Mechanism and pathophysiology of spinal and spinal cord injury

R. Braalanan
Rotterdam, the Netherlands
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This is a surnmarized review of those aspects of INJURIES OF THE CERVICAL SPlNE

the biomechanics and the pathopyhsiology of injuries
to the spine that are of practical significance for a
General
neurosurgeon. There is not space enough in this survey
for a detaled description of biomechanical studies, Elunt injuries of the cervical spine may be caused
autopsy fmdings, cadaver experiments on spinal injuries by direct or indirect force.
nor on traumatic spinal cord damage in animal ex- Direct forces, such as from a falling object hitting
periments. the neck are relatively rare. They act directly on a
Aspects of radiological or MRI diagnosis will vertebra. Cornmonly, the result is a fracture of a
not be discussed in this paper, nor treatment of spinal spinous process or vertebral arch. Lesions resulting
injuries: these subjects will be dealt with in other from indirect forces are caused by movements of the
papers. spine that extend beyond the physiological range. Hyper
Biomechanical studies,(19, 25., 28) autopsy (17, 18) and (ante) flexion results in compression of the vertebral
cadaver experiments (28) have· established the fun- body and disc and dictraction of the posterior elements.
damental relationship between mechanisn of injury Hyperextension (sometimes indicated as hyperretroflex-
-vector force- and acute injuries of the spine, in par- ion or hyperdeflexion) results in compression fractures
ticular the cervical spine. The mechanism of injury is of the spinous processes and the arches and in tearing
of major importance in the complete understanding and of the anterior longitudinalligament and in elderly pa-
management of spinal trauma. In controlled laboratory tients of the disco (1,9) Indirect forces may also be shear
experiments pure vector forces such as flexion- forces which displace the vertebrae parallel to each
extension, vertical compression, lateral flexion or com- other, or forces acting along the axis of the cervical
binations have been shown to produce injuries peculiar spine, such as compressive forces that approximate the
th each vector force or combination of forces. skull and the trunk or distractive forces that separate
However, a single vector force may cause different in- them. (1,9) Lateral hyperflexion and hyperrotation also
juries. The greater the force, the more severe the play a part in cervical spinal injury.
injury .(28) There are ofien combinations of these excessive
In clinical practice the causative force can only movements, 8uch as hyperflexion and axial compres-
be inferred on the basis of the history of the accident sion or axial,distraction that act to injure the cervical
and clinical and radiological evidence, since the spine. These combinations determine the type of in-
conditions of the mechanis of injury are certainly not jury to the cervical spine.
controlled and usually not even directly observed. As an example: compressive axial forces may in
Because of the close pathologic and radiographic one case produce compression of the atlas, and in
similarity of the experimentally produced and clinical another produce compression of a vertebral body of
lesions, the knowledge obtained from controlled the lower cervical spine - differences that are probably
laboratory models may be reasonable applied to the in- due to the action of additional forces.
juries seen.(1,9) Sometimes a series ofunphysiological movements,
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 Mechanism and pathophysiology of spin:¡l and spinal cord injury Neurocirugía

such as hyperflexion followed by hyperextension, or An atlas fracture is usually the result of compressive
vice versa, causes the injury. (9) hyperextension, wich causes the type-I fracture, con-
Although there are many c1assifications of acute cer- fined to the posterior arch. It may also be due to pure
vical spine injuries, the supposed mechanísm of injury vertical compression resulting in a type TI-fracture, in-
is the most common basis for such c1assification. An volving both rarches and crossing the equator of the
ofien used c1assification of injuries of the lower cer- atlas.
vical spine is presented in table 1. Jefferson's fracture is a fracture of the anterior and
posterior bony arches of e 1 with lateral displacement
of the lateral masses of e 1 onto e 2 (fig. 1). Although
atlas fractures are generally dismissed as relatively in-
Table 1
nocuous injuries, follow-up studies have revealed that
many patients have persisting symptoms of dysaesthesia,
Narrowing sagittal neckpain and/or neck stiffness. (20)
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diameter of spinal canal

Distractive hyperflexion
- hyperflexion sprain none
- unilateral facet interlocking moderate
- bilateral facet interlocking usually severe

Compressive hyperflexion
- hyperflexion fracture dislocation usually severe
- tear-drop fracture ofien severe

Distractive hyperextension
- hyperextension dislocation common
- hyperextesion sprain temporary, sometimes
severe
Figure l.-A drawing of the «Jeffersons's fracture» (1920).
Compressive hyperextension
- hyperextension fracture dislocation commonly not
Type I
Axial compression
- wedge-like fracture of vertebral body none
- burst fracture varying, usually severe

Common ciassification of injuries ofthe lower cervical spine with their

influence on the sagittal diameter of the spinal canal.

Type 11

Upper Cervical Spine

The atlas functions as a bony meniscoid between

the occiput and the axis. The transverse ligament whích
originates bílaterally from the medial aspect of the
lateral mass of the atlas keeps the odontoid process in Type 111
its place. (9,15)
In interior atlantoaxial dislocations, most probably
due to shear forces, the distance between the anterior
arch of the atlas and the intact odontoid process exceeds
2 to 3 mm. in adults and 4 to 5 mm in children. If,
as in the rare case, the cord is involved, the trauma is Figure 2.-Classification of fractures of the odontoid process according to
usually fatal. (9,15) Anderson and d'Alonzo.

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Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

FraGtures of the odontoid process account for 10 % Pain in the posterior part of the neck and limited
of all cervical spine fractures. The most cornmon causes motion of the neck are the most common symptoms
of fractures of the odontoid process are falls on the head in these fractures. (23)
and traffic accidents, especially motor-vehicle ac- Neurologic sings and symptoms -mainly signs of
cidents. (23) pyrarnidal tract damage- are encountered in only a
These fractures are c1assified according to Ander- minority of cases, because the space in the spinal canal
son and D~lonzo (fig. 2).(3) The type I fracture is an is relatively large in the upper cervical spine: compres-
oblique avulsion fracture of the tip of the odontoid pro- sion of the spinal cord is less likely to occur with frac-
cess - an extremely rare injury. The most common type tures of the odontoid process than in injuries of the lower
II fracture is localized at the base of the odontoid pro- cervical spine.
cess. In the type III fracture, the «low» type, the frac- In the hangman's fracture, or traumatic spon-
ture line is mainly localized in the vertebral body of dylolisthesis of C2, the fracture occurs at the base of
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the axis. the pedicles (fig. 4) and results in an anterior disloca-

These fractures are usually associated with tion of the body of C2 in relation to C3. This type of
prevertebral soft tissue swelling. Fractures of the odon- fracture dislocation is very common nowadays, occur-
toid process may be associated with atlas fractures, in ring in motor-vehic1e accidents, in which the patient's
particular Jefferson's burst fracture. Many patients with face comes in contact with the windshield and the neck
odontoid fractures have head injuries or mandibular is subsequently sharply extended and axially compress-
fractures. ed (compressive hyperextensión). The cord usually
Howorth and Petrie ascribe odontoid fractures to escapes demage, because the sagittal diameter of the
suden forward or backward movements of the head with spinal canal is not reduced. (9.15)
respect to the trunk (fig. 3).(Í~ The direction of the
displacement suggests the mechanism of injury. In case
of anteflexion of the head, the broken-off odontoid pro-
cess appears to be sheared off by the transverse liga-
ment, whereas in retroflexion it seems to be sheared
off by the anterior arch of the atlas. This is, however,
probably a too simplistic explanation.

Figure 4.- The location of the fracture in the arch of C2 in the hangman's
fracture. The ~agittal diameter of the spinal canal is not reduced. :

A fracture through the posterior part of the

arch of the axis and chip fractures at the tip of the
spinous process of C2 are usually a result of
Figure 3.-0dontoid fractures with anterior or posterior displacement of hyperflexion.
the broken-off odontoid process.
An avulsion fracture of the antero-inferior
margin of the body of the axis indicates a hyper-
In children flexion injuries cause no real fracture extension injury. It may be an additional injury
of the odontoid process, but an epiphysiolysis of the hangman's fractures, but isolated avulsion fractures are
odontoid process. also seen.

234
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

Lower Cervical Spine The most common causes of bilateral and unilateral
interlocking are falls from steps or stairs, traffic ac-
Distractive hyperflexion. In distractive hyperflex- cidents, and athletic injuries. (9) The destruction of
ion, e.g. by a blow on the occiput from below, the ligaments and disc is usually less extensive in unilateral
spinous processes are separated and the posterior than in bilateral facet interlocking. In either case,
ligaments and capsules of the intervertebral articula- fragments of a ruptured disc may be found in the spinal
tions are overstretched and may be torno A hyperflex- canal. (9. 29)
ion sprain (8. 9) may develop, in particular when the The neurological deficit in case of facet interlock-
posterior portion of the annulus fibrous and the posterior ing varies from neck pain without neurologic impair-
aspect of the intervertebral disc are torno Hyperflex- ment to a complete and permanent cord lesiono The
ion sprains are radiologically characterized by an neurologic deficit is, in general, more severe in bilateral
kyphotic angulation at one particular cervical segmento than in unilateral interlocking owing to greater narrow-
This lesion is usually located between C2 and C4 in ing of the segittal diameter of the spinal canal in the
younger and between C4 and C7 in adult subjects. The former condition. About half of all patients with
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diagnosis should not be made in case of a posttraumatic bilateral facet interlocking have a complete cord lesiono
smooth continuous arcual kyphosis due to muscle Additional unfavourable factors in facet interlocking
spasm. Because the sagittal diameter of the spinal canal predisposing to cord lesions are a small natural width
is not reduced, hyperflexion sprains only very rarely of the spinal canal and cervical spondylosis, with con-
produce cord deficit. Temporary root deficit, however, sequent narrowing of the spinal canal.
may occur, probably as a result of stretching of roots. In elderly patients there is a more parallel displace-
Hyperflexion sprains are also called «anterior ment of the dislocated cranial vertebra due to
subluxations», with the term subluxation being com- degenerative bi-section of the intervertebral disco The
monly used to cover a situation in wich there is partial sagittal diameter of the spinal canal is then severely
disruption of the articular surfaces. It is, however, very reduced, so that almost all elderly patients with bilateral
difficult to establish a borderline between maximal facet interlocking have a complete cord lesiono
physiological excursion and partial disruption ofthe sur- Most patients with facet interlocking have root le-
faces, and the diagnosis of «subluxation» has therefore sions too, but in case of a complete cord lesion it is
led to much confusion and to the incorrect treatment very difficult clinically to distinguish the root lesion
of spinal injuries. Consequently, we prefer not to use from the cord lesiono
this term, particulary if the traumatic nature of a par- Compressive hyperflexion. In compressive
tial disruption is definite. hyperflexion there exists a combination of a hyperflec-
Facet interlocking occurs if the articular facets loose ting and an axially compressing force, for instance by
contact, override, and, while springing back after in- a blow on the back of the head and neck. This force
jury, become interlocked (fig. 5). This interlocking may is transmitted along the spine and may result in a
be unilateral or bilateral. Facet interlocking is an ex- hiperflexion fracture dislocation. In the more severe
ample of a «dislocation», a complete and permanent forms of compressive hyperflexion the anterior part of
disruption of the normal contact -between articular the vertebral body tends to be pinched off (teardrop frac-
surfaces. ture), while the posterior part displaced backwards into

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\f~.·ú52.~
·.• .·•'~.-'•· . ,
/fíl·.··
\,¿:;}
' L-.5-,. ~
I ..

Figure 5.-Facet interlocking. Left: in a younger patient with an intact anterior longitudinal ligament the pincer's mechaninsm of cord compression is
not so evident as Right: in case of older patients with more parallel displacement of the dislocated vertebra.

235
Mechiínism and pathophysiology of spinal and spinal cord injury Neurocirugía

the spinal canal (fig. 6). (9,15,31) The backward displace- tures the posterior ligamentous complex is not so
ment of the posterior part of the vertebral body is seriously damªged or may be intacto (1,9,15)
facilitated by a rupture of the caudally bordering disco Traumatic Disc Prolapse. Many cases of traumatic
The vertebral body ofien shows vertical fractures. disc prolapse in the lower cervical spine have been
reported in connection with cervical spine injuries
although the incidence of this injury remains uncertain.
Such prolapse occurs particularly in combination with
distractive and compressive hyperflexion injuries. (9,31)
These disc prolapses can be revealed on CT-
myelography and on MRI. (15)
Figure 6,- The mechanism in a compressive hyperflexion injury. Note the
In hyperextension injuries the disc is ofien tom but
backward displacement ofthe posterior part ofthe vertebral body, resulting this tearing is mainly anterior, and it is highly im-
in sagittal narrowing of the diameter of the spinal canal. There is also a
teardrop fracture on the antero-inferior border of the vertebral body.
probable that in these injuries the disc ever prolapses
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into the spinal canal. The traumatic disc prolapse has

been linked with the anterior cervical cord syn-
Compressive hyperflexion injuries are notorious drome. (29) However, we have seen such prolapses in
for producing a high incidence of severe spinal cord combination with all types of cord injury.
lesions due to sagittal narrowing of the spinal canal with Distractive hyperextension. The relative weakness
«contact pressure» of the ~ord. More than half of our of the intervertebral disc is an important contributing
patients with such injuries had complete cord factor in the genesis of distractive hyperextension in-
lesions. (9) juries of the cervical spine. They occur particularly in
Axial compression. In the case ofaxial compres- elderly patients with spondylotic changes ofthe spine.
sion (with slight anteflexion) of the lower cervical spine, The disc has been bisected by the process of
the simplest type of injury is a slight wedge-compression degenerative secondary joint formation. Forced
fracture of the vertebral body, which may result in sorne hyperextension of the cervical spine may result in rup-
kyphotic angulation. ture of the anterior longitudinalligament and of the in-
Such wedge-compression fractures must be differen- tervertebral disc, with a significant backward displace-
tiated from the flartening of vertebral bodies that results
from the degenerative changes in cervical spondylosis.
The larter «platyspondylia» is particularly observed in
the vertebral bodies of CS, C6 and C7.
Such degenerative changes, and the super-
imposition of transverse processes on the lateral
radiograph, may cause errors in interpretation and
simulate nonexistent compression fractures of vertebral
bodies. These wedge-fractures have usually an intact
posterior ligament complex and intervertebral disco a
Therefore these fractures are commonly stable, do not
narrow the spinal canal, and are not accompanied by
neurological deficit unless there is an additional
traumatic disc prolapse.
More severe axial forces produce burst fractures.
Most burst fractures are also stable because the posterior
ligaments and capsules have remained intacto The bone
fragments, however, may impinge upon the cord,
resulting in transient to permanent severe neurological
deficit. b
In compressive hyperflexion injuries the posterior
Figure 7,-Distractive hyperextensio(l may result in tearing ofthe anterior
ligament complex is usually tom, resulting in an addi- longitudinal ligament and subsequendy in posterior displacement of the
tionallocal kyphotic angulation. In typical burst frac- cranial vertebra with pinching of the cord,

236
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

ment of the cranial vertebral body. The portion of the of the vertebral body (fig. 8), a bony pincer's
spine above the separation moves backwards and pin- mechanism that would compress the cord in the sagit-
ches the cord between the inferior posterior border of ta direction does not occur. (15) Therefore, the
the dislocating body and the leading edge of the arch neurologic deficit in the majority of cases is either rnild
ofthe vertebra below (fig. 7). When the traumatic force or non-existent, in contrast with the situation in com-
is removed, however, there is commonly spontaneous pressive hyperflexion injuries in which the arch rernains
realignment of the spine. Radiographs made subsequent- intact and the cord is ofien subjected to bony pinching
ly to this usually appear normal, although there may or contact pressure (fig. 8). -
be a widening of the shadow of the prevertebral soft
tissues, outlined anteriorly by the airway and posteriorly
by the cervical skeleton. (26) In the injured spondylotic
segments the sagittal diameter of the spinal canal is - INJURIES üF THE THÜRACIC,
due the spondylotic osteophytes- smaller than average, THORACOLUMBAR AND LUMBAR SPINE
and as a result of this the cord has less «play» within
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the spinal canal, with consequent earlier pinching of

and damage to the cord. (9) These distractive hyperex- Nowadays the most common c1assification ofthese
tension injuries (hyperextension dislocations and injuries is based on the three column concept by Denis
hyperextension sprains) may also occur in younger pa- (fig. 9) (table 2).(11)
tients wo have canals that are constitutionally narrow.
This predisposes to serious neurologic damage in minor
spine injuries. .
Hyperextension injuries can be recognized because
many of these patients have facial wound, broken man-
dibles, and fractures of the nasal bone.
Compressive hyperextension injuries are
characterized by compression fractures of the articular
processes of the vertebrae and anterolisthesis of the up-
per vertebral body relativeto the lower body
(fig. 8).(1, 9, 15) Such compressive hyperextension
fracture-dislocations occur particularly in younger pa-
tients who have intact intervertebral discs.

Figure 8.-A compressive hyperextension injury. There are fractures ofthe

articular facets. The upper vertebral body shows anterolisthesis relative to
the lower body. There is no narrowing ofthe spinal canal, no bony pincer's
mechanism.

The hangman's fracture is an example of such

hyperextension fracture-dislocation, but in the upper
cervical spine. These injuries also occur in the lower
cervical spine. Since the arch of the dislocated vertebra Figure 9.- The three columns in the concept of Denis. Top: anterior col-
usually fractures before there is anterior displacement umn. Middle: middle column. Bottom: posterior column.

237
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

Tabla 2 injuries of the thoracic and lumbar spine. They result

from axial compression with damage to the anterior and
middle column of the spine. The nucleus pulposus im-
type columns mechanism vertebral ring neurology plodes through the end-plates of the adjacent vertebral
bodies, in particular the supra-adjacent vertebral body.
wedge a-m+p+ compressive intact none
Posteriorly displaced bone fragments may impinge
compression fiexion
on or penetrate the ventral surface of the cord or cauda.
fracture axis: middle
Burst fractures may be stable, if the interfacetal joints
and the posterior ligament complex remain intact.
burst a-m-p axial broken, often in 50%
The spinal canal is narrow and in a relatively large
fracture compression repulsion of neuro!.
percentage of patients with a burst fracture there is
axis: posterior bone fragments deficit,
neurological involvement, which may be incomplete or
in spinal canal sometimes
complete.
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complete
The fracture-dislocation is another common
type of injury. All three columns of the spine are
fracture a-m-p- translation with obstruction neuro!.
disrupted, due to translation forces in combination with
dislocation distraction, spinal canal deficit in
axial compression or distraction and/or torsion.
compression, 75% about
Radiologically there is usually an anterior dislocation
torsion 50% comp.
and angulation of the cranial vertebra with detachment
axis: varying
of an anterosuperior wedge fragment from the body of
the lower vertebra. This results in a marked deforma-
seat-belt a+m-p- distraction intact sometimes
tion of the spinal canal. About half of the patients have
injury fiexion deficit
complete cord or cauda lesions, and in another 25 per-
axis: anterior
cent of these cases partial cord or root involvement
Classification of injuries of the thoracic and lumbar spine according to Denis. (11) exists.
= anterior column
a The so-called seatbelt injury is a characteristic
= middle column
m injury, commonly occurring at L2 or L3. The person
p = posterior column retained in the seatbelt suffers a sudden deceleration
+ = intact in an automobile or airplane crash with the kynetic
- = lesion energy of the upper trunk and torso, causing sudden
flexion and distraction centred at the mid-Iumbar
spine about the fulcrum of the seatbelt on the anterior
abdominal wall. (32) Patients with these fractures
Simple compression fractures of the vertebral body, ofien have no cord or cauda demage and for that reason
due to axial forces, usually do not show neurological this type of injury may initially not be diagnosed
involvement because the spinal canal is not compromis- in patients who have concomitant head injuries or
ed (fig. 10). Burst fractures account for about 50% of other severe extracranial injuries. Extension injuries are
rareo
Most injuries to the thorack (Tl-TlO) and
thoracolumbar (TU-U) spine are due to automobile and
motorcycle accidents, falls, suicidal attempts and mine
accidents. (22) Most patients are young. Injury to the
T-I-TlO and TU-U vertebrae occur with about equal
frequency.
Only a small percentage of injuries to the spine
occur between L2 and L5. These injuries are also
mainly burst injuries or fracture dislocations. They
may be due to direct impact or to vehicular acci-
Figure 1O.-Compression fracture ofvertebral body - in this drawing ofthe
cervical spine. There is no sagittal narrowing ofthe spinal canal and therefore dents. Acute traumatic spondylolisthesis is highly un-
no neurological deficit. common.

238
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

INJURIES TO THE CORD AND CAUDA Transient symptoms have been attributed to a relative
vertebral artery insufficiency (30) resulting from com-
The neurological deficit in injuries of the spine may pression or spasm of the vertebral artery or of the
be due to lesions of the cord, cauda, roots or to two anterior spinal artery.
orall three of these. Lesions of the spinal cord and
cauda may be temporary results of spinal shock or per- Pathology
rnanent injuries resulting from structural damage.
The primary traumatic lesion, resulting directly
Primary Damage and at the moment of injury from a mechanical impact
on the spine, includes laceration of the dura and men-
Damage to the cord is a direct result of the impact,
inges, extradural, intradural, and subarachnoid hemor-
the primary damage, but also due to e.g. persisting com- rhage, and damage to the cord and spinal roots. Most
pression of the cord or to intrinsic vascular and spinal cord lesions are spread over more than one
rnetabolic changes in the cord itself, the so-called secon- segmento
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dary damage. Traumatic extradural hemorrhage is rare and is

Primary damage to the cord is usually due to com- hardly ever a primary cause of compression of the cord.
pression, but may also be due to overstretching or to Subdural hemorrhage does occur, but does not com-
insufficient circulation. press the cord. Subarachnoid hemorrhage is common,
The compression of the cord or cauda may occur
particularly when the cord is lacerated or contused or
either from opposite sides (pinching) or from one side when roots are avulsed.
(contact pressure).(I,9) Such compression is common-
In autopsies done in cases in which there was only
ly exerted by bone, but may also be due to a hematoma, brief survival following a spinal injury, microscopic
a prolapsed intervertebral disc, or even infolding changes in the cord are unusual or absent. In cases in
ligaments. In cervical spinal injuries there may be per- which survival lasted' from 1 day to 3 months, the
sistent pinching, such as from bilateral facet interlock- changes seen in the cord consist of wallerian degenera-
ing (fig. 5) or temporary pinching such as from hyperex- tion, macrophage removal of debris, and astrocytic
tension sprains (fig. 7). gliosis. (17) The neural tissue at the site of the injury is
One-sided anterior compression, «contact pressure»,
replaced with dense gliosis and there are on1y limited
may -in the cervical spine- beexerted by a herniated
regeneration phenomena which have no clinical
intervertebral disc, particularly in patients under 45 significance. (17) In surviving patients, a delayed
years of age with disruptive hyperflexion or hyperflexion
myelopathy may occur afier 5 to 10 years, with the for-
compression injuries.(9, 31) This type of compression
mation of cysts in the cord adjoining the site of an acute
may also be due to bone displacement, as in com- traumatic hemorrhagic necrosis in the center of the cord
pressive hyperflexion injuries (fig. 6) and burst
or at a distance from the necrotic site. In paraplegia,
fractures. such as that caused by thoracolumbar injury, these cysts
In thoracolumbar injuries the most common causes (<<posttraumatic syringomyelia») may develop rostral to
of cord and cauda damage are pinching due to defor- the lesion, particularly in the cervical region. (4,5)
mation of the spinal canallike in fracture-dislocations
and compressing bone fragments in the spinal canal,
Secondary Damage
that produce either contact pressure or pinching like
in burst fractures. Evidence from various laboratory experiments in-
Overstretching occurs when the cord is drawn out dicates that following trauma to the spinal cord a se-
over the anterior wall of the spinal canal, like in wedge- quence of events occurs that results in a variable degree
fractures of the thoracic spine, or in the case of a tear- of tissue autodestruction and progressive paraplegia. (2)
drop fracture. (9, 31) It has also been seen in excessive There occurs a progessive decrease in spinal cord
skull traction. blood flow in both grey and white matter within a few
Damage to the cervical cord has also been attributed hours afier asevere spinal cord contusion or compres-
to local impairment of the blood supply to the cord or sion injury. Failure to maintain SCBF leads te ischemic
to impaired venous drainage. (17) However, while the hypoxia and rapid tissue destruction, which is believ-
vertebral artery may be damaged in cervical injuries, ed to be due to the occurrence of oxygen free-radical
ruptures and thrombosis of the artery are rareo (9,18) lipid peroxidative reactions. There is a marked deple-
239
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

tion of high energy phosphate reserves, lactic acidosis Patients who received a regirnen of 2 g of
and tissue edema. (2) methylprednisolone (30 mg per kilogram of body
This degree of ischaemic response is positively cor- weight) as an inmediate loading dose + 5.4 mg per
related with the severity of injury and it is negatively kilogram for the next 23 hours had improvement in both
correlated with the extent of posttraumatic functional motor and sensory scores as compared with those
recovery. (12,33,34) receiving placebo. The improvement was modest but
It is generally accepted that in order to promote also occurred in complete tetraplegia. In patients with
recovery after spinal cord injury, an attempt must be made anterior cord syndromes high dose of corticosteroids
to prevent this process and in particular the posttraumatic had no apparent benefit.
cord ischemia. This is particulary true of the white matter Patients treated with naloxone, or with methylpred-
since functional recovery depends upon the preserva- nisolone more than 8 hours after their injury, did not
tion of the long ascending and descending tracts. differ in their neurologic outcomes from those given
Spinal cord injury involves mechanical damage to placebo.
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axons. Young and co-Workers (34) have stressed that a This advance in the management of the secondary
large proportion of the axons at the lesion site must die damage of acute spinal cord injury is a modest step,
or become disconnected as a direct result of mechanical but welcome,OO) and has stimulated further research in
damage, no matter how attractive the theories concer- this field.
ning secondary nonmechanical injuries to axons may We should not forget, however, that the most fre-
sound. The number ofaxons that can be salvaged by quent and important cause of preventable cord damage
any pharmacological treatrnent must be limited in cases is a persisting cord compression which has not been
of severe spinal cord injury. «However, the finding of detected, due to insufficient use of diagnostic procedures
walking animals with 10 % of spinal axons imparts a and because we did not consider the possibility. Three
breath of optimism in this otherwise dismal pic- examples:
ture». (34) This fact suggests that saving or regeneration 1. A patient with an odontoid fracture and an im-
of as little as 5-10 % ofaxons in the spinal cord may complete cord lesion due to a fracture disloca-
restore sorne function in spine-injured animals. tion C6-C-7, which was missed because of over-
Laboratory fmdings suggest that treatrnents that can pre- projection of the shoulder on the lateral X-rayo
vent 5-10% ofnondisrupted axoris at the lesion site from Incomplete cord lesions are only rarely the result
dying may restore sorne motor and sensory function. of an odontoid fracture: there should be a careful
There are 1ikely to be a large number of phar- scrutiny of the lower cervical spine.
macological approaches to this goal. 2. An elderly patient with a serious incomplete
Here only one approach which has resulted in a transverse cord lesion, due to a detectable
practical and successful application in man will be men- hyperextension sprain C5-C6. This patient was
tioned. treated in supine position without pillow under
Faden et at<'2) has speculated that endogenous the head. This neck position induced repeated
opiates (endoendorphins) might be re!eased by traumatic pinching of the cord.
spinal injury and contribute to the ultimate neurologic 3. A patient with a burst fracture T12-U in whom
impairment by critically reucing spinal cord blood flow through a dorsal approach part of the indriven
during the first hours after injury. To test this hypothesis bone fragments were removed. However,
they did animal experiments in cats inducing an in- anteriorly localized bone fragments were left in
complete cervical spinal cord injury and tested the ef- place as was a herniated intervertebral disc in the
fects of naloxone and TRH. Both drugs were highly spinal canal.
effective in improving neurological recovery in ex-
perimental animals. Others did animal experiments
testing the efficacy of megadose methylprednisolone (60 SPINAL SHOCK
mg/kg/24 hours) and could prove a positive result that
has led to human application. (3) Recently, the results The term spinal shock was introduced by Marshall
of a randomized controlled trial of methylprednisolone Hall in 1841 to indicate the state oftransient inexcitabili-
in the treatment of acute spinal cord injury were ty or hypoexcitability of the isolated spinal cord below
reported. (10) the level of a transection of the cord.(lO) Spinal shock

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 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

may be due to the loss of facilitation from descending patients with such lesions can survive for a considerable
tracts, to persisting inhibition from below the transec- time and even breathe spontaneously during part of the
tion acting upon extensor reflexes, or to the axonal day with the use of their remaining auxiliary respiratory
degeneration of interneurons. (10) The intensity and muscles the trapezius, sternocleidomastoid, and
duration of the shock depend on the level of the platysma. They may also be able to move about in a
organism on the vertebrate scale; the higher the degree specially adapted, electrically driven wheelchair. As
of cerebral development the greater the shock. In spinal a rule, however, the life expectancy of patients with such
shock the motor paralysis below the level of the lesion very high tetraplegic injuries is greatIy shortened.
is at first of a flaccid type, even if the paralysis is of Below C4. In the acute stage of injuries below the
the upper-motor neuron type. All cutaneous and ten- C4 level diaphragm function is usually impaired, but
don reflexes below the level of the shock are greatIy may recover. The arms of the patient are paralyzed and
depressed or abolished, although bulbocavernosus and the shoulders are drawn up by the action of the levator
anal reflexes may persisto When the shock subsides the scapulae and trapezius muscles. The neck and a small
refiexes return. In humans the duration of the arefiex- area of the anterior aspect of the upper arm have nor-
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ia varies, with reflex activity sometimes appearing mal sensation; the rest of the body has a complet loss
within a period of 3 or 4 days in children or after 3 of sensibility.
to 6 weeks in adults. The first refiexes to return are the Below CS. Patients with lesions below C5 may also
anal and bulbocavernosus reflexes. (14) As a rule, fur- need artificial respiration. In such injuries the shoulders
ther refiex return is in a headward direction. However, are elevated, the arms abducted, and the forearms flexed
return of the knee jerk refiex may precede that of the owing to uninhibited action of the deltoid, biceps, and
ankle jerk. brachialis muscles. Contractures of the elbow easily
develop, and the forearms should thus be kept in ex-
tension and the arms in abudction.
TRAUMATIC CORD SYNDROMES Below C6. With injuries below C6 there is usually
sufficient respiratory function for spontaneous
Cord lesions can be differentiated into complete le- breathing; tracheostomy and artificial ventilation are
sions and various types of incomplete lesions. only rarely indicated. The hands show radial deviation
due to the action of the extensor carpi radialis muscles,
Complete cord lesions but are paralyzed.
In the acute stage of complete cord lesions there Below C7. The hand and finger extensors and fiex-
exists a total fiaccid paralysis with fullloss of tendon ors are functional in the case of injuries below the C7
refiexes and of sensibility below the level of the injury. vertebra, but the interossei and sorne opposing muscles
The cremasteryc, sphincter ani, and bulbocavernusos are greatIy reduced in power. This usually results in
refiexes may persist for sorne time after the injury and a claw hand. Most of these patients are able to write,
then disappear. The plantar fiexion response is ofien to feed themselves, to type and, after adequate train-
absent or takes the form of a flexorvariant with a pro- ing, to sit in a wheelchair with good balance, and can
longed interval between the stimulus and the response. even take up wheelchair-bound athletic activities.
Alternatively, it may persist for a few hours after the Thoracic leve!. The lower a transverse lesion is
injury or reappear after 1 or more days usually only localized, the greater number of intercostal muscles that
to disappear again and give way to an extensor plantar function normally. Patients with complete cord lesions
response. (9) aboye T5 have, especially initially, impairment of
The neurologic deficit in complete cord lesions is vasomotor control, which results in postural hypoten-
determined by the level of the lesiono (14) sion when they move from a horizontal to an upright
Cl to C4. With cord lesions at the CI to C4 level position. (14) In patients with complete cord lesions
the diaphragm is paralyzed as a result of interruption below T6 sorne of the abdominal muscles may retain
of the segmental innervation of the phrenic nerve. intact function.
Because all respiratory muscles below the transection Epiconus and Conus. Patients with epiconal and
are also paralyzed, lesions at this level willlead to death conal injuries may have a paralysis of the legs of the
within a short time unless artificial respiration is ap- upper- or of the lower- motor-neuron type. lnitially,
plied irnmediately. With modern management regimes they usually have urinary retention. Ultimately, plan-
241
 Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía

tar extensor responses and spasticity may develop when posterior columns are supposed to contain supranuclear
cord lesion supervenes. fibers for the neck and arms; the lateral parts are sup-
posed to contain fibers for the thoracic, lumbar, and
Incomplete Lesions of the Cervical Cord sacral segments. This explains why a central cord lesion
There are various types of incomplete cervical cord primarily affects the upper part of the body. This theory
lesions. The various clinical syndromes appear to be assumes that the motor impairment of the arms that is
interrelated and extensions of one another. They are not seen in the central cord syndrome is due to supranuclear
due to different mechanisms but represent a progres- lesion; in our experience, however, this may also be
sion in the magnitude of the applied forces with increas- the result of involvement of the anterior horns. (9)
ing severity of injury.(9, 27) A root syndrome is the least Brown-Séquard Syndrome. The Brown-Séquard
serious clinical definable pattern. With greater force syndrome indicates a lesion of one lateral half of the
a central cord syndrome results, followed by the anterior spinal cord. It is characterized by an ipsilateral paresis
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cord syndrome and finally a complete syndrome. Obli- and loss of propioceptive sensation, with sensory ataxia
que forces can produce Brown-Séquard syndromes. below the level of the lesion and contralateral loss of
Variations in clinical syndromes are caused by the pain and temperature sensation. The syndrome is rarely
magnitude and direction of the applied force of injury. encountered in its pure form or with blunt injuries, yet
Anterior Cord Syndrome. The anterior cord syn- it is nevertheless cornmon enough to classify many cord
drome (9, 29) is characterized by inmediate complete lesions as producing the Brown-Séquard syndrome if
paralysis with hypesthesia and hypalgesia below the there is an asyrnmetric paresis of the lower extremities
level of the injury, but with preservation oi the touchy, with analgesia or hypalgesia on the least paretic side.
motion, position, and vibration senses. The syndrome A slowly progressive Brown-Séquard syndrome sug-
is most ofien seen in hyperfl.exion injuries of the cer- gests spinal cord compression on one side, such as by
vical spine and also occasionally in thoracic injuries. a prolapsed intervertebral disco
Central Cord Syndrome. The central cord syn- Contusio Cervicalis Posterior. A reversible traumatic
drome (30) is characterized by disproportionally greater syndrome of the cord, characterized by pain, tinglind,
motor impairment of the upper than of the lower ex- and hyperesthesia in a multisegmental area of the neck,
tremities. There may be bladder dysfunction and vary- arms, and hands, but sometimes also in the trunk, has
ing degrees of sensory loos. In milder variants of the been designated «contusio cervicalis posterior».(9) 1 is
syndrome, paresis of the arms or hands is combined a cornmon, mild, and reversible cord syndrome.
with sorne weakness of the legs; in severe variants the Other Lesions. Besides the patterns described
arms or hands are paralyzed and the legs are paretic.(9) above, there are other, lees cornmon patterns of cer-
In the patients with the latter type there may be sen- vical cord lesions, such as the bulbar cervical dissocia-
sory loss involving all modalities, and urine retention tion pattern, the onionskin pattern, and other patterns
is always presento This form of the syndrome is that are more difficult to categorize. (9,30) Additionally,
predominantly seen in hyperextension injuries, but may one or more cervical roots are ofien involved in cer-
also occur in hyperflexion injuries.(9) vical spine injuries, particulary in cases of unilateral
Several hypotheses have been put forward to explain or bilateral facet interlocking.
the predominant localization of lesions in the central
part of the cord, including sorne based on the relative- Thoracic Cord Lesions
ly loose texture and rich vascularization of the central More than 85 percent of patients with a thoracic
cord region which allows the extension of edema and injury and a cord lesion have a complete cord lesiono (~
hemorrhage along the central canal in a longitudinal 7,21,24) Fewer than 10 percent of these patients show any
direction. Other hypotheses attach signficance to a
further improvement, particulary of a sensory nature.
relative vascular insufficiency in the terminal area of
Incomplete lesions cornmonly produce the anterior
the anterior spinal artery. The discrepancy in motor im- cord syndrome.
pairment of the arms and legs that is seen with central
cord lesions has been explained by Schneider et alYO)
Conus and Cauda Lesions
as being due to the somatotopic division of the lateral
and posterior columns of the cord. The central areas Patients with fracture-dislocations or burst fractures
of the lateral pyramidal tracts, spinothalamic tracts, and of the thoracolumbar area may have cord or cauda

242
 Mechanisrn and pathophysiology of spinal and spinal cord injury Neurocirugía

equina lesions. About 60 percent of these patients have Most late progressive cord lesions are due to a per-
complete lesions and another 40 percent incomplete le- sistent deformation of the spinal canal. The lesion oc-
sions. In the acute state following an incomplete lesion, curs in that segment of the cord that rides over the
it is very difficult to assess whether part of the conus backward-projecting upper margin of a body of a lower
or sorne roots have escaped damage. The fracture- vertebra, as in badly healed cervical compression-
dislocation injury in particular yields a high propor- fracture disolocations with major kyphotic angula-
tion of complete lesions. (6.7.24) tion. (7) Another cause for a late progressive cord le-
The wide variation in the neurologic picture en- sion may be a prolapsed disc or a non-united fractured
countered in thoracolumbar lesions is mainly due to odontoid process with atlantoaxial instability and in-
a variation in the exact vertebrallevel of the conus and termittent pinching of the cord between the
cauda. Moreover, the forro and capacity of the vertebral superoposterior border of the body of the axis and the
canal may vary widely. The common demoninator in posterior arch of the atlas. (9) In 1 10 2 percent of pa-
patients with thoracolumbar injuries and involvement tients with paraplegia the cause of a delayed cord le-
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of the cord, cauda, or both is the presence of bone in sion is the development of an intramedullary cyst. (4.5)
the spinal canal. In such post-traumatic syringomyelia, the simptoms are
In injuries of the lumbar anda lumbosacral spine usually loss of pain and temperature sensation over
the neurologic symptoms result from lesions of the several segments of the cord rostral to the original in-
cauda equina. jury site. In thoracolumbar spinal injuries the cyst may
extend to the cervical region.
Progressive Cord Lesions Initially, most of the symptoms and signs created
Neurologic symptomatology is usually maximal by the cyst are unilateral, but become bilateral latero
directly after an accident with injury to the spinal cord, The pathogenesis of post-traumatic intramedullary cysts
and may then persist or gradually disappear, either com- remains controversial although abnormal pulsations of
pletely or partly. Sometimes, however, neurologic symp- cerebrospinal fluid (CSF) acting on the central canal
toms develop or increase in serverity at sorne time after are considered to be of considerable importance in their
the original injury. This usually happens within the first origino (4.5)
few days, but it may start moríths or even years after
the accidento The most common manifestation of such
progressive injury is an elevation in the level of the le- References
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