Lumbar Spine and SIJ Flashcards

1
Q

Natural history of acute LBP

A

80% of patients with acute LBP have recovery in 6-8 weeks and may not require extensive treatment.

Characterized by periods of exacerbation and remission.

Flare ups are normal and do not necessarily represent a failure of treatments

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2
Q

Natural history of chronic LBP

A

Widely variable
1/3 of patients had full recovery at 12 month follow up
<5% have persistent symptoms with significant disability. High degrees of pain intensity and disability are unfavorable prognostic factors.

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3
Q

Relationship between work-related spinal loading, prolonged sitting, and/or participation in sports and recovery from LBP

A

No relationship

Therefore, these activities shouldn’t necessarily be limited for patients recovering from LBP

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4
Q

Determining pathoanatomical diagnosis

A

We cannot accurately determine specific tissue causing sxs for most patients.
This is likely ok since most spinal tissues work together and will be influenced by any treatment.

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5
Q

3 primary anatomic regions in nervous system which help to modulate pain

A
  1. Spinal cord (dorsal horn neurons have increased excitability and spontaneous discharge nociceptive info)
  2. Brain stem (Periaqueductal gray matter - opioidergic)
  3. Higher brain centers
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6
Q

Consistent recommendations for treatment of patients with acute LBP

A
  1. initiate early treatment that emphasizes resumption of activity and discourages bed rest
  2. Early recognition of psychologic and work related factors (yellow/blue/black flags)
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7
Q

Consistent recommendations for treatment of patients with chronic LBP

A
  • Supervised exercises
  • Cognitive behavioral therapy
    (Recommendations for manual therapy vary)
  • Step care approach - rapid transition from passive to active treatments with encouragement and reassurance
  • Final common pathway should include activity based approach that maximizes patient participation
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8
Q

Is a single red flag enough to warrant referral?

A

No. Nearly all patients have at least one red flag. About 1% of patients with LBP have serious pathology.

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9
Q

Key clinical features predicting metastatic neoplasm of lumbar vertebrae

A
  1. History of cancer
  2. Overall clinician judgment

(others include unexplained weight loss, >50 yo, <17 yo, failure to improve over predicted time interval following treatment, no relief with bed rest)

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10
Q

Strong predictors of vertebral fracture

A
  1. Contusion or abrasion on the back
  2. History of acute trauma
    ~3. Corticosteroid use

CPR - 3 more positive indicates high risk:

  1. > 70 yo
  2. Female
  3. Significant trauma
  4. Prolonged use of corticosteroids
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11
Q

National guidelines re: imaging and LBP

A

National guidelines call for restricting use of lumbar MRI in patients with nonspecific LBP

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12
Q

Lumbar MRI findings which are meaningfully associated with symptoms

A
  1. High intensity zone (HIZ) in the annular region of the disc > associated with diskogenic pain
  2. High T2 signil in and near vertebral end plate (Modic sign) > disruption of end plate with subsequent bone marrow edema> impaired diffusion of nutrients/waste products> may contribute to diskogenic pain
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13
Q

Physical exam test that increases likelihood of diskogenic pain

A

Centralization of sxs

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14
Q

Yellow flags

A

A patient’s personal mistaken beliefs about pain and injury

  • Pain Catastrophizing Scale: Strong predictor of disability
  • Fear-Avoidance Beliefs Questionnaire: Not good predictors of chronicity when used in isolation.
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15
Q

Blue flags

A

Patient’s perception of work and work conditions that may impair return to work

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16
Q

Black flags

A

Patient’s social and financial issues.

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17
Q

Self efficacy

A

Belief one can achieve future goals. Patient’s beliefs about how pain can be controlled appear to be a powerful predictor of disability.

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18
Q

Spinal manipulation therapy

A
  1. Recommended in most guidelines, early on in treatment of patient with acute (sometimes chronic).
  2. Unlikely that use of SMT in isolation will provide optimal benefit
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19
Q

Motor control exercises

A

Superior to minimal intervention at short- and long-term follow up

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20
Q

CPR for lumbar manipulation

A
  1. No sxs distal to knee
  2. Sxs <16 days
  3. Score of <19 on Fear-avoidance beliefs questionnaire
  4. At least 1 hypomobile segment
  5. At least 1 hip with greater than 35 deg of internal rotation

(Generalizability of this rule has been questioned)

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21
Q

Evidence for lumbar extensor strengthening

A

Not sufficient. Appears to be more effective than no treatment, no comparison to other exercise approaches.

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22
Q

Benefit of aerobic training

A

Appears to reduce increased awareness of neural stimulus (central sensitization)

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23
Q

Weight training and LBP

A
  1. Reduces frequency of acute LBP

2. Properly performed weight training is very unlikely to result in reinjury of spinal tissues

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24
Q

McKenzie Exercises

A

Likely to reduce pain and increase mobility in individuals with acute/ subacute/ chronic LBP

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25
Q

Patient education (Back pain)

A

Key component of care.

  1. Avoiding bedrest
  2. Understanding difference between god pain and bad pain
  3. Physiology of pain and neuroplasticity
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26
Q

Evidence for pain neuroscience education and dry needling

A
  1. No data for PNE

2. Data inconclusive for DN

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27
Q

Peripheral and central events that occur with spinal manual therapy

A

Peripheral: Increased diffusion of water within discs and skeletal muscle; maybe rapid changes in concentrations of inflammatory mediators.

Central: Activation of pain modulatory circuitry; autonomic responses e.g. changes in cortisol levels.

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28
Q

Which part of the disc contains most of the neurovascular structures?

A

Outermost annulus.
Sensory information from these nerves travels to spinal cord via two possible routes - possibly contributing to somewhat vague and diffuse spatial location of people with disc pain.

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29
Q

Tissue fluid exchange within discs

A
  1. Influenced by physical activity

2. Needed to synthesize collagen and proteoglycans

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30
Q

How common are findings of DDD on imaging?

A

Signs are present for most people by third decade of life. Almost universal by 7th/8th decades.

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31
Q

Relationship of smoking and heavy physical loading with DDD

A

Not meaningful etiologic factors.

In the absence of trauma, competitive weight lifters have a lower than expected degree of degeneration.

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32
Q

Strongest known predictors of DDD development

A

Genetic factors

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33
Q

Relationship between OA and DDD?

A

DDD has the highest prevalance in those people with OA involving the extremities.
Age-related changes in discs are similar to those observed in articular cartilage and are not necessarily related to pain.

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34
Q

What part of spine usually gets injured with axial trauma to the spine?

A

Vertebral end plate.

Disruptions in end plate have a strong correlation with DDD.

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35
Q

How to annular tears heal?

A

Limited capacity for healing.
Heal through inflammatory processes > poorly remodeled scars> Increased area of disc that is innervated > decreased threshold to stimulation of pain-sensitive fibers.

Heterogeneity in vascularization of healing annular tears may contribute to variations in recovery from LBP.

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36
Q

Process leading to development of spondylosis

A

DDD> dehydration of nucleus > decreased internal stiffness of disc > micromotion during loading and slackening of supporting tissues due to loss of disc height> facet overload> osteoblastosis

> Further loss of disc height and reduction in ROM > cycle that further reduces threshold for nociception during loading.

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37
Q

Exercise prescription for DDD depending on stage:

A

Mild/ early stage: No additional treatment precautions
Later stage: Avoid exercises that stress vigorous or sustained loading at the end of trunk ROM. Avoid early-morning lumbar flexion for approximately 2 hours. Avoid prolonged flexion including sitting. Work on improving hip ROM.

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38
Q

Why is delayed onset of pain common with DDD?

A

Swelling from micro-hemorrhage and associated edema

39
Q

Are pelvic bones symmetrical?

40
Q

Primary intervention for SIJ dysfunction

A

Motor control.

Hip muscle activation can increase stiffness of SIJs.

41
Q

Evidence for form closure theory

A

No real evidence to support this. There is better evidence to support the biotensegrity model.

42
Q

Total SIJ and pubic symphysis motion with position changes

A

SIJ: Rotation = 1.15-2.5deg. Translation - 0.4-0.9mm

Pubic Symphysis: Rotation = 2 deg. Translation vertical = 0.8 mm males, 1.6 mm females. Translation AP = 0.5-0.7 mm

43
Q

SIJ ligaments relevant to pain

A

Short posterior ligament is often a source of pain. Multidirectional fibers so most any motion can stress it.

Pain with palpation of long posterior (distal) ligament is highly sensitive.

44
Q

Relationship between posture and sacrotuberous ligament

A

Optimal sitting posture engages the sacrotuberous ligament by positioning the sacrum in flexion (enabling stabilizing influence on SIJ).

45
Q

SIJ innervation

A

Upper portion: L5
Lower portion: Sacral plexus

(SIJ can refer pain to L5 and sacral dermatomes)

46
Q

Which parts of SIJ refer where?

A

Upper section: upper buttock, middle buttock, lateral thigh
Lower section: Middle buttock, lower buttock, thigh and lower leg

Groin pain also common for SIJ. SIJ rarely occurs above L5 region.

Note: Pain location not a reliable tool for identifying pain generating structure.

47
Q

“Triangulation of forces” with three muscles at lumbar spine

A

Deep erector spinae
Quadratus lumborum
Psoas
(page 13 of current concepts)

48
Q

Changes to multifidus with LBP

A

Fibrosis after surgery

Atrophy in relation to LBP

49
Q

Quadratus lumborum

A

Highly involved with stabilization during every loading mode of the spine.

50
Q

Importance of glute max in SIJ stabilization

A

Tensions thoracolumbar fascia ipsilaterally and contralaterally.

Glutes often inhibited with LBP. Hip extension becomes hamstring dominant.

51
Q

An important muscle to strengthen for pubic hypermobility

A

Adductors due to working with contralateral rectus sheath.

52
Q

Characteristics of “acute lbp with mobility deficits”

A
  • Restricted spinal ROM and segmental mobility.
  • LBP reproduced with provocation of involved segments
  • Unilateral pain
  • onset of sxs often linked to a recent unguarded/awkward movement or position
53
Q

Characteristics of “subacute LBP with mobility deficits”

A
  • May report sensation of back stiffness
  • Unilateral pain
  • Symptoms reproduced with end-range spinal motions
  • Sxs reproduced with provocation of involved segments
  • Demos at least 1: Limited thoracic ROM and associated segmental hypomobility, “ lumbar, “ lumbopelvic
54
Q

Characteristics of “acute lbp with movement coordination impairments”

A
  • Acute exacerbation of recurring lbp that is commonly associated with referred LE pain
  • Pain at rest or produced with initial to mid-range movements
  • Pain reproduced with provocation of involved segments
  • Movement coordination impairments of lumbopelvic region with flexion/extension movements
55
Q

Characteristics of “subacute lbp with movement coordination impairments”

A
  • Subacute, recurring lbp that is commonly associated with referred LE pain
  • Lumbosacral pain with mid range motions that worsens at end range
  • Pain reproduced with provocation of involved segments
  • Lumbar segmental hypermobility
  • Decreased thoracic and/or lumbopelvic/hip mobility
  • Decreased trunk and/or pelvic region muscle strength and endurance
  • Movement coordination impairments while performing self-care/home management activities
56
Q

Characteristics of “chronic lbp with movement coordination impairments”

A
  • Chronic, recurring low back pain often with associated LE pain
    At least one of the following:
  • Pain worsens with sustained end-range movements/positions
  • Lumbar segmental hypermobility
  • Thoracic and/or lumbopelvic/hip hypomobility
  • Decreased trunk/pelvic strength and endurance
  • Movement coordination impairments while performing community/work-related recreational or occupational activities.
57
Q

Characteristics of “acute lbp with related/referred LE pain”

A
  • Acute LBP + LE pain
  • Sxs often worsened with flexion activities and sitting
  • Centralization-
  • Reduced lumbar lordosis
  • Limited extension mobility
  • Possible lateral trunk shift
  • Clinical findings consistent with subacute or chornic LBP with movement coordination impairments.
58
Q

Characteristics of “acute lbp with radiating pain”

A
  • LBP and narrow band of lancinating pain in LE
  • LE paresthesias, numbness, weakness possible
  • Radicular sxs present at rest or produced with initial to mid-range spinal mobility, lower limb tension testing
  • Signs of nerve root involvement may be present

(Common for these sxs and impairments to also be present in pts with related/referred LE pain)

59
Q

Characteristics of “subacute LBP with radiating pain”

A
  • Subacute, recurring back and LE pain
  • Possible paresthesias, numbness, weakness
  • Pain reproduced with mid-range and worsen with end-range lower limb tension tests
  • Possible neuro deficits
60
Q

Characteristics of “chronic lbp with radiating pain”

A
  • Chronic, recurring back and LE pain
  • Possible paresthsias, numbness, weakness
  • Pain reproduced with sustained end-range lower limb tension tests
  • signs of nerve root involvment may be present
61
Q

Characteristics of “acute/subacute lbp with related cognitive or affective tendencies”

A

At least 2:

  • 2 + responses to mental disorder screen, affect consistent with individual who is depressed
  • High FABQ score, behavioral processes consistent with an individual who has excessive anxiety or fear
  • High pain catastrophizing scores
  • Exam doesn’t follow initial/mid-range/ end-range movement/pain relationship reflective of tissue stress/inflammation/ irritability
62
Q

Characteristics of “chronic lbp with related generalized pain”

A
  • LBP > 3 months
  • Generalized pain not consistent with other impairment-based classification criteria
  • At least 1: Positive responses on depression screen, high FABQ score, high pain catastrophizing scores.
  • Exam doesn’t follow initial/mid-range/ end-range movement/pain relationship reflective of tissue stress/inflammation/ irritability
63
Q

CPR for stabilization classification

A
  1. Age <40 yo
  2. Positive prone instability test
  3. Aberrant movements with motion testing
  4. SLR > 90 deg
64
Q

Treatment for acute lbp with mobility deficits

A
  1. Manual therapy
  2. Therex for mobility
  3. Pt ed encouraging activity
65
Q

Treatment for subacute lbp with mobility deficits

A
  1. Manual therapy
  2. Ther ex for mobility
  3. Ther ex (treat impairments) and education to prevent recurrence
66
Q

Treatment for acute lbp with movement coordination impairments

A
  1. NMR for stability in mid-range positions
  2. Temporary external devices for restraint
  3. Self care/home management training
67
Q

Treatment for subacute lbp with movement coordination impairments

A
  1. NMR and Ther ex for stability in mid-range positions and during self-care related functional activities
  2. Manual therapy/ ther ex for thoracic or hip mobility deficits
  3. Self care/ home management strategies maintaining the involved structures in mid-range positions
68
Q

Tretament of chronic lbp with movement coordination impairments

A
  1. NMR and ther ex for stability at all ranges and during household, occupational, and recreational actvities
  2. Manual therapy for thoracic or hip mobility deficits
  3. Community work/ re-integration
69
Q

Treatment for acute lbp with related/referred LE pain

A
  1. Ther ex, MT, traction to promote centralization and lumbar extension mobility
  2. Progress to interventions for subacute/chronic movement coordination impairment as able.
70
Q

Treatment for acute lbp with radiating pain

A
  1. Pt education in positions that reduce strain or compression to involved nerve roots
  2. Manual or mechanical traction (prone?)
  3. MT to mobilize joints/soft tissues adjacent to the involved nerve root that has impaired mobility
  4. Nerve mobility exercises in pain-free non-symptomatic range
71
Q

Treatment for subacute lbp with radiating pain

A
  1. MT to mobilize joints/soft tissues adjacent to the involved nerve root that has impaired mobility
  2. Traction
  3. Nerve mobility exercises in mid-end range
72
Q

Treatment for chronic lbp with radiating pain

A
  1. MT and TE for thoracolumbar and LQ nerve mobility deficits
  2. Pt education on pain managemnet strategies.
73
Q

Treatment for Acute/Subacute LBP with related cognitive or affective tendencies

A
  1. Pt education and counseling to address specific classification exhibited by patient
74
Q

Treatment for chronic lbp with related generalized pain

A
  1. Pt education and counseling to address specific classification exhibited by patient
  2. Low-intensity, prolonged aerobic exercise activities.
75
Q

Relationship between pelvic rotation and hip flex/ext

A

Anterior rotation + hip extension

Posterior rotation + hip flexion

76
Q

Cluster of exam findings to diagnosis pubic joint hypermobility

A
  1. Excessive motion on 3 WB radiographs
    • ASLR
  2. Tenderness of superior pubic ligament
77
Q

Hip flexion test for pelvic fracture

A

ASLR. + = unable to complete.

78
Q

Metrics for crossed SLR

A

97% specific for herniated disc or lumbar radiculopathy

79
Q

Metrics for Fortin finger test

A

Sensitive, not specific.

80
Q

Stork test for normal SIJ movement

A

Standing unilateral hip flexion. Should only see sagittal plane motion. Abnormal would be motion in other planes, e.g. hip hike or rotation.

81
Q

Best imaging for pelvic fracture (traumatic)

82
Q

Risk factors for chronic destructive pyogenic sacroiliitis

A

IV drug use
Inflammatory bowel disease
Post-op infection
(can have insidious onset)

83
Q

2 most useful criteria for ruling out zygapophyseal origin of pain

A

Absence of pain during coughing or sneezing

No pain when arising from a flexed seated posture

84
Q

2 Laslett’s tests with highest sensitivity and specificity (should be performed first)

A

Thigh thrust

Distraction

85
Q

What type of manipulations were most effective for SIJ pain?

A

SIJ manipulation combined with lumbar manipulation more effective than SIJ alone.
Manipulation improves muscle function and is effective when combined with stabilization exercises.

86
Q

Purpose of shotgun approach after manipulation

A

Moving joint through passive, active, and resisted range of motion.

87
Q

Principles of stabilization program

A
  • Keep exercises bilateral and functional whenever possible.
  • Train every muscle that works to stabilize SIJ/pelvis
  • Focus on motor control and endurance over strength. Building strength can come at the end (phase 5)
88
Q

Do SIJ belts decrease muscle activity?

A

No. There seems to be no change in muscle activity with belts. They act on the passive systems of the pelvis.

89
Q

When to consider prolotherapy or surgery for SIJ dysfunction

A

After failed conservative treatment (and pain is consistent with SIJ pathology, e.g. positive but temporary response to SIJ injection).

90
Q

Relationship between lumbar fusion and future SIJ degeneration

A

75% of patients with L45 and/or L5S1 fusion had SIJ degeneration unilaterally or bilaterally in 5 years. Fusion to sacrum increases rate of degeneration and likelihood that degeneration will be bilateral.

SIJ degeneration may be accelerated on side that had the iliac crest harvesting.

91
Q

Ankylosing spondylitis diagnosis CPR

A

Berlin criteria

  1. Alternating buttock pain
  2. Pain with rest relieved with exercise
  3. PM pain in second half of night
  4. Morning stiffness >30 minutes

IBP criteria:

  1. <40 yo
  2. Insidious onset
  3. Improvement with ex
  4. No improvement with rest
  5. PM pain which improves with getting up
92
Q

Lumbar stenosis diagnosis CPR

A
  1. Bilateral symptoms
  2. Leg pain > back pain
  3. Pain during walking/standing
  4. Pain relief upon sitting
  5. > 48 years old
93
Q

Vertebral compression fracture CPR

A
  1. Age > 52 years
  2. No presence of leg pain
  3. Body mass index < 22
  4. Does not exercise regularly
  5. Female gende