Spinal Pathology & Clinical Patterns Flashcards

1
Q

What is the MOI for a lumbar muscle strain?

A

Often overexertion. Direction dependent.

Note: isolated strain not common in the low back.

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2
Q

What is the MOI for a herniated lumbar disc?

A

i) Traumatic onset: flexion and rotation.

ii) Insidious onset: prolonged or repetitive flexed posture.

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3
Q

What is the source of pain in the case of a disc herniation?

A

The outer 1/3 fibres of the annulus as this is the only neurally innervated components of the disc OR muscle loading imbalances from resultant instability.

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4
Q

What are the functions of the intervertebral disc?

A

i) transmit forces
ii) resist compression, torsion and shear
iii) allow spinal movement

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5
Q

What is the biochemical composition of nucleus pulposus?

A

i) some elastin & collagen
ii) high concentration of proteoglycans (therefore high water content - 85/90% but decreases w/ age)
- The result is an incompressible semi-fluid.

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6
Q

What are the functions of the nucleus pulposus?

A

i) shock absorption
ii) transmit mechanical stresses
iii) fulcrum for movement
iv) weight bearing: resists compression
v) nutrition

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7
Q

What are two age-related changes that occur within the nucleus pulposus?

A

i) decreased proteoglycan (# and effectiveness) and water content
ii) increased collagen
- Grows more similar to annulus.

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8
Q

What is the biochemical composition of the annulus fibrosis?

A

i) 50-60% collagen content

ii) small # of proteoglycans and water content

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9
Q

Describe the orientation of layers of lamellae in the annulus fibrosis.

A

i) Concentric lamellae in which each layer is perpendicular to the adjacent
ii) 65’ from vertical
iii) thick anterolaterally and thin posteriorly

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10
Q

What are the functions of the annulus fibrosis?

A

i) contain nucleus pulposus
ii) enhance mobility
iii) weight bearing
iv) shock absorption
v) resist shear and torsion
vi) vertebral stability (holds VBs together)

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11
Q

What is the composition of the vertebral end plate?

A

1 mm of cartilage. Hyaline cartilage closer to the vertebral body and fibrocartilage closer to the disc.

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12
Q

What is the coverage of the vertebral end plate relative to the IV disc?

A

i) covers NP entirely
ii) does not fully cover AF
ii) covers area encircled by ring apophysis

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13
Q

Is the vertebral end plate more strongly bound to the disc or vertebral body?

A

Disc.

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14
Q

What are the functions of the vertebral end plate?

A

i) growth plate
ii) nutrition for IVD
iii) protection

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15
Q

Upon axial compression, which part of the intervertebral system is most likely to fail?

A

The vertebral end plate. Upon axial compression:

i) hydostatic pressure of NP rises
ii) tensile force in AF rises allowing radial NP expansion
iii) compressive forces exerted upward and downward from NP onto end plate to redistribute force.
iv) trabeculae fracture first, followed by end plate fracture

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16
Q

Which nerve root would a posterolateral herniation at L4/5 impact? L5/S1? Large central L4/5 herniation?

A

i) L5 (often the lower VB)
ii) L5 and S1
iii) cauda equina

17
Q

Is disc herniation a mobility or stability issue?

A

Stability. Disc injury restributes forces to other structures (esp. facets).

18
Q

Which structures reinforce the z-joint capsules anteriorly and posteriorly?

A

i) anterior: ligamentum flavum

ii) posterior: multifidus

19
Q

What special intra-articular features to z-joints possess?

A

i) subcapsular pockets (superior and inferior)
ii) fat pads
iii) meniscoid structures
- these structures can cause locking

20
Q

What is spondylolithesis pathology?

A

Anterior displacement of one vertebra or the vertebral column relative the vertebra below. Often secondary to a fracture of the pars interarticularis following repetitive trauma or increased training.

21
Q

What is the MOI for a pars interarticularis fracture?

A

Flexion/distraction.

22
Q

Describe the grading system for spondylolithesis.

A
I: <25% slippage
II: 25%-50% slippage
III: 50% -75% slippage
IV: >75% slippage
Note: Grade III, IV and high level IIs require surgical stabilization prior to therapy.
23
Q

Define clinical instability.

A

Pathological increase in translatory movement that interferes with joint function. It is NOT synonymous with hypermobility or joint laxity.

24
Q

What are the expected subjective reports associated with clinical instability?

A

i) catching/clunking and positive physical exam
ii) history of dislocation/joint slipping
iii) apprehension loading the region or with movement

25
Q

What is the source for pain in DDD?

A

i) circumferential tears through the outer 1/3 of annular fibres.
ii) inflammation

26
Q

What is degenerative spondylolithesis pathology?

A

Development of laxity in capsule and disc due to early degeneration which allow for anterior translation of superior vertebra (<30%) often resulting in stenosis.

27
Q

What is the pattern of stenosis that often develops from degenerative spondylolithesis?

A

Lateral +/- central (often L4/5 causing L5 nerve root compression). This pathology is not likely to progress.

28
Q

What symptoms would arise from lateral stenosis?

A

Nerve root signs (myotomes, dermatomes, reflexes).

29
Q

What symptoms would arise from central stenosis?

A

Cord signs (cauda equina, hyperreflexivity, spasticity etc.)

30
Q

What symptoms would arise from foraminal stenosis?

A

May affect movement if z-joint articular surface implemented.

31
Q

What are the three components of the Panjabi model of stability?

A

i) passive: vertebrae, discs, ligaments, capsules etc.
ii) active: muscles & tendons.
iii) neural/control: proprioception, descending control, motor coordination etc.

32
Q

What is Panjabi’s neutral position?

A

Position of the spine that requires minimal internal stress and muscular effort to hold (high laxity).

33
Q

What is Panjabi’s neutral zone?

A

The part of spinal ROM in which motion is produces with minimal internal resistance.

34
Q

What is Panjabi’s elastic zone?

A

The part of spinal ROM from the end of the neutral zone into up to physiological limit characterized by significant degree of internal resistance (high stiffness).

35
Q

What is Panjabi’s definition of clinical instability?

A

A decrease in the ability of the spinal stabilization system to maintain the neutral zone within the physiological limit such that no pathology occurs.

36
Q

What are the components of Hertel’s model of instability?

A

i) mechanical insufficiencies: ligamentous, articular, degeneration, synovial changes etc.
ii) functional insufficiences: weakness, neuromuscular control, proprioception, postural control etc.
- The result is RECURRENT episodes of pain secondary to instability.