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 belowthis 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 cont’d

• 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?

What’s 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-Séquard 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 he’s got “the

rheumatism some bad in his legs” with the crazy weather these days

• His wife tells you “he’s wetting himself” which is unlike him

• He seems to be having lots of trouble riding his bike because he thinks the bike seat isn’t 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. Treatment must begin within 8h of injury2. Methylprednisolone 30mg/kg bolus iv over 15

minutes3. 45 minute pause post bolus4. 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

3-8h of injury• Worse outcome if started 8h post injury• Conflicting evidence re benefit therefore

more trials required

Pros Cons• Believed to inhibit

formation of free radical-induced peroxidation

• May increase spinal cord blood flow

• Increase extracellular calcium

• Prevent potassium loss from cord

• Pneumonia• Sepsis• Wound infection• GIB• Delayed healing

NASCIS IBracken 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 IIBracken 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 IIIBracken 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 0.45-

35.58)– 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