clinical
SPINAL CORD INJURY: CAUSATION
AND PATHOPHYSIOLOGY
In the second of three articles on spinal cord injury, FINTAN SHEERIN describes some of the causes
and effects of spinal cord trauma
T he incidence of spinal cord injury
worldwide stands at about 20 new
cases per million of population a year
(Glass 1999), but is double this figure in
the US (DeVivo 2002).
In the western world, the greatest
causes of spinal and spinal cord injuries
are related to risk taking incidents, such as
drink driving and non-adherence to safety
procedures (DeVivo 2002, Grundy et al
2001, Healy et al 2004). As such, these
may be preventable through educative
strategies and by enforcing road safety
and health and safety measures.
Spinal cord trauma can lead to different
degrees of motor and sensory loss. This
article will examine the effects of injury
events on the spinal cord by relating the
biomechanics of injury to the anatomy of
the vertebral column.
It will also consider the neurological
sequellae of injury and describe some of
the presentations classified under the Inter-
national Standards for Neurological Class-
ification of Spinal Cord Injury (American
Spinal Injury Association 2002).
THE VERTEBRAL COLUMN
There are three points along the vertebral
column that are particularly susceptible
to injury: the junctions of C7 and T1
and that of T12 and L1, and vertebra
T7. To understand why these areas are
susceptible, it is important to be familiar
with the anatomy of the vertebral
column.
The vertebral column comprises 33 vert-
ebrae that are held firmly together by
ligaments forming a ‘fortress’ around the
spinal cord.
Most of the vertebrae conform to the
standard model, with a large vertebral
body, spinous and transverse processes,
laminae and pedicles.
vol 12 no 9 february 2005 emergency nurse
Those of the upper cervical spine
however, namely the atlas and the axis,
and those in the sacrococcygeal region,
Fintan Sheerin BNS, PgDipEd,
RMHN, RGN, RNT is a lecturer
practitioner in spinal cord injury,
are unusual. National Spinal Injuries Unit,
The upper cervical spine is the only region Mater Misericordiae University
where significant rotation is needed. This is
Hospital, Dublin, and school
facilitated by the odontoid, or peg, process
of nursing and midwifery,
that protrudes upwards from the body of
University College Dublin
the axis and articulates with a facet on the
posterior surface of the anterior ring of the
atlas, acting as a pivot for the latter.
The vertebrae in the sacrococcygeal
region, meanwhile, are fused into a solid
mass, but with intervertebral foramina
persisting between the sacral vertebrae.
Table 1. Types of spinal ligament
> Ligamentum flavum: between laminae
> Supraspinous ligament: between the tips of spinous processes
> Interspinous ligament: between spinous processes
> Anterior longitudinal ligament: on the anterior surface connecting the body of
one vertebra to that of another
> Posterior longitudinal ligament: on the posterior surface connecting body to body
> Intertransverse ligament: between transverse processes
> Ligamentum nuchae: between cervical spinous processes
> Radiate ligaments: connecting vertebrae to ribs.
Schneck 2002
The spinal column is comprised of more
than bone. Each vertebra must articulate
with other vertebrae and bones, and there
needs to be some flexibility and mobility
in the intervertebral joints. This is provided
by the intervertebral discs between the
junction of C1 and C2 and that of L5 and
S1, which also help to absorb shock.
There are eight types of spinal ligaments,
which connect vertebrae throughout the
column, either to other vertebrae or to
other bone such as the ribs, and help to This article has been subjected
keep the column stable (Table 1). to double blind peer review
29
 clinical

Cervical region
Fig. 1. Vertebral column divisions and characteristics
Of the five regions, the cervical is most flex-
ible and mobile. The vertebrae here are small
with superior articular facets facing posterio-
medially and upwards (Barker 2001).
The nearly horizontal direction of the
spinous processes in this region allows
for greater extension, with the exception
of C1 and C2, which articulate differently
and which have only rudimentary spinous
Cervical processes.
> flexible Force applied to the cervical spine does
> allows movement not always result in localised vertebral
> seven verterbrae damage, however, because the flexibility
> small bones of the region, and the ability of the neck to
move in anteriorposteriolateral directions,
can help transfer the force downwards to
Thoracic
the thoracic spine where there is little or
> inflexible and rigid no flexibility.
> allows little movement
> 12 verterbrae Thoracic region
> larger bones The thoracic spine has larger vertebrae
and thinner interverterbal discs than the
cervical region, and has inferiorly directed
spinous processes (Tortora and Grabowski
1996). The superioposteriolateral orient-
Lumbar ation of superior articular facets and the
> slightly flexible articulation with the ribs create a relatively
> allows some movement rigid and immobile structure (Chiles and
> five verterbrae Cooper 1996).
The junction between C7 and T1 represent
the border between the flexible cervical
spine and the rigid thoracic spine, and is
the most susceptible to vertebral column
Sacral damage. This is because, when force is
> inflexible: fused applied to the cervical spine, it is directed
> no movement downwards because of the latter’s flexibility,
> five verterbrae and is focused on the cervical-thoracic
junction. The region must be examined on
Coccygeal X-ray therefore before it is given the all-clear
(Prendergast and Sullivan 2000, Walker
PETER GARDENER

1998, Young and Shea 1998).

The vertebral column can be described
therefore as a stable structure that supports
the upper appendicular skeleton and head,
while protecting the delicate neurological
tissues of the spinal cord.
It can be divided into five principle
regions: cervical, thoracic, lumbar, sacral
and coccygeal. Each has specific structural
variations and properties (Fig. 1).
The cervical and thoracic regions are the
most common sites of spinal injury.
A similarly important junction exists
between T12 and L1, which is between
the rigid thoracic and more mobile lumbar
regions. This is the second most common site
of spinal injury (Chiles and Cooper 1996).
Another significant injury site is T7,
the apex of the largest primary curve of
the vertebral column. Primary curves are
remnants of the spinal curve present at
birth (Sheerin 2004).
This vertebra is at risk of injury because it
provides a ‘buckling’ point if compressive
forces are applied directly along the axial
skeleton.

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CAUSATION OF SPINAL CORD INJURY These two events allow the vertebrae
The main causes of spinal cord injury fall to ‘ride over’ those below them, resulting
into the following categories: in spinal cord contusion or transection
> Traumatic: motor vehicle accidents caused by the loss of vertebral alignment.
(MVAs), falls, sports injuries, objects These injuries usually involve the low
falling onto the head, assault cervical region, namely C5 to C7 (Hickey
> Non-traumatic: degenerative, infective 2003).
or oncogenic spinal lesions. It is important to remember that during
Of the principal mechanisms of injury, an MVA there may be other forces at play
however, MVAs (Guin 2001) and falls that can cause different injuries. If the
(DeVivo 2002) account for the vast vehicle turns over for example, the driver’s
majority. head can rotate leading to displacement
of facet joints.
Motor vehicle accidents The forces involved in MVAs can cause
Motor vehicle accidents account for such severe damage to vertebrae C1 and
around 39 per cent of spinal cord injuries C2 that the cord is affected, so that the
in the UK (Harrison 2004). person involved cannot self-ventilate. In
The mechanism of injury in MVAs such circumstances, death is the most
can be simple or can involve a complex common outcome (Schoen 2000).
combination of forces focused on the
vertebral column. These forces are limited
by safety devices such as side impact bars, Fig. 2. Mechanism of injury in motor vehicle accidents
airbags and head rests.
When a vehicle is travelling at, say,
70mph, everything in the vehicle,
including the driver, is travelling at the
same speed. The impact of the vehicle
with another vehicle or object leads to a
sudden deceleration to 0mph. Because it is
secured to the vehicle by the seatbelt, the
driver’s body achieves this sudden velocity
change, but the head does not.
Instead, the head continues to travel
forward until the vertebral structure
prevents it from any further displacement.
It then travels downwards causing severe
distraction – or pulling apart – of the
posterior vertebral column, and damage
to the ligamentous complex between,
and covering, the spinous processes: a
hyperflexion injury.
At the same time, there is severe
compression along the anterior vertebral
column with the potential for vertebral
body damage (Fig. 2). The force of the
forward moving vehicle creates an equal
and opposite force when it suddenly stops.
This violently ‘whips’ the driver’s head and
neck in the opposite direction.
If the headrest is absent or ineffective, the
driver’s head moves back over the upper edge
of the seat and then downwards leading
to severe anterior distraction with anterior
longitudinal ligamentous damage, and
posterior compression with fractures of the
HARRISON

spinous processes: a hyperextension injury.

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 clinical
Fig. 3. Injury following fall from height
Falls
Falls account for about 46 per cent of spinal
cord injuries in the UK (Harrison 2004).
There are many types of fall, including
those from a height, at ground level, from
the ground into a hole, on a flat surface,
or up stairs or steps.
Each of these types of fall involves a force
being imposed onto the vertebral column,
each from a different angle.
Typically, falls from a height are from
second or third storey levels (National
Spinal Injuries Unit 2005). They might be
suicide attempts, or be caused by a loss
of balance from a window, ladder, roof or
scaffold (Fig. 3).
The forces involved in falling from a
height are similar to those involved in
32
MVAs. The individual falls and the fall
is broken by contact with a solid barrier
causing a sudden change in the velocity of
the body to 0mph.
On impact, an equal and opposite
force is created and meets the impacting
individual.
If the person falls on the feet, the two
forces travel longitudinally along the
vertebral column, which causes ‘axial
loading’, and meet at a point where the
forces are concentrated.
This can compress vertebrae and the
spinal cord, cause burst fractures, and
force bone fragments to enter the spinal
canal. There may also be fractures to the
lower extremities.
If the person falls on the buttocks, a
hyperflexion injury to the lumbar area may
result, again with compression fractures.
Similar injuries are also found in diving,
which is one of the sports most associated
with spinal cord injury.
In this scenario, however, it is the person’s
head that hits a solid surface, potentially
leading to a mid-thoracic injury and
possible hyperextension or hyperflexion
in the cervical region, depending on the
position of the head.
Falls up stairs are commonly associated
with hyperextension injuries to the neck.
Hyperextension occurs when a person
climbing stairs unbalances and falls onto
them face first (Fig. 4).
Typically, the person hits their chin
on a stair, which forces the neck into
hyperextension. This is also found in
bathroom falls when a person steps out of
a bath or shower onto a tiled surface and
falls face first.
These injuries are often seen in older
people (Hickey 2003) and, while the events
themselves may not lead to spinal cord
injuries, they can cause rupture in anterior
longitudinal ligaments resulting in anterior
vertebral column weakness.
Decisions regarding the clearance of the
cervical spine in such patients should not be
made without magnetic resonance imaging
(Young and Shea 1998), because patients
are at high risk of further injuries due to
bone movement and displacement.
Sports related injuries
Ten per cent of spinal cord injuries in the
UK are sports related (Harrison 2004).
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They result from the same mechanisms as

Fig. 4. Hyperextension injury due to a fall on stairs
MVAs and falls: compression, distraction,
hyperflexion, hyperextension and
rotation.

PATHOPHYSIOLOGY
When the spine is subjected to the sort of
events described above, it undergoes an
exaggerated range of normal movements,
including forced flexion, extension and
rotation.
Flexion involves movement towards
the midline, with the chin coming down
onto the chest, while extension involves
movement away from the midline, with
the occiput being forced onto the back.
Both flexion and extension involve
compression and distraction to specific
parts of vertebrae, but vertebrae may also
experience severe generalised compression
and distraction due to some of the injury
events outlined above.
If spinal cord injury occurs, the resulting
presentation is produced by both the
primary event and a ‘cascade of secondary
pathophysiological mechanisms’ (Young
and Shea 1998).
Table 2 shows that primary injury is
caused essentially by trauma and results
in haemorrhagic changes that lead to
ischaemia and necrosis (Hickey 2003).
Secondary injury though results from
various chemical and vascular changes.

Table 2. Primary and secondary spinal cord injuries

Time after injury Pathophysiology Observed change

Primary
Immediately Traumatic structural damage Disruption of spinal cord and surrounding vascular components with
resulting compromise of vascular supply, leading to ischaemia
Secondary
Few minutes to Release of vasoactive agents, and cellular Changes to microvessels in the central grey matter
few hours enzymes Multifocal haemorrhages
Infiltration of site by neutrophils and Postcapillary venule distension
macrophages
Increase in intracellular calcium levels Damage to vascular endothelium
Leakage of erythrocytes into perivascular spaces
Increase in extracellular potassium levels Conduction block
and resulting depolarisation of cells
By between four Hypoxia induced catecholamine release Further haemorrhage and necrosis
and eight hours Elevated calcium remains Appearance of aneurysms and vessel rupture in lateral columns of
the spinal cord
By 24 hours Thrombi formation in capillaries

Sapru (2002)

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Spinal and neurogenic shock

Table 3. Autonomic effects on specific organs
The first article in this series (Sheerin
2004) explains that the spinal cord is the
Organ and Action Parasympathetic effect Sympathetic effect
reflex centre for the body. For example,
Respiratory System the classic tendon reflex occurs when
Bronchioles Constricted Dilated the spinal cord interpretes sensory input
Rate of ventilation Decreased Increased signifying a risk to the body’s integrity, and
initiates a protective motor response.
Secretions Increased No direct effect
But not only somatic reflexes pass
Cardiovascular System through the spinal cord. The cord is
Rate and force of heartbeat Decreased Increased associated intimately with the autonomic
Coronary vessels Constricted Dilated nervous system and is the integrating
centre for autonomic reflexes.
Skeletal vessels No direct effect Dilated
The autonomic nervous system acts
Visceral and dermal vessels No direct effect Constricted continuously, through its sympathetic and
Blood pressure Decreased Increased parasympathetic divisions, to maintain
Digestive System
an equilibrium in the functioning of the
smooth muscle, cardiac muscle and the
Peristalsis Increased Decreased
glands. The scope of this control can be
Muscular sphincters Relaxed Contracted seen in Fig 5.
Salivary glands Thin, watery saliva Viscid saliva The effects of each division on specific
Gastrointestinal secretions Increased No direct effect organs and vessels is described in Table 3.
The sympathetic division has a particular
Glycolysis and gluconeogenesis No direct effect Increased
relationship with the cord because they are
Urinary System linked by the communicating branches of
Bladder muscle Contracted Relaxed the spinal nerves in the thoracolumbar
Sphincters Relaxed Contracted region (Fig. 5). These links are described as
the ‘thoracolumbar outflow’.
Skin The parasympathetic outflow is, how-
Secretion of sweat No direct effect Increased ever, only partly related to the spinal cord
Erector pili muscles No direct effect Contracted because it has its greatest outflow from the
brainstem, via the cranial nerves, with a
Hickey (2003)
smaller part located in the sacral region of
the cord. This part of the parasympathetic
outflow is therefore described as the
Table 4. Physiology of neurogenic shock
‘craniosacral outflow’. Up to 80 per cent
of the parasympathetic outflow emanates
Zedjlik (1992)

Spinal cord injury above T6

through cranial nerve X, the vagus nerve.
When the spinal cord is injured, there is
a sudden loss of conduction due to the
Spinal shock
migration of potassium ions from inside
the cells into the extracellular spaces.
Sympathetic This is associated with a transient loss
Sympathetic outflow with unopposed of somatic and autonomic reflex activity
outflow to systemic
parasympathetic stimulation to heart
vascular system below the level of neurological damage.
This is termed ‘spinal shock’.
Most spinal cord injuries affect the cervical
Passive dilation of Reduced Reduced and high thoracic region (DeVivo 2002) so
Reduced Reduced
systemic vascular stroke heart
preload afterload there is often relative loss of sympathetic
system volume rate
outflow with continued unopposed
parasympathetic, namely vagal, activity.
Reduced cardiac output
The signs of this imbalance are:
> Hypotension: due to passive dilation
of abdominal blood vessels, caused by
loss of sympathetic tone, and decreased
Neurogenic shock: hypotension, bradycardia, altered thermoregulation
cardiac output

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Fig. 5. Autonomic nervous system

Sympathetic division Parasympathetic division

Eye

Salivary
glands

Trachea

Bronchi
Postganglionic Postganglionic
fibres fibres

Heart
Preganglionic
fibres

Preganglionic
Liver
fibres
Stomach

Gallbladder

Kidney

Adrenal
gland

Alimentary
tract

Urinary
bladder

> Bradycardia: due to unopposed vagal This autonomic initiated cardiovascular

stimulation of the heart
> Loss of thermoregulation, poikilo-
thermia: due to passive dilation of
dermal blood vessels and consequent
inability to maintain body heat, and to
loss of sweat gland activity in neurologic-
ally impaired skin.
condition is termed ‘neurogenic shock’
and is typically seen between four and
six hours after injury in patients with cord
lesions above T6 (Table 4).
Spinal and neurogenic shock are transient
conditions that can last between 48 hours
and six weeks post-injury.

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 clinical
Fig. 6. Anterior cord syndrome
Variable loss of motor function and of pin prick and
temperature sensation below the level of the lesion
Area of cord damage
Assessment of resolved spinal shock is
based on the return of the sacral reflexes,
in particular the bulbocavernosus and
anocutaneous reflexes (Hickey 2003). These
are somatic reflexes, the earliest to return
after spinal shock has passed.
CLINICAL SYNDROMES
The absence of spinal activity that
characterises the period of spinal shock
makes it impossible for clinicians to assess
actual neurological status.
Fig. 7. Posterior cord syndrome
Loss of impulses relating to light touch, deep pressure,
vibration and proprioception and kinaesthetic awareness
Area of cord damage
36
This only becomes clear after resolution
of spinal shock, when a diagnosis of
complete or incomplete spinal cord injury
can be made.
According to the American Spinal Injury
Association (ASIA), complete spinal cord
injuries are defined as those involving the
most sacral segments of the cord, S4 and
S5 (ASIA 2002).
Incomplete injuries do not involve these
two sacral segments and can lead to a
diagnosis of one of the four classic cord
syndromes, or a diagnosis that comprises
elements of several (American Spinal
Injuries Association 2002).
The classic cord syndromes, as described
by Bing (1921), are: anterior cord
syndrome, posterior cord syndrome, central
cord syndrome, and Brown-Séquard’s
syndrome.
Anterior cord syndrome
Anterior cord syndrome typically results
from damage to the anterior two thirds
of the spinal cord, but can also be due to
damage to the anterior spinal artery.
The resulting ischaemia leads to variable
loss of motor function and of pin prick and
temperature sensation below the level of
the lesion (Hayes et al 2000). Sensibility
to light touch, deep pressure, vibration
and proprioception are preserved (Hickey
2003) (Fig. 6).
Anterior cord syndrome has a 10 to
20 per cent potential of motor recovery
(Kirschblum and Donovan 2002).
Posterior cord syndrome
This rare presentation is, in a sense,
complementary to anterior cord syndrome,
because it involves the posterior third of
the spinal cord, known as the dorsal
column.
This region is sensory in nature, and
provides pathways for transmitting
impulses relating to light touch, deep
pressure, vibration and proprioception
and kinaesthetic awareness. These senses
are lost, while motor function and sense
of pain and temperature are preserved
(Fig. 7).
The preservation of motor function,
however, can be countered by loss of
positional senses, leading Kirschblum and
Donovan (2002) to conclude that the
potential for ambulation is poor.
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Central cord syndrome

Fig. 8. Central cord syndrome
This is a syndrome usually involving the
cervical region of the spinal cord, and is
Loss of of motor function and of pin prick and temperature
one that tends to affect older people with
sensation below the level of the lesion
cervical spondylosis who have experienced
hyperextension injuries (Chiles and Cooper Incomplete loss of
1996, Kirschblum and Donovan 2002, the above
Nelson et al 2001).
It is suggested that spondylosis and
hyperextension injuries cause anterior-
posterior compression of the cord with
inward bulging of the ligamentum
flavum, which places pressure on the cells
of the anterior horn. This will predispose
the person to developing oedema in the
central cord region (Hickey 2003).
To understand this more fully, a basic
review of the anatomy of the lateral
corticospinal tract may be useful. This
tract, which controls voluntary movements
Area of cord damage
in the contralateral limbs, is organised so
that the cervical fibres are located medially
to the thoracic, lumbar and sacral fibres. This asymmetrical presentation is due
Because of this positioning, in people to the levels at which the ascending and
with spondylosis and hyperextension descending pathways cross over.
injuries, central pressure is exerted on In ascending pathways, which are con-
cervical as well as thoracic fibres, leading cerned with pain and temperature, first
to greater motor loss in the upper limbs order neurones enter the cord via the
than the lower limbs, and variable bowel posterior nerve root and synapse with
and bladder dysfunction (Fig. 8). second order neurone in the posterior
The involvement of the lower motor grey horn.
neurones, which supply the upper limbs, The second order neurones then cross
explains the characteristically flaccid arms over at this level before ascending in the
of the person with central cord syndrome, lateral spinothalamic tract.
while damage to upper motor neurones,
which supply the lower limbs, can cause Fig. 9. Brown-Séquard syndrome
spasticity there. There may also be variable
sensory loss below the level of the injury. Loss of voluntary motor control on same side as cord damage
Loss of pain and temperature sense on opposite side
Cervical cord syndrome has good potential
for recovery, especially in younger patients
(Kirschblum and Donovan 2002).

Brown-Séquard’s syndrome
The classic description of this syndrome
involves a hemisection of the spinal cord
due to a penetrating injury, for example
from a knife or gun.
This is a rare condition, and most
patients present with Brown-Séquard
plus syndrome, characterised by relative
ipsilateral hemiplegia, which is loss of
motor function on the same side of
the body, with relative contralateral
hemianalgesia, which is sensory loss to
the opposite side of the body (Hayes et al Area of cord damage
2000, Roth et al 1991).

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 clinical
Damage to this pathway, therefore,
results in contralateral hemianalgesia
below the level of the injury.
Ninety per cent of the fibres in the
descending pathway, which concerns
voluntary movement, cross over at the
level of the medulla oblongata, and travel
in the lateral corticospinal tract.
Because the crossing over occurs at a
level above the spinal cord, any damage to
the pathway below this results in ipsilateral
hemiplegia below the level of the injury
(Fig. 9).
Similarly, fibres of the dorsal white
columns of the cord, which concern
touch, deep pressure, vibration and
proprioception, remain uncrossed until
they reach the medulla. Loss of these
sensations will, therefore, be ipsilateral.
Recovery from Brown-Séquard’s
syndrome is very likely, with between 75
and 90 per cent of patients being able to
walk independently after rehabilitation
(Roth et al 1991).
CONCLUSION
There are diverse manifestations of spinal
cord injury and it is helpful to relate
mechanism of injury to the likely or
potential pathophysiology.
Although presentation varies, there
are principles underpinning the nursing
management of patients with this type of
trauma.
The third and final article on spinal cord
injury applies these principles to the care of
patients immediately after the injury period
but before admission to specialised spinal
cord injury units.
References
American Spinal Injury Association (2002) International
Standards for Neurological Classification of Spinal
Cord Injury. Revised edition. Chicago, ASIA.
Barker E (2001) Anatomy and physiology of the
spine and spinal cord. In Nelson A et al (eds) Nursing
Practice Related to Spinal Cord Injury and Disorders:
A core curriculum. New York NY, Eastern Paralyzed
Veterans Association.
Bing R (1921) Compendium of Regional Diagnosis
in Affection of the Brain and Spinal Cord. Second
edition. New York NY, Rebman.
Chiles B, Cooper P (1996) Acute spinal injury. The
New England Journal of Medicine. 334, 8, 514-520.
Dawodu S (2001) Spinal Cord Injury: Definition,
epidemiology, pathophysiology. emedicine. www.
emedicine.com/pmr/topic182.htm (Last accessed
December 9 2004)
38
DeVivo M (2002) Epidemiology of traumatic spinal
cord injury. In Kirshblum S et al (eds) Spinal Cord
Medicine. Philadelphia PA, Lippincott Williams and
Wilkins.
Glass C (1999) Spinal Cord Injury: Impact and
coping. Leicester, BPS Books.,
Grundy D et al (1991) Diving into the unknown.
British Medical Journal. 302, 6778, 670-671.
Guin P (2001) Advances in spinal cord injury care.
Critical Care Nursing Clinics of North America. 13,
3, 399-409.
Harrison P (2004) Spinal cord injury incidence update:
UK database summary 2001. Spinal Cord Injury Link.
3, 2, 4.
Hayes K et al (2000) Classifying incomplete spinal
cord injury syndromes: algorithms based on the
international standards for neurological and functional
classification of spinal cord injury patients. Archives of
Physical Medicine and Rehabilitation. 81, 5, 644-652.
Healy D et al (2004) Speed and spinal injuries. Injury.
35, 9, 908-912.
Hickey J (2003) The Clinical Practice of Neurological
and Neurosurgical Nursing. Fifth edition. Philadelphia
PA, Lippincott Williams and Wilkins.
Kirschblum S, Donovan W (2002) Neurologic
assessment and classification of traumatic spinal cord
injury. In Kirshblum S et al (eds) Spinal Cord Medicine.
Philadelphia PA, Lippincott Williams and Wilkins.
National Spinal Injuries Unit (2005) NSIU Database.
Dublin, Mater Misericordiae University Hospital.
Nelson A et al (2001) Nursing Practice Related to
Spinal Cord Injury and Disorders: A core curriculum.
New York NY, Eastern Paralyzed Veterans Association.
Prendergast V, Sullivan C (2000) Acute spinal cord
injury. Critical Care Nursing Clinics of North America.
12, 4, 499-508.
Roth E et al (1991) Traumatic cervical Brown-Séquard
and Brown-Séquard-plus syndromes: the spectrum
of presentations and outcomes. Paraplegia. 29, 9,
582-589.
Sapru H (2002) Spinal cord: anatomy, physiology, and
pathophysiology. In Kirshblum S et al (2001) Spinal
Cord Medicine. Philadelphia PA, Lippincott Williams
and Wilkins.
Schneck C (2002) Anatomy, mechanics, and imaging
of spinal injury. In Kirshblum S et al (eds) Spinal Cord
Medicine. Philadelphia PA, Lippincott Williams and
Wilkins.
Schoen D (2000) Adult Orthopaedic Nursing.
Philadelphia PA, Lippincott.
Sheerin F (2004) Spinal cord injury: anatomy and
physiology of the spinal cord. Emergency Nurse. 12,
8, 30-36.
Tortora G, Grabowski S (1996) Principles of Anatomy
and Physiology. Eighth edition. New York NY, Harper-
Collins College Publishers.
Walker M (1998) Protection of the cervical spine in the
unconscious patient. Care of the Critically Ill. 14, 1, 4-7.
Young W, Shea M (1998) Acute management of spine
and spinal cord injury. Trauma Quaterly. 14, 1, 21-42.
Zejdlik C (1992) Management of Spinal Cord Injury.
Second edition. Boston MA, Jones and Bartlett.
emergency nurse vol 12 no 9 february 2005