Spinal Cord Syndromes

Resident Rounds
April 12, 2007
Juliette Sacks

Anatomy
Spinal cord ends as
conus medullaris at
level of first lumbar
vertebra
lumbar and sacral
nerve roots exit below
this and form the
cauda equina

Neuroanatomy
Corticospinal tracts
Spinothalamic tracts
Dorsal (posterior) columns

Corticospinal Tract
Descending motor pathway
Forms the pyramid of the medulla
In the lower medulla, 90% of fibers decussate
and descend as the lateral corticospinal tract
Synapse on LMN in the spinal cord
10% that do not cross descend as the ventral
corticospinal tract
Damage to this part cause ipsilateral UMN
findings

Spinothalmic Tract
Ascending sensory tract from skin and
muscle via dorsal root ganglia to cerebral
cortex
Temperature and pain sensation
Damage to this part of the spinal cord causes:
Loss of pain and temperature sensation in the
contralateral side
Loss begins 1-2 segments below the level of the
lesion

Dorsal (Posterior) Columns

Ascending neurons that do not synapse until
they reach the medulla at which point they
cross the midline to the thalamus
Transmits vibration and proprioceptive
information
Damage will cause ipsilateral loss of vibration
and position sense at the level of the lesion

Complete vs Incomplete
Incomplete:

Sensory, motor or both functions are partially

present below the neurologic level of injury
Some degree of recovery

Complete:

Absence of sensory and motor function below the

level of injury
Loss of function to lowest sacral segment
Minimal chance of functional motor recovery

Light touch
Transmitted through both the dorsal
columns and the spinothalamic tracts
Lost entirely ONLY if both tracts are
damaged

Case #1

33 yo F fell off a 20 cliff snowboarding

C/o inability to move both legs
GCS 15 BP 130/68 HR 89 regular
Normal UE exam
No power in LE
Vibration and position sense normal in LE
Sensation normal in LE
No rectal tone or perianal sensation

Anterior Cord Syndrome

Damage to the corticospinal and
spinothalamic tracts
Dorsal column function is intact
Loss of:
Motor function
Pain and temperature sensation

Vibration, position and crude touch are

maintained

ACS contd
Causes:

Direct injury to anterior spinal cord

Flexion injury of cervical spine causing a
cord contusion
Bony injury causing secondary cord injury
Thrombosis of anterior spinal artery

Symptoms
Complete paralysis below the level of
the lesion with loss of pain and
temperature sensation
Preservation of proprioception and
vibration sense

What to do?
Urgent CT/MRI
Surgical decompression may be an
option
Prognosis: POOR

Case #2
24 y.o. M came off motorcycle at high speed
Wore no helmet and sustained severe head
injury
C-spine films were unremarkable apart from a
narrow spinal canal
Once conscious, he was quadriparetic with
2/5 power in most muscle groups
No other neurological findings

Where is the lesion?

Whats the deal?

MRI:

Mild swelling of the cord at C3/4

Prevertebral soft tissue swelling and
disruption of anterior longitudinal ligament

Prognosis:

Within 48h, power in UE 3/5 and LE 4/5

At 2/12, further but not full recovery

Central Cord Syndrome

Older patients
Preexisting central
spondylosis
Hyperextension injury
Injury affects central cord>
peripheral cord
Damage to corticospinal
and spinothalamic tracts
Upper extremities>thoracic
>lower extremities>sacral

CCS
Present with:

Decreased strength
Decreased pain and temperature sensation
Upper>lower extremities
Spastic paraparesis/quadriparesis
Maintain bladder and bowel control

Prognosis: GOOD

Although fine motor recovery of the upper

extremities is rare

Case #3
24 y.o. M stabbed in the
neck during stampede
argument over whose
doolie tires were bigger
No LOC
C/o inability to pick up his hat with his left
hand
Unaware of his girl holding his right arm

Brown-Squard Syndrome
Hemisection of the cord
Ipsilateral loss of:

Motor function
Proprioception and vibration sense

Contralateral loss of:

Pain and temperature sensation

BSS
Caused by:

Penetrating injury
Lateral cord compression from:

Disk protrusion
Hematomas
Bone injury
Tumours

Prognosis: GOOD

Case #4
76 y.o. Grandpa says hes got the
rheumatism some bad in his legs with the
crazy weather these days
His wife tells you hes wetting himself which
is unlike him
He seems to be having lots of trouble riding
his bike because he thinks the bike seat isnt
under him when it actually is

Cauda Equina Syndrome

Peripheral nerve injury to lumbar, sacral and
coccygeal nerve roots
Symptoms:
Variable motor and sensory loss in lower
extremities
Sciatica
Bowel and bladder dysfunction
Saddle anaesthesia

Prognosis: GOOD

ED Stabilization
ABCs
Airway:

Low threshold for definitive airway in

patient with cervical spine injury especially
if higher then C5
Spinal immobilization very important

Spinal Shock
Loss of neurological function and
autonomic tone below level of lesion
Loss of all reflexes
Resolves over 24-48h but may last for
days
Bulbocavernosus reflex returns first

Spinal Shock
Symptoms:

Flaccid paralysis
Loss of sensation
Loss of DTRs
Bladder incontinence
Bradycardia
Hypotension
Hypothermia
Intestinal ileus

Hypotension
Must determine cause:

Spinal cord injury

Blood loss
Cardiac injury
Combination of above

Blood loss is the cause of hypotension until

proven otherwise!
Vitals are often non specific
R/O other causes with: CXR, FAST, CT

Neurogenic Shock
Neurogenic Shock:

Warm
Peripherally vasodilated
Bradycardic

Bradycardia may be caused by something

other than neurogenic shock
Cervical spine injury may cause sympathetic
denervation
Resuscitate with fluids +/- vasopressors

Corticosteroids
Controversial
Based on NASCIS trials
Methylprednisolone improved both
motor and sensory functional outcomes
in complete and incomplete injuries
Benefit dependent on dose and timing
of dose

Corticosteroids

NASCIS recommends:

1.
2.
3.
4.

Treatment must begin within 8h of injury

Methylprednisolone 30mg/kg bolus iv over 15 minutes
45 minute pause post bolus
Maintenance infusion 5.4mg/kg/h methylprednisolone
is continued x 23h

Evaluated in blunt injury only

Large doses of steroids in penetrating injury may
be detrimental to recovery of neurological
function

Steroid Therapy as per NACSIS

Attributed to antioxidant effects
Treat for 24h in patients treated within
3h of injury
Treat for 48h in patients treated within 38h of injury
Worse outcome if started 8h post injury
Conflicting evidence re benefit therefore
more trials required

Pros
Believed to inhibit
formation of free
radical-induced
peroxidation
May increase spinal
cord blood flow
Increase extracellular
calcium
Prevent potassium loss
from cord

Cons

Pneumonia
Sepsis
Wound infection
GIB
Delayed healing

NASCIS I

Bracken et al. 1984. Efficacy of

methyprednisolone in acute spinal cord injury,
JAMA, 251:45-52

Prospective, randomized double blind trial

with 330 patients
2 treatment arms:
100 mg bolus MP, then 25 mg q6h x 10 d
1000 mg bolus, then 250 mg q6h x 10 d
No sig difference in primary outcomes
4x increase in wound infections in high dose
group
Trend towards increased sepsis, PE, death
in higher dose group

NASCIS II

Bracken NEJM 1990; 322: 1405-11

DBRCT of methylprednisone vs naloxone

vs placebo (total N=487)
Methylprednisone 30 mg/kg bolus then 5.4
mg/kg/hr X 23 hours
Outcome = neurological function at 6
weeks and 6 months assess by a neuro
function score
NO benefit of naloxone

NO benefit of steroids overall

NO difference in mortality
Trend to more infections and GI bleeds with
steroids

NASCIS II
Post hoc SUBGROUP ANALYSIS
showed a benefit at 6 months in the
subgroup treated within 8 hrs

Improved motor score: 4 points (p < 0.03)

Improved Touch score: 5 points (p < 0.03)
Improved pin-prick score: 5 points (p < 0.02)

Concluded that steroids were indicated if

started within 8hrs
One year data showed similar improvement
in motor score but no difference in sensory
scores (Bracken. J Neurosurg 1992; 76; 23-31)

NASCIS III

Bracken JAMA 1997: 277(20); 1597-1604

DBRCT of methylprednisone 24hrs vs 48

hrs vs Tirilazad (total N=499)
NO placebo arm

Overall, NO difference between the

three groups
Post-hoc subgroup analysis: 48 hour
steroid group showed improved motor
scores at 6 weeks and 6 months if started
between 3-8hrs
6 weeks: 5 points motor score (p <0.04)
6 months: 4.4 points (p <0.01)

NASCIS III
Adverse outcomes

Severe pneumonia higher in 48hr group

2.6% vs 5.8% (p<0.02)

Severe sepsis higher in 48hr group

0.6% vs 2.6% (p< 0.07)

They concluded

Steroids indicated for SCI

If started within 3hrs, treat for 24hrs
If started within 3-8hrs, treat for 48hrs

Cochrane Review
the randomized trials of MPSS in the

treatment of acute SCI provide evidence for a

significant improvement in motor function
recovery after treatment with the high dose
regimen within 8 hours of injury
Bracken November 2000
Update in Spine 2001 by Bracken
4 trials and 797 patients randomized to get high
dose methylpred vs placebo for 24 hours

Cochrane Review Results

Primary outcome = neurological

improvement at 6 weeks, 6 months, 1
year
Complicated motor and sensory exam
High dose methylpred associated with
4/70 point increase in motor function
at 6 weeks, 6 months but not one year

SCI and Steroids

Clinical relevance?

4 points spread over 14 muscle segments unilaterally

Not validated score
No inter-rater reliability

Conclusions based on post-hoc analysis of small

subgroup from 1 trial
65 patients per arm
Data drudging
High risk of alpha error

Serious complications (not statistically significant)

GI bleed and wound infection (RR 4.00, 95% CI 0.4535.58)
Severe pneumonia (RR 2.25, 95% CI 0.71-7.15)
Range of values in CI huge do the risks outweigh the
benefits??

SCI and Steroids

Author consultant for Pharmacia (they
make methylprednisolone)
Weak support for use of high dose
methylpred in acute SCI + may be
increased risk of severe adverse
outcomes.

Bottom Line
CAEP position statement : steroids are NOT
STANDARD OF CARE
There is insufficient evidence to support the use
of high dose methyprednisolone within 8 h of
acute SCI
Significant harm to using steroids
NASCIS subgroup data needs to be validated in
prospective, randomized, blinded trials
No new literature to argue for or against this

Neurological Examination
LOC
Deteriorating course
Neck, back pain and/or bladder, bowel incontinence
should increase suspicion of sc injury
Define level of lesion
Motor function
Sensory level
Proprioception testing
DTRs
Anogenital reflexes

DI
C-spine films as per c-spine rules/nexus
CT
MRI: better for visualizing neurological,
muscular and soft tissue
If CT negative and patient has positive
neurological findings, this is next step
Important to image entire spine as 10%
have 2nd injury

Treatment
Prevent secondary injury
Alleviate cord compression
Establish spinal stability
Assess the neurological deficit and spinal
stability
Imaging
Consult spine/neurosurgery

Other cord lesions

Malignancy
Epidural hematoma
Abscesses

At the end of my rope

Urgent care necessary
MRI is better than CT for imaging spinal cord
Comprehensive serial neurological exams
important re management options
Steroids are not the standard of care in
Canada
Consider spinal shock, neurogenic shock and
other causes of shock in someone with a
spinal cord injury