SPINAL INJURIES
Spinal cord trauma:
pathophysiology,
classification of spinal
cord injury syndromes,
treatment principles and
controversies
George I Mataliotakis
Athanasios I Tsirikos
Abstract
Acute spinal cord trauma is a devastating injury which often leads to
severe disability. The tissue response following the initial insult ex-
tends the cord damage, while there is limited repair potential with
regards to axon regeneration resulting in permanent neurological def-
icits. Management of acute cord injury is an area of active research in
order to stabilize the spine in a timely manner, minimize the secondary
insult and promote regeneration. Methyl-prednisolone administration
for limitation of the secondary injury phase and acute versus late oper-
ative treatment are areas of current debate among several authors.
This article is an overview of all aspects of early and long term spinal
cord injury management. It focuses on the patho-physiological mech-
anisms of the acute injury phase and the different clinical types of cord
injury syndromes. The treatment principles are described along with an
updated view on the controversial issues.
Keywords cord syndromes; methyl-prednisolone; neuro-plasticity;
neuro-protection; spinal cord trauma
Introduction
The neural tissues forming the spinal cord are highly susceptible
to injury and have little capacity for self-repair. Reversal of spinal
cord injury continues to be one of the greatest challenges in
medicine. Knowledge of patho-biology is rapidly evolving and
components once thought to be detrimental such as glial scarring
and inflammation are now believed to have beneficial effects.1,2
Traumatic spinal cord injury (SCI) is typically caused by a con-
tusive force to the spinal cord leading to activation of numerous
mechanisms that both extend and limit the injury.3
George I Mataliotakis MD Fellow in Spinal Deformity Surgery,
Scottish National Spine Deformity Centre, Royal Hospital for Sick
Children, Edinburgh, UK. Conflicts of interest: none declared.
Athanasios I Tsirikos MD FRCS PhD Consultant Orthopaedic and
Spine Surgeon, Honorary Clinical Senior Lecturer, University of
Edinburgh; Clinical Lead, Scottish National Spine Deformity Centre,
Royal Hospital for Sick Children, Edinburgh, UK. Conflicts of interest:
none declared.
ORTHOPAEDICS AND TRAUMA 30:5
Neurons are especially vulnerable to injury because of the
length, complexity and specificity of their connection. In addi-
tion, the receptor and membrane specializations that enable
chemical and electrical neuronal transmission cause a high ca-
pacity for and vulnerability to major ionic shifts. The spinal cord
components are rarely exposed to inflammatory cells and there is
a specialized barrier between endothelial cells supported by
astroglia that restricts movement of proteins and other
molecules.1
Spinal cord salvage and repair are two primary goals of
therapy.2 Traditionally, the role of the Spinal Surgeon is in post-
traumatic spinal cord salvage focussing on acute care, surgical
decompression, vertebral stabilization and management of
chronic complications, such as syringomyelia, tethering and
deformity.2,4 Neuro-protective and repair strategies are based on
understanding of the temporal evolution of injury mechanisms.
Spinal teams with surgical and scientific expertise will translate
new advances from experimental studies into clinical studies
aiming to design and apply new treatments.1e3
Epidemiology
The estimated annual incidence of acute SCI in the United States
among those who survive a traumatic event is 40 per million
population or approx. 12 500 per year.1,5 The distribution of age
at injury is bimodal; the first peak (approximately 50% new in-
juries) involves young adults and the second peak involves
adults older than 60 years.5,6 The average age of young adults
has increased from 28.7 to 42 years.5 Adults older than 60 are
vulnerable to SCI due to age related bony changes, such as cer-
vical spondylosis and stenosis, the effects of medication and
sensory loss.5 The clinical outcome in patients >60 years is
considerably worse than that in younger patients. Approximately
50% of patients have cervical, 35% thoracic or thoracolumbar
and 11% lumbar injury; the location of the remaining 4% is
unknown or unreported. The single most commonly affected
level is C5. The most frequently reported post-SCI neurologic
category is incomplete tetraplegia (39.5%); complete paraplegia
accounts for 22.1%, complete tetraplegia for 21.7% and incom-
plete paraplegia for 16.3%.5 At least 20% of patients with SCI
have other major injuries such as cerebral contusions or flail
chest.5
Mechanisms of cord injury
The spinal cord may be injured by compression, contusion,
laceration or vascular insult.3 The impact of injury depends on
the magnitude of initial insult and the underlying condition of the
spinal cord. The difference between compression and contusion
is in the rate of deformation.1 In cord contusion, the compressive
force exceeds the tissue components tolerance leading to
disruption of axons and damage of neuron cell bodies, myeli-
nating cells and vascular endothelium.
Mechanical failure of the osseo-ligamentous spinal column
structure may lead to SCI by abrupt physical deformation of the
cord substance (contusion) and/or by direct laceration/
compression by bone fragments.6 Gunshot injuries may cause
direct laceration of the cord by the projectile or indirect injury by
the bone/disc fragments.6e8 Abrupt distortion and shearing by
the blast cavitation of the projectiles’ kinetic energy may also
440 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES

cause injury to the cord.7 Knife injuries may cause direct com-
plete or partial laceration of the cord.9 Key-stages of the spinal cord response to closed
Based on the macroscopic findings, SCI can be classified into trauma1,6,11e16
four groups: (a) solid cord injury, the least common type, is Acute phase C Cord oedema, intracellular swelling
associated with normal appearance of the cord after injury; (b) (up to 72 hours) C Haemorrhage
contusion, the most common type, is associated with areas of C Regional cord perfusion shifts
haemorrhage and expanding necrosis/cavitation but with no C Inflammatory response: free radical
disruption of the surface of the cord; (c) laceration, where is a production, lipid peroxidation and
clear-cut disruption of the surface anatomy; and (d) massive cytokine release
compression, where the cord is macerated to varying degrees.10 C Membrane instability: shifts in
In most instances, the anatomic degree of spinal cord damage electrolytes and accumulation of
does not correlate with the degree of functional loss. neurotransmitters
C Demyelination
Pathophysiology-neurological insult C Cell necrosis and apoptosis
Intermediate phase C Proximal and distal extension of
The predominantly lipid structure of the spinal cord partially
(days to weeks) oedema, necrosis and apoptosis
accounts for its vulnerability to injury. Aside from the pia matter
C Continued inflammatory response
there is very little connective tissue in the spinal cord in com-
C Vascular angiopathy
parison with the peripheral nerves, which are much more
C Peak levels of astrocyte and
resilient.
macrophage activity
C Initial scar formation
Primary injury
C Neuroplasticity
After the SCI the spinal cord is contused, may be partially C Spasticity
lacerated but is rarely transected. The maximal neurologic deficit Chronic phase C Formation of fluid e filled cavity
is observed immediately after a SCI because axonal transmission (months to years) C Wallerian degeneration
is disrupted or blocked by abrupt neuronal cellular damage, C Glial scar formation
endothelial and blood vessel damage, haemorrhage and massive C Demyelination
shifts in membrane potential and ionic concentrations.1 This is C Schwann cell proliferation
mostly irreversible.6 C Syringomyelia
C Tethered cord
Secondary injury C Neurite sprouting, altered
The secondary injury phase begins immediately and may extend neurocircuits and chronic
for several days. The tissue damage continues during that phase pain syndromes
substantially extending the size of the injury. Oedema and hae-
Table 1
morrhage within the cord may spread from the primary site of
impact over several rostral and caudal levels. Haemorrhage is
more evident in the gray matter because of its rich vascularity. Endothelial damage is the primary event that initiates the
Endothelial damage leading to increased permeability and cascade of SCI inflammation. Mechanical gaps between endo-
intracellular oedema, is a key factor in the recruitment of in- thelial cells develop within 1.5 minutes of injury leading to
flammatory cells.6 damage of perivascular basement membrane, red blood cell
The secondary injury response can be divided into acute, in- extravasation, platelet aggregation and fibrin deposition. Platelet
termediate and chronic phases. The intermediate phase starts a few aggregates occlude vessels leading to ischaemia. Endothelial gaps
days after injury and lasts for several weeks. The events of each promote influx of fluid and proteins thus producing oedema.
phase are summarized in Table 1; however there is close interre- Subsequent events promote microglial activation and leucocyte
lation among all phases without distinct borders between them. infiltration. The basal laminae are further degraded due to
increased endothelial expression of vascular cell adhesion
Vascular injury/inflammatory response molecule. These events further exacerbate the loss of endothelial
The spinal cord is not exposed to inflammation like tissues as integrity, increasing vascular permeability and leucocyte influx.
skin, bone, lungs, which frequently undergo healing process. The prominent cytokines present at SCI include IL-1, IL6,
Endothelial cells normally form a barrier that excludes the active TNF-a, and TGF-1. Early expression of TNFa and IL1 by micro-
blood components from the Central Nervous system (CNS).1,17 glia enhances the recruitment of inflammatory cells to the injury
This blood-CNS barrier is characterized by tight junctions be- site. IL1b is upregulated within one hour of injury, peaks at eight
tween endothelial cells and strong interactions between the hours after injury and persists at least seven days.1,11,17
surrounding astrocyte foot processes and basal lamina.1,17 Thus The four general classes of inflammatory cells that respond to
macrophages, lymphocytes and poly-morpho-nuclears are SCI are microglia, neutrophils, macrophages and lymphocytes.
seldom observed in the normal spinal cord and the intrinsic Microglia, neutrophils, macrophages offer innate immunity and
microglia is quiescent. Also, CNS cells are rarely exposed to in- lymphocytes offer adaptive immunity.6 Neutrophils enter the
flammatory cytokines (Table 2). damaged spinal cord immediately after injury and reach peak

ORTHOPAEDICS AND TRAUMA 30:5 441 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES
Patient function recovery according to spinal cord injury
level
Level Patient function
C1eC3 C Ventilator dependent
C Limited talking
C Electric wheelchair with head control
C3eC4 C Initially ventilator dependent; may become
independent
C Electric wheelchair with head control
C5 C Ventilator independent
C Present biceps, deltoid, and elbow flexion
C No wrist extension and supination (cannot
feed him/her self )
C Electric wheelchair with hand control,
minimal manual wheelchair function (in-
dependent ADL’s)
C6 C Better function than C5
C Wrist extension and supination intact (can
feed him/herself )
C Manual wheelchair, transfers with sliding
boards, drive car with manual controls
(independent)
C7 C Triceps strength present
C Manual wheelchair and independent
transfers
C8-T1 C Hand and finger strength present
C Manual dexterity
C Fully independent transfers
T2eT6 C Normal upper limbs function
C Improved trunk control
C Wheelchair
T7eT12 C Abdominal muscle control
C Seated activities unsupported
L1eL5 C Variable lower limb function
C Variable bowel and bladder function
C Variable requirement of assisting devices
and bracing
S1eS5 C Variable bowel and bladder function
C Variable sexual function
C Walking with minimal or no assistance
Table 2
numbers within six hours. Macrophages follow and peak within
two to seven days persisting as long as 2 weeks after injury.11,17
Lymphocytes entry is delayed and protracted; the cells are
detectable several months after injury. The acute inflammatory
response lasts approximately 10 days. Inflammatory cell counts
are generally not elevated in CSF later than three weeks after
injury. Neutrophil depletion reduces histologic recovery from
injury.
The activation of microglia (intrinsic inflammatory cells of the
cord) begins almost immediately after injury and is correlated with
increase in tissue damage.12 Upregulation of TNFa, IL1b and IL6 is
detectable within minutes of injury and increases during the first
four days after injury.12 Microglia gets activated during the early
acute inflammation phase and during the neurotrophin
ORTHOPAEDICS AND TRAUMA 30:5
production phase (glial cell line derived neutrophilic factor).
Blockade of metabotropic glutamate receptor subunit 5 on
microglia is associated with reduced microglial activation and
improvement in tissue and functional outcome after SCI.
Macrophages and microglia are removing the growth inhibi-
tory components of myelin debris promoting regeneration.12
However, macrophages are associated with chondroitin sul-
phate proteoglycan deposition, which may inhibit axon growth.
Experimental studies showed that reduced T lymphocyte
response resulted into less extensive tissue loss and decrease in
secondary SCI.12,13
Ionic dysregulation
Ionic homoeostasis is lost immediately after SCI. Failure of the
cell membrane and the transmembrane adenosine pumps causes
loss of regulation of extracellular concentrations of sodium,
glutamate and other molecules.14 Subsequently, the mitochon-
drial membrane breaks down and various receptors become
activated, leading to numerous changes in gene regulation and
production of free radicals. Glutamate excitotoxicity damages the
oligodendrocytes (myelinating cells of the CNS) and axons.11,17
Free e radical mediated damage
Oxidative damage may continue as long as five days. Molecular
oxygen causes damage to membranes, proteins and nucleic acids
by lipid peroxidation, protein nitration and activation of redox
esensitive signalling cascades.1,6 Lipid peroxidation coincides
with the initial influx of neutrophils, macrophage and microglia
activation. Neutrophils and activated microglia are the major
source of nicotinamide adenine dinucleotide sulphate oxidase-
derived reactive oxygen in the injured cord.17 Oxidation of
membrane lipids increases permeability to ions and causes fail-
ure of the transmembrane adenosine triphosphate-driven pump
function.
The glial scar
Proliferation of astrocytes to the SCI site leads to the develop-
ment of glial scar. The reactive astrocytes secrete chondroitin-
sulphate proteoglycans which is the main glial scar compo-
nent.18 Its formation is regulated by the TGFb and acts as a
physical barrier to regenerating axons.11,16
Chronic changes
Local disruption of CNS connections after SCI is followed by
trans- and retro-grade neuronal degeneration, segmental
sprouting of axons, plasticity and alterations in neuronal excit-
ability. The clinical manifestations include spasticity, autonomic
dysreflexia and neuropathic pain.6 A syrinx secondary to SCI can
cause delayed neurologic dysfunction such as ascending paraly-
sis, brainstem symptoms and pain. Myelomalacia and spinal cord
tethering may also complicate the chronic lesion.
Endogenous reparative process
Animal studies showed that new stem cells are formed around
the ependyma, which actively replace some depleted cells,
especially oligodendroglia.18 In-migration of Schwann cells may
also lead to functional myelin repair of CNS axons. Administra-
tion of sonic hedgehog protein or transduced transcription fac-
tors may further increase new cell formation.
442 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES

SCI associated conditions

The nine elements of inflammatory response
1. Neurogenic shock is the acute complication following SCI
leading to disruption of autonomic pathway. There is tem- 1 Endothelial damage and activation
porary loss of sympathetic tone while the parasympathetic 2 Activation of resident microglia
tone is maintained. The neurogenic shock may last for one to 3 In migration of polymorphonuclear leukocytes
three weeks and manifest over hours to days, due to the 4 In-migration of macrophages
secondary injury.6 This condition manifests with hypoten- 5 Dysregulated oxidative metabolism and
sion, bradycardia and circulatory collapse due to decreased release of free radicals
systemic vascular resistance.4,6,19 It can be treated with: a) 6 Free radical mediated damage of membranes,
fluid resuscitation until the dilated intravascular volume is proteins and nucleic acids
filled to the normal central venous pressure and b) use of 7 Propagation of excitotoxicity, toxic calcium
vasopressors with both a and b adrenergic actions to counter and sodium concentrations
the loss of sympathetic tone and provide inotropic/chrono- 8 Necrotic and apoptotic cell death
tropic support. Swan-Ganz catheter is recommended to 9 Local and systemic activation and recruitment
monitor the central venous pressure (CVP) and prevent of anti CNS antigen reactive T and B cells
overload.4,6,19 Apart from sinus bradycardia, orthostatic hy-
Table 3
potension may also be due to loss of sympathetic tone in the
acute phase.
Council Grade, MRC Grade) distal motor and 0/2 distal sensory
2. Spinal shock is an acute post-injury neurophysiologic con-
scores (absent perianal sensation). In an incomplete SCI there is
dition affecting the cord, caused by hyperpolarization of the
some preserved motor or sensory function below the injury level
neurons rendering them unresponsive to brain stimuli.20,21 It
and it is classified as ASIA B, C or D (Table 3). This includes
is manifested as temporary loss of cord function and reflex
voluntary anal contraction (sacral sparing), palpable or visible
activity below the injury level. It is characterized by flaccid
muscle contraction below injury level or present perianal
areflexic paralysis, loss of sympathetic tone causing brady-
sensation. The level of neurologic injury is the lowest segment
cardia, hypotension and absence of the bulbocavernosus
with intact sensation and antigravity muscle strength (3/5 grade
reflex.20,21 The extent of neurologic deficit cannot be fully
MRC or more). In regions where no myotomal testing exists, the
evaluated in the presence of the spinal shock. The initial
motor level is presumed to be the same as the sensory level.
clinical picture usually resolves within 48 hours and is
Injury to the cervical spinal cord may lead to tetraplegia
signified by the return of the bulbocavernosus reflex.21
causing impaired function in the upper limbs, trunk, lower limbs,
Conus or cauda equina injuries may lead to permanent loss
bowel and bladder. Upper cervical spinal injuries may lead to
of the bulbocavernous reflex. The spinal shock can be
diaphragm paralysis and respiratory compromise. Injury to the
divided into four phases: (a) areflexia/hyporeflexia; (b)
thoracic cord, conus or cauda equina may lead to paraplegia. In
initial reflex return; (c) early hyper-reflexia; (d) late hyper-
paraplegia, there is sparing of the upper limbs and impaired
reflexia, which is due to the underlying neuroplasticity after
function in the trunk, lower limbs, bowel and bladder depending
SCI. Over subsequent weeks and months after the return of
on the level of injury.
reflexes, reflex axons grow new synapses to mediate hyper-
Depending on the cord involvement following injury, the
reflexia. The synapse growth appears to be axon-length,
patient can develop different types of cord syndromes:
activity-dependent and competitive.20
A. Central cord syndrome is the most common SCI. It usually
Both neurogenic and spinal shock need to be differentiated in the
happens in older individuals sustaining hyperextension in-
acute setting from hypovolemic shock which is caused by
juries to the cervical spine.22,23 It occurs from an abrupt
decreased cardiac preload due to blood loss and results in hy-
contusion of the cord with a pincer type mechanism between
potension associated with tachycardia.
the hypertrophied ligamentum flavum posteriorly and the
3. Other injuries manifesting with altered neurology and inter-
osteophytes anteriorly.23 It involves the grey matter and
fering with the examination are: a) closed head injuries; b)
central portion of the cord more than the peripheral.22
other non-contiguous or unstable spinal fractures; c) verte-
Because of the anatomical arrangement of the motor tracts
bral artery injuries. Vertebral artery injuries may be caused
to the upper limbs being more medial followed by thoracic,
by cervical spinal fractures/dislocations, can be diagnosed
lumbar and sacral components this syndrome manifests with
with Magnetic Resonance (MR) Angiography, and can pro-
greater weakness of the upper than the lower limbs.22,23 The
duce basilar artery insufficiency which is an indication for
majority of patients will have bowel and bladder control.
stenting.
The prognosis is good with 75% recovery; although spas-
ticity may remain, almost all young and 50% of elderly pa-
Classification of SCI
tients will regain ambulatory function. Most of the patients
SCI is divided into complete and incomplete. Complete is a SCI will not recover fine motor use of the hands.24
when there is no spared motor or sensory function below the B. Anterior cord syndrome is the second most common SCI
affected level. A SCI can only be characterized as complete after syndrome and involves the anterior two thirds of the spinal
resolution of the spinal shock and is further classified as Amer- cord. It is either of vascular origin or due to a retro-pulsed
ican Spinal Injury Association (ASIA) grade A (Table 3). This fracture fragment onto the cord.6,8,24 It manifests as com-
includes no voluntary anal contraction, 0/5 (Medial Research plete motor and sensory loss below the level of the injury.

ORTHOPAEDICS AND TRAUMA 30:5 443 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES
Only the dorsal columns are spared which provide deep
touch, proprioception and vibration sensation. The motor
loss is greater in the lower than the upper limbs.8 The
prognosis is poor with only 10% neurological recovery.6,24
C. Brown-S
equard syndrome occurs with damage of the lateral
half of the cord (hemisection).6,25,26 It is manifested as
ipsilateral motor, position and proprioception loss and
contralateral loss of pain and temperature, which affects two
levels below the injury.6,25 It is usually the result of a
penetrating injury. The prognosis is very good with almost
90% recovery of bowel/bladder function and ambulation.26
D. Posterior cord syndrome is rare and involves loss of posterior
column function, which provides deep touch, proprioception
and vibration sensation.6,24 These patients maintain the
ability to ambulate but they rely on visual input for spatial
orientation.6,24
Persistent spinal cord compression
Continued compression of the injured spinal cord by disc, bone
or blood clot in the epidural space may exacerbate the magnitude
of the ischaemic and secondary injury cascades.6,23 Persistent
compression is common after SCI and may be caused by a
ruptured disc, bony fragmentation or dislocation. Ischaemia is
the presumptive mechanism of persistent compression.1 Persis-
tent compression after contusive SCI causes potentially reversible
additional injury in animal studies and decompression improved
the outcome in mild and moderate but not in severe SCI.1,6
Neurological recovery was inversely related to the duration of
compression.23
Neuroprotection
The primary injury usually does not transect the spinal cord;
post-mortem studies of acutely injured spinal cords found that a
sub-pial rim of spared but damaged long tract axons frequently
spans the lesion. It is found in animal studies that significant
neurological function can be maintained if only 1.4e12% of the
total number of axons is spared across the injury.3 Neuro-
protection aims to reduce the secondary injury and limit the
injury to the level of damage initially done by the trauma.
Diverse compounds ranging from hormonal receptor agents such
as tamoxifen and oestrogen to polyethylene glycol have neuro-
protective effects on numerous mechanistic pathways.3,27 Repair
of inadequately myelinated residual axons is an important target
of therapy aimed at improving conduction of spared axons. The
inflammatory response has also a major role in the expansion
and resolution of SCI and is a key target for neuroprotection.
Spinal cord inflammation is a topic of current active research.
Experimental studies showed that chondroitinase enzyme
degraded the glial scar leading to partial restoration of sensory
function.16
Treatment
The goals of management of an acute SCI are to prevent further
injury, maintain blood flow, relieve neural compression and
provide vertebral stabilization in order to allow early rehabili-
tation, whereas attention to systemic physiology influences the
final outcome. The treatment can be subdivided into prevention,
ORTHOPAEDICS AND TRAUMA 30:5
initial assessment, acute treatment, definitive treatment
(including non-operative and surgical) and rehabilitation.
Despite the ongoing advances in trauma prevention with the
use of helmets, protective garments, airbags etc 50% of SCIs are
still due to Road Traffic Accidents (RTA). The treatment starts at
the site of injury and attention should be drawn towards proper
immobilization of the patient with rigid collars, standard log roll
techniques and transportation on a firm spinal board. Upon
reaching the Trauma Centre, the primary and secondary surveys
are based on Advanced Trauma Life Support (ATLS) protocol.2,6
Absence of posterior midline tenderness in the awake, alert pa-
tient predicts low probability of significant cervical injury.
Emphasis should be given to SCIs proximal to C5, which may
require intubation.6 Abdominal bruising following a high energy
injury should raise suspicion of flexion-distraction injuries of the
thoracolumbar spine. Rotational deformity may indicate a uni-
lateral facet dislocation.
Neuroprotective drugs
The American National Acute Spinal Cord Injury Study (NASCIS)
phases IeIII studied the use of methylprednisolone sodium suc-
cinate (MPSS) in various protocols regarding dose and timing of
administration following an acute SCI. Post-hoc analysis of the
NASCIS II data revealed that those patients receiving MPSS within
eight hours of injury had significant improvement in sensory and
motor function after one year.2,28,29 Post-hoc analysis of the
NASCIS III data demonstrated that if the treatment starts within
three hours from injury there is no need to extend treatment
beyond 24 hours, whereas if it starts after three hours the motor
recovery is better if the treatment extends to 48 hours.30
The MPSS administration protocol requires a loading dose of
30 mg/kg over the first hour and an infusion of 5.4 mg/kg/hour
for 23 hours if started in less than three hours post-injury or for
47 hours if started three to eight hours post-injury. Indication for
MPSS administration is non-penetrating SCIs within eight hours
of injury and contraindications include: a) pregnancy; b) age
under 13 years; c) brachial plexus injuries; d) more than eight
hours after injury. However, patients treated with MPSS have
increased incidence of wound infections pneumonia, sepsis and
death from respiratory complications.28,30 Partly for this reason
in 2013 the AANS/CNS Guidelines for the Management of Acute
Cervical Spine and Spinal Cord Injury released a level one
recommendation that the administration of MPSS for the treat-
ment of acute SCI was not recommended.2 The controversy still
exists as recent evidence suggests that surgery within 24 hours of
injury in conjunction with 24 hours of MPSS may improve
neurological recovery and reduce adverse events.31,32 The Na-
tional Institute of Clinical Excellence (NICE) guidelines do not
recommend the standard use of methylprednisolone following
the acute stage after traumatic SCIs.33
Encouraging results have been found with Riluzole, a drug for
patients with Amyotrophic Lateral Sclerosis, which was shown to
reduce motor neuron degeneration and prolong survival. The
phase I study showed significant improvements in recovery of
motor function and a multicentre clinical trial has commenced.2
Also minocycline, a chemical derivative of tetracycline has been
shown to reduce apoptosis and increase neuroprotective effects
in animal SCI models but is not ready for clinical use.2 Similarly
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 SPINAL INJURIES
other agents, such as tirilazad mesylate, gangliosides and gluta-
mate antagonists have been investigated for the treatment of
acute SCI, which require further trials before introduction to
clinical practice.
Support of spinal cord perfusion
The autoregulation is altered after SCI so that the cord is
increasingly vulnerable to systemic hypotension.1 The mean
spinal cord perfusion pressure is equivalent to the mean arterial
(MAP) minus Cerebro-Spinal Fluid (CSF) pressure.1 Appropriate
fluid resuscitation and use of vasopressors to keep the MAP
above 90 mmHg is mandatory in order to maintain tissue
perfusion.34 Intensive Care Unit (ICU) level of care for cardio-
pulmonary management is most appropriate in the acute phase
to facilitate careful haemodynamic monitoring and implement
pulmonary protocols.1 Additionally, fever or hyperthermia are
harmful for cord tissue preservation.
Treatment of spinal injury
Injuries to the spine tend to occur at areas of maximal mobility
and are closely related to the spinal cord trauma.6 Injuries occur
when significant forces to the spinal column cause fractures,
ligamentous disruption or combined injuries that result in direct
compression and injury to the spinal cord. Injuries to the verte-
bral column are commonly classified by location (craniocervical,
subaxial cervical or thoracolumbar) and mechanism of injury
(flexion, extension or axial load). White and Punjabi defined
spinal stability as “the loss of the ability of the spine under
physiological loads to maintain relationships between vertebrae
in such a way that there is neither damage nor subsequent irri-
tation to the spinal cord or nerve roots, in addition, there is no
development of incapacitating deformity or pain due to structural
changes”.35 The ‘‘three column’’ concept of thoracolumbar spine
injuries was described by Denis in 1984 and dictates that at least
2e3 spinal columns need to be disrupted to be considered un-
stable and subject the spinal cord to risk of damage.36 More
recently, the Thoraco-Lumbar Injury Classification score (TLICS)
included the neurological post-injury function in a classification
system for spinal injuries to assist on defining indications for
surgical treatment of a thoracolumbar spinal injury (Table 4).37
Acute-non operative treatment of SCI
In case of a fracture or dislocation with spinal cord injury in an
alert oriented patient it would be indicated to apply axial traction
for closed reduction and cord decompression. The technique
involves application of GardnereWells tongs and/or a Halo ring.
4.54 Kg traction weight is applied and then weight is added in
2.27 Kg increments with serial lateral radiographs until the cer-
vical spine is aligned. The general guideline is 4.54 Kg for the
head and 2.27 Kg for each level until the level of injury. There
must be about 15e20 minutes between each increment in order
to allow for the ligaments to relax, the patient to be examined for
any change in neurology and an X-ray to take place. Small doses
of diazepam may contribute to muscle relaxation, whilst keeping
the patient alert. Even though recent reports mention that even
63.5 Kg of weight can be tolerated, most surgeons would not
exceed 22.68e31.75 Kg of maximum traction. Once the facet gets
disimpacted the manoeuvres for reduction can be applied. If at
ORTHOPAEDICS AND TRAUMA 30:5
any point the patient develops neurology, the radiographs show
over-distraction or there is failure of reduction the process should
be discontinued.
Operative treatment-clinical evidence on the timing for
decompression
Most incomplete SCIs have an indication for decompression in
order to preserve as much as possible of the spared function. The
aim is to relieve the spinal cord from continuous pressure and
micro-trauma caused by the fracture or disc fragment, and
realign/stabilize the injured area providing a stable environment,
therefore limiting the effect of the secondary injury to the cord.1
The goals of surgery are to remove the compressive forces on the
spinal cord, restore anatomical alignment and re-establish spinal
stability.1 Decompression should take place if the patient is
deteriorating neurologically or if there is a foreign body retained
into the spinal canal (i.e. gunshot wounds).
Controversy exists regarding the timing of surgical intervention
in non-deteriorating patients, as initial prospective studies
demonstrated no benefit from decompression within 72 hours
post-injury.1 The Spine Study Trauma Group recommended that
patients with acute SCIs but no other life threatening injuries
should receive decompression within 24 hours of injury.38 Pre-
liminary results indicated that 24% of patients who received
decompressive surgery within 24 hours had an improvement of at
least two grades of the ASIA scale compared to 4% in those who
had later surgery. Also, the overall rate of complications among
those who received early decompression was 20% lower than that
of patients who received treatment later. The Surgical Timing in
Acute Spinal Cord Injury Study (STASCIS), a multicenter, inter-
national, prospective cohort study showed that at six month
follow-up a 2-grade ASIA improvement was 2.8 times higher
among those who had surgical intervention within 24 hours post-
injury.31 A prospective study by Wilson et al.39 showed superior
motor neurological outcomes at six months in patients who had
decompressive surgery within 24 hours after SCI.
There is insufficient evidence (level III) regarding timing of
treatment of traumatic central cord syndrome. This entity pre-
sents no spinal instability and shows spontaneous clinical
improvement with good prognosis despite myelomalacic cord
changes being present.2,22 Similarly, there is no substantive ev-
idence for decompression in the thoracic cord. In complete SCIs,
surgical treatment should take place to stabilize the spine and
facilitate early rehabilitation with as less external devices as
possible. In the long term and following the final neurological
status of the patient, appropriate tendon transfers should be
considered in order to maximize function.
Stem cells-future operative treatments
More than half of the astrocytes in the glial scar are generated by
ependymal cells, the neural stem cells in the cord.18 Also, mul-
tipotent endogenous progenitor cells exist in the sub-ventricular
zone throughout the neuraxis and can be harvested during
neurosurgical procedures. The neural stem cell-derived scar
component has several beneficial functions, including restricting
tissue damage and neural loss after SCI.18 Following differenti-
ation guidance to the oligodendrocyte lineage in experimental
SCI models, it was found that they can re-myelinate the cord.
However, ineffective tissues and cells connectivity in the cord
445 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES

mechanical and pharmacological prophylaxis. The first consists

The American Spinal Injury Association (ASIA) of anti-embolism stockings, foot impulse or intermittent pneu-
impairment scale classifies the extent of spinal cord matic compression devices. The second is based on administra-
injury in five categories tion of low molecular weight (LMWH) or un-fractioned heparin
ASIA impairment scale (UFH) for patients with severe renal impairment. The VTE pro-
phylaxis continues until the patient resumes mobility.42
A Complete No motor or sensory function is
preserved in the sacral Skin problems
segments S4eS5 Pressure sores are a common cause of deep infection and
B Incomplete Sensory function preserved but sepsis.43 The patient must be removed from the immobilization
not motor function is preserved board as soon as possible. Regular log rolling and use of pressure
below the neurological level and redistributing air mattresses have reduced skin complications.43
includes the sacral segments S4eS5
Autonomic dysreflexia (AD)
C Incomplete Motor function is preserved below the
neurological level, and more than
AD is a potentially fatal clinical syndrome which develops in
half of key muscles below the
patients with SCI and presents with uncontrolled hypetension.44
neurological level have a muscle
It is caused by injuries proximal to T6 level most likely due to
grade less than 3
imbalanced sympathetic discharge. Lesions below T6 allow
D Incomplete Motor function is preserved below
enough descending parasympathetic control to modulate
the neurological level, and at least
splachnic tone and prevent hypertension. Apart from the unop-
posed autonomic equilibrium, the increased responsiveness of
half of key muscles below the
the peripheral blood vessel alpha-adrenergic receptors may also
neurological level have a muscle
explain the development of hypertension. These receptors
grade of 3 or more
decrease their threshold secondary to low resting catecholamine
E Normal Motor and sensory function is normal
following a SCI.44 Another possible mechanism includes loss of
Table 4 supraspinal inhibitory control of the medulla-oblongata bulbo-
spinal pathways over serotonin in the inter-medio-lateral nucleus
of the spinal cord. The unabated serotonin causes strong vaso-
injury environment is still a major hindrance for application of
constriction. This syndrome is considered medical emergency
stem cells in clinical practice.
and if left untreated may cause seizures, retinal haemorrhage,
pulmonary oedema, renal insufficiency, myocardial infarction,
Neurological and functional recovery following SCI
cerebral haemorrhage and death. Ageing decreases the AD
The more severe the SCI the less the anticipated neurological symptoms and the magnitude of diastolic blood pressure eleva-
recovery. Similarly, less severe initial ASIA grade and score >50 tion possibly due to decreased baroreceptor sensitivity.44
predicted better functional status; whereas worse functional The treatment of AD should be etiologic and symptomatic.
outcome was predicted in older patients and in the presence of Continuous blood pressure monitoring is required. The patient
oedema or haemorrhage on MRI.40 Apart from the severity of should be sat more upright in bed if possible. The patient should
neurological injury and patient age other predictors of long-term be catheterized and checked that any indwelling urinary catheter
functional outcome include the injury level and reflex pattern.41 is working properly. The patient should also be checked for
Only 10e15% of complete lesions will develop sensation and/or faecal impaction and manual evacuation is recommended. In all
motor function distal to the level of injury.2 Regarding incom- these steps the blood pressure should be assessed. Short acting
plete injuries, 30% of ASIA B patients will end up to ASIA C and anti-hypertensives, such as nifedipine or nitrates are recom-
another 30% to ASIA D; whereas 70% of ASIA C will improve to mended if the systolic blood pressure is above 150 mmHg.
ASIA D. Very few patients though will reach ASIA E level. Recurrence should be anticipated if the causative factor is not
Complete injuries in the cervical spine seem to have better identified. In inability to control the symptoms intensive care
neurological recovery than those in the thoracic level; similar treatment is advised.19,44
recovery rates are expected in incomplete injuries.40,41
After the initial therapeutic window for neuroprotection, Psychological disorders
repair strategies have been used for treating severe SCIs with the Approximately 11% of patients with SCIs suffer from major
aim of restoring CNS communication above and below the depressive disorders, which may lead to suicidal ideation in both
injury. These strategies focus on the residual autonomous func- the acute and chronic phases. A supportive environment
tion of the spinal cord, rehabilitation and prevention of long-term providing explanations and reassurance in a familiar atmosphere
complications. is important. Interventions, such as pain relief, adequate sleep
and pharmacological treatment are indicated to improve patient’s
Complications in patients with SCI psychological status during rehabilitation.4,41

Deep venous thrombosis

Rehabilitation
There is anticipation of a prolonged recumbent period in SCI
patients. Unless there is coagulopathy or active bleeding, all Traumatic SCIs may cause long lasting impairment in many
patients should receive venous thromboembolism (VTE) organ systems and together with permanent changes in function

ORTHOPAEDICS AND TRAUMA 30:5 446 Ó 2016 Elsevier Ltd. All rights reserved.
 SPINAL INJURIES

with flaccid a-reflexic paralysis and bradycardia due to loss

Three predictors of thoraco-lumbar injury severity score of sympathetic tone. It usually resolves within 48 hours
1 Morphology C Compression 1 X-rays signified by the return of the bulbo-cavernosus reflex;
(immediate C Burst 2 CT thereafter the extent of the SCI may be assessed. Differ-
stability) C Translation/ 3 ential diagnosis with hypovolemic shock is needed.
rotation  Central cord syndrome is the most common SCI. It is
C Distraction 4 caused by a pincer type cord contusion following hyper-
2 Integrity of PLC C Intact 0 MRI extension of the cervical spine. It affects the motor function
(long-term C Suspected 2 of the upper more than the lower limbs. It has 50e75%
stability) C Injured 3 prognosis with regards to return of ambulation; fine hand
3 Neurological C Intact 0 Clinical motor function does not recover in most patients.
status C Nerve root 2 examination  The goal of treatment is to reduce the insult of the sec-
C Complete 2 ondary injury mechanisms on the cord, to decompress and
cord stabilize the spine.
C Incomplete 3  Spinal autoregulation is altered following SCI rendering the
cord cord vulnerable to systemic hypotension. Tissue perfusion
C Cauda Equina 3 maintenance is mandatory by keeping the MAP above
Operative 0e3 C Non-surgical 90 mmHg with the use of appropriate fluid resuscitation
management 4 C Surgeons’ and vasopressors.
choice  Neuroprotection: Initial studies regarding the use of high
>4 C Surgical dose methylprednisolone within three to eight hours of
injury showed significant improvement of sensory and
Table 5 motor function after one year. Subsequent studies showing
increased systemic complication rate suggested not regular
use of methylprednisolone in SCI patients.
lead to higher morbidity and lower quality of life.4 The goal of
 Persistent compression is common after SCI due to a
rehabilitation is to assess and identify mechanisms for reinte-
ruptured disc, bony fragmentation or dislocation. It may
gration into community based on functional level and daily
exacerbate the magnitude of ischaemic and secondary
needs.45 Milestones in rehabilitation are transferring techniques,
injury cascades if left untreated. Recent evidence suggests
self-care, mobilization and hand function (Table 5). In patients
that patients showed improved motor function at six
with neurological improvement potential, electrical stimulation
months follow up if they were surgically decompressed
techniques are utilized to keep the muscles activated until final
and stabilized within 24 hours from injury.
neurological recovery. Physiotherapy and joint mobility preser-
 Complications in patients with SCI include: a) deep venous
vation is of utmost importance to keep the limbs functional.
thrombosis; b) pressure sores; c) urinary sepsis; d) auto-
Tendon transfers can be used to improve function in affected
nomic dysreflexia; e) neuropathic pain; f) myelomalacia;
upper limbs and hands.
g) syrinx; h) psychological disorders.
 Milestones in rehabilitation are transferring techniques,
Conclusion
self-care, mobilization and hand function. A
 Cord contusion is the most common mechanism of injury.
Partial laceration may be present but cord transection is
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