CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY 27

Due to the onion-skin or Déjerine pattern of

topographic representation, a perioral distribu-
tion of sensory loss denotes a lesion in the lower
medulla and upper cervical cord, whereas a
more peripheral facial distribution of sensory
loss involving the forehead, ear, and chin denotes
a lesion in the cord at C3-4. Cervicomedullary
injuries often mimic the central cord syndrome
because of a greater weakness in the arm than
the leg.

Acute Central Cord Syndrome

Figure 3: Central cord syndrome. The drawing
depicts a case of cervical spondylosis with
osteoarthritis of the cervical spine including ante-
rior and posterior osteophytes and hypertrophy of
the ligamentum flavum. Superimposed is an acute
hyperextension injury that has caused rupture of
the intervertebral disc and infolding of the liga-
mentum flavum. The spinal cord is compressed
anteriorly and posteriorly. The central portion of
the cord shown in rough stippling sustained the
greatest damage. The damaged area includes the
medial segments of the corticospinal tracts pre-
sumed to subserve arm function. Reprinted with
permission from Tator.23
Schneider21,22 described the acute central cer-
vical cord injury syndrome characterized by a
disproportionally greater loss of motor power in
the upper extremities than the lower extremities
with varying degrees of sensory loss. He hypoth-
esized that acute compression was an etiological
factor in many cases such as cord compression
between bony bars or spurs anteriorly and in-
folded ligamenta flava posteriorly (Figure 3).
Table 5 shows the similarities and differences
between the central cord syndrome and the syn-
drome of cruciate paralysis. Clinically, it may be
very difficult to make this distinction. Fortu-
nately, the combination of plain films, computed

TABLE 5
CENTRAL CORD SYNDROME VS. CRUCIATE PARALYSIS WITH ARMS WEAKER THAN LEGS
Central Cord Syndrome Syndrome of Cruciate Paralysis

Site of Lesions Mid to lower Lower medulla and upper cervical cord,
Anterior horn cells anterior aspect
Lateral corticospinal tract Corticospinal decussation caudal to the pyramids
(medial part)
Clinical Arms weaker than legs Arms weaker than legs
Manifestations Flaccid arms acutely Flaccid arms acutely
Legs normal or variably weak Legs normal or variably weak
Lower motor neuron deficits Upper motor neuron deficits in upper limbs develop
in upper limbs persist ± Trigeminal sensory deficit (onion skin, spinal tract
of 5th cranial nerve)
± Cranial nerve dysfunction
(9th, 10th, or 11th cranial nerve)
Prognosis for Variable Usually good
Neurological
Recovery
28 CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION

tomography (CT), and magnetic resonance

imaging (MRI) can usually accurately localize
the lesion to either the mid to lower cervical
spine in the central cord syndrome or to the cer-
vicomedullary junction in the syndrome of cru-
ciate paralysis.7
There is recent evidence that syndromes
characterized by greater weakness of the arm
than leg are not based on previously enunciated
mechanisms such as the presumed differing lo-
cations of the arm and leg fibers in the corti-
cospinal tract.13 In contrast, the new explanation
is derived from careful clinical-pathological-
MRI correlations17 and of cases of SCI. The new
understanding is based on the finding that the
corticospinal tract subserves mainly distal limb
musculature and, thus, the functional deficit
Figure 4: Anterior cord syndrome. A large disc
would be more pronounced in the hands when herniation is shown compressing the anterior
the tract is the primary site of damage. aspect of the cord and resulting in damage (rough
It is of interest that Schneider initially ad- stippling) to the anterior and lateral white matter
tracts and to the grey matter. The posterior
monished against operating on individuals with columns remain intact. Reprinted with permission
central cord syndrome because of their good from Tator.23
prognosis for spontaneous recovery. Indeed, in
some instances, his patients showed very rapid
spontaneous clinical recovery. Furthermore,
Schneider reported deterioration following lam-
view, was “a syndrome for which early operative
inectomy in some patients. Although it is true
intervention is indicated.” The anterior aspect of
that a considerable number of patients with cen-
the cord is damaged and, in severe cases, there
tral cord syndrome make a substantial recovery
may only be sparing of the posterior columns
without surgery, many remain with significant
(Figure 4). In less severe cases, there may be
deficits,3 especially with serious impairment of
some retention of motor function due to sparing
the hands due to a combination of severe weak-
of some fibers in the lateral corticospinal tracts.
ness and severe proprioceptive loss. When there is
persistent compression, instability, or neurologi-
cal deterioration, a patient with central cord syn- Posterior Cord Syndrome
drome should be considered a surgical candidate. Posterior cord syndrome is a rarely seen type
of incomplete SCI syndrome. Many researchers,
Anterior Cord Syndrome including the author, have doubted its existence.
It supposedly occurs after major destruction of
Anterior cord syndrome was originally de- the posterior aspect of the cord but with some
scribed in the setting of acute cervical trauma by residual functioning spinal cord tissue anteriorly
Schneider,20 who presented two patients with (Figure 5). Thus, clinically, the patient has re-
“immediate complete paralysis with hyperesthe- tained spinothalamic function but lost move-
sia at the level of the lesion and an associated ment and proprioception due to damage to the
sparing of touch and some vibration sense.” posterior half of the cord, including the corti-
Both patients, one of which was a young football cospinal tracts and posterior columns.
player, had a ruptured disc (the football player
also had bone fragments in the canal), and both
made a substantial recovery following surgical
Brown-Séquard Syndrome
removal of the intracanalicular space-occupying The Brown-Séquard syndrome is caused by a
lesions (Figure 4). This syndrome, in Schneider’s lesion of the lateral half of the spinal cord (Fig-
 CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY
Figure 5: Posterior cord syndrome. A laminar frac-
ture is depicted with anterior displacement of the
fractured bone and compression of the posterior
aspect of the spinal cord. The damaged area of the
cord (roughly stippled in the upper diagram)
includes the posterior columns and the posterior
half of the lateral columns including the corti-
cospinal tracts. Reprinted with permission from
Tator.23
ure 6) and is characterized by ipsilateral motor
and proprioceptive loss and contralateral pain
and body temperature loss. The syndrome can
be associated with a variety of mechanisms of
injury, but in the series of Braakman and Pen-
ning4 was most often observed with hyperexten-
sion injuries; also reported were cases with flex-
ion injuries, locked facets, and compression
fractures.
The Brown-Séquard syndrome may be pres-
ent at the onset of injury in some patients; in
others, it may become apparent only several days
after injury as a gradual evolution from a bilat-
eral incomplete injury. Hybrid combinations
of Brown-Séquard and other incomplete syn-
dromes may occur. For example, the author has
seen examples of central cord injuries that are
quite asymmetric, with the more severely dam-
aged side of the cord showing features of a
Brown-Séquard syndrome. The Brown-Séquard
syndrome occurs most often following cervical
injuries and less frequently in the thoracic cord
and conus medullaris. In milder cases, there may
be no sphincter deficit.
29
Figure 6: Brown-Séquard syndrome. A burst frac-
ture is depicted, with posterior displacement of
bone fragments and disc, resulting in unilateral
compression and damage (rough stippling) to one-
half of the spinal cord. Reprinted with permission
from Tator.23
Conus Medullaris Syndrome
Almost all of the lumbar cord segments are
opposite the T12 vertebral body, and almost all of
the sacral cord segments are opposite the L1 ver-
tebral body with the cord ending opposite the
L1-2 disc space (Figure 7). Because injuries at
T11-12 and T12-L1 are relatively common due to
the mobility of these segments compared with
the relatively immobile thoracic segments, in-
juries to the conus medullaris are frequent. These
injuries usually produce a combination of lower
motor neuron deficits with initial flaccid paraly-
sis of the legs and anal sphincter. This is followed
in the chronic phase by a combination of some
degree of muscle atrophy and spasticity or reflex
hyperactivity with, possibly, an extensor plantar
response. The sensory picture may be variable,
and in some cases the only evidence of incom-
pleteness is retention of some perianal sensation,
which is an example of sacral sparing. In the
more severe conus lesions, bowel and bladder
deficits may be profound with the ultimate devel-
opment of a low-pressure, high-capacity neuro-
genic bladder.
30 CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION

Figure 7: Conus medullaris syndrome. A burst fracture of T12 is depicted

with posterior dislocation of bone fragments from the vertebral body into
the spinal canal resulting in compression of the conus medullaris. Almost
all the lumbar cord segments are opposite the T12 vertebral body, so that a
severe compression injury at this level could affect all lumbar and sacral
segments of the cord. Reprinted with permission from Tator.23

S1 roots may be present as well. Thus, these pa-

CAUDA EQUINA INJURIES
With the spinal cord normally terminating
opposite the L1-2 disc space (Figure 7), injuries
at this level or below involve the roots of the
cauda equina, although injuries one or two levels
above also involve the origins of some of the
roots comprising the cauda equina. Clinically,
these injuries may be complete (Grade A on the
new ASIA/IMSOP scale), whereas incomplete
injuries vary in severity and range from Grades
B to D. Similar to SCI, the motor fibers tend to
be more susceptible to trauma so that incom-
plete cases always have sensory preservation with
or without some motor preservation. Cases with
only motor preservation are extremely rare. The
degree of bowel and bladder deficits parallels
those found with cord injury. It is believed that
cauda equina injuries have a much better prog-
nosis for neurological recovery compared with
SCI because the lower motor neuron inherently
has more resilience to trauma, with fewer sec-
ondary injury mechanisms and greater regener-
ative capacity than the upper motor neuron and
its tracts.
One interesting and dangerous cauda equina
syndrome is associated with acute central disc
herniation at L4-5 or L5-S1 and results in major
damage to the sacral roots that lie centrally
within the dural sac (Figure 8). Partial or com-
plete sparing of the lumbar roots and often the
tients may have total preservation of leg strength
but complete bowel and bladder paralysis as well
as perineal anesthesia. The sacral roots are very
delicate and sometimes may not recover, even
when decompressed reasonably expeditiously.
REVERSIBLE OR TRANSIENT
SYNDROMES
There are a number of complete or incom-
plete SCI syndromes that are reversible or tran-
sient (Table 4). One of the most interesting is the
“burning-hands syndrome,” which frequently
occurs in athletes.28 The syndrome is character-
ized by transient paresthesiae and dysesthesiae in
the upper limbs, especially the hands. It may
exist with or without long-tract signs, which, if
present, are usually evanescent. Biemond2 found
pathological changes in the posterior horn of
one case and termed the condition “contusio
cervicalis posterior.” Braakman and Penning5
found that hyperextension was the most fre-
quent mechanism of injury. Intramedullary le-
sions may be demonstrable by MRI.28 Torg et al26
described a transient incomplete spinal cord
syndrome with sensory and motor deficits that
lasted up to 48 hours in football players and used
the inappropriate term “neurapraxia.” They
found that all of the patients had radiological
 CLINICAL MANIFESTATIONS OF ACUTE SPINAL CORD INJURY
Figure 8: Cauda equina syndrome. The drawing
shows an acute central disc herniation of L4-5 with
major compression of the central aspect of the
cauda equina. The medially placed sacral roots
from S2 downward sustain the maximal compres-
sion, whereas the more laterally located L5 and S1
roots are completely or partially spared. Reprinted
with permission from Tator.23
spinal abnormalities such as ligamentous insta-
bility, disc disease, or spinal stenosis. These tran-
sient cord injury syndromes are usually bilateral,
which distinguishes them from the other syn-
drome of “stingers” or “burners” in athletes due
to unilateral nerve root or brachial plexus lesions
(especially traction injury), most of which are
also transient.28
Spinal cord concussion is a transient loss of
motor or sensory function of the spinal cord,
with recovery of function usually within min-
utes but always within hours. In most instances,
the patient reports that the symptoms are rap-
idly diminishing and a normal neurological
examination is found. The exact pathophysiol-
ogy of spinal cord concussion is unknown, but
most likely is caused by a biochemical abnor-
mality in the cord such as leakage of potassium
from the intracellular to the extracellular space
due either to direct mechanical injury or sec-
ondary to a vascular mechanism. The latter pos-
sibility was suggested by Schneider et al.21
Acute Spinal Cord Syndrome
without Radiological Evidence
of Trauma
The syndrome of SCI without radiological
abnormality (SCIWORA) is more common in
31
children than in adults and represents a signifi-
cant percentage of pediatric SCIs.16 Children
with SCIWORA tend to be less severely injured
than those with definite evidence of bony injury,
although complete injuries have been described.
By definition, the negative radiological examina-
tion includes only plain films and tomography,
either conventional or CT. If a negative MRI was
included in the definition, the number of cases
would diminish dramatically, because of the
extreme sensitivity of MRI in detecting mild
cord injury and spinal column injuries such as
torn ligaments and ruptured discs. Children are
more susceptible to these injuries, presumably
because of the laxity of their spinal ligaments
and the weakness of their paraspinal muscles.
True SCIWORA can also occur in adults, but
is much less frequent than the syndrome of SCI
without radiological evidence of trauma (SCI-
WORET). In patients with SCIWORET, radio-
logical examinations are abnormal but x-rays
show no evidence of trauma. Prior to the use of
CT in spinal trauma, the incidence of SCI-
WORET in adults was approximately 14%.24 The
addition of CT has reduced the reported inci-
dence of SCIWORET to about 5%. There has
been a recent analysis of the incidence of SCI-
WORET in a Japanese study of acute SCI18 which
shows that many of these patients have demon-
strable compression by myelography or MRI and
should be considered for early surgical decom-
pression. It is likely that very few SCIs will re-
main undetected by MRI, because of its high
sensitivity for detecting mild SCI and nonbony
spinal column lesions. Cervical spondylosis is the
most common associated condition in adults
with SCIWORET, but other arthropathies (e.g.,
spinal stenosis, ankylosing spondylitis, and disc
herniation) may on rare occasion be associated
with SCI and not show radiological evidence of
trauma.
Trauma Patients with an Acute
Spinal Cord Syndrome but Without
Direct Trauma to the Spine
In some trauma patients, there is an acute
spinal cord syndrome but no direct trauma to
the spine. This relatively rare syndrome differs
from SCIWORET and SCIWORA in that these
32 CONTEMPORARY MANAGEMENT OF SCI: FROM IMPACT REHABILITATION
patients sustain a lesion of the spinal cord that
manifests as an acute spinal cord syndrome and
is associated with trauma although the trauma
is not to the spine. The syndrome can occur in
both children and adults and produces the clini-
cal findings known as the “anterior spinal artery
syndrome.” Keith11 described several cases in
children with major abdominal, thoracic, or
limb trauma and concluded that many had sus-
tained an aortic injury that caused occlusion of
intercostal or lumbar arteries with subsequent
occlusion of medullary arteries and spinal cord
infarction. Rarely, penetrating injuries such as
gunshot wounds can interrupt major arterial
feeders to the cord without direct trauma to the
spine. Severe hypotension and systemic shock in
trauma patients can also result in spinal cord
ischemia and infarction, even without causing
concomitant cerebral ischemia.
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