Spine Flashcards
What is mechanism and deficit of central cord syndrome
Best prognosis of incomplete SCI
Associated with spondylosis and hyper extension
Injury due to osteophytes and flavum or from haematoma.
Weakness - upper > lower, distal > proximal
Variable
Sensory loss
Loss of bladder and bowel
Sacral sparing.
What is the mechanism and deficit of anterior cord syndrome?
Worst prognosis of incomplete syndromes
Flexion and compression injury affecting anterior cervical artery.
Loss of lateral and ventral Spinothalamic and Corticospinal - pain, temp, light touch. Paralysis lower> upper
Maintain proprioception, vibration and gross touch.
10-20% chance of motor recovery
Causes of Lunbar spinal stenosis
Congenital - short pedicels, failure of formation of posterior elements.
Idiopathic, achondroplasia, osteopetrosis
Acquired DDD/spondylolisthesis Inflammatory Neoplastic Traumatic Iatrogenic - laminectomy
Definition of Schuermann’s
Structural rigid kyphosis of the thoracic Spine defined as anterior wedging of 3 or more adjacent vertebrae with at least 5 degrees
(Sorenson criteria)
Non operative indications for thoracolumbar fractures
<25 degrees kyphosis
Based on stability of PLC
Compression - TLSO 6-12 weeks
Burst - 6 weeks bed rest and 6 weeks TLSO
Bony chance with no PLC injury - TLSO 12 weeks
What is the distribution of MSD?
Lumbar > thoracic > cervical
Thoracic most symptomatic - cord compression
Cervical highest rate of mortality
Most in anterior and middle columns, rarely posterior.
What are the spinal red flags?
Weight loss, night pain and fevers
Hx and Examine
Breast lumps, cough, urinary problems.
What is a reflex? Definition
A reflex is an involuntary response to a stimulus via a reflex arc
What is difference between spinal shock and neurogenic shock?
Spinal shock (Whytt 1750) loss of sensation and motor paralysis with initial loss but gradual recovery of reflexes following a SCI. 4 phases. Polysynaptic reflexes return in phase 2
Disruption of autonomic pathways within spinal cord leading to hypotension and bradycardia. (Loss of sympathetics and unopposed vagal tone)
What is the classification used for C2 cervical spine injuries? - Hangman’s
Levine and Edwards
Type I - 3mm. Signif angulation. Vertical fracture line. C2/3 disc and PLL disrupted. Unstable. 5mm
SURGERY OR PROLONGED TRACTION.
Type IIa no horizontal displacement. Horizontal fracture line. significant angulation.
AVOID TRACTION. REDUCE IN HYOEREXTENSION THEN HALO 6-12
Type III - type I with associated bilateral C2/3 facet dislocation. Rare
SURGICAL REDUCTION OF FACET DISLOCATION AND STABILISATION.
What level of change is concerning on neurophysiology testing during spine surgery?
> 50% reduction in SSEP
> 75% reduction in amplitude for MEP
Also free running EmG - burst and train response and stimulus evoked EMG - low current depolarisation (7mA) of pedicle screws concerning
4 causes of scoliosis
1) Neuromuscular -
CP, Musc dystrophy, NF, Marfan’s, Arthrogryposis, EDS
2) Congenital -
failure formation, segmentation, mixed
3) Idiopatic -
Infantile, juvenile, adolescent, Adult
4) Syndromal - Skeletal Dysplasias
Approach to Infantile Idiopathic Scoliosis
Age & Thoracic deformity Characteristic RVAD Other reasons -MRI if not idiopathic Mx - cast 5, surgery if progresses
break it down into two groups: early-onset before age 5 : late- onset after age 5
The key - if significant thoracic deformity present before 5 - real risk of subsequent cardiopulmonary compromise down the road
Characteristics -
- Males more commonly affected than females
- 3/4 convex to LEFT, unlike adolescent idiopathics where the vast majority is convex right
- In general, most curves resolve spontaneously
- Thoracic and thoracolumbar curves tend to resolve, but DOUBLE structural curves with a thoracic component have a definite progressive potential
- Initial curve size and amount of associated rotation are prognostic factors
If Mehta RVAD exceeds 20°, curve is likely to be progressive - single most important factor predicting progression
Start searching for other reasons for the deformity
- Dysraphism?
- Tethered cord?
- Syrinx?
- Congenital failure of formation or segmentation?
- Look for other visceral abnormalities
- X-rays to see if this is a congenital curve
- Then measure the RVAD
- If any suspicion that this is not an “idiopathic” curve, get an MRI!
Treatment
- Most resolve on their own
- Serial casting
(elongation derotation flexion casting) is the conservative treatment of choice - The indications for casting are unclear, but any low-weight floppy child with a big curve and an RVAD over 20° should be casted
- Casting is usually done in the OR under GA
- No point in casting past 5 years of age (growth velocity has plateaued). Can be braced after this
- Surgery when serial casting has failed to halt progression -– requires anterior discectomy over four or five apical segments, then growing rod posteriorly
Response to bracing for Juvenile Idiopathic scoliosis
Treatment
- Curves less than 25° are observed
- Curves that progress beyond 25° are braced (Milwaukee brace)
Curves greater than 45° at the beginning of brace treatment tend to require surgery eventually
- Curves greater than 35° at the beginning of brace treatment have a 50% chance of requiring surgery
Milwaukee brace
- Patients with curves less than 35° and RVAD of less than 20° tend to do well with brace
- Patients with curves greater than 45° and RVAD of greater than 20° tend to do poorly with brace
- Patients between 35 and 45° were unpredictable
Risks of progression in Adolescent Idiopathic scoliosis
Curve Progression – 4 Growth Factors, 2 Curve Factors
- The younger the patient at diagnosis, the higher the risk of progression
- Presentation prior to menarche portends a higher risk of progression
- The lower the Risser grade at curve detection, the higher the risk of progression
- Females with comparable curves to males have 10 times the risk of progression
- Double curves have a greater tendency to progress than single
- The larger the curve at detection, the higher the risk of progression
Formula for shortening with scoliosis surgery
A basic formula: cm of shortening = 0.07 x number of segments fused x number of years of growth remaining
So if you were going to fuse 8 segments in a 7 year old who has 7 more years to grow, the predicted cm of shortening would be 0.07 x 8 x 7 = 3.92 cm
Bracing indications in Idiopathic adolescent scoliosis
Bracing Indications – In principle, works on growing spine (don’t use if almost finished growing)
- Patients should be skeletally immature –- R0-1, and premenarchal or postmenarchal by < 1 year
- The 30-40o curve should have bracing started immediately
- The 20-30o curve can be watched, and bracing started if there is progression of 5o
- Curves less than 20o should be watched for progression
- Basically, you have to be R0-1 and premenarchal or just recently postmenarchal even to be considered
- Do not send away the 30-40o curve for observation –- they need bracing NOW.
Location classification of Scoliosis
⇨ CERVICAL (C2-C6) ⇨ CERVICOTHORACIC (C7-T1) ⇨ THORACIC (T2-T11/12 Disc) ⇨ THORACOLUMBAR (T12-L1) ⇨ LUMBAR (L1/2 Disc-L4)
Age classification of Idiopathic scoliosis
to complete
Characteristics of Infantile IS
Rare Most Left sided Increased incidence of neural axis abnormalities Impaired respiratory function main issue Low rate of progression - 10%
Characteristics of Juvenile IS
Second most common
Higher incidence of neural axis abnormalities
Most Right sided
High rate of progression - 95%
Characteristics of Adolescent IS
Most common
Girls around 13yo most common
All right sided
What are concerns with painful scoliosis?
ROT
⇨ RAPID PROGRESSIVE CURVE
⇨ OVEREXERTION
⇨ TUMOUR (OSTEOID OSTEOMA)
What are features of a scoliosis exam?
• ASYMMETRY of the SHOULDERS, SPINE & PELVIS.
• SPINAL DYSRAPHISM such as MIDLINE hairy patches, dimples, naevi or tumours.
• RIB PROMINENCES (rib rotational deformity).
• CAFÉ-AU-LAIT spots suggesting NF (indicating a neuromuscular scoliosis).
• CAVOVARUS FOOT deformity, which suggests a neurological causes (such as neural axis abnormalities – therefore warrant an MRI)
• LLD (possible compensatory scoliosis).
•LLD ASSESSMENT.
•Perform ADAMS FORWARD BENDING TEST.
(Positive if there is axial plane deformity indicating a structural curve)
•If concerned scoliosis is a secondary compensatory scoliosis due to LLD, ask patient to SIT (which will eliminate the cause).
•Perform NEUROLOGICAL EXAMINATION lower limbs.
•Perform ABDOMINAL REFLEXES, looking for ASYMMETRIC ABDOMINAL REFLEXES.
Absence or asymmetry of abdominal reflexes is associated with a SYRINX.
- Ligamentous laxity (Marfan’s/EDS), absent joint creases (arthrogryposis)
Classification of Cervical myelopathy
Ranawat
1 - no neurological deficit
2 - subjective weakness, dysaesthesias, hyperreflexia
3 - objective weakness, UMM signs.
3a - ambulatory
3b - non-ambulatory
What factors need to be assessed on a scoliosis x-ray series?
- NUMBER OF CURVES
- LOCATION OF CURVE
- APEX OF CURVE
- COBB ANGLE
- Sagittal balance
- EVIDENCE OF CONGENITAL SCOLIOSIS
- RVAD + PHASE RIB HEAD (INFANTILE / JUVENILE)
- RISSER STAGE
- TRI-RADIATE CARTILAGE
Classic radiology of Schuermann’s
Schmorl’s nodes, vertebral end plate abnormalities, loss of disc height, wedge vertebrae
Location & Gender distribution of isthmic spondylolisthesis
L5/S1 - 87-95%
L4/5 - <3%
Males affected more commonly
Females FOUR times more likely to develop high-grade slip
Classification of Spondylolisthesis
Wiltse - DID TIP
Meyerding - 5 grades
Grade - low or high
Level
Dysplastic (CONGENITAL TYPE 1) - assoc Spina bifida
Isthmic ( ACQUIRED TYPE 2) - Lytic stress #, Elongation (healed pars defect, acute
Degenerative - rare greater than 30%
Traumatic - other than pars
Iatrogenic - facetectomy or transition syndrome
Pathological -
Generalised - TB, Pagets, Osteopetrosis, arthrogryposis, RA
Local - Tumours (GCT), infection
What is normal Slip angle when measuring spondylolisthesis?
20-30 degrees
Risks for Spondylolistheis progression
⇨ HIGH GRADE SLIP (GRADE III OR MORE) ⇨ SLIP ANGLE > 30 ⇨ SACRAL INCLINATION > 60 ⇨ FEMALE ⇨ DYSPLASTIC SPONDYLOLISTHESIS
Define spondylosis
anatomic defect (seen on xray as a radiolucent gap) in the pars interarticularis with adjacent bone sclerosis.
Risks of progression in Isthmic Spondylolisthesis
- YOUNG PATIENTS 50% SLIP (GRADE III, IV)
- L4/5 SLIPS - less common but lack of IL legs
- ADULT ISTHMIC SPONDYLOLISTHESIS
Specific Examination points for Isthmic Spondylolisthesis
- Look for LUMBAR HYPERLORDOSIS.
- Feel for a PALPABLE STEP over the SPINOUS PROCESS.
- There is ↓ LUMBAR ROM (FLEXION / EXTENSION).
- SLR TEST may be positive.
- NEUROLOGICAL EXAMINATION of the lower limbs.
MANAGEMENT OF PAEDIATRIC ISTHMIC SPONDYLOLISTHESIS
ASYMPTOMATIC NO SLIP
⇨ NO TREATMENT (OBSERVATION every 6-12 months)
ASYMPTOMATIC < 50% SLIP
⇨ ACTIVITY MODIFICATION (AVOID CONTACT SPORTS)
SYMPTOMATIC SPONDYLOLYSIS NO SLIP
⇨ ACTIVITY MODIFICATION
⇨ TLSO BRACE (6-12 WEEKS) IF ACUTE (bone scan)
SYMPTOMATIC SPONDYLOLYSIS SLIP
⇨ ACTIVITY MODIFICATION
⇨ TLSO BRACE (6-12 WEEKS) IF ACUTE
ALL PATIENTS >50% SLIP or PROGRESSIVE NEUROLOGY or FAILURE NON-OPERATIVE
⇨ SURGERY
pars defect repair, in-situ fusion, reduce and fuse
Epidemiology of Degenerative spondylolistheis
- Increasing incidence with age (typically > 50 years of age).
- Incidence of 8% of the population.
- More common in BLACKS and DIABETICS.
- F>M (6-10:1) due to ↑ LIGAMENTOUS LAXITY (hormonal).
- More common in patients with a TRANSITIONAL L5 VERTEBRA and with SAGITTALLY ORIENTATED FACET JOINTS.
Why are degenerative spondylolistheses rarely more than grade 1 or 2
- As the listhesis progresses with the narrowing of the intervertebral disc, subsequent changes in the motion segment include SPUR FORMATION, SUBCHONDRAL SCLEROSIS, LIGAMENT HYPERTROPHY and FACET JOINT HYPERTROPHY.
- These secondary changes have a tendency to restabilise the motion segment.
Differentiate Neurogenic and vascular claudication
- Neurogenic claudication is worsened with standing up or walking.
- Neurogenic claudication is improved with spine flexion / leaning forward.
- Vascular claudication is relieved with cessation of walking.
- Stationary cycling worsens vascular claudication whilst not changing neurogenic claudication
Associations of Klippel Feil
Failure of segmentation of in cervical spine Sprengel deformity - 33% short, broad neck Torticollis scoliosis jaw anomalies
Define basilar invagination
Potrusion of dens above McRae line or 5mm beyond McGregor line
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Present in : Klippel-Feil Hypoplasia of atlas bifid posterior arch of atlas Occipitocervical synostosis Systemic - Morquio, achondroplasia, OI, spondyloepiphyseal dysplasia
Radiological definition of Atlantoaxial instability
ADI >5mm
Power’s ratio - basion to posterior margin of atlas / opsithion to anterior arch of atlas.
Normal = <1.0
Occipitocervical synostosis (50%)
Paediatric cervical spine injury - <8 yo increased risk because
Ligamentous laxity, large head to body ratio, horizontal facet joints
87% of <8yo C3 or higher
How to diagnose pseudosuubluxation on lateral x-ary
Swischuk line connecting spinolaminar junction of C1-3
Spinolaminar junction of C2 must be <1mm anterior to this
Reduces on extension radiographs
Radiological signs of Ank Spond
Dagger sign - inter spinous lig on ap
Anderson lesion - discovertebral
Romanus lesion - lyric erosion anterior corner of vertebra from annulus. Becomes ossified syndesmophyte
Atypical granulomatous infections of spine
TB Actinomyces Israelii Nocardia Brucella Fungal Spirochetes
What conditions are disc sparing?
TB - Potts
Tumours
Infection - disc involving
C1/C2 instability causes
Adult traumatic
- atlas fracture
- transverse ligament injury
- type 1 odontoid fracture
Adult degenerative
- RA cervical spondylitis
- Os Odointoideum
- Down syndrome
Paediatric trauma
- Rotatatory instability
Paediatric degenerative
- Downs
- JRA
- NF-1
- Morquios syndrome
What are the measurements for stall to-axial instability?
AADI - norm 3 adults , 5 Paeds
3.5 -7 instability - loss of transverse ligaments
7-10 loss of all 3 ligaments
>10 high risk of neurology
PADI - normal 14mm
17mm normal <0.8 narrow
Management of C1-C2 instability
Myelopathic - decompress and stabilise
Halo
C1-2 fusion
C0-2 fusion
What are the non-organic signs of LBP? Back pain
Waddell’s
1) Pain on axial compressor or rotation spine
2) Over reaction
3) Regional disturbances with no dermatome
4) Negative SLR with distraction
5) Superficial and non-anatomical tenderness
What is the scoring system for TL spinal fractures?
TLICS - TL injury classification and severity score - modified TLISS
3 non-op
4 unclear
5 surgery
Post ligaments - intact, suspected, injured 0,2,3
Morphology - wedge, burst, translational/rotational, distraction 1-4
Neurology - none, root, complete, incomplete/cauda 0,2,2,3/3
=5 op
TLISS was mechanism not morphology
General Criteria for treating C2 dens fracture
Age Medic comorbs Type Displacement Body habitus Neurology
Classification of dens fractures
Anderson and D’Lonzo
1 top avulsion - alar ligaments
2 base - unstable and 25-75% nonunion
3 body fracture. Stable and unite
Grauer modification
2a - transverse <1mm displace
2b - oblique (AS/PI) downhill from anterior
2c - reverse oblique (AI/PS) uphill
Treatment of Dens fractures
1&3 - non op
1- hard collar. No halo as distracts
3- hard collar
2- surgery depending on 6 criteria -
Collar - elderly with CI. 12 weeks
Halo - undisplaced. 12 weeks
Screw - minimally displaced. NOT 2c. Anterio approach
Fusion - wiring, trams articular screws, c1LM and C2 pedicel screws.
Elderly - 35% mortality >70yo
42% mortality in halo >65yo - cardioresp limitations
Surgery - Odontoid screw or C1/C2 fusion
Hard collar risks pseudarthrosis
Non-union risks >40yo >1mm displace Post displace >5mm Angulation>11 degrees Comminution Neurological defects Reverse oblique Loss of position 2 mm
