spinal cord syndromes
DESCRIPTION
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 - PowerPoint PPT PresentationTRANSCRIPT
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Spinal Cord Syndromes
Resident Rounds
April 12, 2007
Juliette Sacks
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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
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Neuroanatomy
• Corticospinal tracts
• Spinothalamic tracts
• Dorsal (posterior) columns
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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
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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
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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
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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
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Light touch…
• Transmitted through both the dorsal columns and the spinothalamic tracts
• Lost entirely ONLY if both tracts are damaged
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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
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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
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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
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Symptoms
• Complete paralysis below the level of the lesion with loss of pain and temperature sensation
• Preservation of proprioception and vibration sense
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What to do?
• Urgent CT/MRI
• Surgical decompression may be an option
• Prognosis: POOR
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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
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Where is the lesion?
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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
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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
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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
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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
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Brown-Séquard Syndrome
• Hemisection of the cord
• Ipsilateral loss of:– Motor function– Proprioception and vibration sense
• Contralateral loss of:– Pain and temperature sensation
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BSS
• Caused by:– Penetrating injury– Lateral cord compression from:
• Disk protrusion• Hematomas• Bone injury• Tumours
• Prognosis: GOOD
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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
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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
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ED Stabilization• ABCs• Airway:
– Low threshold for definitive airway in patient with cervical spine injury especially if higher then C5
– Spinal immobilization very important
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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
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Spinal Shock• Symptoms:
– Flaccid paralysis– Loss of sensation– Loss of DTRs– Bladder incontinence– Bradycardia– Hypotension– Hypothermia– Intestinal ileus
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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
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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
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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
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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
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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
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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
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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
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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
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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)
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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)
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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
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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
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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
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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??
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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.
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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
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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
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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
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Treatment• Prevent secondary injury• Alleviate cord compression• Establish spinal stability• Assess the neurological deficit and spinal
stability• Imaging• Consult spine/neurosurgery
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Other cord lesions…
• Malignancy
• Epidural hematoma
• Abscesses
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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