Spine- Thoracolumbar IV- Acute IDDs Flashcards

1
Q

Which is more common, acute or persistent IDDs?

A

Persistent IDD

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2
Q

Which region of the spine is an IDD rarely found in?

A

Thoracic

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3
Q

Why are there greater consequences if there is an IDD in the thoracic spine?

A

Narrowest canal

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4
Q

What percentage of symptomatic disc herniations are in the thoracic region?

A

<1%

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5
Q

Where is an acute IDD most common?

A

Lumbar region

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6
Q

What percentage of IDDs are symptomatic?

A

1-3%

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7
Q

What percentage of LBP cases are caused by acute IDD?

A

<5%

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8
Q

What age group are acute IDDs mostly in?

A

30-50 year olds

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9
Q

What segments are 94% of the acute IDDs in the spine in?

A

L4-S1

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10
Q

What portion of the disc is the most common area for an acute IDD?

A

Posterolateral portion of the disc

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11
Q

Why is the posterolateral disc more susceptible to an acute IDD? (think fibers)

A

weaker, thinner, with MORE vertical and LESS oblique annular fibers

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12
Q

What is the acute IDD placement in the posterolateral disc just lateral to? Why does this matter?

A

The PLL, which means less reinforcement

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13
Q

What kinds of trauma can cause an acute IDD?

A
  • axial compression
  • forward bending or stooping with or without twisting/lifting
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14
Q

What is not happening with forward bending?

A

Lumbar spine NOT fully flexing

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15
Q

What does forward bending or stooping without or with twisting/lifting lead to?

A
  • less circumferential disc compression
  • MORE anterior segmental shearing force due to the pull of gravity, except less at L5,S1
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16
Q

Why is the less circumferential disc compression with forward bending or stooping trauma?

A
  • unevenly distributed annular tension
  • increased and asymmetrical stress on weaker and thinner POSTEROLATERAL annular and end plate fibers
  • LESS fixated end plate
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17
Q

Where is there less anterior segmental force in bending/stooping without twisting?

A

at L5,S1

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18
Q

What structures are MORE commonly torn in acute IDD?

A

OUTER annular tearing and end plate avulsion

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19
Q

What structures are LESS commonly torn with acute IDD?

A

INNER annular tearing and NPH

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20
Q

What is the vascularity and innervation of the inner annulus?

A

Aneural and avascular

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21
Q

What is the vascularity and innervation of the outer annulus?

A

vascular and neural - heals better

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22
Q

What is the role of disc?

A

Shock absorption and load distribution

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23
Q

What happens to disc structures once damaged?

A

Immunoreactive - large AUTO immune inflammatory response occurs

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24
Q

What happens along with the large AUTO immune inflammatory response we see with acute IDD?

A
  • Excessive osmotic pressure OR increased static fluid pressure in and around disc and spinal nerve
  • Static fluid that consists of increased inflammatory chemicals that sensitizes spinal nerve and structures to pressure/tension
  • radiculopathy/radicular S&S
  • NO lymphatic veins in PNS or CNS so drainage is poor
  • EXTENDED Inflammatory phase
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25
Q

What are typical posterolateral IDD symptoms?

A
  • Dull/achy spinal pain
  • Radiculopathy
  • Referred pain into glutes and groin
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26
Q

Why is the pain with posterolateral IDD dull and achy?

A
  • annulus highly innervated so very painful
  • significantly MORE swelling than cervical disc due to higher number of GAGs
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27
Q

Why is there radiculopathy along with acute posterolateral IDD?

A
  • possible segmental paresthesias within 24hours into distal extremity
  • worse situation
    > presence of radiculopathy
    > presence of coldness indicating greater circulatory compromise
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28
Q

When is there typically reduced pain with typical posterolateral IDD?

A

reduced pain when unloaded
- lying and standing/walking

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29
Q

When is there typically increased pain with posterolateral IDD?

A

Increased LBP and paresthesias
- FB/sitting/lifting
- coughing/sneezing (increased pressure in the trunk since it is a forceful activity)

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30
Q

Why is there increased pain in the mornings with typical posterolateral IDD?

A

Increased pain in the AM due to pooling of swelling from static sleeping position

31
Q

What are a lot of the early symptoms of posterolateral IDD due to?

A

Pressure and chemicals from swelling

32
Q

What type of posture may we see with posterolateral IDD?

A

A lateral shift of the shoulders on the pelvis
- SB away from the pain
- counter contralateral SB to level eyes

33
Q

What (aside from posture) can we observe with severe spinal nerve compression with posterolateral IDD?

A

Smaller calf girth
- wasting likely at 4-6 weeks and indicative of severe spinal nerve compression
- MORE of a sign for a persistent radiculopathy

34
Q

What can we find with ROM with postlat IDD?

A

All may increase pain

35
Q

Why will flexion and possibly SB away from the injured area of the disc be painful?

A

Swelling being pushed toward spinal nerve like water balloon
- tension on torn annulus, endplate, and dura

36
Q

What is MOST limited with postlat IDD?

A

Flexion and possibly SB away from injured area of the disc
- increases extremity and LBP

37
Q

What other directions are possibly less limited with postlat IDD?

A

Extension and possibly SB toward the injured area

38
Q

Why can Ext and SB be painful with postlat iDD?

A

May increase LBP due to increased hydrostatic pressure on end plate fractures and high osmotic pressure of disc

39
Q

Why can ext and SB centralize extremity pain?

A
  • by squeezing swelling away from spinal nerve, causing centralization
40
Q

What ROM is NOT consistent with postlat IDD?

A

ROTation

41
Q

What is the centralization of symptoms?

A

Abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motions or sustained postitions

42
Q

What will we find in our scan with typical postlat IDD?

A
  • resistance and MMT - variable
  • Stress tests:(compression/distraction/PA/torsion) - possibly positive due to acuity
  • neuro tests: possibly positive depending on severity and timing
43
Q

What order will we have positive neuro tests?

A
  • Diminished dematomes
  • DTR: hyporeflexive
  • Myotomal fatigue
  • positive dural mobility tests
44
Q

What will we find in our biomechanical exam?

A

Possibly positive stability tests

45
Q

What are some unique S&S with rare central and posterior IDD?

A
  • cord or cauda equina S&S depending on level
46
Q

What do we do with a central and posterior IDD?

A

IMMOBILIZATION AND EMERGENCY REFERRAL

47
Q

Where is the typical lowest level of spinal cord?

A

L1/L2 segment

48
Q

Who was mechanical diagnosis and therapy developed by?

A

Robin Mckenzie

49
Q

What is the mechanical diagnosis and therapy based on?

A

The belief that most spinal pain comes from injuries to the disc which is not supported in the research

50
Q

What is the classification system with mechanical diagnosis and therapy based on?

A

primarily on symptoms
- location
- positions that increase symptoms

51
Q

What does mechanical diagnosis and therapy determine?

A

A directional preferance

52
Q

What can directional preference be associated with?

A

Centralization, decreasing severity, and improving function

53
Q

What is the MOST common directional preferance?

A

Ext/hyperextension (>70%)

54
Q

What are the three classification syndromes?

A
  • postural
  • dysfunction
  • derangement
55
Q

What is postural classification syndrome focusing on?

A

Correcting poor posture

56
Q

What is dysfunction classification syndrome focusing on?

A

Stretches to improve end range motion

57
Q

What is derangement classification syndrome focusing on?

A

Using end range motion to improve the theoretical nucleus deformation in disc herniations

58
Q

What is the dynamic disc theory of mckenzie therapy?

A

Deformation NOT migration in a normal disc

  • sitting/flexion decreased anterior disc height, increased posterior disc height and the nucleus deforms posteriorly
  • sitting/extension causes increased anterior disc height, decreased posterior disc height and an anteriorly deformed nucleus
59
Q

When is the dynamic disc theory predictable?

A

ONLY In asymptomatic lumbar spines when the annulus is intact and with normal hydration

60
Q

What can happen with altered fluid dynamics with mechanical diagnosis and therapy?

A
  • high osmotic pressure with large AUTO immune swelling response
  • increasing hydrostatic pressure through repetitive motions - MOST OFTEN in ext
61
Q

When is there limited and contradictory findings with the dynamic disc theory?

A

In symptomatic discs and age related disc diseases with annular changes

62
Q

What happens with increasing osmotic pressure through repetitive motions?

A
  • spinal pain initially increases from resistance of high osmotic pressure being overcome by increased hydrostatic pressure
  • Swelling squeezed away from spinal nerve into the nucleus and the end plates for draining
  • CENTRALIZES pain, LE symptoms decrease which is a priority
63
Q

Is mechanical diagnosis and therapy superior to other treatments for acute LBP/disability?

A

NO

64
Q

What else needs to be done aside from mechanical diagnosis and therapy?

A

Stabilization and proliferation of tissues

65
Q

How many reps and how often should we do directional preference with acute IDD?

A

10-20 reps every 1-2 hours

66
Q

When can intermittent traction be helpful with acute IDD?

A

With radiculopathy, especially if no centralization

67
Q

What else can we do for an ext preferance?

A

Postural/ergonomic education/taping or bracing
- limited to no sitting
- limited to no driving/FB

68
Q

What can we do to avoid counterproductive sitting with driving with ext preference acute IDD?

A

Possible HEP for 1-2 weeks to avoid sitting while driving

69
Q

What is MET ultimately for with acute IDD?

A

Tissue proliferation and stabilization particularly of local muscles

70
Q

How can we do unweighted walking?

A
  • unloader
  • aquatic
  • antigravity systems
71
Q

What is the prognosis for acute IDD?

A

90% start to improve by 6 weeks and symptoms resolve by 12 weeks

72
Q

Will acute IDD require surgery most of the time?

A

NO

73
Q

How are the outcomes comparing sx and without for acute IDD?

A

Slower but the overall same outcomes after two years