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spine - trauma, mets and BG anatomy > CVJ, occipital condyle, AOD, rotatory sublux, ant atlan-axial sublux, C1# > Flashcards

CVJ, occipital condyle, AOD, rotatory sublux, ant atlan-axial sublux, C1# Flashcards

1
Q

List 4 ligaments that join C1 to the occiput

A

1) Ant atlant-occipital membrane (Ext of ALL, ant. arch C1 to ant FM)
2) Post atlanto-occipital membrane (post FM to post arch C1)
3) Lateral atlanto-occipital ligaments (TP of C1 to jug foramen bilateral)
4) O-C1 articular capsules

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2
Q

List 4 ligaments that join C2 to the occiput

A

1) Apical ligament (tip of dens to ant FM margin)
2) Alar ligament (back of dens to occip condyles)
3) Cruciate ligament, vertical part (back of dens to ant. FM margin)
4) Tectorial membrane, extension of PLL (to clivus)

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3
Q

List 5 ligaments that join C1 and C2

A

1) ALL
2) PLL
3) transverse lig TAL (dens to C1, tubercles on medial side of lat mass)
4) C1-C2 articular capsules
5) Post atlanto-axial lig / lig flavum (arch of C1 to arch of C2)

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4
Q

What is the blood supply and venous drainage of the odontoid?

A

2 sources of blood supply:
VA – supply anterior and posterior ascending vessels – anastomose in apical arcade near alar ligaments
- carotid arteries also contribute to ant. asc. vessels
- pharyngovertebral venous drainage

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5
Q

What is the lymphatic drainage of the CVJ?

A

retropharyngeal nodes - upper deep jugular cervical chain (which also receive nasopharynx, sinuses)
- therefore, retrograde infection can cause Grisel’s syndrome

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6
Q

what are the biomechanics of the O-C1 junction?

A

up to 25° flex/ext only (5-10 lateral)

  • flex limited by: - tectorial membrane
    - dens hitting basion
  • ext limited by: - tectorial membrane
    - post arch hitting opisthion (also C1 lateral mass in posterior condylar recess)
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7
Q

what are the biomechanics of C1-2?

A

C1-2 - up to 10° flex/ext

- up to 42° rotation  - to rotate the neck 90°, the subaxial spine contributes in decreasing amounts
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8
Q

What is the normal ADI in adults and children?

A

up to 3mm in adult

up to 5 mm in kids

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9
Q

what ligaments should one consider if increased ADI?

A

TAL (join c1 and c2)

alar (dens to condyle)

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10
Q

What is a sclerotome and how is it derived?

A

Paraxial mesoderm forms into bilaterally paired blocks termed somites - these somites subdivide into sclerotomes, myotomes and dermatomes.

Dermatome - dorsal paraxial mesoderm - gives rise to skin
Myotome - part of a somite that forms muscle

Sclerotome - forms vertebrae, rib cartilage and part of occipital bone

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11
Q

What sclerotomes contribute to the formation of the O-C junction? And what are the major bony formations?

A

Occ 1,2 - basiocciput
Occ 3 - jugular tubercles
Occ 4 - part of clivus, apex of dens, apical ligaments, alar and cruciate ligaments, occipital condyles, C1 post arch (superior) and lateral mass

Spinal 1 - C1 ant arch, dens, C1 post arch (inferior portion)

Spinal 2 - C2 body, C2 facets and post arch

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12
Q

Describe the relationship of the dens to the C2 body at birth

A

at birth, the dens is separated from body C2 by neurocentral synchondrosis

  • lies below the level of the sup art. facets
  • disappears by 8 years
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13
Q

At what age does the tip of the dens become visible?

A

at birth, tip of dens not visible - seen by 3 years of age = ossiculum terminale

  • fuses by 12 years
  • if fails to fuse = ossiculum terminal persistens (no significance)
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14
Q

What are 4 considerations when there is a gap in the odontoid?

A
  1. Os odontoideum – odontocentral synchondrosis fails to fuse (after age 5-7), at risk for AA instability
  2. Ossiculum terminale – non-union of secondary oss center at tip, above TAL (no significance)
  3. Nonunion of dens fracture
  4. Nontraumatic unfused odontoid synchondrosis – same as #1 above but normal (before age 5-7)
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15
Q

What are 4 congenital malformations of the occipital bone?

A
  • manifestations of occipital vertebrae
  • basilar invagination
  • condylar hypoplasia
  • assimilation of atlas
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16
Q

What are 4 congenital malformations of the atlas?

A
  • assimilation of atlas
  • AA fusion
  • aplasia of atlas arches
  • failure of ring fusion if both ant/post arches are bifid > age 3 pathological, cranial settling occurs, needs tx
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17
Q

What are 3 congenital malformations of the axis?

A
  • irregular AA segmentation
  • dens dysplasias e.g., hypoplasia-aplasia, os odontoideum
  • C2-3 segmentation failure
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18
Q

List 6 conditions that can lead to AA instability

A
  • errors of metabolism e.g., Morquio
  • Downs
  • infection – Grisel’s
  • inflammatory – RA
  • traumatic OA, AA dislocations, os odontoideum
  • tumours
  • miscellaneous
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19
Q

What is Grisel’s syndrome?

A 
o	inflammatory, spontaneous subluxation at atlantoaxial joint following parapharyngeal infection, d/t
♣	tonsillitis
♣	mastoiditis
♣	retropharyngeal abscess
♣	otitis media
most
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20
Q

How does Grisel’s syndrome present? and how is a diagnosis confirmed?

A

Presentation:
o torticollis, neck pain, or neurological deficit
o if severe subluxation S/S of cervical cord compression

Diagnosis:
o ESR
o MRI/CT confirm parapharyngeal soft tissue mass, dislocation, osteomyelitis, bone erosion
o KEY: needle biopsy of prevertebral mass confirm pyogenic focus, obtain specimen for C+S

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21
Q

How is Grisel’s syndrome managed?

A

o appropriate abx ASAP
o reduction of dislocation by cervical traction reserved for gross dislocations only
o occipitocervical dislocation requires halo
o otherwise immobilization in a SOMI (sternal-occipital-mandibular immobilizer) is sufficient
o only rarely necessary to perform fusion

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22
Q

What are c spine abnormalities in Down’s syndrome?

A

o 14-24% atlantoaxial instability symptomatic in 1%
o os odontoideum
o hypoplastic odontoid process incomplete cruciate ligament
o rotary atlantoaxial luxation

treat as per usual indications but caveat avoid halo (v. problematic in this population), use internal fixation/instrumentation

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23
Q

What is a typical presentation of occipital condyle fracture?

A

Closed head injury and lower CN palsies (1/3 of patients with occipital condylar fracture will have lower CN palsy)

neck pain - must get ct

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24
Q

How are occipital condyle fractures classified?

A

Anderson & Montessano

Type I:
non-displaced, comminuted condylar #
no displacement of FM
mechanism = axial load of condyle onto C1 lateral mass
stable IF tectorial membrane and contralateral alar ligament are still intact
Rx = collar

Type II:
# thru base of skull extending into occipital condyle (i.e. alar, tectorial ligaments intact)
no displacement of FM
stable
Rx = collar
Type III:
avulsion # of condyle by ipsilateral alar ligament
mechanism = rotation/lateral bending
may be unstable 
Rx = HALO-vest orthosis for 12 weeks
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25
Q

How does Tuli classify occipital condyle #s?

A

Type I - undisplaced - no immobilization required

Type II - displaced
IIa - no imaging evidence of instability - hard collar
IIb - imaging evidence of instability - halo or surgery

26
Q

What imaging evidence does Tuli use to determine instability?

A

CT
> 8 degrees of axial rotation of O-C1 to one side
> 1mm of O-C1 translation
> 7mm of overhang of C1 on C2
> 45 degrees of axial rotation of C1-C2 to one side
> 4mm of C1-C2 translation

27
Q

What are 4 factors that predispose young people (

A
  1. ligaments are more lax
  2. weaker muscles
  3. head is disproportionately larger w.r.t. body
  4. plane between occipital condyles and C1 superior facets is horizontal/shallow (deepens/vertical with age)
28
Q

What osseus / ligaments limit hyperflexion, hyperextension and lateral flexion at the A-O region?

A
  • hyperflexion limited by contact between ant. lip foramen magnum and the odontoid.
  • hyperextention limited by the tectorial membrane. (and posterior FM hitting C1 posterior arch)
  • lateral flexion/rotation limited by the alar ligaments
29
Q

What are common associated injuries in persons with Atlanto-occipital dislocaton?

A
  • initial injury may injure carotid or vertebral arteries – consider angio in survivors
  • associated severe head injury
  • look for associated odontoid fractures
30
Q

How is atloanto-occipital dislocation classified?

A

Traynelis

Type I - Anterior O relative to C1 (2nd most common)

Type IIa - longitudinal between O-C1 (most common)
Type IIb - longitudinal between O-C1 and C1-2

Type III - Posterior O relative to C1

can also have mixed i.e. anterior and longitudinal

31
Q

How does A-O dislocation present?

A
  • intact
  • dead (bulbar-cervical dissociation) or period of VSA
  • coma
  • lower cranial n. deficit
  • long tract signs
32
Q

What measurements can you use on CT to diagnose A-O dislocation?

A

May see traumatic SAH around brainstem

A. Wackenheim’s line
line drawn as caudal extension of clivus should tangentially intersect tip of dens in normal pt

B. Dens-basion relationship
1 (0.77 in normal pt)

D. X-line method
line between basion-postC2 should tangentially intersect tip of dens

line between opisthion-posteroinferiorC2body should tangentially intersect rostral limit of C1 spinolaminar line

MOST SENSITIVE:
CCI (Condyle-C1 interval)
Should be suggests AOD

33
Q

What is the treatment for AOD?

A
  1. ventilatory/CV support
  2. urgent halo application
  3. if severe cord/brainstem/head injury
    a. treat these with usual measures
    b. proceed with fusion only if viable
  4. FUSION – occipito-cervical fusion (do this urgently if pt presents intact)
34
Q

What are typical outcomes after AOD?

A
  • 60% mortality – most die within 3 weeks

- depends on neurological deficit

35
Q

How is rotatory atlanto-axial subluxation defined?

A
  • pathological fixation of the atlas on the axis in position that is normally accomplished during head rotation

almost always children (girls)

36
Q

Why is this a condition of children?

A
  • children: larger head, shallow & horizontal facets, loose ligaments, weaker muscles
  • excessive rotation is usually limited by alar ligaments
37
Q

what conditions is RAA sublux associated with?

A

o trauma
o URTI – Grisel syndrome – inflammation weakens TAL & articular capsule
o Down’s, Morquio, Marfan, JRA
o after H&N surgery

38
Q

How do these patients present?

A

head-tilt – “cock-robin” deformity
- limited, painful neck ROM

three clinical signs of Sudek:

  • palpable deviation of C2 spinous process in same direction as head
  • spasm of ipsilateral SCM muscle
  • inability to turn head past midline
39
Q

what is the ideal imaging modality to diagnosis RAA sublux?

A

CT with reconstruction
- imaging of choice, can get 3 CTs with head neutral, looking L, looking R and demonstrate fixed relationship of C1 to C2
MR
- can show amount of ligamentous damage

40
Q

how does the status of the TAL affect interpretation of RAA sublux?

A

disrupted TAL = C1 can sublux anteriorly and facets of C1-2 can lock with 42 degrees

41
Q

How is the VA affected by RAA sublux?

A

rotation > 35 degrees = angulation, then stretching, of contralateral VA

rotation > 45 degrees = angulation and possible occlusion of ipsilateral VA

42
Q

what is the treatment algorithm for RAA sublux?

A

Initial management:
o soft collar (usually unable to fit hard collar)
o anti-inflammatory
o muscle-relaxants

Try for 1-2 weeks – don’t delay too long, or else it will become irreducible – if fails:

cervical traction, e.g. Halter traction
physiotherapy for neck ROM
benzodiazepines

  • After reduction:
    o collar for 6 weeks
  • If fails or recurs:
    o try closed reduction again
  • If fails or recurs again:
    o open reduction & C1-2 fusion with graft
43
Q

what are the 3 criteria by which RAA sublux is classified?

A

Displacement of C1 arch relative to dens
Degrees of rotation
ligaments involved

type I = no ant displacement of C1 arch vs dens (most common)

type II = 3-5 mm of ant displacement of C1 arch to dens, >35 deg of rotation with TAL involved - treat with reduction and halo

type III = >5 mm of ant displacement of C1 arch rel to dens, > 40 deg of rotation; TAL + alar lig is involved - treat with reduction and fusion

type IV = posterior displacement C1 arch relative to dens - treat with reduction and fusion

44
Q

what are the important ligament and osseous structures in a diagnosis of anterior atlanto-axial subluxation?

A
  • most important lig structure is the transverse atlantal ligament (TAL)
  • alar ligaments, accessory atlanto-axial ligament, and tectorial membrane assist the transverse ligament
  • osseous structures are the dens and anterior arch of atlas.
45
Q

what is the normal ADI in adults and children?

A
  • up to 3mm in adult
  • if TAL cut, but alar OK – can be up to 5mm
  • up to 5mm in kids
  • if TAL and alar cut >5mm
46
Q

what is the normal amount of flexion / extension at C1/2 and what limits this flexion / ext?

A

up to 10 deg flex / ext

hyperflexion is limited by the tectorial membrane

  • hyperextension is limited by ant. arch of C1 abutting on the odontoid
47
Q

what is the normal amount of rotation at C1/2

A

up to 42 deg.

to rotate neck to 90 deg - the subaxial spine contributes in decreasing amounts

48
Q

what conditions are associated with AAS?

A

o trauma
o Down’s
o RA
o errors of metabolism (Morquio), Marfans, Hurlers

49
Q

what are ligament and bony anomalies associated with Down’s syndrome?

A

increased lig. laxity
20% have ADI >5mm, but:
o only about 1% are symptomatic
o symptoms begin at 7-12 y/o

inc. incidence of bony anomalies:
o os odontoideum
o odontoid hypoplasia (with incompetent cruciate lig)
o condylar hypoplasia
o atlantal hypoplasia*** important for type of fusion needed

also predisposed to OA instability and AA rotatory instability

50
Q

How is AAS treated if the patient suffers from neuro deficits from compression?

A

first see if reducible in either fl/ex or with halo traction:
- if no then decompress, e.g., trans-oral, then posterior OCF

  • if yes then fuse either C1-2 or OCF
  • be aware of potential hypoplastic C1 – may need to fuse occiput
51
Q

How is AAS treated with evidence of radiographic instability?

A

need fusion, since immobilization will not result in ligamentous improvement

o at risk for severe deficit from minor trauma

o first line should be C1 lat mass and C2 pars screw construct, or
- C1-2 transarticular screws, if feasible, supplemented with Brooks/Gallie

o must assess need for occiput fusion

52
Q

what is the mechanism commonly associated with atlas fractures?

A
  • atlas squeezed between occipital condyles and axis = pure axial load
  • fracture occurs at site of VA groove - where the bone is thinnest
53
Q

How are atlas fractures classified?

A

Landells and Van Peteghem

  1. single arch fractures - anterior or posterior

a. stable
b. isolated anterior is rare

  1. both arches fractured - posterior + anterior
    a. classic Jefferson’s, disconnects lateral masses from each other
  2. lateral mass fracture
    a. fracture line may extend into a single arch
54
Q

what is the most important element of C1 fractures to consider when planning treatment?

A

TAL intact = fracture likely stable - 6-8 wks collar

TAL disrupted = fracture unstable = 8-12 wks halo, surgery if it fails

  • Any lateral mass # must raise the suspicion of injury to transverse ligament
  • look for evidence of boney avulsion on thin-cut axial CT
  • get MRI to assess TAL
55
Q

what is the rule of spence?

A
  • If on plain x-ray, sum of distance of excursion of lateral masses is 7mm or more, there is a transverse ligament rupture
56
Q

what is the most common association with C1 fractures?

A

50% have assoc. C2 fracture – treat these according to the need for C2 fracture surgery

57
Q

What is the Barrow classification for TAL injury?

A

Type
IA - TAL disruption at its midportion
IB - TAL disruption at its periosteal insertion

Type
IIA - comminuted C1 lateral mass fracture
IIB - avulsion of TAL tubercle with intact C1 lateral mass

58
Q

How is this classification used to guide treatment?

A
  • Type I injuries never heal unless do instrumented C1-2 fusion = soft tissue injury
  • Type II injuries can be tried in halo vest first, but 25% will need C1-2 fusion - bony injury
59
Q

How are unilateral anterior or posterior ring C1 #s managed?

A

collar

60
Q

How are bilateral anterior ring or Jefferson’s # managed?

A

intact TAL = collar for 8-12 weeks

disrupted TAL = halo 8-12 weeks
 OR go directly to fusion:
 C1-2 fusion = transarticular screws (ventral or posterior); C2 pars + C1 lat mass screws
 if not feasible d/t vertebral artery anatomy, then need to do O-C2 fusion

61
Q

How are type I TAL disruption managed?

A

C1-2 fusion…if not feasible d/t fracture of C1 post elements, then OCF needed

62
Q

How are type II TAL disruption managed?

A

halo vest (25% will eventually need C1-2 fusion)

spine - trauma, mets and BG anatomy (3 decks)

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