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11,500 cases per year in US
1994: 207,000 SCI patients
2.6% of all admitted trauma
Summa 1999, Burnley 1993, Lasfargues 1995
#1 : Male teenagers and young adults
Relative increase in 60-70 y/o MVA (44.5%) Falls (18.1%) Violence (16.6%)
Summa 1999
Cervical 50-64% Thoracic 17-19% Lumbar (cauda equine)
20-24%
C1-C2 Facet Joints› Horizontal plane› Facilitates axial rotation
Tectorial Membrane› Continuation of PLL› Major occip- cervical
stabilizer› Secondary restraint for
extension of occiput on atlas
Alar Ligaments
Netter’s Anatomy
Lateral mass: Consists of ipsilateral
sup/inf. facets Upward inclination of ~
400
Facet joint complex resists anterior translation and rotation
Vertebral artery Traverses foramen in TP Does not traverse C7
Netter’s Anatomy
Ribs and sternum limit thoracic spine movement; increase stability
Spinal cord takes up the majority of the canal space
Facet joints in coronal plane
Lordotic sagittal alignment (20-600)
Significant (F/E) motion at each level
Biplanar facet joints
L2 -L5: Cauda Equina
Netter’s Anatomy
FG Fasc. Gracilis (Sensory, lower part of cord, Proprioceptive, Deep pain, Vibration, Ipsilateral)
FC Fasc. Cuneatus (Sensory, Upper part of cord, Proprioceptive, Deep pain, Vibration Ipsilateral)
PH Posterior Horn (Sensory cell bodies)
AH Anterior Horn (Motor Cell Bodies)
LCS Lateral Corticospinal Tract (Crossed Pyramidal Upper Motor Neurons to ipsi AH)
ACST Anterior Corticospinal Tract (Direct Pyramidal go to contra AH)
PSCT ASCT Spinocerebellar Tracts
LST Lateral Spinothalamic Tract (Sensory, Pain and Temp: cell bodies in contra PH)
AST Anterior Spinothalamic Tract. (Sensory, Touch: cell bodies in contra PH)
Exits through intervertebral foramen C1 exits between skull and atlas C2 to C7 exit above corresponding vertebrae C8 exits below C7, above T1 Below T1; all nerves exit below corresponding
numbered vertebral pedicle
Spinal nerves that have exited from the cord
L1-L5: Nerve cell bodies lie in the cord behind T11-T12
S1-S5: Nerve cell bodies line within the region of the conus medullaris
Cauda equina nerves are more like peripheral nerves withstand trauma better than CNS
Damage to this region causes LMN signs
Primary mechanical insult Rapid compression due to bone
displacement from burst or dislocation Distraction *** Shear *** Penetration
Primary injury leads to cascade of secondary injury mechanisms
*** Portends poor prognosis !!!
Vascular changes› Diminished blood
flow› Hemorrhage› Vasospasm › Thrombosis
Electrolyte shifts Free radical
production Inflammatory
cascade
Final pathway is neuron death by:
Cell necrosis with structural dissolution
Apoptosis: chemical trigger initiates process that removes non-functioning neurons but also kills normal neurons in zone of injury
Aggressive field resuscitation› Maintain systemic BP› Maintain optimal oxygenation
Steroids› NASCIS-2 8 hour window› NASCIS-3 < 3 hrs---24 hrs; 3-8 hrs---48 hrs.
30mg/kg bolus then 5.4mg/kg/hr Surgical decompression? Timing ?
Complete Cervical tetraplegia Thoracic and lumbar paraplegia
Incomplete syndromes Anterior cord Central cord Brown-Sequard Posterior cord Conus medullaris
Definition No motor or sensory function more than three
segments below the neurological level of injury
There is absence of sacral sparing
Absent limb function
Ventilator dependence
C4 level may be vent independent
C5 deltoids, biceps
C6 biceps, wrist extension
C7 wrist extension, triceps
C8 functional grasp
T1 intrinsic hand fct
4
5
Better respiratory and trunk control with injury at more caudal levels
Thoracolumbar most commonL1
T12
12
L1
L2 hip flexion L3/4 knee
extension L4 foot
dorsiflexion L5 EHL S1
gastrocsoleus
L2
L2
Indicates some continuity of long tract fibers
Sacral structures are most peripheral in both posterior columns and lateral corticospinal tracts
Continued function of sacral LMNs in conusSkeletal Trauma
Perianal sensation (S4-S5) dermatome
Voluntary external anal contraction
Great toe flexor activity
Skeletal Trauma
Affects the anterior 2/3 of cord Preserves the posterior column:
proprioception, vibratory sensation May be due to persistent retropulsed
bone or disc material/ mechanical insult Vascular component
Loss of all motor and sensory below injured level
Deep pressure sensation only
Poor prognosis for motor recovery
Older patients with preexisting spondylosis
MOI: Hyperextension injury: fall, whiplash Spinal cord pinched by osteophytes
anteriorly and the underlying hypertrophic ligamentum flavum posteriorly; leads to significant injury to the “central portion” of the cord
Best prognosis among common patterns
Upper extremity > lower extremity involvement
Distal > proximal Earliest and greatest
recovery in legs followed by bladder
Hand dexterity often slow to return, full recovery variable
Results from functional hemisection of cord, projectile or penetrating wound
Loss of ipsilateral motor Loss of contralateral
pain, temperature, and light touch sensation
75% regain independent ambulation
80% recover bowel and bladder function
Rare Loss of
proprioception Maintain
ambulation but rely on visual input
Direct injury to conus region (L1-L2) Presents as mixed lesion of cord and
nerve root damage Bowel, bladder, and sexual dysfunction Injury to CM can disrupt the
bulbocavernosus reflex arc Therefore, the absence of a bulbocavernosus
reflex unreliable indicator of spinal shock in this clinical setting
Modified From: Lockhart RD; Hamilton GF; Fyfe FW. Anatomy of the Human Body. JB Lippincott Company
Lower motor neuron lesion (not cord)
Sacral segments more affected than lumbar
Saddle anesthesia with incontinence
Lumbar sparing
Common mechanism for central cord injury in elderly—hyperextension with a spondylolytic neck
MRI findings impressive SCI protocol followed by observation until
recovery plateaus Treatment : same as central cord syndrome.
Be aware of the clinical triad of
neurological injury and
concomitant lamina fracture with
burst pattern (Cammisa, 1989)---trapped roots
Decompression rarely of benefit except forINTRA-CANAL BULLET AT THE T12 TO L5 LEVELS with incomplete injury
(better motor recovery than non-operative)
Fractures usually stable, despite “3-column” injury
More favorable prognosis than cord injuries
In c-spine injuries: frequently see complete cord injury with varying levels of root injury Good chance of recovery of one level Recovery dependent on level of injury
ATLS guidelines: A-B-C’s Examine for head, neck, or back
trauma –need to logroll Paradoxical diaphragmatic breathing Priapism Neurogenic shock: hypotension and
bradycardia Loss of sympathetic tone
Log roll !!!!! Palpate
Tenderness Gap/ Step-off Crepitus
Motor: 0-5 Sensory Rectal exam: sacral sparing? DTRs: LMN function Spinal reflexes: UMN function
Biceps C5 Brachioradialis C6 Triceps C7 Quadriceps L4 Gastroc-soleus S1
Perianal/perineal sensation Rectal tone Big toe flexion Implies partial structural continuity of
white matter long tracts May be only evidence of incomplete
injuryhigher chance of recovery Essential to check and document
Bulbocavernosus reflex: Pull glans or press
clitoris anal contraction (int. sphincter) around gloved finger
Absence is indicator of spinal shock
Skeletal Trauma
Scapulohumeral reflex (C3) Tap on spine of scapula =>abd and
elev arm Hoffman’s Inverted Radial Reflex Tap BR =>finger flexion (C6 root) Superficial abdomenal Cremaster Crossed adductor response Tap Medial Fem Condyle =>add contra
leg
Temporary loss of all or most spinal reflex activity below level of injury
Lasts around 24 hours (max 48 hrs) Ends when bulbocavernosus reflex and/or
anal wink returns An injury cannot be considered complete
until resolution of spinal shock
Neurologic level of injury (NLI)› Most caudal level
with bilateral normal motor and sensory function
Complete/Inc› Importance of
sacral levels Zone of partial
preservation
A Complete:
B Incomplete:C Incomplete:
D Incomplete:
E Normal:
No motor or sensory below lesion
Sensory only below lesion to S4-5Preserved motor below lesion, key
muscle strength < 3Preserved motor below lesion, key
muscle strength > 3
Normal motor and sensory below lesion -ASIA
1992
X-rays CT MRI MRA
Lateral C-spine in trauma room› Must include down to C7-T1› Swimmer’s view or pull-down if necessary› Single most important radiographic
examination C-spine series
› AP, Open mouth (dens) T-L-S spine films as indicated (one
spine fracture mandates full spine radiographic evaluation) › T-L junction: 50% of injuries occur at T11-L1
Lordosis Unreliable sign of
injury Prevertebral soft
tissues Unreliable No agreed upon
measure 6 mm at C3 22 mm at C6
Anterior spinal line› Anterior aspect of vertebral
body along ALL
Posterior spinal line› Posterior aspect of
vertebral body along PLL
Spinolaminar line› Joins the anterior margins
of the junction of the lamina and spinous processes
Spinous process line› Joins tips of spinous
processes
– Lateral masses of C1 Lateral masses of C1 should align over should align over facet joints of C2facet joints of C2
– combined lateral combined lateral mass displacement mass displacement over 7 mm suggests over 7 mm suggests transverse ligament transverse ligament tear (Spence’s Rule)tear (Spence’s Rule)
Injury suspected on plain films Better visualize fracture (specificity and
sensitivity) Unable to adequately assess on plain
films Sagittal and/or coronal reconstructions
can be helpful (particularly at Oc.-cervical and C-T jcts.)
Fracture or soft tissue injury in the plane of the CT can be missed
Invaluable for assessing cord and soft tissues
R/O associated disc herniation ( facet dislocations)
Hemorrhage vs edema in soft tissues ???? Ligamentous tears and facet capsule
disruptions visualized with fat suppression May allow prognostic assessment of final
motor function› Intrasubstance hematoma
T1 T2 GRE
Roaf, 1960 – pure axial load or pure flexion leads to little posterior ligamentous injury
Nagel, 1981 – 20 degrees of kyphosis or 10 degrees lateral angulation implies incompetence of PLL and posterior elements, thus inferring instability
Panjabi, 1981 – it takes sectioning of PLL and posterior annulus to destabilize a motion segment with the addition of facet capsule and interspinous ligament disruption
James et al, ’94 – middle column offers little additional resistance to kyphosis with increasing axial load
The Issues Often difficult to diagnose Missed or delayed diagnosis can lead to
catastrophic neurologic disability No agreed upon protocol in the intoxicated,
multiply-injured, or head-injured patient
The Problems Unnecessary imaging?
Should every patient with blunt trauma gets x-rays?
Overzealous consultation When and who should ‘clear the c-spine’ ??
The Hard Collar Dilemma: Prolonged hard collar use leads to decubiti as
well as neck pain
Hoffman, Mower, et al., NEJM 2000 Multicenter study 34,069 patients with blunt trauma AP/Lat/Open Mouth on all patients 810 with positive x-rays Only 8 with false-negative x-rays
Only 2 clinically significant
Harris, Kronlage, et al. Spine 2000 Polytrauma, intoxicated, CHI patients IRB Protocol: Includes intra-op flex/ext with
fluoro after all films read as normal Goal: Identify ligamentous injuries 3/ 153 (+) --- all required surgical stabilization
Criteria for clinical clearance› No posterior midline
tenderness› Full pain-free active ROM› No focal neurologic deficit› Normal level of alertness› No evidence of intoxication› No ‘distracting injury’
If x-rays negative, but patient c/o neck pain, active flexion/extension x-rays when able. Rarely helpful in acute setting
If neurologic deficit attributable to neck injury, immediate MRI
Controversy over the polytrauma or intoxicated patient remains EAST practice guidelines: trauma series and
thin cut axial CT through C1-2 CT of cervical –thoracic junction if poor
visualization on plain and swimmer’s
15-30% incid. uni-/bilat
Neuro intact: MRI prior to reduction attempt
Neuro injured: Reduction prior to MRI
Neuro unknown: MRI first
Attempt reduction without MRI ONLY if able to accurately monitor neurologic exam throughout process
Experimental evidence Clinical evidence
Non-operative Operative
Numerous studies Classic: Tarlov 1954 Delamarter 1995 Dimar 1999 Experimental models: Balloons, clips, cables,
spacers Beagles, rabbits, rats
Severity of SCI dependent on: Force of compression Duration of compression Displacement, canal narrowing
Surgical decompression does attenuate the deleterious effects of acute SCI Persistent compression is a potentially
reversible form of secondary injury
Most studies uncontrolled and retrospective analyses
Spontaneous recovery unpredictable, but generally occurs
Timing to reduction is important Most dramatic benefit in bilateral jumped
facets
Surgical benefit must be weighed against limited non-operative benefit
Numerous studies, almost exclusively retrospective
Timing: early, late, and later
The only prospective randomized trial 62 patients with cervical SCI
34 “Early” (< 72 hrs) surgery 28 Late (> 5 days) surgery
ASIA assessment No difference in neurological outcome
Most studies retrospective with historical controls
No clear consensus on timing No statistical evidence that surgical
decompression influences neurologic outcome
Tator et al 1999 Retrospective, multicenter (36) Examined use and timing of surgery in
acute SCI 9 month period 1994 to 1995 All within 24 hours of injury 16 to 75 years old Non-penetrating trauma
585 patients Complete SCI in 57.8% Traction 47% Surgery 65.4%
< 24 hrs: 23.5% 25-48hrs: 15.8% 48-96hrs: 19% > 5 days: 41.7%
C-spine vs. T-L spine Partial vs. complete
› Spinal shock Definition of early surgery Role of steroids Type of decompression
› traction vs. anterior vs. posterior
High energy vs. low energy
Associated injuries
There is strong experimental evidence in animals to indicate:
Decompressive surgery of the spinal cord improves recovery after SCI
Earlier surgery yields more improvement
There is strong experimental evidence that suggests early decompression (<6-8 hrs) leads to a higher likelihood of neurological recovery.
Extrapolating animal data to clinical practice may be a leap, but this data comprises the majority of current scientific evidence.
The sole prospective randomized study concluded that there is no difference between early (<72 hrs) and late (> 5 days) surgical decompression with respect to neurological recovery.
Vaccaro, et al. Spine 1997