Spine- Thoracolumbar IV- Acute IDDs Flashcards
1
Q
Which is more common, acute or persistent IDDs?
A
Persistent IDD
2
Q
Which region of the spine is an IDD rarely found in?
A
Thoracic
3
Q
Why are there greater consequences if there is an IDD in the thoracic spine?
A
Narrowest canal
4
Q
What percentage of symptomatic disc herniations are in the thoracic region?
A
<1%
5
Q
Where is an acute IDD most common?
A
Lumbar region
6
Q
What percentage of IDDs are symptomatic?
A
1-3%
7
Q
What percentage of LBP cases are caused by acute IDD?
A
<5%
8
Q
What age group are acute IDDs mostly in?
A
30-50 year olds
9
Q
What segments are 94% of the acute IDDs in the spine in?
A
L4-S1
10
Q
What portion of the disc is the most common area for an acute IDD?
A
Posterolateral portion of the disc
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
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
13
Q
What kinds of trauma can cause an acute IDD?
A
- axial compression
- forward bending or stooping with or without twisting/lifting
14
Q
What is not happening with forward bending?
A
Lumbar spine NOT fully flexing
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
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
17
Q
Where is there less anterior segmental force in bending/stooping without twisting?
A
at L5,S1
18
Q
What structures are MORE commonly torn in acute IDD?
A
OUTER annular tearing and end plate avulsion
19
Q
What structures are LESS commonly torn with acute IDD?
A
INNER annular tearing and NPH
20
Q
What is the vascularity and innervation of the inner annulus?
A
Aneural and avascular
21
Q
What is the vascularity and innervation of the outer annulus?
A
vascular and neural - heals better
22
Q
What is the role of disc?
A
Shock absorption and load distribution
23
Q
What happens to disc structures once damaged?
A
Immunoreactive - large AUTO immune inflammatory response occurs
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
25
What are typical posterolateral IDD symptoms?
- Dull/achy spinal pain
- Radiculopathy
- Referred pain into glutes and groin
26
Why is the pain with posterolateral IDD dull and achy?
- annulus highly innervated so very painful
- significantly MORE swelling than cervical disc due to higher number of GAGs
27
Why is there radiculopathy along with acute posterolateral IDD?
- possible segmental paresthesias within 24hours into distal extremity
- worse situation
> presence of radiculopathy
> presence of coldness indicating greater circulatory compromise
28
When is there typically reduced pain with typical posterolateral IDD?
reduced pain when unloaded
- lying and standing/walking
29
When is there typically increased pain with posterolateral IDD?
Increased LBP and paresthesias
- FB/sitting/lifting
- coughing/sneezing (increased pressure in the trunk since it is a forceful activity)
30
Why is there increased pain in the mornings with typical posterolateral IDD?
Increased pain in the AM due to pooling of swelling from static sleeping position
31
What are a lot of the early symptoms of posterolateral IDD due to?
Pressure and chemicals from swelling
32
What type of posture may we see with posterolateral IDD?
A lateral shift of the shoulders on the pelvis
- SB away from the pain
- counter contralateral SB to level eyes
33
What (aside from posture) can we observe with severe spinal nerve compression with posterolateral IDD?
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
What can we find with ROM with postlat IDD?
All may increase pain
35
Why will flexion and possibly SB away from the injured area of the disc be painful?
Swelling being pushed toward spinal nerve like water balloon
- tension on torn annulus, endplate, and dura
36
What is MOST limited with postlat IDD?
Flexion and possibly SB away from injured area of the disc
- increases extremity and LBP
37
What other directions are possibly less limited with postlat IDD?
Extension and possibly SB toward the injured area
38
Why can Ext and SB be painful with postlat iDD?
May increase LBP due to increased hydrostatic pressure on end plate fractures and high osmotic pressure of disc
39
Why can ext and SB centralize extremity pain?
- by squeezing swelling away from spinal nerve, causing centralization
40
What ROM is NOT consistent with postlat IDD?
ROTation
41
What is the centralization of symptoms?
Abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motions or sustained postitions
42
What will we find in our scan with typical postlat IDD?
- 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
What order will we have positive neuro tests?
- Diminished dematomes
- DTR: hyporeflexive
- Myotomal fatigue
- positive dural mobility tests
44
What will we find in our biomechanical exam?
Possibly positive stability tests
45
What are some unique S&S with rare central and posterior IDD?
- cord or cauda equina S&S depending on level
46
What do we do with a central and posterior IDD?
IMMOBILIZATION AND EMERGENCY REFERRAL
47
Where is the typical lowest level of spinal cord?
L1/L2 segment
48
Who was mechanical diagnosis and therapy developed by?
Robin Mckenzie
49
What is the mechanical diagnosis and therapy based on?
The belief that most spinal pain comes from injuries to the disc which is not supported in the research
50
What is the classification system with mechanical diagnosis and therapy based on?
primarily on symptoms
- location
- positions that increase symptoms
51
What does mechanical diagnosis and therapy determine?
A directional preferance
52
What can directional preference be associated with?
Centralization, decreasing severity, and improving function
53
What is the MOST common directional preferance?
Ext/hyperextension (>70%)
54
What are the three classification syndromes?
- postural
- dysfunction
- derangement
55
What is postural classification syndrome focusing on?
Correcting poor posture
56
What is dysfunction classification syndrome focusing on?
Stretches to improve end range motion
57
What is derangement classification syndrome focusing on?
Using end range motion to improve the theoretical nucleus deformation in disc herniations
58
What is the dynamic disc theory of mckenzie therapy?
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
When is the dynamic disc theory predictable?
ONLY In asymptomatic lumbar spines when the annulus is intact and with normal hydration
60
What can happen with altered fluid dynamics with mechanical diagnosis and therapy?
- high osmotic pressure with large AUTO immune swelling response
- increasing hydrostatic pressure through repetitive motions - MOST OFTEN in ext
61
When is there limited and contradictory findings with the dynamic disc theory?
In symptomatic discs and age related disc diseases with annular changes
62
What happens with increasing osmotic pressure through repetitive motions?
- 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
Is mechanical diagnosis and therapy superior to other treatments for acute LBP/disability?
NO
64
What else needs to be done aside from mechanical diagnosis and therapy?
Stabilization and proliferation of tissues
65
How many reps and how often should we do directional preference with acute IDD?
10-20 reps every 1-2 hours
66
When can intermittent traction be helpful with acute IDD?
With radiculopathy, especially if no centralization
67
What else can we do for an ext preferance?
Postural/ergonomic education/taping or bracing
- limited to no sitting
- limited to no driving/FB
68
What can we do to avoid counterproductive sitting with driving with ext preference acute IDD?
Possible HEP for 1-2 weeks to avoid sitting while driving
69
What is MET ultimately for with acute IDD?
Tissue proliferation and stabilization particularly of local muscles
70
How can we do unweighted walking?
- unloader
- aquatic
- antigravity systems
71
What is the prognosis for acute IDD?
90% start to improve by 6 weeks and symptoms resolve by 12 weeks
72
Will acute IDD require surgery most of the time?
NO
73
How are the outcomes comparing sx and without for acute IDD?
Slower but the overall same outcomes after two years
