1. Spinal Cord Syndromes Resident Rounds April 12, 2007 Juliette Sacks

2. 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

3. Neuroanatomy Corticospinal tracts Spinothalamic tracts Dorsal (posterior) columns

4. 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

5. 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

6. 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

8. 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

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

11. 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

13. 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

14. 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

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

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

17. 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

18. Where is the lesion?

20. 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

22. 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

23. 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

24. 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

26. Brown-Séquard Syndrome Hemisection of the cord Ipsilateral loss of: –Motor function –Proprioception and vibration sense Contralateral loss of: –Pain and temperature sensation

27. BSS Caused by: –Penetrating injury –Lateral cord compression from: Disk protrusion Hematomas Bone injury Tumours Prognosis: GOOD

28. 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

29. 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

30. ED Stabilization ABCs Airway: –Low threshold for definitive airway in patient with cervical spine injury especially if higher then C5 –Spinal immobilization very important

32. 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

33. Spinal Shock Symptoms: –Flaccid paralysis –Loss of sensation –Loss of DTRs –Bladder incontinence –Bradycardia –Hypotension –Hypothermia –Intestinal ileus

34. 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

35. 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

36. 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

37. Corticosteroids NASCIS recommends: 1.Treatment must begin within 8h of injury 2.Methylprednisolone 30mg/kg bolus iv over 15 minutes 3.45 minute pause post bolus 4.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

38. 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

39. 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

40. 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

41. 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

42. 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)

43. 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)

44. 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

45. 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

46. 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

47. 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??

48. 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.

49. 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

50. 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

51. 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

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

53. Other cord lesions… Malignancy Epidural hematoma Abscesses

54. 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