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Mechanism and Pathophysiology of Spinal and Spinal Cord Injury
Mechanism and Pathophysiology of Spinal and Spinal Cord Injury
R. Braalanan
Rotterdam, the Netherlands
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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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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
Type 11
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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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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. :
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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
.,.f\~' ~
\f~.·ú52.~
·.• .·•'~.-'•· . ,
/fíl·.··
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' L-.5-,. ~
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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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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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237
Mechanism and pathophysiology of spinal and spinal cord injury Neurocirugía
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.
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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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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
240
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
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