Trauma 2006; 8: 29–46

Traumatic spinal cord injury: the relationship

between pathology and clinical implications
WS El Masri(y)

The pathological effects of traumatic spinal cord injuries (SCI) encompass the
pathology affecting the spinal cord. As a result of the interruption of spinal cord
conduction, one or more pathological and patho-physiological processes affect
almost every system of the human body. Knowledge of the pathological
processes that affect the spinal cord and the various systems of the body is
essential for the safe and good management of these patients. The small
incidence (10–15 per million per year) of these highly complex conditions makes
it difficult for skills and experience to develop in District General Hospitals in the
management of these patients. The associated sensory impairment or loss
present diagnostic challenges to the clinician in almost every aspect of paralysis
and throughout the patient’s life.
In the acute stage simultaneous good management of the multi-system
impairments and malfunctions giving equal attention to all systems including that
of the traumatized spine is the key to good quality outcome. Concentrating
resources at any one time on any one particular aspect of paralysis is unlikely to
yield a similarly good outcome. The neurological outcome does not depend only
on the quality of the management of the SCI. The traumatized physiologically
unstable spinal cord is vulnerable and unable to protect itself from non-mechanical
complications outside the spinal canal, many of which can easily develop in
patients with SCI adding to the threats from the biomechanical instability.
To date there are many controversies in the management of many aspects of
paralysis at all stages following injury. One of the main current controversies is in
the management of the SCI itself. There are many reasons that seem to
perpetuate this controversy. Some of the reasons may be related to different
interpretations of the pathological processes that affect the vertebral axis and the
spinal cord as well as their effects on neurological outcome. The natural history
of neurological recovery following SCI is not always duly acknowledged.

Key words: clinical implications; pathology; traumatic spinal cord injury

Introduction A spinal injury (SI) with bony and ligamentous

Traumatic spinal injuries are potentially catastrophic
injuries with wide ranging effects depending on the
pathology sustained at the time of the accident.
Consultant Surgeon in Spinal Injuries Director Midlands Centre for
Spinal Injuries The Robert Jones & Agnes Hunt Orthopaedic
Hospital, Oswestry, UK
Address for correspondence: WS El Masri(y), RJ & AH Orthopaedic
Hospital Gobowen, Oswestry, Shropshire SY10 7AG, UK. E-mail:
Waghi.ElMasri@rjah.nhs.uk
injury/ies but without cord damage can cause tempo-
rary pain, physical limitation, anxiety, temporary
psychosocial and emotional disturbances as well as
financial loss. Most of these effects are however
short lived and reversible. With good management,
of the injured bony spine and its soft tissues the
patient is able to regain confidence and resume life
in a manner to which he/she was accustomed within
weeks from injury.
The effects of SI with neurological damage are
truly catastrophic in the short term both medically

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30 WS El Masri(y)
and non-medically. With good management and
appropriate support this catastrophe need not neces-
sarily be permanent. Sudden paralysis as well as
the devastating medical, emotional, psychological,
social, financial and economic consequences usually
affect not only the patient but also the partner,
family and friends, employer and the community in
general. The magnitude and permanency of these
effects however vary, depending on the level and
magnitude of the initial damage of the neural tissues,
the quality of the management offered to the patient,
the quality and intensity of education given to the
patient and carers; as well as the frequency and
quality of monitoring and response to the needs of
the patient on an ongoing basis. The medical conse-
quences of a spinal cord injury (SCI) are those of a
multi-system patho-physiological impairment and
malfunction, multiple disabilities and a potential for
the development of a wide range of complications.
Patho-physiology and
characteristics of spinal
cord injuries
In general, the functioning of the systems of the
body depends largely on the reflex activity of the
cord segments below the level of the lesion. Since
this reflex activity is almost never static in magni-
tude nor in frequency (except in cases of infarction
of the spinal cord segments below the level of the
injury), the physiological impairment and conse-
quent functioning of the various system of the body
remain labile throughout the individuals’ lives.
Although the abnormal reflex activity and reflex
functioning of the various systems of the body can
be clinically predicted by an experienced clinician
during the stage of spinal shock and, perhaps, the
transition phase of return of reflex activity, many of
the changes in reflex functioning remain unpre-
dictable beyond the stage of return of reflex activity
and throughout the patient’s life.
Furthermore, because of the disconnection of the
higher co-ordinating influences of the brain over
spinal cord activity, complications that in normal
circumstances are usually localized and limited to
the area affected can become a source of unusual far
flung and remote effects in various related and unre-
lated systems of the body. A ureteric calculus for
example, is unlikely to cause dysuria or painful renal
colics in a complete paraplegic or tetraplegic
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patient. In such a patient however it will be a source
of excess reflex neural activity in the segments distal
to the cord lesion and manifested as excess spastic-
ity. This excess spasticity could cause falls from the
wheel chair or bed resulting in fractures of long
bones and/or damage to skin and other soft tissues.
If this excess spasticity affects the pelvic floor
muscles, it could also cause urinary retention and
infection. Urinary retention in a tetraplegic or a
paraplegic patient above the level of D5 is likely
to cause excess unregulated sympathetic activity
known as autonomic dysreflexia with marked
increases in both systolic and diastolic blood pres-
sure and cerebro-vascular accidents. Any other
potentially painful pathology in an area innervated
by the spinal cord segments below the level of the
lesion is likely to result in the same cascade of
pathological events.
The impairment and/or lack of spino-thalamic
protective sensation can cause diagnostic as well as
management challenges. Any injury or pathology
such as lower limb fracture, urinary calculi,
hydronephrosis, intra-abdominal catastrophies and
so on, will not present with the expected pain or dis-
comfort, often causing delay in diagnosis. Indeed
injuries such as pressure sores, burns and scalds are
likely to develop as the result of sensory impairment.
Such challenges are minimized when patients are
treated in large numbers in dedicated SCI centres
where the clinical expertise as well as the adequate
infrastructure are available.
SCIs also result in depression of the immune
system. Patients are at particularly high risk of
developing respiratory, urinary and skin infections
as well as septicaemia. Therefore meticulous care is
required in the management of the multi-system
malfunction of these patients. Prophylactic antibi-
otics are strongly discouraged.
The principles of management of most pathologi-
cal conditions often have to be modified and individ-
ualized to patients with SCI. It is not advisable to
choose the same principle of management that is
applied to the general population (for whatever
pathological condition) and apply it automatically to
a paraplegic or tetraplegic patient. Consideration of
the level, density and the prognosis of the cord
injury; associated patho-physiological processes
operating at the time and how they will be affected
by and affect the outcome of the particular treat-
ment; the age of the individual and his/her level of
independence; the level of care and support that is

required and will be required after the treatment
usually influence the choice of the preferred option
of management. The dose of pharmacological agents
may also require modification in a paralysed patient.
The non-medical, emotional, psychological,
social, psycho-sexual, financial and vocational
pathological effects of a spinal cord injury are at
least as devastating to patients and carers as the
medical effects are. It is likely to take the patient just
as long to come to terms with these effects as with
the paralysis and the multi-system malfunction.
The direct and indirect inter-effects between the
medical, social, psychological, financial aspects and
so on, cannot be overemphasized. For example,
financial difficulties can result in matrimonial
disharmony which in turn can result in depression,
self-neglect and the development of pressure sores,
urinary infections and/or constipation. Conversely
complications such as pressure sores or contractures
interfering with comfortable seating or excess spas-
ticity are likely to add to the burden of the
partner/carer and result in extra strains on the rela-
tionship and disharmony.
Pathology and diagnosis
Accurate diagnosis of the SI is required in order to
initiate safe management. The diagnosis does not
only depend on the level and density of the SI/SCI
but also on the cooperation and the level of con-
sciousness of the patient, both of which can pose
significant diagnostic challenges to the clinician. An
understanding of the pathological multi-system
effects of the paralysis is also important for the
holistic management of the patient with SCI.
Diagnosis of SI/SCI in the conscious patient
In general, conscious patients who have sustained a
SCI will present with spinal pain, rigidity and ten-
derness over the site of the injury all of which are
related to the damage of the bony vertebra and soft
tissues. Fisher suggested that a conscious alert
patient who is able to communicate and has no
symptoms of pain, rigidity or tenderness in the spine
following trauma is unlikely to have sustained a
spinal column injury (Fischer, 1984). Although this
is true in the great majority of cases the author has
witnessed some elderly patients with pure ligamen-
tous damage to the spine presenting without pain or
rigidity. Extreme pain from other associated injuries
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Traumatic spinal cord injury 31
may also mask pain from a spinal fracture with con-
sequences for the timely diagnosis of a SI (Nichols,
Young, Schiller, 1987).
The clinical diagnosis of a SCI in the conscious
patient without major associated injuries can be
made without difficulty. Loss or impairment of
motor power, sensation and reflexes are indicative
(individually or in combination) of a spinal cord or
cauda equina injury.
It is essential to determine at the earliest stage
possible both the level and the density of the pathol-
ogy (neural tissue damage). The level of the injury is
defined by the last normal dermatomal and
myotomal distribution which is likely to coincide
with the last normal spinal cord segment. It is now
internationally accepted by experts in the field that
the dermatomal and myotomal distributions may be
abnormal for three segments below that level ie, both
sensation and motor power could be present but
impaired in three segmental distributions below the
last normal segment. For example, if the last normal
sensation is at the dermatomal distribution of C5 but
there is hypoaesthesia or analgesia in the der-
matomal distribution of C6, C7 and C8 the level of
the injury would be defined as C5. Because however,
there is some impairment of sensation in the der-
matomal distribution of C6, C7 and C8 it can be
logically assumed that the spinal cord segments C6,
C7 and C8 are only partially damaged and that some
of their functions are preserved. These segments
are therefore known as the ‘zone of partial
preservation’.
The density of the damaged area in the spinal cord
is defined by the presence or absence of sparing of
sensation with or without sparing of motor power
below the zone of partial preservation.
Absence of motor power, including voluntary
contraction of the anal sphincter, and loss of
sensation, including anal sensation below the zone
of partial preservation, may be indicative of a
clinically complete cord injury at the time of the
examination. It is important however, to appreciate
that not all clinically complete injuries in the
early hours or days following SCI remain clinically
complete (Boerger, Limb, Dickinson, 2000;
Bohlman, 1979). Spinal shock can also mimic an ini-
tially complete injury following which significant
recovery can occur. The density of the spinal cord
lesion can be expressed clinically using the Frankel
classification (Figure 1). Frankel, Hancock, Hyslop
et al. (1969) described five grades of severity of the
Trauma 2006; 8: 29–46
32 WS El Masri(y)
Figure 1 This figure is based on the data of Frankel
et al. (1969).
cord lesion from A to E which became subsequently
known as Frankel grades or Frankel Classification.
Frankel A being the most severe with complete
somato-sensory loss; while Frankel E being neuro-
logically intact. In between Frankel B, C and D
describe various degrees of motor and sensory loss.
The American Spinal Injury Association (ASIA) has
modified the Frankel classification (ASIA impair-
ment scale) and added a numerical element for
motor power and sensation. This is currently known
as the ASIA/ISCOS Classification (Figure 2).
The author strongly recommends an as adequate
documentation of motor power, sensation and
reflexes as possible using the ASIA/ISCOS chart
while also documenting the limiting factors, if any,
that would affect reliability of examination and/or
documentation for future comparison.
Diagnosis in the semiconscious
or the unconscious patient
Unconscious or semiconscious patients with head
injuries, and the intoxicated patient following major
trauma, present particular challenges to the clini-
cian. This can result in delays in the diagnosis of a
SI with potential major consequences. It is therefore,
in my opinion, imperative that such patients are
managed with the assumption that they have sus-
tained a SI until otherwise proven, clinically (when
the patient becomes alert) as well as radiologically.
Sitting up patients in bed with unstable SIs and/or
mobilizing them out of bed are in my experience the
commonest causes of neurological deterioration and
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litigation in this field. Further mechanical and/or
non-mechanical damage to the spinal cord is rela-
tively unlikely to occur in recumbency but can easily
occur when patients with a biomechanically unstable
spinal column and/or physiologically unstable spinal
cord are verticalized prematurely.
In semiconscious or unconscious patients follow-
ing major trauma, the absence of obvious clinical
signs of neurological impairment does not exclude
the presence of a spinal column nor of a spinal cord
injury. Unless the clinician is absolutely confident
that there is no spinal column and/or cord injury, I
would suggest a clear entry in the medical records to
the effect that the patient’s neurological assessment
could not be made because of the poor level of
consciousness. This fact should also be communi-
cated verbally to the nursing staff looking after
the patient.
I would recommend the following instruction: DO
NOT SIT THE PATIENT UP IN BED NOR MOBI-
LIZE THE PATIENT OUT OF BED PRIOR TO THE
EXCLUSION OF A SPINAL INJURY CLINI-
CALLY AND RADIOLOGICALLY. Such documen-
tation can result in the prevention of further
neurological deterioration and/or paralysis as well
as avoid litigation against the clinician and/or the
institution.
The general examination of the unconscious
patient can yield clinical signs which, in combina-
tion, can increase the clinician’s level of suspicion
regarding the presence of a neurological impair-
ment of spinal cord origin. The following signs are
strongly suggestive of a cervical spinal cord
injury: facial or scalp lacerations; myosis of one or
both pupil(s) due to the interruption of the sympa-
thetic outflow to the pupils; bruising or swelling of
the neck; absence of chest expansion during inspi-
ration associated with increasing abdominal girth
and retraction of intercostal muscles (diaphrag-
matic breathing caused by paralysis of intercostals
and abdominal muscles); presence or absence of
spontaneous movement in each limb; difference in
tone between proximal and distal muscles of all
limbs as well as difference in tone between the
upper and the lower limbs; response to painful
stimulus by pressure over bony prominences in the
form of limb withdrawal and/or facial grimacing.
The stimulus must be applied systematically to
each and every dermatomal distribution, prefer-
ably commencing distally in the lower limbs and
proceeding cranially to identify a level of injury.
 Traumatic spinal cord injury 33

Loss of active movement in the elbows, wrists, or
hands, with loss of response to painful stimuli in
the upper limbs are likely to be due to a cervical
cord injury. The presence of priapism in a truly
semi-conscious or an unconscious patient is also
suggestive of a high SCI. A combination of
hypotension and bradycardia due to sympathetic
nervous system areflexia is strongly suggestive of
a cervical SCI.
Bruising over the chest or thoraco lumbar spine in
the absence of diaphragmatic breathing, with
absent responses to painful stimuli applied to the
bony prominences of the lower limbs, in association
with absent tendon reflexes of the lower limbs could
be indicative of a lower thoracic cord or cauda
equina injury.
Unlike the patient with head injury who is likely to
be incontinent of urine on presentation at the accident
and emergency department, a patient with combined
head and SCI is likely to be dry and develop retention
of urine for some time before developing overflow
incontinence. This is due to the loss of bladder
reflexes and detrusor inactivity during the stage of
spinal shock. Any combination of the aforementioned
clinical signs is diagnostic of a SCI. Unfortunately, to
date there has been no attempt to rank these clinical
signs which, in the author’s opinion, would further
reduce problems with diagnosis.

Figure 2 ASIA/ISCOS Classification. ASIA (American Spinal Injury Association); ISCOS (International Spinal
Cord Society)

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34 WS El Masri(y)

cervical injuries are initially diagnosed as upper

Figure 2 Continued
Pitfalls in the neurological
assessment and general
management of patients with SCI
One of the commonest problems encountered by cli-
nicians who subsequently see the patients in Spinal
Injuries Centres is the mis-diagnosis of the level of
injury. Often patients with mid-cervical or lower
thoracic injuries, even when the patient has been
fully conscious, alert and co-operative. It is impor-
tant to remember that sensory preservation in the
sub-clavicular area is likely to be due to intact inner-
vation from the fourth cervical dermatomes through
the supraclavicular nerves rather than the third and
fourth thoracic dermatomes. It is therefore advisable
to assess the sensation in the upper trunk along the
mid-axillary line rather than in the mid-clavicular
line of the chest.
In a busy accident and emergency department it is
easy to mistake passive movements for active move-
ments. For example, a patient with a C5 lesion in
spinal shock will be able to actively move the
deltoid and biceps muscles resulting in active
abduction of the shoulder and flexion of the elbow.
This active movement will invariably result in
passive movement of the wrist and fingers. If
voluntary and reproducible wrist and finger active
movements cannot be demonstrated such move-
ments should not be interpreted as normal move-
ments. This applies to most muscle groups around
distal joints of limbs.
Involuntary twitching or movement of paralysed
muscles may be seen in the accident and emergency
department soon after a spinal cord injury for a
varying period of time. This does not indicate
preservation of voluntary power.
The presence of the bulbocavernosous reflex
without preservation of sensation and/or voluntary
motor power cannot be relied upon as indicative of
an incomplete lesion. The bulbocavernosous reflex
is often found positive from a very early stage in
complete cord injuries.
An apparently normal Babinski Response (down-
going plantar flexion of the big toe in response to
plantar stimulation) can be seen in patients with
complete and incomplete SCI in association with
absent tendon reflexes for many days or weeks fol-
lowing the injury. This little known and unpublished
observation has been responsible for the delay in
diagnosis in a few cases.
Due to the loss of thermoregulatory mechanisms,
patients with SCIs become poikilothermic and can
easily develop hypothermia or hyperthermia depend-
ing on the ambient temperature. It is important to
ensure monitoring of the temperature especially
during clinical examination since hypothermia can
exaggerate the bradycardia of a tetraplegic or high
paraplegic patient which can lead to cardiac arrest.

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Care should be taken during the resuscitation and
initial management of the patient taking into account
the impaired physiology of the spinal man/woman.
Common causes of death in the first few days are
respiratory failure from pulmonary oedema, reten-
tion of secretions, cardiac arrest or delay in diagno-
sis of associated major injuries.
The association of hypotension and bradycardia
presents temptation to the inexperienced clinician to
over hydrate in the hope of raising the blood pressure.
The temptation is further heightened by the presence
of oliguria in the first few days of injury. Some clini-
cians succumb. The sympathetic nervous system of a
patient with tetraplegia or high paraplegia is unable to
cope with the fluid overload. The patient can therefore
easily develop pulmonary oedema and die. Unless
there are associated injuries and a definite source of
bleeding adult patients with SCI rarely require more
than 2.5 litres of intravenous fluid per day.
Paralysis of the intercostals muscles reduces the
vital capacity of patients with tetraplegia and high
paraplegia. The paralysis or significant paresis of
abdominal muscles further disadvantages the respira-
tory system of these patients as they become unable
to cough and get rid of their bronchial secretions. This
is likely to further reduce vital capacity. Accumulated
secretions become a source of infection. The combi-
nation, left untreated is often lethal. With a good
regime of respiratory physiotherapy consisting of
deep breathing exercises, vibration and percussion of
the chest wall as well as assisted coughing, the great
majority of patients who are able to bend their elbows
(however weakly) ie, patients with C5 cord lesions
and below, do not require ventilation. Less than 5% of
tetraplegic patients admitted to our service within 72
hours of injury require ventilation. Those who do
require ventilation are often elderly and/or with pre-
vious chronic respiratory problems and/or with asso-
ciated severe chest trauma. Bronchodilators and
humidification add further ease to management.
Paralytic ileus is not uncommon in patients with
SCI. The ileus can be neurogenic in origin. It can
also be due to the development of a retroperitoneal
haematoma at the site of the fracture or due to asso-
ciated intraperitoneal damage of a viscus.
Unfortunately in some patients the ileus can be
delayed. Bowel sounds can be heard in the accident
and emergency department only to disappear a few
hours later. Early hydration and feeding of the
patient is likely to cause abdominal distension which
will further embarrass the diaphragm and reduce the
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Traumatic spinal cord injury 35
vital capacity further. It is the author’s practice to
withhold oral fluid and food for 48 hours or longer
until the bowel sounds return.
Patients with SCI at all levels will have impaired
sacral innervation of the sigmoid colon almost cer-
tainly causing constipation. This aspect seems to
receive little attention, leading frequently to great
distress to patients and can contribute to abdominal
distension.
Hypoxia, hypothermia and tracheal suction can
result in the exaggeration of bradycardia, probably
through increased vagal activity leading to cardiac
standstill. Cardiac arrest is less likely to occur in
patients with normal sympathetic activity and/or
following the return of sympathetic reflex activity.
There are many pitfalls in the management of the
various systems of the body affected by the spinal
cord pathology, at all stages following injury and
beyond discharge. In fact the majority of complica-
tions that occur in these patients both in the early
stages and/or during their lifetime are preventable. A
thorough knowledge of the pathology and patho-
physiology of the spinal man/woman is essential to
prevent complications occurring. Unfortunately the
subject is beyond the scope of this article.
Management of the SCI
It is logical to suggest that since all the problems,
medical and non-medical, resulting from the spinal
injury are caused by the cord pathology; anything
that can be done to reverse or minimize the pathol-
ogy, would in turn reduce the neurological impair-
ment and magnitude of these problems.
There are several approaches to the management
of the SI. Most are based on belief, logic and habit.
They are justified by personal conviction regarding
the importance of the various pathologies caused by
the injury. The interpretation of the significance of
secondary changes that occur in the spinal cord fol-
lowing injury, of the level of threat from the bio-
mechanical instability of the spinal column, and of
the significance of the sudden encroachment of the
spinal canal by bony or soft tissue elements varies
between clinicians. The course that is followed in
the management unfortunately depends to a large
extent on such interpretations.
It is attractive to extrapolate from the results
of the experimental laboratory animal and believe
that certain pharmacological agents and/or surgical
Trauma 2006; 8: 29–46
36 WS El Masri(y)
procedures can alter the course of the injury in humans
by manipulating/altering the course of the secondary
changes in the spinal cord following trauma. This
is based on the belief that these secondary changes can
be the cause of further damage to the spinal cord hence
the hypothesis of the ‘secondary injury’. This hypoth-
esis, however, is not universally accepted.
It is legitimate to assume that the potential for
displacement at the site of a biomechanically un-
stable fracture necessitates surgical stabilization.
Biomechanical instability can however be safely
contained with active conservative treatment.
It is also logical to believe that bony fragments
and/or soft tissue in the spinal canal could cause
further damage to neural tissue and therefore have to
be surgically removed. Many reports however have
demonstrated that significant neurological recovery
occurs without surgical decompression and with
good conservative management. The lack of agre-
ement over the interpretation of the pathological
processes and their significance together with the
lack of reliable data are in the author’s opinion some
of the major factors fuelling the controversy in the
management of the SCI.
The hypothesis of the secondary injury
Opinion is divided as to the contribution of the
initial impact to the final neurological outcome in
SCIs. Frankel, Michaelis, Paeslack (1973a), Frankel,
Michaelis, Paeslack (1973b), White, Southwick,
Panjabi (1976) and many others including the author
believe that the fate of the neurological injury is
largely determined at the time of the accident.
Freeman and Wright (1953) did however suggest
that the definitive cord damage could result from the
changes that occur in the spinal cord following
injury rather than from the initial impact.
Secondary changes (vascular, cellular, electro-
physiological, enzymatic, electrolytic, and metabolic)
occur in and around the area in the spinal cord that
sustained the impact. Scientists and clinicians have
for a number of decades tried to direct treatment
during the critical period of these secondary changes
in the hope of preventing further neurological deteri-
oration and/or improving the neurological outcome.
Unfortunately the interpretation of the clinical sig-
nificance of some of these changes in the spinal cord
is not agreed upon (El Masri(y) and Jaffray, 1992). In
the laboratory animal, attempts at manipulating the
secondary changes following sub-threshold force of
impact within a window of opportunity can possibly
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be beneficial. Beyond a certain threshold of force
of impact however these secondary changes cannot
be manipulated successfully and neurological
improvement cannot be demonstrated (Dolan, Tator,
Endrenyi, 1980; Guha, Tator, Endrenyi, 1987). In
other words, there is a threshold of magnitude of
impact beyond which attempts at manipulating the
secondary changes by surgery or other means fail and
no improvement can be achieved nor demonstrated in
the experimental animal. Complications from further
mechanical and/or non-mechanical damage can
occur during the surgical procedure.
In humans, where the force of the impact cannot
be measured, the secondary changes in the spinal
cord cannot be directly observed nor quantified;
where the window of opportunity could be, at least
theoretically, different from that of the laboratory
animal and practically difficult to take advantage of
(because of practicalities of the clinical situation
and/or possible associated life threatening injuries);
it is extremely difficult to but speculate. The results
of surgery and/or pharmacological agents are more
difficult to evaluate and have yet to be convincingly
demonstrated to reflect the experimental findings in
the laboratory situation.
Steroids have been strongly advocated for a
number of years. The rationale for their use is to
arrest the cascade of the secondary injury process.
Their true effectiveness however has, since the first
reports been doubtful (El Masri(y) & Short, 1997;
Short, El Masri(y), Jones, 2000) and they are cur-
rently regarded as an option of treatment. With the
recent results of the multinational Corticosteroid
Randomization After Significant Head injury trial
(CRASH, 2004), which had to be abandoned
because of statistically significant increase in mor-
tality and lack of efficacy associated with their use,
steroids are likely to be administered increasingly
rarely to acute SCI patients. There is early evidence
to suggest that high dose methyl prednisolone causes
myopathy in humans. Currently their use is
regarded as an option of management. Other phar-
macological agents have also been tested in animals
and promoted. To date however, the majority are
limited to laboratory or to clinical trials.
The administration of inotropic medication to
elevate the blood pressure of tetraplegic and high para-
plegic patients in the acute stage as advocated by Levi,
Wolf, Belzberg (1993) is a practice that has not yet
been fully evaluated with regard to its effect on the
secondary injury. The hypotension that occurs as a

result of the sympathetic paralysis has for many
decades been accepted as an occurrence of no signifi-
cant clinical consequences to the acutely paralysed
individual. Some, including the author, regard it as a
possible protective mechanism in prevention of further
bleeding in the spinal cord. Bleeding in the spinal cord
is probably one of the most injurious elements to
neural tissues since release of haemoglobin within
neural tissue triggers a cascade of deleterious reac-
tions. It is possible that by elevating the blood pressure
in an already damaged spinal cord (with disturbed
autoregulatory mechanisms) the bleeding within the
cord could increase. Unfortunately to the author’s
knowledge this has not been tested in the laboratory.
Biomechanical instability of injuries
to the spinal column
Biomechanical instability (BI) causes concern
because of the potential displacement of the frac-
tured elements at the site of the injury which can
damage or further damage neural tissue. The diagno-
sis of BI is usually based on radiological investiga-
tions at the time of the presentation of the patient.
Unfortunately, the function of the muscles, undama-
ged ligaments, supporting bony structures and the
natural history of the repair process that follows are
often not thoroughly considered. It is perhaps worth-
while noting that most vertebral fractures heal
within six to twelve weeks from injury. Ligamentous
injuries however, can take much longer to heal.
In the majority of patients the biomechanical sta-
bility (BS) of the spine is usually restored once the
healing of bone and/or ligament occurs. In other
words, biomechanical instability is time related.
There is no evidence to suggest that surgical
stabilization enhances the speed of healing or
achieves earlier BS. Surgical stabilization should
therefore be regarded as no more than an option for
“Containment” of the BI until natural healing occurs.
Biomechanical stability can be at least equally well
achieved with active conservative treatment.
Unfortunately, the terms non-surgical treatment
and conservative treatment are liberally inter-
changed. Conservative treatment consists of a period
of bed rest ranging between four and twelve weeks
followed by a period of bracing until stability is
achieved. Currently, patients are rarely managed in
recumbency for periods exceeding four to six weeks.
Non-surgical management rarely include such
periods of treatment in recumbency. The poor results
that ‘conservative’ managements are blamed for are
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Traumatic spinal cord injury 37
often described in series where the description of
‘conservative management’ is often lacking and are
probably results of poor selection or inadequate
‘non-surgical management’. It is difficult to contain
the BI with non surgical means during early vertical-
ization and/or early mobilization of the patient fol-
lowing injury. However, some have reported good
results in neurologically intact patients who have
burst unstable fractures with casting in extension
and early mobilization (Chow, Nelson, Gebhard
et al., 1996). Although clinically patients seemed to
do well, the kyphotic deformity tended to recur.
Unstable injuries without
neurological damage
The instability of these injuries can be contained by
either surgical or conservative means until natural
healing occurs. There are no class one studies on long
term outcomes. Since the spinal cord of such a patient
is however not damaged and in all probability ‘phys-
iologically stable’; the risks to the intact spinal cord
from surgery is minimal. This is provided no per-
operative or post-operative complications occur. In
these patients, conservative treatment of four to six
weeks of bed rest (followed by six to eight weeks of
bracing) is relatively more time consuming and prob-
ably more costly than surgical stabilization. Patients
with major ligamentous injuries with no bony injuries
may require even longer periods of bracing before
healing occurs if treated conservatively. It is therefore
reasonable to encourage the patient who is neurolog-
ically intact to undergo surgical stabilization provided
he/she understands there is a small risk of paralysis
(1–3%) from surgery. Loss of surgical fixation prior
to healing and attainment of natural biomechanical
stability due to inadequate or poor instrumentation,
osteoporosis or infection is likely to add an extra risk
to neural tissue.
In my practice I give all patients with and without
neurological damage a choice between surgical and
conservative management following adequate expla-
nation of potential risks and benefits of each of the
two methods of management.
Stable and unstable injuries with
neurological damage
The injured spinal cord is physiologically unstable
probably because of the loss of its autoregulatory
mechanisms, disruption of its blood brain barrier and
of the cell membrane disturbances that occur follow-
ing injury (El Masri(y), 1993). This physiological
Trauma 2006; 8: 29–46
38 WS El Masri(y)
instability renders the spinal cord vulnerable and
unable to defend itself from non mechanical insults
such as hypoxia, sepsis, hypotension, metabolic
changes and anaemia, all of which are at risk of devel-
oping easily in SCI patients as a result of the multi-
system malfunction associated with the paralysis.
Surgical realignment, surgical stabilization and/or
surgical decompression do not offer protection to the
injured spinal cord against these insults. On the
contrary, hypoxia and/or hypotension, technical
difficulties leading to further mechanical damage
and ligation of an important blood vessel to stop
bleeding which is usually difficult to identify
during surgery can potentially cause more harm.
Furthermore, post-operative complications such as
bleeding, chest or urinary infection and/or surgical
wound infection can also cause harm.
Late pain is rare in patients treated conservatively
with four to six weeks periods of bed rest followed
by six to eight weeks of bracing. Adequate analgesia
and support from peers and the staff especially in the
first week following injury is essential.
The spinal column is a segmental structure for
maximum flexibility. Surgical stabilization with
long fusions can restrict the flexibility of the spine
and interfere with the rehabilitation process and the
quality of independence of the patient. Fortunately
in the last decade instrumentation has improved
to involve a minimum number of units of motion
(vertebra). The surgery is however more exacting,
the learning curve longer and the complications
potentially more serious. Considering this and the
small incidence of SCIs, such procedures are best
done when required in SCI test Centres.
There is no evidence to suggest that realignment
and/or surgical stabilization are essential to prevent
late pain at the site of the fracture. The incidence of
pain at the site of fracture with our conservative man-
agement is less than 5%. This is another important
area for research preferably by independent assessors
who are not involved in the patient’s management.
Early mobilization/rehabilitation
Surgical stabilization to enhance early mobilization,
rehabilitation and discharge from hospital is often
advocated. Early mobilization (verticalization) espe-
cially during the stage of spinal shock (areflexia)
may not be safe or beneficial to the neurologically
impaired patient. Further neurological deterioration
in association with postural hypotension during
mobilization has been documented in patients with
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BS spines and incomplete neurological injury (El
Masri(y), 1993). It has been our practice in the last
two decades to carry out tilt table studies: blood
pressure measurements and neurological examina-
tion with increments of 10° of tilt prior to mobiliz-
ing the patient.
Early mobilization of patients with complete upper
thoracic or cervical cord injuries is associated with
reduction of vital capacity (Cameron, Scott, Jousse
et al., 1995; Morgan, Silver, Williams, 1986) and a
potential drop of oxygen saturation which may further
impair cord functions. It is therefore more than prob-
able that the physiological instability (PI) of the
injured spinal cord is at least as threatening to spinal
cord functions as the BI of the spinal column is.
Furthermore, the combination of postural hypoten-
sion and reduced vital capacity which can occur
during early mobilization are unlikely to enhance the
active process of physical rehabilitation which
requires energy, motivation and a sense of well being.
Unfortunately, early mobilization and early reha-
bilitation are often advocated by clinicians who are
rarely directly involved in the rehabilitation process
of the patient.
Canal encroachment and decompression
Some of the first case reports to suggest that canal
encroachment as demonstrated by computerized
tomography does not correlate with the degree of
neurological impairment, does not prevent neurolog-
ical recovery in patients with incomplete cord
injuries and does not result in neurological deteriora-
tion in patients without impairment of cord function
were published by El Masri(y) and Jaffray (1992) and
El Masri(y) and Meerkotter (1992). Since then the
same conclusions have been independently made by
reviewing the outcome of conservative treatment of
50 consecutive patients with canal encroachment
between 10% and 90% in Frankel C, D and E groups
(El Masri(y), Katoh, Khan, 1993; El Masri(y), 1993).
Other groups have since published similar findings
(Limb, Shaw, Dixon, 1995; Rosenberg, Lenger, Weisz
et al., 1996; Boeger, Limb, Dickson, 2002). Surgical
decompression in patients with incomplete injuries is
not necessary for neurological recovery to occur. The
long term outcome of conservative management
without decompression of spinal canal encroachment
is most promising (Figure 3).
Surgical decompression is even more unlikely to
be of benefit if the severity of the initial impact is
beyond a certain magnitude as recovery is most
 Traumatic spinal cord injury 39

Figure 3 (a) Lateral cervical spine X-ray revealing a burst unstable fracture of C5 vertebra with retropulsion in
the spinal canal of a patient following a road traffic accident in 1988. The patient was admitted to the Midlands
Centre for Spinal Injuries on the same day of the accident with C5 Frankel C paralysis and almost complete
paralysis in the left upper and lower limbs. She was treated conservatively with skull traction and bed rest for
seven weeks and required a further period of four weeks in a Minerva for rehabilitation. She did not undergo
surgical decompression nor surgical stabilisation. She recovered significant motor power to ambulate with
minimal arm support and was discharged eleven weeks from injury. (b) Lateral CT scan through a midline cut
to reveal the extent of spinal canal encroachment. (c) Cross-sectional CT at the site of the fracture. (d) Lateral
cervical spine X-ray in 1991 revealing reasonable alignment and good consolidation at the site of the fracture.
(e) Lateral MRI in February 2002 demonstrating a signal in the spinal cord at the level of the lesion as well as
remodelling of the spinal canal. (f) Recovery sustained for the last 18 years

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40 WS El Masri(y)
Figure 3 Continued
unlikely to occur (Dolan et al., 1980; Guha et al.,
1987). The debate, claims and counter claims about
surgical decompression and its timing remain incon-
clusive (Fehlings and Perrin, 2005).
Decompression can be achieved by non-surgical
means with realignment. Traction may or may not be
required depending on the type of injury. The effect
of facet relocation and realignment on pain relief is
impressive. There is no concensus however on the
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value or the timing of realignment on neurological
recovery (Fehlings and Perrin, 2005). In the author’s
experience, closed reduction of facet dislocation and
realignment is safe in experienced hands in the first
24–48 hours from injury. The author has had to
abandon closed reduction of facet dislocation if the
patient presents more than 48 hours from injury. It is
conceivable that oedema of the cord is at its
maximum at 48 hours from injury and for a number
of days beyond. In the process of closed reduction of
a cervical spine dislocation, however experienced
the clinician is, there is likely to be some reduction
in the size of the spinal canal. In the presence of
marked oedema and a swollen cord any reduction
in the size of the canal can cause further damage to
the cord. Elderly people are even more vulnerable.
Cord compression
Cord compression does not appear to prevent neuro-
logical recovery in patients with significant neuro-
logical impairment following spinal cord injuries
(Figure 4). The arguments for surgical decompres-
sion often quote compressive disc disease and other
space occupying lesions. It must be appreciated that
the pathological processes of disc disease and other
slowly growing space occupying lesions are likely to
be different from that of acute traumatic canal
encroachment. In other words while the final radio-
logical picture of neural compression might appear
to be similar, the pathological processes that lead to
this are different.
It is also interesting to note that in a number of
post mortem examinations, many witnessed by the
author, the neural tissue pathology (contusion,
oedema and haemorrhage) tend to extend for a
number of vertebral levels above and below the site
of the fracture. This can also be demonstrated on the
MRI scan. It is difficult to believe that decompres-
sion at the one site of the fracture would alter the
course of the pathology and outcome.
Since the installation of the MRI scanner in our
institution in 1994 we have been prospectively
and restrospectively monitoring the neurological
progress of patients with cord compression treated
conservatively. The preliminary results indicate that
no patient with or without neurological sparing has so
far deteriorated permanently. They also indicate that
the great majority of patients with incomplete cord
injuries in Frankel/ASIA groups B, C and D patients
do recover neurologically significantly without surgi-
cal decompression Figure PW). It appears that the
 Traumatic spinal cord injury 41

same clinical prognostic indicators of recovery apply Some patients make significant neurological recov-
whether there is cord compression or not. We can still ery that enables them to ambulate again without any
assure a patient with a Frankel B acute tetraplegia or surgical or pharmacological intervention (Frankel,
paraplegia (complete motor paralysis but sensory Hancock, Hyslop et al., 1969).
sparing) that the chances of walking out of the depart-
ment varies between 50% and 70% or more depend-
ing on the preservation of pin prick sensation and not
the degree of cord compression. What is not known is
whether there is an advantage to either method of
treatment (conservative or surgical) in terms of speed,
magnitude and or end point of recovery.
Indeed a prospective multi-centre trial with
assessors who are independent from the provider of
management is also overdue to settle this matter.

Natural history of complete

spinal cord injuries
Between the second and fourth day after injury some
ascent of the lesion for up to three segments can
occur in about 10% of the patients. This is temporary
and is probably related to cord oedema which reaches
its peak during this period. Recovery is almost
always assured. The majority of patients recover to
the original level or more within the following few
weeks in the published studies.
Between 5–9% of patients with initially clinically
complete spinal cord injuries make a significant
recovery (Frankel, Hancock, Hyslop et al., 1969).
Many more patients, documented in this publication,
recover cord functions in one or two myotomal dis-
tributions below the level of the injury. Although
there is some debate over the percentage of patients
in Frankel A group who make various degrees of Figure 4 (a) Lateral MRI of a 47. year old patient who
recovery, nevertheless most clinicians who practice sustained a 10 foot fall in 1996. He was admitted to
in SCI Centres have seen these patients. our centre within 24 hours from injury. The MRI
Anderson and Bohlman (1992) suggested that reveals a double injury involving both the spinal axis
anterior surgical decompression and arthrodesis of and the spinal cord at D9 and L3 level. The spinal cord
is compressed at both levels. There is also a degree of
the cervical spine lead to zonal motor improvement. biochemical instability at both levels. The patient pre-
Katoh and El Masri(y) (1994) demonstrated that sented with a Frankel B neurological loss (complete
similar results can be achieved with conservative motor paralysis but sensory sparing). (b) Cross-sec-
management. In a series of 53 patients with com- tional CT views demonstrating significant canal
plete traumatic tetraplegia admitted within two days encroachment at D9. (c) Cross-sectional MRI demon-
strating thecal compression at the cauda equinal level
of injury in our centre there were two prognostic of L3. (d) Demonstrate good painless range of move-
indicators for zonal motor recovery: dermatomal ment and functional recovery without intervention
preservation of sensation and an initial neurological from surgical stabilization, surgical decompression
level higher than the vertebral fracture. These were pharmacological agents or experimental intervention
to achieve and maintain this result for the last 10
good prognostic signs of zonal motor recovery years. The patient was treated conservatively with six
regardless the mechanism of injury or residual canal weeks of bed rest followed by a period of six weeks in
stenosis (Katoh and El Masri(y), 1994). a body cast.

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42 WS El Masri(y)

Figure 4 Continued

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Natural history of incomplete
cord injuries
Patients with incomplete cord injuries (Frankel B, C
and D) make significant neurological recovery
regardless of the degree of canal stenosis (Katoh, El
Masri(y), Jaffray, 1996) or canal encroachment (El
Masri(y) and Meerkotter, 1992; El Masri(y), Katoh,
Khan, 1993; El Masri(y), 1993; Limb, Shaw, Dixon,
1995; Rosenberg, Lenger, Weisz et al., 1996; Boerger,
Limb, Dickson, 2000; Fehlings and Perrin, 2005;
Frankel, Hancock, Hyslop et al., 1969) provided both
the BI of the Hancock, Hyslop spinal column and the
PI of the spinal cord are well contained.
The role of surgery
The role of surgery in trauma remains controversial.
This is due to a number of factors. The relatively
small number of traumatic cases does not readily
allow for good randomized control trials. There is a
lack of objective independent reliable assessment of
outcomes. The differences in the background of
training, experience and expertise of clinicians; dif-
ferences in systems of management of the SCI and of
the multi-system impairment with implications on
neurological and global outcome; the differences
between the methods of funding and methods of
health care provision; the temptation to apply the
principles of management of the neurologically
intact to the neurologically impaired patient; and the
lack of evidence about the superiority of either
methods of management (surgical or conservative)
in terms of outcome are all contributing factors to
the current controversy. The matter is further com-
plicated by a strong belief by some that early surgery
(mainly decompression within a few hours of injury)
can be beneficial.
The microscopic and macroscopic pathological
changes in the spinal cord following trauma have been
studied in depth in the laboratory animal. There is
class one evidence about the beneficial effect of early
decompression in the laboratory animal. In the
author’s opinion this does not justify direct extra-
polation to humans. Scientific methodology dictates
proving that what is class one evidence in the labora-
tory animal is also proven to be class one evidence in
humans before an intervention (pharmacological, sur-
gical or otherwise) is considered to be a necessary
treatment in humans. Although one is very tempted to
accept the class 2 and 3 available evidence in humans,
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Traumatic spinal cord injury 43
the subjectivity of most of the studies is a method-
ological weakness. One cannot confidently exclude a
bias when those who make the selection for surgical
decompression and carry out the surgical procedure
are the same people who carry out the study.
Convincing evidence of the benefits of surgical
decompression on neurological outcome is truly
lacking in humans. At a more basic level, the tempo-
ral neurological changes that occur hour by hour
during the first 24–48 hours following injury have not
been documented nor studied even in the conscious
patient without cognitive impairment. This requires
some urgent attention.
Currently the neurological examination and docu-
mentation in the first few hours of injury does not
provide reliable data for accurate follow up com-
parison. During the stage of spinal shock (are-
flexia) assessment of the Frankel/ASIA grading is
not reliable. Associated pain often requiring anal-
gesia and sedation further undermines the accuracy
of the neurological assessment. It is therefore dif-
ficult to obtain a baseline neurological examina-
tion if early surgery is carried out. Unfortunately,
early neuro-physiological testing remains equally
unreliable in determining if a cord lesion is com-
plete or incomplete and likely to recover or not.
Currently early surgery is therefore based on belief
and hope. Unless the natural history of the various
Frankel/ASIA groups from the first few hours of
injury can be established confidently, temporally
and predictably the matter is likely to remain in the
realm of debate and speculation.
The belief that the BI at the fracture site is difficult
to contain without surgery and that the presence of
canal encroachment by bony or soft tissue is detri-
mental to neural tissues has led to an explosion
of surgical instrumentation and intervention.
Unfortunately, this has been to the detriment of
almost complete loss of skills and expertise with con-
servative management.
Those who promote conservative management of
neurologically impaired patients add more weight-
ing to the physiological instability of the spinal
cord and are able to contain the BI of the spinal
column without difficulty. They consider the risk
of neurological deterioration or lack of neurologi-
cal recovery, with surgery, to be higher than with
expert conservative management as stated earlier.
This is not to mention the technical difficulties that
can be encountered with the more elaborate proce-
dures especially during the learning curve.
Trauma 2006; 8: 29–46
44 WS El Masri(y)
Most of the claims and counterclaims about the
superiority of various methods of management are
based on retrospective studies. The results are
usually inconclusive (Fehlings and Perrin, 2005;
Wilmot and Hall, 1986). Laminectomy has a noto-
riously bad reputation for further destabilizing some
injuries biomechanically and in causing reduction
of spinal cord blood flow. The latter was shown
experimentally by Anderson and Means (1985).
Neurological deterioration following laminectomy
is not unusual and has been documented (Morgan,
Wharton, Austin, 1971; Bohlman, 1979). There is
also controversy about the rate of complications
and the effect of the method of management on
total hospitalization time (Wilmot and Hall, 1986;
Murphy, Opitz, Cabanela et al., 1990; Carvel and
Grundy, 1994). There is evidence however to
suggest that the incidence of complications is
higher and that hospitalization is longer when the
patient’s transfer to a spinal injuries centre (SIC) is
delayed and when surgery to the injured spine is
performed prior to referal to the SIC (Wilmot and
Hall, 1986; Carvel and Grundy, 1994; Aung and
El Masri(y), 1997).
One of the relatively few prospective comparative
studies comparing surgical and conservative man-
agement in 208 patients with acute spinal cord injury
(Tator, Duncan, Edmonds et al., 1987) revealed no
difference in neurological outcome nor in length of
hospitalization. The only parameter found to be sig-
nificant to the length of stay was the severity of the
cord injury.
Despite a significant improvement in surgical
technique and anaesthesia and the appearance of
new surgical instrumentation on average every two
years for over a period of three decades; surgery
remains an option of treatment and there is no class
1 evidence to suggest it is necessary for better
outcome (Fehlings and Perrin, 2005).
At the Midlands Centre for Spinal Injuries of the
Robert Jones and Agnes Hunt Orthopaedic Hospital,
patients are given an informed choice between con-
servative and surgical management of the injury irre-
spective of the radiological appearances on X-rays,
CT scans and/or MRI scans.
The author’s indications for surgical stabilization
are the following:
• Neurologically intact patients. Their rehabilitation
requirement is limited. The majority will be dis-
charged within a few days from surgery.
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• Patients with pure ligamentous injuries associated
with malalignment with or without neurological
impairment. The time to stability restoration is
much longer than when bony structures are
damaged.
• Mentally challenged patients and patients who are
unable or unwilling to co-operate with conserva-
tive management such as patients with uncon-
trolled epilepsy.
• Patients with late painful deformities.
The author’s only indication for surgical decompres-
sion in the acute stage is a neurologically deteriorat-
ing patient with MRI signs of further compression of
neural tissues. Late decompression for post-trau-
matic syringomyelia in the long term is required in
less than 5% of the population of patients with SCI
(El Masri(y) and Biyani, 1996).
Conclusion
Knowledge of the level, density and pathological
processes of the spinal cord lesion and its patholog-
ical and clinical effects on the various systems of the
body is essential for adequate management of these
patients. It is therefore not surprising that the
response to the conventional treatment directed to
the non-traumatic pathologies is often disappointing
when applied to SCI patients.
The prognostic indicators of neurological recovery
have been well documented with expert conservative
management (Katoh and El Masri(y), 1994; Katoh,
El Masri(y), Jaffray et al., 1996; Folman and El
Masri(y), 1989). They seem to have equal signifi-
cance in the presence of biomechanical instability,
canal encroachment and cord compression. To date
there is no convincing evidence to suggest that any
intervention, surgical, pharmacological experimental
or otherwise, provide a better outcome than active
conservative management. The Class 1 evidence for
surgery in the laboratory animal and Class 2 and 3
evidence in humans require urgent further independ-
ent evaluation. Currently all available interventions
are options of management. Furthermore, the effects
of the anaesthetic agents (positive, negative or
neutral) on the injured spinal cord have yet to be
explored (Hickey, Albin, Bunegin et al., 1986).
Prospective well designed studies by independ-
ent assesors are difficult to conduct. It is however,
paramount that they are attempted and that the

important aspects of these trials are independently
assessed. With current knowledge it is essential
that the patient is given an informed choice
between methods of treatment. This is becoming
increasingly important since litigation is on the
increase and justification is likely to be required in
case of mishaps. Considering the small incidence,
wide ranging effects, complexity of diagnosis and
management, the need for an elaborate infrastruc-
ture, the need to offer a choice to patients and the
need to conduct research with appropriate method-
ology in all aspects of paralysis; it is only reason-
able to manage patients with SCI in Spinal Cord
Injury Centres equipped to deal with all clinical as
well as research aspects.
Acknowledgements
The author would like to thank the following: Dr BB
Eldeeb for her help with the research and the
composition of the article; Mrs H Edwards and Mrs
Bridget Thomas for their administrative assistance;
Mr Alun Jones and Mr Andrew Biggs for their help
with the illustrations; Marie Carter and Siobahn
Whitby for their help with the bibliography.
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