with cervical tracts positioned
more centrally and lumbar and sacral tracts located toward the periphery. Because of the
relative sparing of these laterally located tracts, the central cord syndrome is manifested by
greater loss of upper than lower extremity function. The prognosis for central cord syndrome
is good, with an expectation for ambulation, but hand function may be chronically impaired.
The posterior cord syndrome is the loss of the posterior column with sparing of the anterior
cord. These injuries produce loss of vibration, light touch, and position sense, but maintain
pain, temperature, and motor functions.
Brown-Sequard syndrome is a hemicord injury with ipsilateral motor paralysis and loss of
dorsal column function as well ascontralateral loss of pain and temperature. he prognosis for

8
Brown-Sequard syndrome is excellent.
The ASIA Impairment Scale (AIS) assesses the extent of injury and is highly predictive of
outcomes. Complete cord injuries with absence of distal and sensory motor function are
ASIA A. The ASIA B patient has some sensation, but no motor function below the zone of
injury. ASIA C patients have both motor and sensory function below the zone of injury, but
the motor function is less than grade 3. ASIA D patients, like ASIA C patients, have both
motor and sensory function, but motor function is grade 4 or 5. ASIA E patients are intact.
Patients with neurologic deicits should have neurologic exams at least every 2 hours, which
are documented in the record. Neurologic function may change in the initial stages after
spinal cord injury, which will be an important determinant of treatment. herefore, accurate
reporting of the neurologic exams is essential. The ASIA classiication is useful for a
comprehensive report of the neurologic examination.

General Approach to Treatment of Injuries

Each patient is assessed clinically for signs of injury by palpation, checking for tenderness,
and by a detailed neurologic examination. A patient with tenderness or signs and symptoms
of neurologic injury should have a CT to identify injury patterns. If any ligamentous injury is
suspected or unexplained neurologic deicits are present, an MRI scan is indicated. At this
point, the injury is classiied morphologically using the AO system. he severity is then graded
using CSISS or SLIC. Patients who have a score greater than 5 SLIC or greater than 7 CSISS
are treated surgically. In patients with less severe injuries, nonoperative treatment in orthosis
is attempted.

Nonoperative Care of Subaxial Cervical Injuries

Nonoperative care is indicated for those with stable fractures or those who are not otherwise
surgical candidates. For most lower cervical spine injuries, patients are managed in an
orthosis. Choices include sot collar, hard collar (e.g., Miami J [Ossur]; Aspen collar [Aspen
Medical Products], or CervMax [PMT Corporation]), cervicothoracic brace, and halo vest.
The general approach in all orthotic management is similar. The orthosis is fitted by a trained
orthotist. Pads that wick luids away from the skin can help to prevent skin breakdown. he
brace needs to control head-mandible motion relative to the thorax. No brace, including the
halo vest, will completely prevent segmental motion in a fractured cervical spine, as the
spinal column can easily assume snakelike intervertebral motions. Twice-daily skin checks
are ordered while the patient is hospitalized or in a rehabilitation facility.

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Training of patients and family is essential to ensure proper use and to avoid complications of
the orthosis. In patientsolder than 65 years, a swallow consult is obtained to assess aspiration
risk prior to institution of diet. Occupational therapy trains patients to use the brace and in the
activities of daily living while immobilized. Upright radiographs are obtained ater brace
placement and scrutinized for increasing kyphosis and/or subluxation. Any change in these,
or new or worsening neurologic symptoms indicates instability, and surgery is recommended.
Follow-up radiographs are obtained at 2, 6, and 10 weeks. In most subaxial injuries, healing
will occur by 10 to 12 weeks or earlier. Patients are initially informed that their orthosis is a
test of stability and that about 5% to 10% of patients will fail and may require surgery. In
patients without clear surgical indication (such as SLIC scores of 4 or 5 and CSISS scores of
5 to 7), either approach can be chosen. In general, I recommend a trial of nonoperative
therapy with orthosis in these cases. In such cases, shared decision making should occur,
taking into account the patient’s preferences.

Soft Collar
Sot collars provide little stability and are used for comfort but also to alert medical personnel
that injury is present. hese are indicated for frail elderly patients with minimal or stable
fractures or in patients who cannot tolerate even a hard collar.

Hard Collar
Many forms of hard collar are available. Use of extraction collars and Philadelphia collars
should be avoided, as these it poorly and can lead to skin breakdown. It does not appear that
the stabilization efect among well-fitting hard collars varies by manufacturer. It is best that
the orthotist use a single brand so that personnel can become familiar with their use and
maintenance. Hard collars do not provide sufficient stability for unstable fractures, but are
efective, in my experience, in stable SLIC score less than 3 and CSISS score less than 5.

Cervicothoracic Orthosis
The cervicothoracic orthosis (CTO) has anterior and posterior chest pads that are connected
by straps under the axilla and over the shoulder. Vertically, they are connected to occipital
and mandibular pads rigidly. The CTO brace provides greater stability than hard collars,
especially at the cervicothoracic junction. The CTO places increasing pressure on the occiput
and chin, and should be used with caution. I do not recommend its use in spinal cord–injury
patients who lack body control or any patient with cognitive impairment due to the risk of

10
skin ulcerations. I recommend the CTO for patients with injuries at the cervicothoracic
junction, those with multilevel spine fractures where multilevel fusions might be otherwise
utilized, and cervical spine injuries combined with upper thoracic injuries. An alternative
treatment for this injury pattern is the thoracolumbosacral orthosis with chin piece (cervical-
thoraco-lumbosacral orthosis). I have abandoned its use due to risk for skin ulceration and
poor patient acceptance.

Halo Vest
The halo vest is the most rigid external orthosis, although segmental motion can still occur at
the fracture site. Anderson reported in patients with unstable fractures treated in the halo vest
that 1.8 mm of translation and 7 degrees of angulation fracture site motion occur during
position change from supine to upright.20 he use of the halo vest has declined and is rarely
used today in my experience for subaxial injuries. It is indicated for unstable fractures in
which fusion is a poor alternative, such as young patients who are neurologically intact or
those with multilevel injuries. For these cases, the halo vest may provide the best
nonoperative approach, thereby avoiding multilevel fusions.

Treatment of Acute Spinal Cord Injury

The goals of treatment of spinal cord–injury patients are to protect the neural tissues from
further injury, reduce and stabilize fracture-dislocations, and provide a stable long-
termpainless spine.

Transport
Patients presumed to have spinal cord injuries should betransferred to institutions that are
experienced in their management, have advanced imaging available, and can provide
intensive care and urgent surgical services. Treatment of spinal cord injuries in Level 1
trauma centers is shown to reduce rates of complication as well as shorten the length of
hospitalization and rehabilitation time. Spinal cord–injury patients require intensive care to
monitor neurologic state and provide hemodynamic support, assess pulmonary function
(which often deteriorates over time), and prevent adverse events, such as skin breakdown.

Immediate Care of the Spinal-Injured Patient

Once a subaxial fracture is diagnosed, consideration of immediate treatment is entertained.
All patients with spinal cord and nerve root injury as well as those with unstable fractures are

11
candidates for immediate intervention. his includes hemodynamic support, further diagnostic
testing, administration of neuroprotective agents, reduction using tong traction, and urgent
surgery. While the decision-making process for resuscitation is taking place, patients with
subaxial fractures should be immobilized in a hard collar and maintained lat on a bed or
stretcher. Although the backboard is an excellent aid for transport to and within the hospital,
it should be removed as soon as possible to reduce the risk of skin breakdown. In addition,
backboards can be associated with fracture displacement, especially in children or in patients
with thoracic kyphosis.

Hemodynamic Support
The injured or compressed spinal cord is ischemic, which can further exacerbate the spinal
cord injury. If spinal cord injuryis present, there is a loss of vasomotor tone, with resultant
hypotension and bradycardia, causing a condition known as neurogenic shock. In addition,
the spinal cord, like the traumatized brain, loses its ability to autoregulate blood low.
Therefore, intramedullary blood low becomes related to the systemic arterial pressure. Any
hypotension, either from loss of vasomotor control or from blood loss, can worsen or
exacerbate the spinal cord injury. Guidelines recommend resuscitation of a spinal cord–
injured patient to a systolic blood pressure greater than 120 mm Hg (usually with pressor
agents) and maintaining the mean arterial pressure at 85 mm Hg. A high FiO2 should be
administered to maintain O2 saturation greater than 95%. Ventilatory failure may be present
or develop over time and requires intubation and mechanical support. Intubation needs to be
performed carefully so that fracture displacement is minimized. It is best that the surgical
team assist in this task by holding the head while maintaining traction.

Magnetic Resonance Imaging in Acute Spinal Cord Injuries

Early treatment decisions may require further imaging by MRI. Urgent MRI is indicated for
unexplained neurologic deicits, neurologic deterioration, to evaluate ligamentous structures,
or in patients with no or minimal deicits who have facet dislocations to determine the
presence of a traumatic disc herniation. In these cases, neurologic worsening has been
reported ater open reduction when the disc lies behind the vertebral body compressing the
spinal cord ater reduction. Several case reports have documented that disc herniation behind
the vertebral body remains in that location ater reduction, causing signiicant neurologic
deicits. In addition, MRI is useful for preoperative planning.

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Neuroprotection
To address the secondary spinal cord injury caused by vascular, molecular, biochemical,
and/or inlammatory changes, early treatment using neuroprotective agents has been proposed.
Many pharmacologic and cellular agents show promise in laboratory animals. However, only
methylprednisolone is approved for current use. Methylprednisolone, when given within 8
hours of injury, has an antioxidant efect by reducing lipid peroxidation that occurs as part of
the secondary injury pathophysiology.
The clinical evidence for use of methylprednisolone is based on the National Acute Spinal
Cord Injury Study 2 (NACISC2). In this randomized control trial, 454 patients with blunt
traumatic spinal cord injuries were randomized to naloxone, methylprednisolone, and
placebo. All patients had randomization and administration of drugs within 8 hours of injury.
Naloxone was thought to have neuroprotective properties at the time. Patients receiving
methylprednisolone had a statistically signiicant improvement of 5 points of ASIA motor
level. The impact of the NACISC2 study was signiicant; subsequently, almost all spinal cord
injuries were treated using the NACISC2 protocols. However, critical analysis of the
statistical methodology, identification of potential harms, including death, and the minimal
perceived benefits have led many to abandon orlimit the use of methylprednisolone for spinal
cord injury.
Recent guidelines by the American Academy of Neurological
Surgeons and the Congress of Neurological Surgeons recommend against the use of
methylprednisolone in acute spinal cord injury. Unfortunately, the data from the NACISC2
study included mostly patients who did not have surgery or even reduction of fracture
dislocations within 24 hours. Further, hemodynamic support was not utilized routinely at the
time of the original study. Thus, there is a knowledge gap as to whether methylprednisolone
may have a beneicial efect when combined with other current standard practices in care. My
current recommendations are to administer methylprednisolone in select patients with
cervical cord injuries, both complete and incomplete, and in incomplete thoracic cord
injuries. Methylprednisolone is recommended only in patients without other significant
traumatic injuries or comorbidities. I do not recommend its use in geriatric patients with
spinal cord injuries. When used, methylprednisolone is administered as a 30-mg/kg loading
bolus over 1 hour and a continuous infusion of 5.4 mg/kg per hour for 23 hours.

Fracture-Dislocation Reduction

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Early fracture-dislocation reduction is important to remove neural compression and
reestablish blood low to ischemic tissue to prevent deterioration and maximize the chance of
neurologic recovery. This can be achieved by two methods:
cranial tong traction and surgery. Cranial tong traction is a useful and generally safe method
to stabilize the spine and to achieve realignments of fractures and dislocations.26 Indications
for cranial tong traction vary and are being supplanted by immediate surgery where reduction
by traction is avoided.
In a study to evaluate the timing of surgery on the outcomes of spinal cord injury, the authors
found that only one-third of patients were ever treated with tong traction before surgery.
Cranial tong traction is a fast method to reestablish spinal cord blood low through reduction.
In low-energy facet dislocations, such as from sporting accidents, early reduction within 4
hours of injury in patients with quadriplegia was shown to have a reversible efect in 80% of
cases.

Timing of Surgery
The timing of surgery in humans remains controversial, despite a large volume of animal data
that demonstrates early surgery correlates with greater neurologic recovery. Because of
diiculties with study design, heterogeneity, and severity of injury, these beneits of early
surgery have not been proven in humans. A recent observational study, Surgical Timing in
Acute Spinal Cord Injury Study (STASCIS), compared neurologic improvement at 6 months
based on ASIA impairment scale between early (_24 hours) and late (>24 hours). Patients
were stratiied according to whether surgery was performed before or ater 24 hours. here was
no diference for the chance of improving one ASIA level; however, there was a statistically
signiicant and better chance of improving 2 ASIA levels if surgery was performed within 24
hours. In patients with spinal cord injuries, the potential for neurologic deterioration caused
by early surgery has been a concern. he mechanics of this are unclear, but likely are due to
hemodynamic changes that occur during surgery. In the STASCIS study, only one patient
deteriorated neurologically; the authors believe that early surgery was feasible and safe in
patients treated at centers with experience in managing spinal cord injuries.

Cranial Tong Technique

Cranial tongs have a metal or carbon iber arc, two pins which are inserted into the skull, and a
hook for traction rope. The pins are disposable, and one pin has a compression spring that
acts to measure the applied force of the pins into the skull. Both MRI-compatible and non–

14
MRI-compatible devices are available. Unless heavy weights are anticipated, I recommend
the use of MRI-compatible devices. Guidelines for Initial Closed Reduction of Subaxial
Cervical Fractures Gelb reported guidelines based on a systematic review of the use of closed
reduction with tong traction in subaxial fractures and dislocations. Based on a retrospective
case series, the recommends early reduction with cranial tong traction for subaxial injuries in
awake patients without more rostral injuries. Prereduction MRI should be obtained in patients
who cannot be examined during closed reduction or if closed reduction fails. MRI will
identify disc disruptions in up to 50% of cases, but does not appear to inluence outcomes in
awake patients; therefore, their utility is questioned.

Cranial Tong Insertion

The location of tong insertion is 1 cm above the pin and in line with the external auditory
meatus. Placement more anteriorly or posteriorly can change the force vectors, which may
theoretically aid reduction. For consistency, I recommend placement in line with the exterior
auditory meatus. The skin is prepared with chlorhexidine and the subcutaneous tissue and
periosteum is iniltrated with local anesthetic. No shaving of the scalp is required. he surgeon
holds the tongs with pins located just above the correct starting point, which are then
symmetrically tightened into the skin and skull. The pin containing the compression spring is
scrutinized until it protrudes 1 mm out from the surface of the pin. Jam nuts along the side of
the pins are tightened to prevent inadvertent further tightening of the pins. If the traction is to
be continued (unusual today), the pins may be retightened one time at 24 hours. The rope is
attached to the tongs and connected to weights by a pulley at the head of the bed. I prefer to
raise the head of the bed 20 to 30 degrees while keeping the angle of the rope at the same
slope.

Reduction Technique
Reduction of fractures and dislocations requires a rigid protocol to maintain safety. he initial
weight is selected dependingon many factors, including body weight, level of injury, age, and
fracture pattern. For midcervical and lower cervical spine injuries, it is recommended starting
with 10 kg (20–25 lb). Ater the weight has been attached (and ater any increase or decrease of
weight), a radiograph is obtained and a neurologic examination is performed and documented
in the medical record. The radiograph is assessed to determine if reduction has been achieved
and for signs of overdistraction. Overdistraction is assessed by examination of the disc space
and facet joints. Overdistraction may cause excess traction on the spinal cord and vertebral

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arteries, which could result in neurologic deterioration. However, to reduce a facet
dislocation in the absence of fractures, overdistraction of 3 to 5 mm may be required. he
neurologic examination assesses any change in perceived sensations, increasing pain, or
paresthesia in the extremities, or deterioration of sensory or motor function. If reduction is
not achieved, 5 to 7 kg of additional weight is added as long as no neurologic deicits or
radiologic signs of overdistraction occur. A C-arm with the patient on a stretcher or Jackson-
type table can reduce the time required to obtain the reduction. In general, once the reduction
is achieved, weights may be decreased. However, for unstable fractures, reducing weight can
result in displacement and neurologic injury. herefore, if weights are decreased, it is essential
to repeat the neurologic examination and examine new radiographs. Some manipulation may
be required to achieve reduction, which should only be done by experienced surgeons. In
facet dislocations, slight lexion may be required to unlock the impacted dislocated facets. his
is accomplished by adding bolsters underneath the occiput to create neck lexion. Another
method is to manually manipulate the spine while in traction. For bilateral facet dislocations,
an attempt to reduce each facet independently is preferred. The tongs are grasped and a lateral
bending movement and forward lexion is applied, ideally reducing one facet. he same
movements are performed on the contralateral side.
In several conditions, cranial tong traction reduction may lead to neurologic deicits.
Distractive lesions, although uncommon in the subaxial cervical spine, lack any longitudinal
running ligaments, which provide the potential for ligamentotaxis that controls reductions.
Facet dislocations have a disrupted disc complex in almost all cases. In a few cases, however,
the intervertebral disc may be herniated behind the cranial vertebral body. he disc may not
reduce when the spinal column is realigned and the disc behind the vertebral body may
increase compression on the spinal cord, resulting in neurologic deicit. his appears to be a
rare condition and almost exclusively occurs during closed reductions with patients under
general anesthesia. Most surgeons agree that cervical tong traction in awake patients using
the method described earlier is much safer. In patients with signiicant neurologic deicits, I
believe that the beneit of immediate reduction exceeds the potential for worsening due to disc
herniation, and I proceed with rapid reduction when indicated.
In patients who are intact or have mild deicits, it is usually possible to obtain an MRI scan
prior to reduction. If a traumatic disc herniation behind the body of the cranial vertebra is
present, the patient should undergo anterior discectomy and then reduction using direct
vertebral manipulation or intraoperative tong traction. If reduction is achieved, then anterior
interbody fusion with a plate is performed. If reduction is not achieved, the patient is turned

16
prone on a turning frame and open posterior reduction is performed. Lateral mass ixation and
bone grat is applied. The wound is closed and the patient is repositioned supine and anterior
body fusion performed with or without addition of an anterior plate.
Another contraindication to traction reduction is ankylosing spondylitis. hese are highly
unstable injuries in which the ALL and PLL are absent and thus do not provide
ligamentotaxis. Traction in these cases can lead to loss of alignment, overdistraction, and
neurologic deficits.

DAFTAR PUSTAKA
Simeone, R, (2018) Spine Trauma in Basic Science of Spinal Cord injury : Rasouli,
Alexander. Rothamn-Simeone and Herkowitz The Spine, seventh ed. United of State.
Philadelpia. Elsevier

Blom, Ashley, David Warwick, Michael RW (2018) Section 3 in Injuries of The Spine
:Dunn, Robert, Nicholas Krugger . Apley & Solomon’s System of Orthopaedics and Trauma,
tenth ed. United of State. CRC press.

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