Spine Non Trauma — FRCS Quiz

45 slides

▸ Slide 449 · Spine - non traumaSpine Non Trauma · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

Which conditions are listed under 'Spine - non trauma'?
What spinal manifestations of RA are listed on this slide?
Which cervical spine conditions are listed?
Which degenerative/structural topics are listed?
Which infective, neoplastic and miscellaneous topics are listed?

Answers · Q & A

Q1.Which conditions are listed under 'Spine - non trauma'?

RA – C1/2 instability, subaxial involvement, cranial settling
AS – pseudoarthrosis; DISH
Cervical myelopathy, OPLL, PID, dural tear
Spinal stenosis, degenerative scoliosis, spondylolysis, sagittal balance
Vertebroplasty, TB spine, pyogenic spine, spine metastasis, failed back syndrome

Q2.What spinal manifestations of RA are listed on this slide?

C1/2 instability
Subaxial involvement
Cranial settling

Q3.Which cervical spine conditions are listed?

Cervical myelopathy
OPLL
PID
Dural tear

Q4.Which degenerative/structural topics are listed?

Spinal stenosis
Degenerative scoliosis
Spondylolysis
Sagittal balance

Q5.Which infective, neoplastic and miscellaneous topics are listed?

Vertebroplasty
TB spine
Pyogenic spine
Spine metastasis
Failed back syndrome

▸ Slide 450 · Lateral XR of this patients cervical spineSpine Non Trauma · 8 questions 1 check expand

Question list

Q1-Q88 questions — tap to reveal all answerslist

Describe the lateral flexion/extension cervical X-ray findings.
What are the risk factors/causes and symptoms of C1/2 instability?
What do you examine and what further investigations are required?
What is the natural history of C1/2 instability (Boden's classic paper)?
What lines and measurements are used to assess cranial settling?
When do you operate for cranial settling versus C1/2 subluxation?
What is the pattern of cervical spine involvement in rheumatoid arthritis?
What is pannus and how does it destroy structures?

Answers · Q & A

Q1.Describe the lateral flexion/extension cervical X-ray findings.

C1/2 subluxation with increased ADI and decreased PADI
No associated cranial settling
No subaxial cervical spine abnormalities
Cervical height index measured

Q2.What are the risk factors/causes and symptoms of C1/2 instability?

Inflammatory joint disease or crystal arthropathy; signs of infection
Previous trauma (odontoid nonunion / os odontoideum)
Ligamentous laxity (Down's syndrome, MPS)
Symptoms: pain (neck and occiput), myelopathy, vertebrobasilar insufficiency (vertigo, diplopia, drop attacks)
Functional grading (Ranawat): I normal, II subjective weakness, IIIA objective weakness (ambulatory), IIIB no longer ambulatory

Q3.What do you examine and what further investigations are required?

Examination: neurological exam, cranial nerves, RA hand signs, Syndromal features (down, MED, morquio) - e.g. Down's syndrome, MPS
Open mouth C-spine XR for rotatory instability: rule of Spence >8mm = TAL incompetence; controlled F/E to check if reducible
CT: bony anatomy for surgical planning
MRI: compressive pathology; cervicomedullary angle <135deg highly correlated with paralysis; myelomalacia
Bloods to rule out RA if undiagnosed (RF, anti-CCP, EULAR or ACR criteria)

Q4.What is the natural history of C1/2 instability (Boden's classic paper)?

~70 patients with C1/2 instability reviewed
60% developed symptoms; best predictor PADI <13mm
Non-operated: 86% neuro deterioration, all died within 4 years
Operated: 70% symptom relief, none died

Q5.What lines and measurements are used to assess cranial settling?

McRae's line: from basion or opisthion; dens tip should be below it
Ranawat line: centre of C2 pedicle should lie below mid transverse axis of C1 (M 17, F 15; abnormal <13)
Redlund-Johnell: C2 base to McGregor line (34/30mm)
Chamberlain's line: hard palate to opisthion; dens tip should be <3mm above
McGregor's line: hard palate to external occipital protuberance; dens tip <4.5mm above; Clark station: anterior C1 ring level with first third of odontoid
Pannus: soft tissue mass encircling the eroded dens; stabilization leads to decrease in pannus

Q6.When do you operate for cranial settling versus C1/2 subluxation?

Cranial settling: neurological compromise, progressive cranial migration >5mm, cephalomedullary angle <135deg -> C0-C2 fusion +/- transoral odontoid resection
C1/2 subluxation: neurology, SAC <13, ADI >10mm, cord diameter <6mm
Reducible: C1/2 fusion with transarticular screw, wiring, pedicle/rod or segmental screws; non-reducible: C1 posterior arch excision + O-C2 fusion, or C1 laminoplasty + C1/2 fusion (less morbidity)
Subaxial: subluxation >4mm or >20% = cord compression; cervical height index <2.0 almost 100% sensitive/specific for neuro compromise; translation >3.5mm, angulation >11deg; operate if >4mm or neurology

Q7.What is the pattern of cervical spine involvement in rheumatoid arthritis?

Cervical involvement in 90% of RA patients
Atlantoaxial subluxation 80%: anterior subluxation of C1 on C2 from pannus between dens and C1 ring, destroying the transverse ligament and dens
Basilar invagination 40%: cranial migration of dens from erosion and bone loss between occiput, C1 and C2
Subaxial subluxation 20%: pannus and soft tissue instability of facet joints and Luschka joints

Q8.What is pannus and how does it destroy structures?

Latin for 'cloth'
Hypertrophied synovium with fibrovascular tissue and inflammatory cells releasing collagenolytic enzymes
Destroys cartilage, bone, tendons, ligaments and blood vessels
Stabilization leads to decrease in pannus

Fact check

90% of RA patients have cervical spine involvement; atlantoaxial subluxation in 80%, basilar invagination 40%, subaxial subluxation 20% — misleading precision — Prevalence varies widely by cohort and imaging: cervical involvement reported up to ~86%, AAS is the most common form (radiographic rates roughly 16-96%), basilar invagination ~5-34% and subaxial subluxation ~10-44%; fixed 80/40/20 figures overstate certainty — medium confidence — source

▸ Slide 451 · PannusSpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is pannus?
Where does the term pannus come from and what is its composition?

Answers · Q & A

Q1.What is pannus?

A soft tissue mass
It encircles the eroded dens

Q2.Where does the term pannus come from and what is its composition?

Latin for 'cloth'
Hypertrophied synovium with fibrovascular tissue and inflammatory cells releasing collagenolytic enzymes
Leads to destruction of cartilage, bone, tendons, ligaments and blood vessels
Stabilization decreases pannus

▸ Slide 452 · Use of open mouth view in basilar invaginationSpine Non Trauma · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

Which lines are used to assess basilar invagination on this slide?
What are the normal measurements for Fishgold's digastric line?
How is Fishgold's bimastoid line interpreted?
What is the use of the open mouth view in assessing C1/2 instability and basilar invagination?

Answers · Q & A

Q1.Which lines are used to assess basilar invagination on this slide?

Fishgold's digastric (Biventer) line - connects the digastric grooves on the undersurface of the skull, just medial to the mastoid processes
Fishgold's bimastoid line - connects the tips of the mastoid processes

Q2.What are the normal measurements for Fishgold's digastric line?

Odontoid tip normally projects 11 mm below the line
Atlanto-occipital joint normally projects 12 mm below the line
Basilar invagination is present when the atlanto-occipital joint projects at or above this line

Q3.How is Fishgold's bimastoid line interpreted?

Odontoid process should be <10 mm above this line
More than 10 mm above the line indicates basilar invagination

Q4.What is the use of the open mouth view in assessing C1/2 instability and basilar invagination?

Open mouth C-spine XR looks for rotatory instability
Rule of Spence: >8mm = TAL incompetence
Controlled flexion/extension views to see if the deformity is reducible

▸ Slide 453 · Fusion technique of C1 C2Spine Non Trauma · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

Describe the Gallie fusion technique for C1/2.
Describe the Brooks and Jenkins fusion.
What screw-based options are available for C1/2 fusion?
What are the main categories of C1/2 fusion techniques?

Answers · Q & A

Q1.Describe the Gallie fusion technique for C1/2.

Interspinous bone graft with sublaminar wiring around the posterior arch of C1 and wiring over the C2 spinous process
Fusion rate 75%fusion (poor rotational stability)
Requires post-operative external fixation

Q2.Describe the Brooks and Jenkins fusion.

Modification of Gallie to overcome rotational deficiency
Bilateral interlaminar grafts with bilateral sublaminar wiring (C1 and C2)
Fusion rate 93%
Also requires post-operative external fixation

Q3.What screw-based options are available for C1/2 fusion?

Transarticular screw - supplemented with Gallie wiring; stable
Screw-rod structure - stable and allows reduction
OC fusion

Q4.What are the main categories of C1/2 fusion techniques?

Wiring: Gallie; Brooks and Jenkins
Transarticular screw (supplemented with Gallie wiring) - stable
Screw-rod structure - stable, allows reduction
OC fusion

▸ Slide 454 · Landmark of transarticular screwSpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What are the entry landmarks for a transarticular screw (Magerl technique)?
What is the sagittal trajectory of the Magerl transarticular screw?

Answers · Q & A

Q1.What are the entry landmarks for a transarticular screw (Magerl technique)?

Axial: 10 degree medial
Entry point 3-4mm cranial to the C2/3 joint
Midpoint of the pars mediolaterally

Q2.What is the sagittal trajectory of the Magerl transarticular screw?

50 degree cephalad
Passes through the posterior 1/3 of the C1-2 joint

▸ Slide 455 · C2 pedicle screwSpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the entry site for a C2 pedicle screw?
What is the trajectory of a C2 pedicle screw?

Answers · Q & A

Q1.What is the entry site for a C2 pedicle screw?

Cranial leading edge of the C2 lamina
Midpoint of the pars mediolaterally
Starting point 2mm lateral to this midpoint

Q2.What is the trajectory of a C2 pedicle screw?

30-45 degree convergent
Directed cranially

▸ Slide 456 · AP Xray lumbar spine and pelvisSpine Non Trauma · 10 questions expand

Question list

Q1-Q1010 questions — tap to reveal all answerslist

Describe the AP X-ray findings in ankylosing spondylitis.
What are the history and examination findings in AS, and how is it diagnosed?
What are the differentials of multiple syndesmophytes and of SIJ sclerosis?
What is ankylosing spondylitis and what is the role of HLA-B27?
What are the discovertebral lesions in AS and the causes of pseudoarthrosis?
How are deformities in ankylosing spondylitis managed?
How does SIJ involvement progress radiologically in ankylosing spondylitis?
What blood tests and further imaging are requested in suspected AS?
What types of spinal osteotomy are used for AS deformity correction?
What are the key points of cervical spine osteotomy in AS?

Answers · Q & A

Q1.Describe the AP X-ray findings in ankylosing spondylitis.

Squaring of vertebrae with marginal syndesmophytes
Bamboo spine appearance; trolley-track and dagger sign
Bilateral SIJ ankylosed, hips okay, no discovertebral lesion
Frontal alignment good, no osteopenia; need lateral XR for facet joint ankylosis

Q2.What are the history and examination findings in AS, and how is it diagnosed?

Hx: PMHx, FHx, morning stiffness, SOB, pain, other joint or heel pain
PE: gait, loss of lumbar lordosis with increased thoracic kyphosis, horizontal gaze, chin-brow vertical angle, wall-to-occiput, Schober's test, chest expansion
SIJ: Faber and Gaenslen tests; neurological exam of LL; listen to heart and lungs, look at eyes and nails
Diagnosis: modified New York criteria - at least 1 clinical + 1 radiological criterion
Clinical: inflammatory back pain >3 months improved by exercise/worse with rest, reduced spine ROM, reduced chest expansion
Radiological: unilateral grade 3-4 or bilateral grade 2-4 SIJ changes

Q3.What are the differentials of multiple syndesmophytes and of SIJ sclerosis?

Multiple syndesmophytes/ossification: DISH - non-marginal syndesmophytes, disc and SIJ spared, more common in older patients (DM)
SIJ sclerosis: osteitis condensans ilii (young women, iliac side)
Fibrodysplasia ossificans progressiva

Q4.What is ankylosing spondylitis and what is the role of HLA-B27?

A systemic seronegative arthritis mainly affecting the axial skeleton
More common in young male patients with family history (HLA-B27)
Presents with back pain not relieved by rest, spine/hip stiffness, stooped posture, fracture
HLA-B27 is an MHC presenting intracellular protein to T cells, initiating an immune response through TNF
Patho hypotheses: misfolding -> homodimer triggering a pro-inflammatory response; arthritogenic peptide presented to autoreactive cytotoxic T cells

Q5.What are the discovertebral lesions in AS and the causes of pseudoarthrosis?

Romanus lesion (50%): erosion at the anterolateral corner with surrounding sclerosis, posterior column spared
Andersson lesion (4%): erosion at the mid-endplate (anterior + middle column), posterior column spared
Pseudoarthrosis: secondary to fracture/Andersson lesion with posterior column involvement - all 3 columns
Causes (D Fang): acute fracture through fused segment, stress fracture, escape fusion -> need circumferential fusion

Q6.How are deformities in ankylosing spondylitis managed?

Aim: posture (horizontal gaze), visceral function, prevent complications (fracture, pseudoarthrosis)
Medical: physio, NSAIDs, TNF-alpha antagonists (infliximab, adalimumab, etanercept)
Preop: anaesthetic/airway, biologics, lung function test, echo, steroid coverage, PPI; osteotomy site usually lumbar (wider canal, end of conus, no ribs, large correction power)
Osteotomies: SPO, Ponte, PSO, VCR; cervical osteotomy for chin-on-chest at C7/T1, aim CBVA within 10 degrees; PSO closing wedge preferred over SPO opening wedge
Complications: neurologic injury, SMA, aortic rupture, non-union, residual deformity
Instrumentation: U3L3; C8 root decompression; C7 laminectomy + partial lateral mass resection +/- C6 and T1 partial laminectomy

Q7.How does SIJ involvement progress radiologically in ankylosing spondylitis?

X-ray SIJ progression: erosion, sclerosis and ankylosis
Assess with the Ferguson view (~20 degrees cranial)
First radiological sign is squaring of the vertebrae

Q8.What blood tests and further imaging are requested in suspected AS?

Bloods: CBC, ESR, CRP, HLA-B27
XR of the thoracic and cervical spine; whole spine sagittal alignment
Need lateral XR for facet joint ankylosis; watch for vertebral collapse (osteoporosis)

Q9.What types of spinal osteotomy are used for AS deformity correction?

SPO: laminectomy + pars
Ponte: SPO + facets
PSO: posterior elements + pedicle
Vertebral column resection (VCR)
Site usually lumbar: wider canal, end of conus, no ribs, large correction power

Q10.What are the key points of cervical spine osteotomy in AS?

Indications: chin-on-chest; residual upper cervical kyphosis causing downward gaze after lumbar osteotomy
Aim to correct CBVA to within 10 degrees
Level C7/T1: wide canal, mobile root (C8), vertebral artery not entering lateral mass
PSO closing wedge better than SPO opening wedge: instability; oesophageal stretching causing dysphagia
Instrumentation U3L3; C8 root decompression; C7 laminectomy + partial lateral mass resection +/- C6 and T1 partial laminectomy

▸ Slide 457 · AS spine fracturesSpine Non Trauma · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What does the sagittal CT show and what should you suspect?
How do you initially manage a suspected AS spine fracture?
What is the definitive management and why is healing difficult?
What are the pre-operative challenges in AS spine fracture surgery?
What are the intra-operative challenges in AS spine fracture surgery?
What are the post-operative complications and epidemiology?

Answers · Q & A

Q1.What does the sagittal CT show and what should you suspect?

Most of the spine ankylosed with a break at the C6/7 level
No obvious soft tissue swelling; posterior element not involved in this CT cut
Suspect ankylosing spondylitis with fracture/pseudoarthrosis

Q2.How do you initially manage a suspected AS spine fracture?

Start with ATLS and immobilize the spine
Expect shock - at this level it can be neurogenic shock; rule out other causes, give fluid resuscitation and vasopressor
Once stabilized, document neurology
Screen the rest of the CT for noncontiguous fractures
MRI to look for epidural haematoma

Q3.What is the definitive management and why is healing difficult?

Fractures heal poorly as the spine is stiff with high stress
Offer posterior decompression and instrumented fusion

Q4.What are the pre-operative challenges in AS spine fracture surgery?

Risk of GA due to cardiorespiratory comorbidities; adjust medications
Difficult airway and ventilation - may need awake fibreoptic intubation

Q5.What are the intra-operative challenges in AS spine fracture surgery?

Positioning in functional/natural position (sandwich prone), do not reduce, fix in situ/original kyphosis, avoid pressure points
Posterior extensile approach; loss of landmarks - need CT navigation and neuromonitoring
Osteoporotic bone (cement - not in the cervical spine); bleeding
Need decompression? If no neurology, no need as want to save more bone bed for fusion; fixation in situ as heroic reduction risks neuro compromise
Long segment fusion; defer anterior reconstruction and deformity correction

Q6.What are the post-operative complications and epidemiology?

Pseudoarthrosis (may need secondary anterior procedure), infection, instrumentation failure
Wound breakdown (tight skin from kyphosis)
SCI incidence 21.1%; multiple and noncontiguous fractures in 13.1%
ASAS classification for AS (modified from modified NY criteria due to delay in diagnosis)

▸ Slide 458 · DISH Forestier diseaseSpine Non Trauma · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What is DISH (Forestier disease)?
What are the radiological features of DISH?
How is DISH treated?
What is the association between DISH and total hip replacement?

Answers · Q & A

Q1.What is DISH (Forestier disease)?

Diffuse idiopathic skeletal hyperostosis - common disorder of unknown etiology with back pain and stiffness
XR: flowing candle wax; associated with HLA-B8
Defined by non-marginal syndesmophytes over 4 continuous vertebral bodies (3 IVD)
10%, more common in middle-aged males, equal in old; mainly anterolateral
Risk factors: DM, hyperlipidaemia, gout

Q2.What are the radiological features of DISH?

Distribution T (R > L) > C > L
Preserved disc space, no osteopenia, no degenerative changes
SIJ not involved; posterior elements not involved (no facet ankylosis, no intra-articular osseous fusion/sclerosis)

Q3.How is DISH treated?

Activity modification, physical therapy, brace wear
NSAIDs and bisphosphonate therapy

Q4.What is the association between DISH and total hip replacement?

Patients with DISH have double the chance of heterotopic ossification (HO)
This applies to patients undergoing total hip replacement (THR)

▸ Slide 459 · Describe CT/XR:Spine Non Trauma · 14 questions expand

Question list

Q1-Q1414 questions — tap to reveal all answerslist

Describe the CT/XR findings in cervical myelopathy.
Describe the MRI findings in cervical myelopathy.
What are the causes of cervical myelopathy and its poor prognostic factors?
What is the natural history of cervical myelopathy and OPLL?
How do you choose the operative approach (PAINS)?
What are the complications of laminoplasty, and how does it compare with laminectomy and fusion?
What history is taken in cervical myelopathy?
What does the physical examination include in cervical myelopathy?
What investigations are performed in cervical myelopathy?
What is the pathology of OPLL?
What is the neurological recovery after surgery for cervical myelopathy (Cheung 2008)?
What is the pseudoarthrosis rate after anterior cervical surgery?
What is the incidence of adjacent segment disease and the evidence for ADR?
What are the criteria, technique, advantages and disadvantages of ADR?

Answers · Q & A

Q1.Describe the CT/XR findings in cervical myelopathy.

Degenerative changes with osteophyte formation and mixed-type OPLL; kyphosis (K line/ C2-C7 angle)
Canal stenosis: absolute <10mm, relative 13mm
Pavlov ratio <0.8; Penning's jaw diameter <12mm suggests a congenital stenosis component
Occupancy ratio >0.4 = poor prognosis
Mizuno XR classification for OPLL: segmental, continuous, mixed, circumscribed/localized (at disc)

Q2.Describe the MRI findings in cervical myelopathy.

Multi-level stenosis with compression from both anterior and posterior (disc, bulging, ossified PLL/yellow ligament)
Kyphosis
Cord edema

Q3.What are the causes of cervical myelopathy and its poor prognostic factors?

Causes: spondylosis (anterior PID, calcified/buckled PLL, Luschka osteophytes; posterior calcified/buckled YL), OPLL, instability (e.g. C1/2), worsened by congenital narrowing (Pavlov <0.8)
Poor prognosis: age >70, chronic symptoms >6 months, JOA <9, multiple levels, canal <30mm2, cord signal (T1 hypo/T2 hyper), compression ratio <0.4

Q4.What is the natural history of cervical myelopathy and OPLL?

Clark: 70% stepwise, 20% gradual, 10% sudden deterioration then plateau
Matsunaga Spine 2012 OPLL: 20% myelopathy at presentation, 20% develop symptoms, 70% asymptomatic
Risk of myelopathy: >60% canal stenosis by OPLL and laterally deviated-type OPLL on CT
Bad CT: C sign = high risk of dural tear

Q5.How do you choose the operative approach (PAINS)?

Assess: axial neck pain/ radiculopathy, alignment (rigid kyphosis, K line), instability, number of levels, site of pathology
1-2 levels: ASF or ASD if no instability
>3 levels without rigid kyphosis: posterior (laminectomy + fusion if axial neck pain/instability, else laminoplasty)
>3 levels with kyphosis: anterior + posterior (anterior to realign/decompress, posterior to decompress/fuse)
K line: K+ no instability = laminoplasty; K+ instability = laminectomy + fusion; K- = A+P
Conservative: analgesics for neck pain, physio; advise operation if JOA <=13 as symptoms usually progress

Q6.What are the complications of laminoplasty, and how does it compare with laminectomy and fusion?

Complications: fracture hinge, spring back of hinge, C5 palsy, axial neck pain, late kyphosis
Laminoplasty advantages: motion preserving (30-40% motion loss quoted), less morbidity, no instrumentation, shorter rehab
Laminectomy + fusion advantages: may relieve neck pain; OPLL may resolve after stabilisation

Q7.What history is taken in cervical myelopathy?

Age, demand, history of DM, chief complaint and progress
Axial neck pain and radicular pain
Function by JOA: use of chopsticks/spoon, walking on level ground/stairs/walking aids, sphincter condition, numbness of UL, trunk and LL
Trauma and red flag signs

Q8.What does the physical examination include in cervical myelopathy?

Power, sensation, jerks, myelopathy hand signs, long tract signs
Lhermitte, Spurling, Romberg/tandem walking
PR examination and jaw jerk

Q9.What investigations are performed in cervical myelopathy?

XR oblique views and flexion/extension views
CT for extent of OPLL and the double layer sign
MRI for cause, level and severity of stenosis

Q10.What is the pathology of OPLL?

Mass of woven and lamellar bone plus fibrocartilage

Q11.What is the neurological recovery after surgery for cervical myelopathy (Cheung 2008)?

Cheung WY Int Orthop 2008: neurological recovery in 71% of patients
Plateau at 6 months
Best in upper limbs, then lower limbs; worst with sphincter dysfunction

Q12.What is the pseudoarthrosis rate after anterior cervical surgery?

Without anterior plate: one level 0-5%, two level 10-20%, three level 30-60%
With anterior plate: one level 0-5%, two level 0-3%, three level 0-7%

Q13.What is the incidence of adjacent segment disease and the evidence for ADR?

Adjacent segment disease: 25% within the first 10 years
BJJ Findlay 2018: meta-analysis of 14 RCTs, follow-up 2-10 years
TDR as effective as ACDF and superior for some outcomes; TDR > ACDF at 2 years and also 4-7 years
Reduces the risk of adjacent segment disease (ACDF ASD 1.6-4.2% per year)

Q14.What are the criteria, technique, advantages and disadvantages of ADR?

Strict criteria: no significant neck pain, no facet arthritis, anterior compression only, no instability, good bone stock (no osteoporosis)
Technique: alignment of COR in coronal and sagittal planes, accurate sizing and endplate preparation
Advantages: preserve motion, prevent ASD
Disadvantages: implant failure/migration; easy to overstuff -> posterior neck pain (increased facet loading)

▸ Slide 460 · OPLLSpine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What are the classifications of OPLL?
Why is OPLL difficult to treat, and what is the anterior strategy?
What is the indication for treatment of OPLL?

Answers · Q & A

Q1.What are the classifications of OPLL?

XR (Mizuno): focal, segmental, continuous, mixed
CT (Hirabayashi): square, mushroom, hill

Q2.Why is OPLL difficult to treat, and what is the anterior strategy?

Difficult: multi-level, at the level of the vertebral body, high chance of dural tear
If anterior approach needed: decompress the surrounding bone; may need to leave OPLL on the dura (floating technique)
Corpectomy may be required

Q3.What is the indication for treatment of OPLL?

Indication for treatment is the same as for cervical myelopathy
No separate OPLL-specific indications are given in the notes

▸ Slide 461 · Functional classification of cervical myelopathySpine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

Which functional classifications of cervical myelopathy are shown?
Describe the Nurick classification (grades 0-5).
Describe the Ranawat classification.

Answers · Q & A

Q1.Which functional classifications of cervical myelopathy are shown?

Nurick classification - based on gait and ambulatory function
Ranawat classification - based on pain, weakness and ambulatory status

Q2.Describe the Nurick classification (grades 0-5).

Grade 0: root symptoms only or normal
Grade 1: signs of cord compression, normal gait
Grade 2: gait difficulties but fully employed
Grade 3: gait difficulties prevent employment, walks unassisted
Grade 4: unable to walk without assistance
Grade 5: wheelchair or bedbound

Q3.Describe the Ranawat classification.

Class I: pain, no neurologic deficit
Class II: subjective weakness, hyperreflexia, dysesthesias
Class IIIA: objective weakness, long tract signs, ambulatory
Class IIIB: objective weakness, long tract signs, non-ambulatory

▸ Slide 462 · JBJS 1987 by OnoSpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the finger escape sign classification (Ono, JBJS 1987)?
What is the source of this classification and how is the test performed?

Answers · Q & A

Q1.What is the finger escape sign classification (Ono, JBJS 1987)?

Cannot hold
Cannot do
2 finger / cannot do full extension
3 finger
Closing the eyes is not necessary for the test

Q2.What is the source of this classification and how is the test performed?

JBJS 1987 by Ono
Finger escape sign classification
Patient does not need to close the eyes

▸ Slide 463 · Lumber stenosisSpine Non Trauma · 12 questions expand

Question list

Q1-Q1212 questions — tap to reveal all answerslist

Describe the MRI findings in lumbar stenosis.
What must be excluded and assessed in back pain with suspected stenosis?
What are the red flag signs in lumbar stenosis?
How do you differentiate the nature of pain and claudication?
What are the treatment aims and indications for fusion?
What is the evidence for decompression with or without fusion, and the natural history of degenerative spondylolisthesis?
What else should be delineated on MRI in lumbar stenosis?
What are the borders of the lateral recess, midzone and intervertebral foramen?
How can fusion relieve back pain and why choose interbody fusion?
What are the anterior and posterior approaches and operations used to relieve stenosis?
What are the complications of fusion and of each surgical approach?
What is degenerative spondylolisthesis and what do the natural history studies show?

Answers · Q & A

Q1.Describe the MRI findings in lumbar stenosis.

Sagittal T2 image: severe stenosis and grade 1 anterolisthesis at L3/4 and L4/5
Disc bulging and buckling of the thickened ligamentum flavum
No endplate destruction, no collapse

Q2.What must be excluded and assessed in back pain with suspected stenosis?

Rule out infection/tumour, rule out cauda equina syndrome, rule out upper spinal involvement (brisk jerk)
Assess severity of axial symptoms and neurology
Assess instability

Q3.What are the red flag signs in lumbar stenosis?

Extremes of age; history of trauma
History of cancer/drug abuse; constitutional symptoms
Rest pain / night pain waking the patient
Saddle anaesthesia / sphincter disturbance

Q4.How do you differentiate the nature of pain and claudication?

Discogenic: worse with increased intradiscal pressure - flexion, sitting, heavy lifting, sneezing
Facet: pain in extension, radiating to posterior thigh and buttock; instability: forward flexion + extension catch
Inflammatory: relief with exercise, morning stiffness; pathological: persistent/night pain
Vascular claudication: exertion-related, worse walking/upslope, relieved by rest even upon standing, diminished peripheral pulses
Neurogenic claudication: exertion + posture, worse walking/downslope, relieved by sitting, not standing (flexion reduces ligament buckling)

Q5.What are the treatment aims and indications for fusion?

Aims: pain relief (disc, instability, facet), decompression of neural elements, prevent progression
Conservative: anti-lordotic brace, flexion-based exercises
Fusion if: pain (discogenic, facet effusion, foraminal stenosis), severe deformity (degenerative scoliosis), instability (dynamic X-ray, anterolisthesis, iatrogenic >50% facet removal, extensive discectomy)
In anterolisthesis with a very narrowed disc (autostabilization) and no dynamic instability, decompression alone may suffice

Q6.What is the evidence for decompression with or without fusion, and the natural history of degenerative spondylolisthesis?

SPORT trial: surgery better SF-36 and ODI vs non-operative up to 8 yrs
Pro-fusion: Herkowitz 1991, Kornblum 2004, Martin 2007 (revision 28% vs 17%), Ghogawala NEJM 2016 (SLIP) - stable slips – fusion group had better functional outcomes and lower revision rate
Against: Forsth NEJM 2016 - fusion group had significantly higher blood loss, surgical cost, length of stay, no difference in outcomes; authors did not distinguish between stable and unstable slips. Repoperation rate of 20% due to ASD, restenosis
Weinstein commentary 2016: decompression alone reasonable for many; fusion may prevent slip progression and reduce reoperation
Degenerative spondylolisthesis (Johnson): 70% stable, 15% improve, 15% deteriorate
Matsunaga: 30% progressive, no X-ray/clinical correlation; instability risk: translation >5mm, disc height <6.5mm, Facet angle >50 deg

Q7.What else should be delineated on MRI in lumbar stenosis?

Neuroforamen stenosis and which side of the lateral recess/central canal is more stenotic
Facet effusion and facet orientation

Q8.What are the borders of the lateral recess, midzone and intervertebral foramen?

Lateral recess: posterior SAP, anterior disc, medial sac, lateral pedicle
Midzone: posterior pars, anterior VB, medial canal, lateral foramen, superior pedicle
IVF: posterior SAP, anterior disc, superior/inferior pedicle

Q9.How can fusion relieve back pain and why choose interbody fusion?

PL and interbody fusion have similar fusion rates (Levin Spine 2018 meta-analysis: PL 84% vs TLIF 94% radiological fusion; weak data for clinical improvement)
Interbody fusion: compression side gives theoretically better fusion and eliminates the disc pain generator
Better at reducing listhesis and restoration of sagittal balance
Corrects disc height (helps neuroforamen stenosis) and restores ligament tension (flagpost theory)

Q10.What are the anterior and posterior approaches and operations used to relieve stenosis?

Anterior: less muscle dissection and infection, bigger cage, better deformity correction, indirect decompression
Posterior: avoids great vessels, allows foraminal decompression
Central stenosis (claudication): laminectomy, which can selectively increase decompression on the more stenotic side
Radiculopathy (lateral recess/neuroforamen): undercut/medial facetectomy; restore disc height to increase neuroforamen space

Q11.What are the complications of fusion and of each surgical approach?

Fusion complications: pseudoarthrosis, cage migration/subsidence, implant failure
Posterior approach: durotomy and traction injury to the nerve root, posterior muscle pain and spasm
Anterior approach: vascular injury, sympathetic dysfunction, transpsoas injury (ureter, lumbar plexus e.g. genitofemoral nerve)

Q12.What is degenerative spondylolisthesis and what do the natural history studies show?

Result of disc degeneration with decreased disc height, ligament buckling and microinstability
Commonest at L4/5; PE shows stepping at L4/5
76% of patients with no neuro deficits initially remained without deficits; 83% with neuro symptoms experience deterioration

▸ Slide 464Spine Non Trauma · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

What topic does slide 464 cover?
What are the key teaching points of slide 464?

Answers · Q & A

Q1.What topic does slide 464 cover?

Not covered in the speaker notes
The slide image is the only source for this slide

Q2.What are the key teaching points of slide 464?

Not covered in the speaker notes
No content is provided beyond the slide number

▸ Slide 465Spine Non Trauma · 11 questions expand

Question list

Q1-Q1111 questions — tap to reveal all answerslist

Describe the radiographic assessment of isthmic spondylolisthesis.
What are the clinical features of isthmic spondylolisthesis?
What is the natural history of spondylolisthesis (Fredrickson 1984)?
What are the risk factors for progression of an isthmic slip?
What are the treatment options for spondylolisthesis?
What are the causes of symptoms and the etiological classification of spondylolisthesis?
What is the Spinal Deformity Study Group classification for reduction in high-grade spondylolisthesis?
What are the problems of in-situ fusion for high-grade spondylolisthesis?
What is the Gaines procedure and what is its risk?
What are the subgroups of isthmic spondylolisthesis?
What fusion technique is preferred in spondylolisthesis surgery?

Answers · Q & A

Q1.Describe the radiographic assessment of isthmic spondylolisthesis.

Lateral: L5 pars defect with spondylolisthesis; slip severity (Meyerding); L5/S1 disc status; bone morphology (trapezoidal VB, dome sacrum)
Lumbar lordosis (normal 20-45), lumbosacral kyphosis (slip angle), sacral inclination (normal >30)
AP: spina bifida occulta; inverted Napoleon's hat in spondyloptosis
Dynamic lateral: 4.5mm translation or 22deg angulation vs the adjacent motion segment
Scannogram: PI = SS + PT

Q2.What are the clinical features of isthmic spondylolisthesis?

PE (L5/S1): stepping at L4/5, lumbar hyperlordosis, pelvic retroversion + hip flexion contracture + hamstring tightness + knee flexion contracture
Phalen-Dixon sign in severe slip
Phalen-Dixon crisis - high grade slip: sudden severe sciatic pain (L5/S1 root irritation), tight hamstrings, flat sacrum, pelvic waddling gait, cauda equina compression with ischiocrural spasm, scoliosis

Q3.What is the natural history of spondylolisthesis (Fredrickson 1984)?

500 patients at age 6 with 45-year follow-up
M>F
No slip if unilateral; most frequent progression in the adolescent
No association between slip progression and back pain
Conclusion: benign course, with only a small percentage developing symptomatic progression

Q4.What are the risk factors for progression of an isthmic slip?

Patient factors: female, young age at presentation, frequent back extension
Morphology: dysplastic pars, sacral dome, wedging of L5, sacral inclination <30, PI >70, large slip angle (>45)
Slip: high grade

Q5.What are the treatment options for spondylolisthesis?

Conservative: flexion-based exercises, anti-lordotic brace, hamstring stretching, core strengthening
Surgery if: slip progression, high grade, Phalen-Dixon crisis, failed conservative treatment (back pain/radiculopathy)
Pars repair in young patients with no slip and normal disc: Buck's screw (cortical bone trajectory, directly across the fracture), Scott wire, Morscher hook screw, pedicle hook screw
Fusion +/- reduction +/- decompression
Reduction controversial: consider in high grade (>50%) + retroverted pelvis + poor sagittal balance; risk of neuro impairment ~33% (L5 stretch injury), needs neuromonitoring
Reduction advantages: restores sagittal alignment, reduces gait abnormalities, larger fusion bed placing fusion in compression rather than shear

Q6.What are the causes of symptoms and the etiological classification of spondylolisthesis?

Wiltse and Newman: dysplastic, isthmic (lytic, elongated, pars fracture), degenerative, traumatic, pathological, post-surgical
Back pain causes: discogenic, pars defect, instability, facet degeneration (remember asymptomatic slip is common)
Radiculopathy: L5/S1 slip compresses the L5 root (foramen enlarged; root encroached by pedicles/fibrocartilage of the pars defect); L5/S1 PID gives S1 radiculopathy
Isthmic: most common at L5/S1; risk factors repetitive hyperextension (gymnasts, dancers), Eskimo populations, first-degree relative
Reduction: passive (muscle relaxant, prone, facet + discectomy, disc height restoration); active (reduction screws, neuromonitoring, fluoroscopy)

Q7.What is the Spinal Deformity Study Group classification for reduction in high-grade spondylolisthesis?

High grade, balanced pelvis = no need for forceful attempts at reduction
High grade, retroverted pelvis but balanced spine = attempt postural (passive) reduction
High grade, retroverted pelvis and unbalanced spine = reduction/realignment mandatory (active), under neurological monitoring

Q8.What are the problems of in-situ fusion for high-grade spondylolisthesis?

Pseudoarthrosis
Progressive slippage
Persistent lumbosacral deformity
Cauda equina syndrome

Q9.What is the Gaines procedure and what is its risk?

Anterior L5 vertebrectomy + posterior L4 to S1 fusion
75% neurological injury

Q10.What are the subgroups of isthmic spondylolisthesis?

Elongated pars
Fatigue fracture
Acute fracture

Q11.What fusion technique is preferred in spondylolisthesis surgery?

Posterolateral (PL) vs interbody fusion
Circumferential fusion is preferred

▸ Slide 466 · SpondylolysisSpine Non Trauma · 4 questions 1 check expand

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Q1-Q44 questions — tap to reveal all answerslist

What is spondylolysis and what is spondylolisthesis?
What are the radiographic findings of spondylolysis?
What is the pathophysiology and who is affected?
What is the treatment and prognosis of spondylolysis without listhesis?

Answers · Q & A

Q1.What is spondylolysis and what is spondylolisthesis?

Spondylolysis: defect in the pars interarticularis
Spondylolisthesis: forward slippage of one vertebra over another

Q2.What are the radiographic findings of spondylolysis?

Defect in the neck of the 'Scottie dog'
Notes state 80% seen on lateral, 15% on oblique, 5% subtle defect on CT/SPECT

Q3.What is the pathophysiology and who is affected?

Fatigue fracture from repetitive hyperextension stress
Examples: gymnasts, football linemen

Q4.What is the treatment and prognosis of spondylolysis without listhesis?

Activity restriction, flexion exercise, bracing
Nonunion is common
Unilateral defect never progresses to listhesis

Fact check

Spondylolysis on XR: 80% seen on lateral, 15% on oblique, 5% are subtle defects on CT/SPECT — contested — The oblique 'Scotty dog' view is classically the standard projection for spondylolysis, though sensitivity of lateral vs oblique is debated (coned lateral may detect ~85% of bilateral L5 defects). Early stress reactions are commonly invisible on plain XR (detection ~11-23% in early lesions), so more than 5% require CT/SPECT/MRI — medium confidence — source

▸ Slide 467Spine Non Trauma · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

On the oblique lumbar radiograph, which structure forms the 'neck' of the Scottie dog?
Why is the oblique view used in suspected spondylolysis?

Answers · Q & A

Q1.On the oblique lumbar radiograph, which structure forms the 'neck' of the Scottie dog?

The pars interarticularis (isthmus) of the vertebra
Ear = superior articular process, foreleg = inferior articular process, body = lamina and spinous process

Q2.Why is the oblique view used in suspected spondylolysis?

Profiles the pars interarticularis - the neck of the Scottie dog
The radiograph shows the outlined defect: a break in the neck = pars defect (spondylolysis)

▸ Slide 468 · Degenerative scoliosisSpine Non Trauma · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

Describe the X-ray findings in degenerative scoliosis.
What are the causes of degenerative scoliosis?
What is the degenerative cascade of the spine?
What is the management approach for degenerative scoliosis?
How does de novo degenerative scoliosis differ from pre-existing/neglected scoliosis?
What is the rate and what are the risk factors for curve progression?

Answers · Q & A

Q1.Describe the X-ray findings in degenerative scoliosis.

Convexity to the right at the mid lumbar spine with a rotational component
Marked degenerative change at multiple facet joints; pedicles and endplate intact
Need lateral + whole spine XR (coronal and sagittal balance), F/E XR, prone traction views for vertical instability, bending and fulcrum views
MRI also required

Q2.What are the causes of degenerative scoliosis?

Osteoporotic collapse
Spondylolisthesis

Q3.What is the degenerative cascade of the spine?

Disc degeneration with decreased water content and decreased disc height
Buckling of ligaments, decreased stability
Increased stress on facet joints -> osteoarthritis and facet hypertrophy
Facet cannot resist shear -> anterior translation (especially with sagittal-oriented facets)
Can cause spinal stenosis/deformity; some may auto-stabilize

Q4.What is the management approach for degenerative scoliosis?

Define the patient's complaint clearly; assess neurology, spinal stability, sagittal balance
Osteoporosis treatment if related to osteoporotic collapse
Decompression only: leg pain, minimal/no back pain, Cobb <30, <2mm subluxation, no thoracic hyperkyphosis, acceptable balance, poor premorbid
Short fusion: back and leg pain, scoliosis <30, segmental instability, no significant global imbalance, extensive decompression
Long fusion: back and leg pain, scoliosis >45, >2mm subluxation, significant global imbalance (determine UIV and LIV)
Severe deformity with poor balance: corrective osteotomy + long fusion (high OT risk, outcome not guaranteed)

Q5.How does de novo degenerative scoliosis differ from pre-existing/neglected scoliosis?

De novo has less coronal deformity (less Cobb, less L4 tilt, less rotational deformity) but more sagittal pelvic malalignment
Fewer vertebral segments involved; affects the lumbar spine
Disc space wedging, osteoporotic collapse, less bone maldevelopment (pedicles)

Q6.What is the rate and what are the risk factors for curve progression?

3 degrees per year
Prior history of progression; unstable segment (asymmetrical disc degeneration, lateral disc wedging, >5mm lateral osteophyte difference)
Cobb >30 degrees, lateral listhesis >6mm
Intercrestal line through L4/5 disc or lower, rotatory subluxation, loss of lumbar lordosis

▸ Slide 469 · Osteoporotic collapseSpine Non Trauma · 16 questions expand

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Q1-Q1616 questions — tap to reveal all answerslist

Describe the X-ray findings of an osteoporotic vertebral collapse and the initial workup.
What are the aims of management in osteoporotic collapse?
How is osteoporotic collapse managed systemically?
How is osteoporotic collapse managed locally?
When is vertebroplasty considered for an osteoporotic collapse?
What are the prerequisites for vertebroplasty?
What are the complications of vertebroplasty?
Why is kyphoplasty preferred over vertebroplasty?
What did the two NEJM 2009 RCTs show about vertebroplasty and how were they criticised?
What did the VAPOUR and VERTOS IV trials show about vertebroplasty?
What is the AAOS 2010 guideline on treating osteoporotic collapse?
How can adjacent level collapse and non-union be decreased after augmentation?
What other options exist apart from vertebroplasty/kyphoplasty and what are the problems with them?
How can failure at the bone-implant interface be reduced?
What is the mechanism of calcitonin for pain relief?
What is Kummel disease and what are its imaging features?

Answers · Q & A

Q1.Describe the X-ray findings of an osteoporotic vertebral collapse and the initial workup.

Anterior wedge collapse of T12 with no retropulsion
Request AP X-ray to look for widening of the interpedicular distance
Ask about mechanism of injury, cancer history, features of infection/TB, neurological deficit
Bloods: bone profile, tumour markers, SEP and inflammatory markers

Q2.What are the aims of management in osteoporotic collapse?

Pain relief and early mobilisation
Prevent deformity and neurological deficit
Prevent future collapse

Q3.How is osteoporotic collapse managed systemically?

Assess osteoporosis severity and calculate future fracture risk
Quit smoking and alcohol, give calcium and vitamin D, weight-bearing exercise
Anti-osteoporotic medication

Q4.How is osteoporotic collapse managed locally?

Analgesics, calcitonin +/- brace
If failed conservative management or non-union, consider kyphoplasty

Q5.When is vertebroplasty considered for an osteoporotic collapse?

Ongoing pain more than 2 weeks after occurrence of a new fracture despite treatment
Progressive compression fractures of one or multiple vertebrae with subsequent loss of posture
Non-union with persisting instability

Q6.What are the prerequisites for vertebroplasty?

Intact posterior wall
Neurologically intact

Q7.What are the complications of vertebroplasty?

Anaesthesia-related complications
Cannula placement: infection, spinal cord injury, fracture of pedicles/transverse process, lung injuries
Cement injection: cement leakage into the spinal canal causing neurological deficits, pulmonary cement embolism, fat embolism
Late adjacent segment collapse

Q8.Why is kyphoplasty preferred over vertebroplasty?

Better evidence on pain relief and potential kyphosis correction
Fewer complications than vertebroplasty due to decrease in insertion pressure
Mechanism: reduces kyphosis, low-pressure injection, increased viscosity of injection
Greater reduction in kyphotic angle and less extraosseous cement leakage than vertebroplasty

Q9.What did the two NEJM 2009 RCTs show about vertebroplasty and how were they criticised?

Buchbinder et al.: pain, QoL and function same as placebo surgery up to 6 months
Kallmes et al.: pain similar to placebo surgery at 3 months
A JBJS 2009 publication criticised their methodology, mainly the cement volume

Q10.What did the VAPOUR and VERTOS IV trials show about vertebroplasty?

VAPOUR trial (Lancet 2016, Clark): vertebroplasty vs sham - great reduction in pain at 3 and 6 months
It is the only RCT to support vertebroplasty; patients had more severe pain, fracture age <6 weeks, and more PMMA cement was used
VERTOS IV (BMJ 2018): no significant pain relief vs sham
AAOS changed stance in 2014, suggesting limited evidence

Q11.What is the AAOS 2010 guideline on treating osteoporotic collapse?

Moderate evidence: calcitonin for pain relief
Weak evidence: ibandronate and strontium, kyphoplasty
Inconclusive: bed rest, brace, exercise programme, electrical stimulation
Not advised: vertebroplasty
Avoid in fractured posterior wall and neurologically compromised patients

Q12.How can adjacent level collapse and non-union be decreased after augmentation?

Treat osteoporosis
Watch for fracture patterns that increase non-union: split type fracture / large angular motion
Beware of endplate deficit leading to intradiscal cement leakage
Avoid aggressive restoration of vertebral height

Q13.What other options exist apart from vertebroplasty/kyphoplasty and what are the problems with them?

Problems with more extensive surgery: medically fragile patients, poor bone quality at the bone-implant interface
Approach: anterior vs A+P vs posterior
Decompression; reduction?
Instrumentation: short or long, construct type (screw-rod, plate, sublaminar hooks and wiring), augmentation
Fusion and rehabilitation; removal of implant: no

Q14.How can failure at the bone-implant interface be reduced?

Preop: treat osteoporosis with a bone-forming agent such as teriparatide
Intraop: screw type (HA coated, PMMA augmented), diameter, length - pullout strength 60% depends on cortical bone of the pedicle, 20% on trabecular bone of the body; advancing to 80% of the vertebral body is adequate
Self tap screws (stronger pullout force), or undertap (self-tapping screws); diverging screws aimed towards subchondral bone, straightforward technique better than anatomical trajectory
Expandable pedicle screws; circumferential fusion
Postop bracing
Crosslink and increasing the length of fixation only increase construct stiffness, they do not decrease failure at the bone-implant junction

Q15.What is the mechanism of calcitonin for pain relief?

Binds receptors in the CNS/PNS
Releases endorphin and decreases prostaglandins

Q16.What is Kummel disease and what are its imaging features?

Post-traumatic osteonecrosis of a vertebral body
XR: sclerosis of cleft margin and vertebral body, pedicle ossification, stress fracture of spinous process, paravertebral callus
MRI: double line sign
Vertebroplasty more likely to fail due to lack of interdigitation of cement

▸ Slide 470 · AP Xray T spine of patient showing soft tissue fusiform swellingSpine Non Trauma · 20 questions expand

Question list

Q1-Q2020 questions — tap to reveal all answerslist

What did the plain X-rays show in this case of spinal TB?
What are the typical X-ray and MRI features of spinal tuberculosis?
What is the clinical assessment in suspected spinal TB?
How is spinal TB diagnosed?
What are the aims of management in spinal TB?
How does the spinal level affect the management of TB spine?
How is TB spine managed when there is no neurology and no instability?
How is TB spine with neurological involvement or instability managed?
What is the epidemiology of TB spine?
What is the pathophysiology of spinal TB?
What is Pott's paraplegia and what are its early causes?
What are the Rajasekaran types of paediatric spine deformity?
What are the features of healed TB disease?
What was the design of the MRC trial of TB spine?
What was a favourable outcome in the MRC trial and what did it conclude?
What did Prof Luk criticise about the MRC trial?
What are the absolute indications for surgery in spinal TB?
What are the late complications of spinal TB?
What are the surgical approaches and deformity correction options in TB spine?
What are the spine-at-risk signs of Rajasekaran?

Answers · Q & A

Q1.What did the plain X-rays show in this case of spinal TB?

AP T spine: soft tissue fusiform swelling
Lateral T spine: collapse of T7 and T8, obliterated disc space, acute kyphosis
Gibbus = acute structural thoracolumbar kyphosis
No skipped lesion

Q2.What are the typical X-ray and MRI features of spinal tuberculosis?

X-ray: anterior vertebral body collapse, disc sparing, multiple levels +/- skip lesions, kyphosis, +/- calcification
MRI: skip lesions 15%, paravertebral abscess 50%, disc sparing (multicentric and multilevel), subligamentous spread
Ddx: infection (TB > pyogenic > fungus) and tumour (lymphoma)

Q3.What is the clinical assessment in suspected spinal TB?

Symptoms: deformity, pain, neurology
Risk factors of infection: immunocompromised, previous TB infection, contact history
Red flag signs
Rule out other differentials: pyogenic infection, carcinoma, lymphoma

Q4.How is spinal TB diagnosed?

Morning urine and sputum TB PCR
CXR abnormal in 2/3 of cases
Biopsy (low sensitivity)
MRI with gadolinium: low T1, bright T2

Q5.What are the aims of management in spinal TB?

Control infection
Control back pain
Salvage neurology
Prevent/correct deformity

Q6.How does the spinal level affect the management of TB spine?

C spine: low threshold for surgery
Lumbar spine: conservative first
T spine: depends on neurology

Q7.How is TB spine managed when there is no neurology and no instability?

Isoniazid + rifampicin, +/- streptomycin
Expected kyphosis = total vertebral involvement x 30.5 + 5.5 (Rajasekaran)

Q8.How is TB spine with neurological involvement or instability managed?

Debridement only: expected kyphosis 10 degrees
HK operation: anterior radical debridement (extirpation) + fusion with strut graft
No instrumentation if <3 levels; instrumentation if >=3 levels
Advantages: direct visualisation of the lesion, fusion under compression anteriorly

Q9.What is the epidemiology of TB spine?

Extrapulmonary TB in 3% of cases
Skeletal TB in 10% of extrapulmonary TB
Spinal TB in 50% of all skeletal TB
Site: TLJ > T > LS > C

Q10.What is the pathophysiology of spinal TB?

Granulomatous spondylitis with a delayed hypersensitivity reaction
Starts in the metaphysis of the vertebral body
Subligamentous spread under the ALL: contiguous multilevel, skip lesions, paraspinal abscess
Disc is a natural barrier and is usually spared
Acute kyphosis may progress in children due to growth spurt

Q11.What is Pott's paraplegia and what are its early causes?

Neurological involvement found in up to 10% of patients
Inflammatory tissues/sequestrum
Epidural abscess
Prolapsed disc/retropulsed fragment
Pachymeningitis (poor prognosis)
Spinal subluxation due to non-union level

Q12.What are the Rajasekaran types of paediatric spine deformity?

Retropulsion
Lateral translation
Toppling
Facet separation
More than 2 = unstable and should be fused

Q13.What are the features of healed TB disease?

Direct compression by a transverse bone ridge
Kyphus: sequestrum >5mm, adjacent segment stenosis
Cord atrophy (syringomyelia)
Reactivation

Q14.What was the design of the MRC trial of TB spine?

Series of studies since 1965 in multiple centres worldwide; follow-up up to 15 years
Korea - Masan: inpatient 6 months bed rest vs outpatient; Pusan: POP jacket vs no jacket
Hong Kong: radical debridement + graft vs debridement; Bulawayo: nonoperative vs operative debridement
Inclusion: clinical and radiological TB, T1-S1 disease
Exclusions: significant neurological deficit (unable to walk room length), significant extraspinal disease, >3 levels of destruction, C spine, anti-TB drugs >1 year
All had anti-TB drugs (PASINAH)

Q15.What was a favourable outcome in the MRC trial and what did it conclude?

Favourable outcome: no symptoms, full physical activity, no CNS involvement, no sinus/abscess, radiological healing; assessed at 5, 10, 15 years
POP jacket not required (Pusan)
Outpatient antibiotics without bedrest are OK (Masan)
HK procedure: anterior decompression + radical debridement + uninstrumented autogenous strut graft fusion > debridement alone
Quicker pain relief, earlier abscess/sinus resolution, higher fusion rate (85% at 5y, 95% at 15y), Kyphosis (3deg@5 maintained @15)
Nonoperative vs operative: all had favourable outcomes

Q16.What did Prof Luk criticise about the MRC trial?

Patients had mild disease
Only 15-year follow-up
Surgery gave quicker resolution of sinus and abscess, higher fusion rate, less late deformity (kyphosis ~10 degrees)

Q17.What are the absolute indications for surgery in spinal TB?

Failed conservative treatment (3-4 weeks)
Neurological involvement
Instability/deformity: kyphosis more than 60 degrees causes significant morbidity, or spinal instability score >2
Non-compliance or non-diagnostic biopsy

Q18.What are the late complications of spinal TB?

Gibbus due to non-union after central necrosis
Pott's paraplegia: reactivation, adjacent segment disease, cord atrophy
Kyphus with sequestrum >5mm and adjacent segment stenosis
Cord atrophy/syringomyelia

Q19.What are the surgical approaches and deformity correction options in TB spine?

Approach - anterior: above T4 equal from either side (usually from the side with the large abscess); below T4 from the left; thoracotomy with rib resection 2 levels above
Decompression: mild - posterior decompression; severe - costotransversectomy + internal kyphus excision
Stabilisation: anterior fusion with strut graft
Deformity correction: mild - closing wedge osteotomy; severe - halo pelvic traction

Q20.What are the spine-at-risk signs of Rajasekaran?

Spine toppling sign
Lateral translation
Posterior facet widening
Retropulsion
More than 2 signs = unstable and should be fused

▸ Slide 471Spine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What topic does this slide cover?
What key teaching point is illustrated on this slide?

Answers · Q & A

Q1.What topic does this slide cover?

Spine Non Trauma (from the slide topic)
Not covered in the speaker notes

Q2.What key teaching point is illustrated on this slide?

Not covered in the speaker notes

▸ Slide 472 · XR showing T9 collapseSpine Non Trauma · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What is the initial X-ray finding in this case?
What history and examination points are important in a patient with a collapsed vertebra?
What is important about the pain history in a collapsed vertebra?
What investigations are used for suspected TB spine (T9 collapse)?
How is an open biopsy of the spine performed?
What are the indications for surgery in TB spine and what is the medical regimen?

Answers · Q & A

Q1.What is the initial X-ray finding in this case?

T9 vertebral collapse

Q2.What history and examination points are important in a patient with a collapsed vertebra?

PMHx and premorbid mobility
Neurology and sphincter function
Costal margin pain
PE: neurological examination

Q3.What is important about the pain history in a collapsed vertebra?

Nature of pain - rest/nocturnal vs mechanical
Onset, progression and alleviating factors

Q4.What investigations are used for suspected TB spine (T9 collapse)?

Routine lymphocytosis
Bone profile and tumour markers
Urinary TB and sputum TB
CT to see the extent of bony destruction
Tissue biopsy: caseating granuloma, AFB, giant cells

Q5.How is an open biopsy of the spine performed?

Transpedicular approach
Costotransversectomy

Q6.What are the indications for surgery in TB spine and what is the medical regimen?

Indications: debilitating pain, deformity, instability
Nonoperative: TLSO brace
DOT: isoniazid, rifampicin, ethambutol, pyrazinamide (intensive phase and continuation phase)
Follow-up to monitor for complications; MRC trial

▸ Slide 473 · jjSpine Non Trauma · 12 questions expand

Question list

Q1-Q1212 questions — tap to reveal all answerslist

Describe the X-ray findings in spondylodiskitis.
What are the risk factors and assessment findings in spondylodiskitis?
What investigations establish the diagnosis and extent of spondylodiskitis?
What MRI features favour infection over tumour?
What are the goals of management in spondylodiskitis?
What are the goals and indications for surgery in spondylodiskitis?
What is the nonoperative management and expected success rate in spondylodiskitis?
What is the pathophysiology of spondylodiskitis?
What is the anatomical distribution of spondylodiskitis?
Which organisms cause spondylodiskitis and how long are antibiotics given?
What are the operative approaches and strut graft options in spondylodiskitis?
What is the role of instrumentation in active spinal infection?

Answers · Q & A

Q1.Describe the X-ray findings in spondylodiskitis.

L4 lower and L5 upper endplate destruction
Decreased disc height and decreased lordosis
Ddx: spondylodiskitis (pyogenic/TB) and malignancy
Less likely TB because the disc is usually spared

Q2.What are the risk factors and assessment findings in spondylodiskitis?

Immunocompromised: IVDA, DM, steroids, malnutrition
Recent systemic infection: UTI, GI, respiratory; recent spine operation
Neurology and pain
Femoral stretch and psoas stretch = psoas abscess
Constitutional symptoms suggest malignancy

Q3.What investigations establish the diagnosis and extent of spondylodiskitis?

CBC, ESR, CRP
Blood cultures positive in ~33%; if positive, ~85% accurate for isolating the correct organism
CT-guided biopsy sent for aerobic, anaerobic, fungal and acid-fast culture
Contrast MRI: loss of T1 body contrast, T2 disc enhancement, contrast-enhancing paravertebral exudate, epidural/psoas abscess

Q4.What MRI features favour infection over tumour?

Disc space involvement
end plate erosion
Significant inflammation
Look for epidural abscess, paraspinal collection and psoas abscess

Q5.What are the goals of management in spondylodiskitis?

Optimise host
Establish microbiological diagnosis
Control of infection
Monitor and prevent neurological deficit, instability and late deformity

Q6.What are the goals and indications for surgery in spondylodiskitis?

Operative goals: eliminate infection (debridement), prevent/improve neurologic deficits (decompression), maintain stability (instrumentation +/- fusion)
Failure to obtain microbiological diagnosis from closed needle biopsy (e.g. C spine)
Poor response to conservative treatment, abscess, neurological deficit
Extensive disease: 2 adjacent VB or single VB with more than 50% collapse, +/- deformity

Q7.What is the nonoperative management and expected success rate in spondylodiskitis?

Nonoperative treatment is the mainstay
IV antibiotics + corset if collapse
Success rate 60-90%

Q8.What is the pathophysiology of spondylodiskitis?

Haematogenous seeding of the endplates (low-flow vascular anastomosis) -> direct extension into the disc -> second endplate
Arterial: diffusion (children/adolescents via intermetaphyseal artery, adults via metaphyseal artery) and septic emboli
Venous via the Batson plexus
Contiguous spread from local infection (retropharyngeal and retroperitoneal abscesses)
Direct inoculation

Q9.What is the anatomical distribution of spondylodiskitis?

Lumbar spine 60% > thoracic 30% > cervical 10%

Q10.Which organisms cause spondylodiskitis and how long are antibiotics given?

Staphylococcus aureus and epidermidis; Gram-negative organisms
E. coli, Pseudomonas in immunocompromised patients
Salmonella in sickle cell anaemia
Duration: 6 weeks vs 12 weeks - no difference (Bernard, Lancet 2015)

Q11.What are the operative approaches and strut graft options in spondylodiskitis?

Single stage: anterior - debridement + reconstruction with strut graft
Two stage: delayed posterior instrumentation and fusion after anterior debridement
Epidural abscess: laminectomy
Strut graft: autogenous tricortical iliac crest, rib or fibula are safe and effective in acute infection
Titanium mesh cages filled with autograft improved deformity correction (Carragee, Spine 2008), followed by posterior instrumentation)

Q12.What is the role of instrumentation in active spinal infection?

Spinal instrumentation in active infection is controversial
Studies show stability of the spine is important for suppression and eventual elimination of infection
Titanium is preferred over stainless steel

▸ Slide 474 · Gadolinium contrast MRISpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the role of gadolinium contrast MRI in spinal infection?
How is an epidural abscess managed?

Answers · Q & A

Q1.What is the role of gadolinium contrast MRI in spinal infection?

Differentiate infection from tumour
Differentiate epidural abscess from CSF - both are high signal on T2
Gadolinium enhance pus in T1, CSF remains low signal

Q2.How is an epidural abscess managed?

Laminectomy and drainage because pus is predominantly posterior
Anterior and posterior decompression if concomitant vertebral osteomyelitis

▸ Slide 475 · XR:Spine Non Trauma · 14 questions 1 check expand

Question list

Q1-Q1414 questions — tap to reveal all answerslist

What X-ray signs suggest spinal metastasis?
What history is important in suspected spinal metastasis?
What examination is needed in suspected spinal metastasis?
What is the Bilsky ESCC score used for?
What imaging and classification systems are used for metastatic spine disease?
What are the treatment goals and principles in metastatic spinal disease?
What medical treatment is given for metastatic cord compression?
What is the evidence for surgery plus radiotherapy in metastatic cord compression?
What is the epidemiology of spinal metastasis?
What is the difference between osteolytic and osteoblastic metastases?
How is hypercalcaemia of malignancy managed?
What are the components and interpretation of the Tokuhashi score?
What are the components of the Tomita score?
What is the principle of tumour separation surgery?

Answers · Q & A

Q1.What X-ray signs suggest spinal metastasis?

Collapse and kyphosis
Winking owl sign (pedicle destruction)
Fusiform swelling
Lung mass

Q2.What history is important in suspected spinal metastasis?

Premorbid status
History of malignancy
History of HIV, IVDU, travel to endemic countries
Nature of pain: tumour infiltration, cortical expansion, instability/fracture, neurocompression
Neurology: direct invasion, epidural seedling, fracture, deformity; also expectations

Q3.What examination is needed in suspected spinal metastasis?

Full neurological examination
Systems exam: lungs, abdomen, PR, breast, thyroid

Q4.What is the Bilsky ESCC score used for?

Grading epidural spinal cord compression on MRI
0: bone only
Ia/b/c: out of bone, deformation of thecal sac, touching cord
II: cord compression with CSF still visible; III: cord compression with CSF not visible
Determines high grade (2,3) vs low grade (1) compression

Q5.What imaging and classification systems are used for metastatic spine disease?

Whole spine MRI with the Bilsky ESCC score
Weinstein, Boriani, Biagini (WBB) classification

Q6.What are the treatment goals and principles in metastatic spinal disease?

Treatment is palliative in intent: salvage neurology, stabilise spine, maintain ambulation, pain relief
Always biopsy if no confirmed bone met
Look for other spinal/skeletal mets, other primaries and other ddx (infection, TB, benign tumour, MM)
Manage by the NOMS framework with a multidisciplinary approach

Q7.What medical treatment is given for metastatic cord compression?

Dexamethasone for neurocompression (50mg loading then 4mg Q6H, with PPI coverage)
Treat hypercalcemia
Bisphosphonate can reduce skeletal events: Zometa 4mg IV every month

Q8.What is the evidence for surgery plus radiotherapy in metastatic cord compression?

Patchell, Lancet 2005: better outcomes with surgery + RT vs RT alone
Adjunct treatment includes preoperative embolisation for vascular tumours

Q9.What is the epidemiology of spinal metastasis?

Bone metastasis is common after lung and liver primary
Spine is the most common site, then proximal femur and humerus (Batson's valveless venous plexus allows seeding like red marrow)
Primary sites: breast > lung > prostate/renal/thyroid; liver also common
Survival is variable (6 months to 5 years)

Q10.What is the difference between osteolytic and osteoblastic metastases?

Osteolytic: osteolysis caused by tumour-induced activation of osteoclasts (RANK, RANKL and OPG)
Osteoblastic: tumour secreted endothelin 1 (90% prostate, 60% breast)

Q11.How is hypercalcaemia of malignancy managed?

A metastatic emergency
Hydration
Loop diuretics
Bisphosphonate

Q12.What are the components and interpretation of the Tokuhashi score?

General condition
Primary tumour
Number of vertebral body foci
Number of extraspinal foci
Major organ involvement and neurology (palsy)
Score 0-15; 9-11 predicts >=6 months, >=12 predicts >1 year survival for excisional surgery; PF FONG mnemonic

Q13.What are the components of the Tomita score?

Primary tumour
Mets to vital organs (treatable/untreatable)
Bone mets
Score 2-10; >6 = palliative decompression/no surgery

Q14.What is the principle of tumour separation surgery?

Circumferential decompression to allow a safety margin for tumoricidal radiation doses without toxicity to the cord

Fact check

Dexamethasone 50mg loading dose for metastatic spinal cord compression (slide notes) — non-standard dose, likely error — Guidelines recommend an initial 10mg IV loading dose followed by 4mg (or 6-10mg) every 6 hours; a 50mg bolus is not a recognised regimen — medium confidence — source

▸ Slide 476 · XR: C6 collapse with vertebral plana deformity. Acute kyphosis and increase in vSpine Non Trauma · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

What are the X-ray findings in this case?
How do you differentiate infection from malignancy on X-ray of the spine?
What history, examination and blood tests are needed for a C6 collapse?
What staging is required once malignancy is confirmed?
What are the four components of the NOMS framework as applied to this case?
What are the components of the Tokuhashi score?

Answers · Q & A

Q1.What are the X-ray findings in this case?

C6 collapse with vertebral plana deformity
Acute kyphosis
Increase in vertebral shadow

Q2.How do you differentiate infection from malignancy on X-ray of the spine?

Infection starts in the disc, malignancy in the vertebral body
More endplate erosion in infection
Posterior elements less commonly involved in infection

Q3.What history, examination and blood tests are needed for a C6 collapse?

Red flags, recent infection (e.g. UTI), risk factors for infection, pain, neurology
Systems screening: breast, abdomen, thyroid, chest, PR
Local tenderness and neurological examination
Bloods: WCC, CRP, CaPO4, ALP, tumour markers

Q4.What staging is required once malignancy is confirmed?

Local and systemic staging
MRI and CT
Managed in a multidisciplinary team according to the NOMS framework

Q5.What are the four components of the NOMS framework as applied to this case?

Neurology: clinical motor deficits; radiological Bilsky stage on MRI - high or low grade cord compression
Oncologic: radioresistant or radiosensitive tumour
Mechanical stability: SINS
Systemic: traditionally Tokuhashi score, now NESM or SORG nomogram

Q6.What are the components of the Tokuhashi score?

General condition
Number of spine metastases
Number of extraspinal metastases
Internal organ metastases
Tissue of origin and neurology
Score 0-15; >9 predicts surgery

▸ Slide 477 · Primary spine tumorsSpine Non Trauma · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

How are benign primary spine tumours classified by Enneking stage?
What are the malignant primary spine tumours?
Which other classification systems are used for spine tumours?

Answers · Q & A

Q1.How are benign primary spine tumours classified by Enneking stage?

Enneking 1 (self-limiting) = osteoid osteoma, ABC, haemangioma
Enneking 2 (active) = osteoblastoma
Enneking 3 (aggressive) = giant cell tumour

Q2.What are the malignant primary spine tumours?

Chordoma
Osteosarcoma
Chondrosarcoma
Ewing's sarcoma (EWS)

Q3.Which other classification systems are used for spine tumours?

Tomita
Weinstein, Boriani, Biagini (WBB)

▸ Slide 478 · Posterior approachSpine Non Trauma · 7 questions expand

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Q1-Q77 questions — tap to reveal all answerslist

How is the patient positioned for a posterior lumbar approach?
How is the level confirmed and the incision/dissection performed?
Describe the decompression steps in a posterior lumbar approach.
What are the boundaries of Kambin triangle?
What is the traditional safe triangle for nerve root injection?
What are the steps of discectomy in the posterior approach?
What does the 2014 Cochrane review show for minimally invasive versus open discectomy?

Answers · Q & A

Q1.How is the patient positioned for a posterior lumbar approach?

Prone on an OSI table
Wilson frame or 4 posters
Pressure areas well padded

Q2.How is the level confirmed and the incision/dissection performed?

Surface landmark: intercrestal line = L4/5
Midline incision along the spinous processes through the lumbar fascia
Subperiosteal dissection laterally to the facet joints (to the transverse process if fusion, but not beyond the intertransverse ligament)
Cobb used to strip laterally along the lamina until facet capsules identified but not violated

Q3.Describe the decompression steps in a posterior lumbar approach.

Remove spinous processes of operative levels with rongeur
Blunt dissection between the lamina of the level above and the ligamentum flavum with an angled curette to create a working window
Thin the cephalad lamina with a burr, complete with a Kerrison rongeur to expose the ligamentum flavum, leaving at least 7mm pars
Extend caudally to the superior most 3mm of the inferior lamina
Dissect the ligamentum flavum from the medial facet edge and remove; facetectomy (medial 3mm vs total)

Q4.What are the boundaries of Kambin triangle?

Exiting nerve root
Medial margin of the superior articular process (SAP)
Superior endplate of the caudal vertebra
Also a landmark for nerve root injection

Q5.What is the traditional safe triangle for nerve root injection?

Inferior margin of the pedicle
Exiting nerve root
Lateral margin of the vertebral body

Q6.What are the steps of discectomy in the posterior approach?

Retract the traversing nerve root
Epidural vein hemostasis
Confirm the level with a needle
Annulotomy with a discectomy knife
Discectomy

Q7.What does the 2014 Cochrane review show for minimally invasive versus open discectomy?

MIS: higher leg pain
Reoperation/readmit rate due to recurrent disc herniation higher (18 vs 13%)
Lower risk of infection
Long-term functional and clinical outcomes show no difference

▸ Slide 479Spine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

Which MRI study and planes are shown on this slide?
What abnormality is demonstrated on the axial T2 image?
What is the purpose of the dashed and yellow lines drawn on the sagittal image?

Answers · Q & A

Q1.Which MRI study and planes are shown on this slide?

Sagittal T2-weighted MRI of the whole spine (printed label: whole-spine survey)
Axial T2 MRI labelled T3-T8, cut at the plane marked by the yellow line

Q2.What abnormality is demonstrated on the axial T2 image?

A discrete rounded mass (intermediate-to-high T2 signal) posterolateral to the thoracic vertebral body
It lies in the paraspinal/epidural region; the diagnosis is not stated in the speaker notes (read from the slide image)

Q3.What is the purpose of the dashed and yellow lines drawn on the sagittal image?

The yellow line marks the plane of the axial cut shown on the right
The dashed white lines mark other reference levels across the whole-spine survey

▸ Slide 480Spine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

Which spinal region and MRI views are displayed on this slide?
What normal structures can be identified in the spinal canal on the axial T2 image?
Why is sagittal imaging combined with an axial image when reporting a lumbar MRI?

Answers · Q & A

Q1.Which spinal region and MRI views are displayed on this slide?

Sagittal T2-weighted MRI of the lumbosacral spine
Paired axial T2 image at the level marked by the yellow line

Q2.What normal structures can be identified in the spinal canal on the axial T2 image?

The canal contains bright (high T2) CSF between the vertebral body and the posterior elements
Dark dots within the bright CSF are the nerve roots traversing the canal
Findings are read from the slide image; the speaker notes do not cover this slide

Q3.Why is sagittal imaging combined with an axial image when reporting a lumbar MRI?

Sagittal shows the level and cranio-caudal extent of disease
Axial shows cross-sectional relationships to the canal, foramina and nerve roots

▸ Slide 481 · What is fail back syndrome?Spine Non Trauma · 8 questions expand

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Q1-Q88 questions — tap to reveal all answerslist

What is failed back syndrome?
What history and risk factors are important in failed back syndrome?
What is the 4W+1 approach if pain never resolved after surgery?
What is the RIPIE differential if pain recurred after initial relief?
How can symptoms of failed back syndrome be classified?
How do leg pain and back pain differ in their causes after lumbar surgery?
What specific postoperative diagnoses can present after lumbar surgery?
How are failed back syndrome and adjacent segment disease investigated?

Answers · Q & A

Q1.What is failed back syndrome?

Recurrent or residual back pain following previous surgery on the lumbar spine
Causes are multifactorial, often the result of poor patient selection
Contributors: patient (physical/psychological), disease (recurrent disease), surgical (indication/technical)

Q2.What history and risk factors are important in failed back syndrome?

Initial indication for surgery, preoperative symptoms, perioperative complications
Postoperative pain relief and current nature of pain; background history
Risk factors for poor outcome: IOD, smoking, obesity, psychiatric history

Q3.What is the 4W+1 approach if pain never resolved after surgery?

Wrong patient (Waddell signs - DONTS) or wrong diagnosis
Wrong indication
Wrong level
Wrong procedure done
Poor surgical technique - inadequate decompression, iatrogenic instability, implant malposition

Q4.What is the RIPIE differential if pain recurred after initial relief?

Recurrent disease (recurrent disc, adjacent segment)
Infection
Pseudoarthrosis
Instrumentation failure
Epidural fibrosis

Q5.How can symptoms of failed back syndrome be classified?

Mechanical symptoms: recurrent disc herniation, discogenic pain, instability, spinal stenosis
Non-mechanical symptoms: local scar tissue formation (arachnoiditis, epidural fibrosis), psychosocial issues, abdominal/pelvic/systemic disease

Q6.How do leg pain and back pain differ in their causes after lumbar surgery?

Leg pain: prolapsed intervertebral disc (PID), stenosis
Back pain: discogenic pain, instability

Q7.What specific postoperative diagnoses can present after lumbar surgery?

Arachnoiditis: inflammation of the arachnoid layer, no effective treatment
Epidural fibrosis (3 months): responds poorly to re-exploration
Diskitis (3-6 weeks postoperatively): rapid onset severe back pain - bedrest, bracing, antibiotics

Q8.How are failed back syndrome and adjacent segment disease investigated?

Bloods to rule out infection; long film
CT: fusion status, implant loosening, bone regrowth, incomplete decompression
MRI: recurrent disc, perineural scar; Scarring can be differentiated from recurrent HNP with a gadolinium-enhanced MRI
ASD risk factors: obesity, preop disc protrusion/adjacent disc degeneration, poor restoration of sagittal balance, facet joint violation, long segment fusion (incidence 5-19%; JBJS article)

▸ Slide 482Spine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

According to this slide, what is the most common structural cause of failed back surgery, and how does it arise?
What frequency does the slide quote for pain disc, pseudarthrosis and neuropathic pain?
Which structural causes are listed at 12% or less, and at what rates?

Answers · Q & A

Q1.According to this slide, what is the most common structural cause of failed back surgery, and how does it arise?

Foraminal stenosis (25-29%) - the single commonest structural cause
Up-down stenosis from loss of disc space; front-back stenosis from facet hypertrophy and osteophyte formation

Q2.What frequency does the slide quote for pain disc, pseudarthrosis and neuropathic pain?

Pain disc: 20-22%
Pseudoarthrosis: 14%
Neuropathic pain: 10%

Q3.Which structural causes are listed at 12% or less, and at what rates?

Recurrent disc herniation: 7-12%
Iatrogenic instability: 5%; facet pain: 3%; sacroiliac joint pain: 2%

▸ Slide 483 · Non organic causes suggested if 3 or above +veSpine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

How many positive non-organic signs suggest a non-organic cause?
List the five non-organic signs.
Which mnemonic is used for the five non-organic (Waddell) signs?

Answers · Q & A

Q1.How many positive non-organic signs suggest a non-organic cause?

3 or more positive signs suggest non-organic causes

Q2.List the five non-organic signs.

Distraction
Overreaction
Non-dermatomal distribution
Tenderness
Simulation

Q3.Which mnemonic is used for the five non-organic (Waddell) signs?

DONTS
Distraction, Overreaction, Non-dermatomal distribution, Tenderness, Simulation

▸ Slide 484 · Paintbrush/ meniscusSpine Non Trauma · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

Which two named signs are listed on this slide?
What do these signs represent?

Answers · Q & A

Q1.Which two named signs are listed on this slide?

Paintbrush
Meniscus

Q2.What do these signs represent?

Not covered in the speaker notes

▸ Slide 485 · MyelogramSpine Non Trauma · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

How is a myelogram performed?
How do you interpret an extradural space-occupying lesion on myelogram?
How do you interpret an intradural, extramedullary lesion on myelogram?

Answers · Q & A

Q1.How is a myelogram performed?

Under fluoroscopy
Spinal needle at L3/4, withdraw CSF, inject contrast
Table tilt to allow contrast to fill up and down
Then XR/CT

Q2.How do you interpret an extradural space-occupying lesion on myelogram?

Examples: PID, metastasis, TB abscess
Paintbrush appearance

Q3.How do you interpret an intradural, extramedullary lesion on myelogram?

Examples: neurofibroma, meningioma
Meniscal sign (can outline the SOL)

▸ Slide 486 · PI is the angle formed from two lines. One from centre of sacrum to femoral headSpine Non Trauma · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

How is pelvic incidence (PI) measured?
What is the relationship of pelvic incidence to spondylolisthesis?
How does the body compensate when lumbar lordosis reduces?

Answers · Q & A

Q1.How is pelvic incidence (PI) measured?

Angle between a line from the centre of the sacrum to the femoral head and a line perpendicular to the S1 endplate through its midpoint
PI = PT + SS

Q2.What is the relationship of pelvic incidence to spondylolisthesis?

Direct relationship to the severity of spondylolisthesis
High PI: more shearing across L5/S1 and less lumbar lordosis
Body tries to keep sagittal balance by increasing lumbar lordosis

Q3.How does the body compensate when lumbar lordosis reduces?

Pelvis rotates posteriorly, reducing the sacral slope
When the sacrum is vertical, the knee flexes to further compensate

▸ Slide 487 · Diagram showing measurements for spinal sagittal balanceSpine Non Trauma · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

How is sagittal vertical axis (SVA) measured?
What is the relationship between sacral slope, pelvic tilt and pelvic incidence?
What are the target values for spinopelvic harmony?
Why does sagittal imbalance matter?

Answers · Q & A

Q1.How is sagittal vertical axis (SVA) measured?

On standing long film X-ray
Line from the centre of C7 vertebral body perpendicular to the ground; measure horizontal distance from the posterosuperior corner of S1
Normal = within 5cm

Q2.What is the relationship between sacral slope, pelvic tilt and pelvic incidence?

Sacral slope + pelvic tilt (positional) = pelvic incidence (morphology)

Q3.What are the target values for spinopelvic harmony?

Lumbar lordosis = PI +/- 9 degrees
PT < 25
SVA < 50mm
Spinal curvature (spinopelvic harmony / cone of economy)

Q4.Why does sagittal imbalance matter?

Imbalance leads to pain and progressive deformity

▸ Slide 488 · When to use this table?: Think of the following question.Spine Non Trauma · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

What clinical question is the Bordeaux classification used to answer?
What determines the type in the Bordeaux classification?
How does the Bordeaux classification guide implant choice?

Answers · Q & A

Q1.What clinical question is the Bordeaux classification used to answer?

How to decide acetabular position/implant in a patient with spinal deformity

Q2.What determines the type in the Bordeaux classification?

Type of lumbo-pelvic complex (LPC): type 1 = PI <40, type 2 = PI >40
Then subclassified A/B/C/D

Q3.How does the Bordeaux classification guide implant choice?

Increasing constraint required for types B, C and D
Based on LPC type: PI <40 (type 1) or PI >40 (type 2)

▸ Slide 489 · SRS (scoliosis research society) Schwab classification for Adult Spine DeformitySpine Non Trauma · 3 questions 1 check expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What is the SRS (Schwab) classification used for?
What does the Ascani 1986 natural history study report for adult scoliosis?
What features indicate a poor prognosis in adult spine deformity?

Answers · Q & A

Q1.What is the SRS (Schwab) classification used for?

Classification for adult spine deformity (Scoliosis Research Society)
Includes parameters relevant to OLIF/degenerative scoliosis surgery

Q2.What does the Ascani 1986 natural history study report for adult scoliosis?

3 degrees per year progression (per slide notes)
All curves increase after skeletal maturity

Q3.What features indicate a poor prognosis in adult spine deformity?

>30 degree Cobb angle
>30% apical rotation
6mm lateral listhesis
Poor quality bone

Fact check

Ascani 1986 Spine natural history study: adult scoliosis progresses 3 degrees per year — mismatch with cited source — Ascani 1986 reported an average progression of 0.4 degrees per year after skeletal maturity; most curves progress at less than 1 degree per year, though larger curves progress faster — source

▸ Slide 490 · SDSG L5-S1 slip classificationSpine Non Trauma · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

What is the SDSG L5-S1 slip classification used for?
How are high and low grade slips defined in the SDSG classification?
What is the management principle for high grade dysplastic slip?

Answers · Q & A

Q1.What is the SDSG L5-S1 slip classification used for?

The current recommended simple classification for dysplastic slip
Balanced pelvis = low pelvic tilt, high sacral slope

Q2.How are high and low grade slips defined in the SDSG classification?

High grade = >50% slip
Low grade = <50% slip

Q3.What is the management principle for high grade dysplastic slip?

Consider partial reduction in high grade slip
Restore normal lumbosacral/pelvis relationship

▸ Slide 491 · Sacral agenesisSpine Non Trauma · 4 questions expand

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Q1-Q44 questions — tap to reveal all answerslist

What is sacral agenesis associated with?
What is the Renshaw classification of sacral agenesis?
How is Renshaw type 1/2 sacral agenesis managed?
How is Renshaw type 3/4 sacral agenesis managed?

Answers · Q & A

Q1.What is sacral agenesis associated with?

Rare; associated with maternal diabetes
Part of caudal regression syndrome
Gastrointestinal disorders e.g. imperforate anus
Genitourinary and cardiovascular disorders
Lower extremity deformities and progressive kyphosis

Q2.What is the Renshaw classification of sacral agenesis?

Type I: unilateral
Type II: partial, bilaterally symmetrical
Type III: ilium articulating with vertebra present
Type IV: fused both ilia or iliac amphiarthrosis

Q3.How is Renshaw type 1/2 sacral agenesis managed?

Conservative physical therapy for Renshaw type 1/2
Most become community ambulators
Foot and knee deformities to be addressed

Q4.How is Renshaw type 3/4 sacral agenesis managed?

Operative management for Renshaw type 3/4
Spinal stabilization procedures for progressive kyphosis and/or scoliosis
Limb amputation for non-functional lower limb deformities

▸ Slide 492 · Bartolotti syndromeSpine Non Trauma · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What is the Castellvi classification of Bertolotti syndrome?
Which Castellvi type is associated with lumbar disc herniation?
What are the reported rates of sacralization and lumbarization?
In the Castellvi classification, what do the suffixes a and b mean?

Answers · Q & A

Q1.What is the Castellvi classification of Bertolotti syndrome?

Type I: enlarged transverse process >= 19 mm (a unilateral, b bilateral)
Type II: pseudoarticulation of transverse process and sacrum (a/b)
Type III: transverse process fuses with sacrum (a/b)
Type IV: type IIa on one side and type IIIa contralateral

Q2.Which Castellvi type is associated with lumbar disc herniation?

Type II
Not associated with types I, III or IV

Q3.What are the reported rates of sacralization and lumbarization?

Sacralization: 7%
Lumbarization: 5%

Q4.In the Castellvi classification, what do the suffixes a and b mean?

a = unilateral
b = bilateral

▸ Slide 493 · Cervical cord injury rehabSpine Non Trauma · 7 questions expand

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Q1-Q77 questions — tap to reveal all answerslist

What is the ventilator weaning success rate after cervical spinal cord injury?
Why does vital capacity decrease on sitting in cervical cord injury?
What is the motor recovery prognosis after traumatic spinal cord injury?
What is the ambulatory potential by ASIA grade?
What are the functional goals at C5 and C6?
How does sphincter function differ in suprasacral vs cauda equina lesions?
Which 1999 consensus published the traumatic spinal cord injury rehabilitation potential data?

Answers · Q & A

Q1.What is the ventilator weaning success rate after cervical spinal cord injury?

C3: 51%
C4: 78%

Q2.Why does vital capacity decrease on sitting in cervical cord injury?

Increased dead space as the abdominal organs drop down when sitting
Can be improved with a corset

Q3.What is the motor recovery prognosis after traumatic spinal cord injury?

Muscles with some motor power below an antigravity muscle have a better prognosis than muscles with no motor power
Grade 1 or 2: 90% reach grade 3 by 1 year
Grade 0: 64% reach grade 3 by 2 years
Recovery is faster in incomplete injuries
Median time to antigravity strength: 2 months motor complete vs 2 weeks motor incomplete (Ditunno 1992)

Q4.What is the ambulatory potential by ASIA grade?

3% / 50% / 75% / 95% in ASIA A / B / C / D (van Middendorp, Global Spine J 2011)

Q5.What are the functional goals at C5 and C6?

C5: use of power wheelchair
C6: manual wheelchair, feeding well
Consider tenodesis grasp/transfer at C6

Q6.How does sphincter function differ in suprasacral vs cauda equina lesions?

Suprasacral: detrusor-sphincter dyssynergia, spastic bladder, reduced volume, may develop reflux/HN, finally incontinence
Cauda equina: flaccid bladder that stretches out, can develop stress incontinence

Q7.Which 1999 consensus published the traumatic spinal cord injury rehabilitation potential data?

Consortium of Spinal Cord Medicine 1999

FRCS Quiz — private