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DPT 730/1: MSK > Exam 1- LBP- Facet jt Impingement > Flashcards

Exam 1- LBP- Facet jt Impingement Flashcards

1
Q

what components of a thorcaolumbar scan are done in standing

A

A/PROM with overpressure
combined motion
myotome- L4/5 heel walk and S1/2 toe walks

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2
Q

what components of a thorcaolumbar scan are done in sitting

A

stress test - stress fractures
dural mobility - SLR and slump test
DTR - L2/3 patella and S1/2 achilles
dermatome

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3
Q

what are the dermatome pattern for the thoracolumbar scan

A

L1/2 - antlat hip, upper antlat hip
L3- medial knee
L4- ant knee, medial malleolus
L5- fibular head
S1- lateral malleolus
S2- heel

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4
Q

what components of a thorcaolumbar scan are done in supine

A

dural mobility - SLR
stress test - lumbar and sacroiliac
myotome

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5
Q

what is the myotome pattern in the thoracolumbar scan that is done in supine

A

L1/2- hip FLX
L3/4- knee EXT
L4/5- dorsiflexion
L5/S1- eversion
S1- knee FLX
S2- curl toes

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6
Q

what are the stress tests done for the lumbar region in the thoracolumbar scan in supine

A
  1. compression- gather legs and push towards head or strike ischial tuberosity
  2. distraction- trap feet and pull calves
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7
Q

what are the stress tests done for the sacroiliac region in the thoracolumbar scan in supine

A
  1. compression - press ASIS
  2. distraction - push ASIS outward
  3. thigh thrust - place hand under sacrum, hip in flexion, push through long axis
  4. Gains Levenes test - drop one leg off table into EXT and lift other leg into hip FLX, push each respectively
  5. PRONE, press sacrum on posterior aspect
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8
Q

what components of a thorcaolumbar scan are done in sidelying

A

myotome- L3 ADD hip, L5 ABD hip, L5-S2 hyperext
dural mobility- femoral nerve

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9
Q

what components of a thorcaolumbar scan are done in prone

A

dural mobility- femoral nerve
stress test - PA pressure lumbar and torsional stress
DTR- semitendinosis

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10
Q

What are the variables for stabilization

A

Jt integrity
Passive stiffness
Neural input
Muscle function

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11
Q

What muscles increase contraction of multifidus

A

Pelvic floor and transverse abdominus

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12
Q

what are the S&S of spondylogenic pain

A

non segmental pain
vague, deep, achy, boring pain
referred pain- not specific
neuro scans normal
can’t reproduce pattern with motion

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13
Q

what is viscerogenic pain S&S

A

cannot produce mechanically
neuro scan normal

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14
Q

what are the S&S of radicular pain

A

electrical shock pain
derm/myotomes, DTRs=normal
dural mobility= ++++
imaging helpful

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15
Q

what are the S&S of radiculopathy pain

A

segmental paresthesia- constant/long duration, slow progression
possible weakness
neuro scan ++++
imaging helpful

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16
Q

what are the S&S of peripheral pain

A

non segmental paresthesia- short/intermittent, fast progression of numbness
possible weakness
derm/myotomes, DTRs,= normal
dural momility= ++++

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17
Q

Name the pain:
referred pain
sensory, DTR, dural= normal
can’t reproduce pain with motion

what is the source/description

A

viscerogenic
referred pain from organ

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18
Q

name the pain:
Sensory, DTR= normal
can’t reproduce pain with motion
dural mobility= ++++
quick pain

what is the source/description

A

radicular
highly inflammed spinal n

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19
Q

name the pain:
Sensory, DTR, dural= ++++
possible weakness
slow progression

what is the source/description

A

radiculopathy
spinal n, blocked conduction

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20
Q

name the pain:
Sensory, DTR, dural= normal
can’t reproduce entire pain with motion

what is the source/ description

A

spondylogenic
local/referred spinal pain

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21
Q

name the pain:
Sensory, DTR= normal
dural= +++
possible weakness
short, intermittent pain

what is the source/description

A

peripheral
peripheral n, decreased conduction in extremity

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22
Q

Why does pain, swelling, inflammation, and disuse cause increase stress on non contractile tissues

A

the force of the global muscles can end up damaging structures around the jt. because stabilization isn’t there to manage the force. therefore putting stress on noncontractile tissues

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23
Q

Once a passive, non contractile tissue has healed, how do we make the jt more stable

A

By improving muscle function and creating more control of the smaller/deeper muscles

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24
Q

what is the peripheral patho of nociplastic pain

A

thinning myelin sheaths
a delta and c fibers get excited easily making it hard to override pain with motion

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25
Q

what is the central patho for nociplastic pain

A

increased excitability of dorsal horn
loss of descending anti-nociceptive mechanism- less pain control - no endogenous opiate released

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26
Q

what are the S&S for possible nociplastic pain

A

less than or equal to 3 months of pain
regional or spreading
Pain can not be explained
pain is hypersensitive or allodynia

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27
Q

what criteria if present can be probable nociplastic pain

A

sensitivity to light, sound, or odor
sleep disturbance
fatigue
cognitive problems

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28
Q

what are ANS S&S for nociplastic pain

A

pitting edma
decrease sebaceous gland
sweaty hands/feet
coldness/clamminess- decrease peripheral arterial shunting
loss of laterality
increased erector pili muscles

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29
Q

what is the general Rx for nociplastic pain

A

JM
MET
neuroscience education/behavioral therapy

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30
Q

why is JM the best treatment in CNS

A

stimulates descending inhibitory pain mechanisms- release endorphins
induce presynaptic inhibition
reduce dorsal horn excitability
decrease inflammatory mediators

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31
Q

what is the MET parameters for nociplastic pain

A

low to moderate intensity global aerobic and resistance
2-3x/wk
30-90 minute sessions
7 weeks duration

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32
Q

what are the benefits of MET with nociplastic pain

A

endogenous analgesia
helps pt to interpret pain and motion as non threatening
reorganize homunculus

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33
Q

why is neuroscience education/behavioral counseling beneficial for nociplastic pain pts

A

explain increased sensitivity and misinterpretation to reduce stress and anxiety
transition to adaptive pain coping

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34
Q

what are risk factors for LBP

A

previous LBP
co morbidities
poor mental health
smoking, obesity, low activity levels
awkward posture

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35
Q

what ROM is required for sit to stand

A

35-42 deg flexion

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36
Q

what ROM is required for picking up objects from the floor

A

60 deg flexion

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37
Q

what abnormal findings can be found with MRI with a chief complaint of LBP

A

IDD
age related disc changes
N compression
facet hypertrophy

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38
Q

who should get imaging with LBP

A

> 50 years of age with a hx of cancer
saddle paresthesia
bowel and bladder dysfunction
specific neurological deficits
progressive/disabling symptoms
no improvement after 6 weeks of conservative RX

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39
Q

what are preventative measures for adults with LBP

A

exercise

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40
Q

what are preventative measures for children with LBP

A

ergonomic furniture

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41
Q

what is the first line Rx for LBP

A

education, cognitive behavioral therapy, stabiization

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42
Q

what do we need to educate the pt on that has LBP

A

spinal structure ad structural strength
neuroscience explanation
overall favorable prognosis
active coping mechanism
stay active with early resumptions of ADL
emphasis on function

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43
Q

why is education important for prognosis of LBP

A

greater emotion = greater pain
improve emotion = less pain

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44
Q

what treatments give short term benefits at best for LBP

A

modalities- heat, electrical stimulation, ultrasound
soft tissue mobilization

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45
Q

when are treatments with only short term benefits best used

A

used for opening a window for MET or MT

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46
Q

what can we do as providers to better our practice for LBP

A

increase consultation time and follow up
reward quality and not volume with reimbursement
increased provider knowledge of evidence and guidelines

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47
Q

what is centralization

A

abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motion

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48
Q

when is intermittent traction the most beneficial for pt with LBP

A

performed in prone and when….
18-60 yrs of age
paresthesia in last 24 hrs distal to knee
oswestry questionairre score >30
+ n root compression, crossed SLR, and centralization

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49
Q

what factors favor stabilization to confirm treatment

A

younger age
postitive prone instability test
aberrant motion
greater SLR ROM
hypermobility with spring testing
increasing episodes

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50
Q

what factors favor directional preference to confirm treatment

A

strong preference for sitting or walking
centralization with motion testing
peripheralization in oppositie direction

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51
Q

what classifies the patient for directional preference

A

centralize with 2 or more movements in the same direction

centralize in one direction and peripherilize in the opposite direction

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52
Q

what classifies the patient for manipulation

A

have recent onset of symptoms <16 days
AND
no symptoms distal to the knee

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53
Q

what classifies the patient for stabilization

A

average SLR ROM >90 deg
positive prone instability test
positive aberrant motion
less than 40 years of age

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54
Q

what is directional preference

A

a position, motion, and factor that alleviates symptoms

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55
Q

what subgroup is most effective for LBP

A

mobilization/manipulation

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56
Q

what are the predicators for a manipulation of LBP

A

no symptoms distal to knee
< 16 days of symptoms
lumbar jt hypomobility
FABQ at work <19
greater than or equal to 1 hip with more than 35 deg IR

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57
Q

what is the most effective treatment for stabilization of LBP

A

motor activation/coordination and stabilization
aquatic therapy, pilates, yoga
trunk balance
progressive aerobic endurance exercise

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58
Q

explain williams flexion exercise/protocol

A

deforming the spine by forcing ourselves to stand
reduce lordosis
involved posterior pelvic tilt and trunk and hip flexion
weak evidence

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59
Q

what is cognitive behavioral therapy

A

helping patients understand and manage all biopsychosocial elements contributing to their symptoms

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60
Q

what is the prognosis of LBP

A

rapid improvements in one month
most improve substantially in 6 wks

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61
Q

how should medications be used with LBP

A

recommend only with an inadequate response to exercise and cognitive behavioral therapy

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62
Q

how does epidural injections affect LBP

A

recommend only for radicular pain
if no benefit by 4 weeks

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63
Q

what is acute IDD

A

annulus and end plate tear
least common is acute herniations

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64
Q

where is IDD most common

A

lumbar region
95% at L4-S1

65
Q

what part of the disc is most common for IDD and why

A

posteriorlateral
weaker, thinner, with more vertical and less oblique annular fibers

66
Q

how can acute IDD occur in the lumbar spine

A

FB with or without twisting cause:
non- symmetrical tension
limited stabilization
more anterior shearing
increase stress on weaker structures

67
Q

what is the immunoreactive response once the disc is injured

A

excessive osmotic pressure or increase in static fluid pressure
more fluid = more chemicals which sensitizes the spinal n (radiculopathy/radicular)
no lymph drainage
extended inflammatory phase

68
Q

what are typical postlat IDD symptoms

A

dull/achy spinal pain
radiculopathy- segmental paresthesia in the first 24 hours into distal extremity
referred pain into glutes and groin due to swelling

69
Q

why is there more swelling with lumbar IDD than cervical

A

more GAGs so there is more significant swelling

70
Q

what pain behaviors would the patient describe about lumbar postlat IDD

A

increase pain with FB, sitting, coughing, lifting
decrease pain with unloading, standing, walking
increase pain in the AM

71
Q

what would we observe with postlat IDD in the lumbar region

A

lateral shift of shoulders on pelvis
smaller calf girth not until 4-6 weeks after injury - spinal n compression 80% conduction loss

72
Q

what would we find in a scan for ROM for acute postlat IDD

A

increase pain with FLX and SB away from injured area - peripherlization of symptoms
decrease pain with EXT and SB toward injured area - centralization

**directional preference

73
Q

why might spinal pain increase with EXT, but nerve symptoms centralize for a patient with postlat IDD

A

due to increase of hydrostatic pressure on disc with high osmotic pressure due to swelling. this is squeezing the inflammation out.

74
Q

what other things can be found in a scan for acute postlat IDD

A

ST- + for compression, distraction, PA, torsion
neuro- fatiguing, hyporeflexive, diminished dermatome, + dural
BE- + stability test

75
Q

what are the classification syndromes with Mckenzie method

A

postural- correct posture
dysfunction- stretch to improve ROM
derangement- use end range ROM to improve theoretical nucleus migration in disc

76
Q

what is the treatment priority for acute IDD

A

get n pain and LE symptoms under control to prevent n damage

77
Q

what is the PT Rx for acute postlat IDD

A

POLICED
directional preference
intermittent traction
postural/ergonomic edu
neural mob
MET

78
Q

how should we prescribe for directional preference

A

10-20 reps every 1-2 hours as needed

79
Q

what is our posture edu for acute IDD patients

A

limited to no sitting
limited to no driving/FB

80
Q

what is our MET for acute IDD patients

A

tissue proliferation and stabilization
unweighted walking

81
Q

what can cause persistent IDD

A

acute IDD
mixed findings with age
lower strength
sedentary lifestyle
heavier occupational lifting
smoking
genetics

82
Q

how can persistent IDD occur from persistent inflammation

A

growth of nociceptive fibers from acute IDD healing can lead to nociplastic pain
brings excessive and destructive enzymes and low grade infection to the disc

83
Q

what does persistent inflammation limit

A

limits proliferation

84
Q

what is the patho for persistent IDD

A

less gags more fibrotic nucleus
more acidic disc - limits proliferation
annular disorganization
thinning/loss of cartilage and end plates
increased inflammation and fatty deposits
persistent herniations

85
Q

what is protrusion

A

bulge
nucleus migrates but remains in annulus

86
Q

what is extrusion

A

nucleus migrates thru the outer annulus

87
Q

what is free sequestration

A

nucleus migrates and breaks away from annulus

88
Q

what is schmorl’s nodes

A

where nucleus migrates into the vertebral body

89
Q

why is the disc not white in a T2 MRI when the patient has persistent IDD

A

low grade inflammation is black
acute (high grade) inflammation is white

90
Q

how might persistent IDD due to narrowing affect the spine

A

loss of disc height/integrity
jt hypermobility during sagittal/frontal plane
foramen narrowing = stenosis

91
Q

why might the patient not have symptoms with RT if they are presenting with persistent IDD due to narrowing

A

the lumbar spine does not have much RT so there isnt as much stress on the spine like EXT or SB

92
Q

what 3 conditions can be caused by persistent IDD when disc height and integrity are lost

A

hypermobility
ARJC
stenosis

93
Q

how do persistent IDD symptoms compare to acute IDD

A

slow change allows tissues to adapt without symptoms

94
Q

how do you treat persistent IDD

A

acute IDD Rx if inflamed
Mckenzie exercises not as effective due to the theory affecting inflammation more than the disc
consider primary driver of symptoms

95
Q

what is the prognosis of IDD

A

3-5 weeks initial strength
8-12 weeks greater tensile strength and dense fibrous tissue

start to improve by 6 wks and symptoms resolve by 12 wks

96
Q

what are negative predictors for prognosis with IDD

A

perpheralization
mental depression
pain behaviors
fear of work

97
Q

why might antibiotics be prescribed for IDD

A

potential infection with persistent IDD due to chronic inflammation

98
Q

when would a steroid pack be given for IDD

A

for a large inflammatory response

99
Q

when is spinal decompression sx indicated for a pt with IDD

A

persistent or worsening radiculopathy
use when symptoms are unresponsive to non-sx treatments

100
Q

why is TDR a better option with persistent IDD

A

better load distribution
preserves facets, foramen, and stability

101
Q

Which of the following is a change in the persistent internal disc derangement?

More glycosaminoglycans
Annular disorganization
Less acidity in the disc
Thickening of end plates

A

annular disorganization

102
Q

During your scan, you note positive neurological signs and symptoms for lower motor neuron involvement. Which of the following is the correct term for these findings?

Nociplastic
Radiculopathy
Spondylogenic
Viscerogenic

A

radiculopathy

103
Q

Once a herniation occurs, which of the following categories indicates the nucleus migrates through the annulus?

Bulge
Protrusion
Extrusion
Sequestration

A

extrusion

104
Q

Which of the following tissues and mechanisms is involved with an acute internal disc derangement?

Increased inflammation of disc
inner annular fibrosis tissue tearing
Migration of nucleus pulposus
Outer annular and end plate tearing

A

outer annular and end plate tearing

105
Q

Which direction preference is the MOST common with an acute internal disc derangement?

A

Extension

106
Q

Which of the following should you be MOST concerned with a central internal disc derangement in the lower lumbar spine?

Cauda Equina Syndrome
Spinal nerve compression
Peripheral nerve compression
Spinal Cord compression

A

causa equina syndrome

107
Q

Which of the following are risk factors for low back pain?

Regular exercise
Previous neck pain
Awkward postures
Light lifting

A

awkward posture

108
Q

Which of the following general expectations should we have for our patients with low back pain?

Most will improve within four to six weeks of onset
Beliefs and behaviors do not influence outcomes
Pain levels are more influential than fear avoidance behaviors
Higher education and income contribute to persistent low back pain

A

most will improve within 4-6 weeks of onset

109
Q

what changes IAR

A

abnormal movement of spinal segment under loaded conditions, resulting in pain or disability

110
Q

what can cause hypermobility

A

trauma
ARDC
repetitive activities
creep
adjacent jt hypo
connective tissue disorder

111
Q

what is the most common place for hypermobility in the lumbar region

A

L4-S1

112
Q

why is L4-S1 the most common region for hypermobility

A

L4/5 are more sagittal plane but L5/S1 transition to more frontal plane to limit ant shear

113
Q

what are symptoms of functional instability in the low back

A

predictable pain
spine and referred pain
decrease pain with positional changes
increase pain with prolong position
catching
self manipulation

114
Q

what can be seen with ROM from a pt with functional instability if acute

A

limited with aberrant motion
EXT due to increase of ant shearing
FLX with Gowers sign

115
Q

what can be seen with ROM from a pt with functional instability if persistent

A

PROM > AROM when NWB vs WB
WNL or excessive, EXT still could be limited plus creasing

116
Q

What can be found in a SCAN for functional instability

A

CM- inconsistent block
ST- + PA, mixed distraction
neuro- neg, possible hyperesthesia

117
Q

what is aberrant motion

A

painful arc
uncoordinated motion
Gowers sign - UE assistance from FB
LE/pelvis compensation

118
Q

what would show in accessory motion with functional instability

A

possible hypomobility (stuck drawer)
adjacent jt hypo from T10-12 RT, SI jt motion, hip hyperextension

119
Q

what would show in stability test with functional instability

A

+ possible prone LE ext test
+ linear stability - most likely ant shearing
+ ASLR
inhibited local m

120
Q

how can the LBP lead to an over recruited psoas m

A

psoas maintains lordosis
excessive recruitment can lead to lumbar hyperext and ant shearing most often occuring with instability

121
Q

what are the symptoms for mechanical instability

A

unpredictable pattern
worsening symptoms with more frequent episodes
increased pain with trivial or lesser ADLs

122
Q

how does mechanical instability differ in a SCAN

A

+ stability test wont stabilize in closed pack postion

123
Q

what can show on a radiograph for mechanical instability

A

vertebral position in various position
spondylolisthesis

124
Q

how do we treat functional and mechanical instability

A

rx for lig
POLICED
postural activities to activate local m
JM - adjacent hypo
bracing/taping
MET

125
Q

what should MET emphasize on with instability

A

stabilization, local m (neutral or FLX and progress into EXT)
hip exercise - EXT, ER, IR decrease LBP
hyperextension is contraindicated

126
Q

what can cause ARJC

A

prior trauma
age
genetics
other disease
sedentary lifestyle with underloading

127
Q

what happens to synovial jt structures in ARJC

A

ARTICULAR CARTILAGE frays or blisters causing the JT CAPSULE to narrow
FIBROUS CAPSULE slackens then thickens/stiffens
SYNOVIAL MEMBRANE produces less SYNOVIAL FLUID and nutrients

128
Q

what are symptoms a pt may tell you when experiencing ARJC in lumbar spine

A

gradual onset of LBP
pain with prolong, particular in standing, prefer FLX
morning stiffness or after prolong position less than 30
possible paresthesia
some movement helps but too much is worse

129
Q

what can be in the SCAN for a pt with ARJC in lumbar spine

A

ob- possible FB
ROM- painful/limited EXT, ipsi SB, contra RT
CM- consistent block or opposing quadrants
ST- pain with compression, torsion, PA
neuro- negative could be positive for radiculopathy if spur

130
Q

how can we treat ARJC in lumbar spine

A

improve integrity and mobility
POLICED- edu and orthotics
JM for pain, integrity and mobility
MET improve motion, integrity and neuromuscular

131
Q

why could pure strengthening parameters be a problem for LBP early on in PT

A

cant overload the jt
too much stress all at once
work up MET parameters as jt integrity increases

132
Q

what can compression of a nerve from outside in be due to

A

ARD/JC
instability
enfolding of lig flavum

133
Q

What can compression of a nerve from inside out be due to

A

sheath around n is fibrotic due to persistent inflammation
increased blood supply to nerve with activity, particularly walking, causes n to enlarge

134
Q

what are stenosis symptoms

A

unilateral LE
decrease pain in LE with FB/sitting/AM
increase pain in LE with standing/walking

135
Q

what can you observe with a patient with stenosis

A

slouched
possible scoliosis

136
Q

what can you find in a SCAN for stenosis

A

ROM- FLX/contra SB decrease pain but still could limited due to not being able to open foramen. EXT/ipsi SB increase pain
CM- consistent block
ST- (+) after 10 sec hold PA, torsion
neuro- (+) radiculopathy

137
Q

what can you find with accessory motion if a patient has stenosis

A

hypomobility- FLX/contra SB
possible adjacent jt

138
Q

what can you find in special test if a patient has stenosis

A

stability test- shearing
LE discrepancies
balance deficits

139
Q

how do you differentiate whether stenosis is due to neural or vascular disease

A

Ankle brachial index test for possible peripheral arterial disease
bicycle test

140
Q

how can the bicycle test indicate stenosis or PAD

A

cycle upright for 3 minutes then bend to lean over handle bars for 3 min
if calf pain still exists after leaning over = PAD
if not= stenosis

141
Q

how do we treat stenosis

A

pt education
directional preference - flx
intermittent traction
manual therapy
neural mob
MET
corsets

142
Q

how can manual therapy be effective for stenosis

A

jt mob in FLX and contra SB direction
manipulation - most effective with exercise

143
Q

how is MET directed for a patient with stenosis

A

aerobic- repetitive stress gains integrity and circulation
balance training
local m stabilization

144
Q

what are indications for sx with stenosis

A

presence of constant and or worsening symptoms
failure to obtain relief with 3-6 months of non sx treatment

145
Q

what is spondylolysis

A

bony defect or fx of pars interarticularis unilateral or bilateral

146
Q

what can cause spondylolysis

A

congenital
repetitive stress, EXT and RT
direct trauma

147
Q

what structures are most common with spondylolysis

A

L5-S1

148
Q

what are S&S of spondylolysis

A

acute- fx S&S plus + bilateral torsion test
persistent- asymptomatic or instability S&S

149
Q

what is spondylolisthesis

A

anterior vertebral seg slippage due to mechanical instability

150
Q

what are 2 most common types of spondylolisthesis

A

isthmic or adolescent with spondylolysis
degenerative

151
Q

what is isthmic or adolescent with spondylolysis spondylolisthesis

A

most common
most rapid slipping
repetitive or traumatic EXT

152
Q

what is degenerative spondylolisthesis

A

due to ARDC
no fx

153
Q

what are S&S of spondylolisthesis

A

worst case instability
possible lateral or central stenosis S&S with slippage
no correlation with slippage and degree of symptoms

154
Q

how do we treat spondylolysis/listhesis

A

worst case instability
MET- local m stabilization

155
Q

what is a meniscoid

A

facilitate the spread of synovial fluid

156
Q

what is facet jt impingement

A

meniscoid becomes wedged due to prolong position or quick movement

157
Q

what are S&S of facet jt impingement

A

woke up or made a quick movement and couldn’t move
acuity with ARJD S&S
instability S&S

158
Q

how do we treat facet jt impingement

A

isometrics to pull meniscoid out of the way
gapping manip

DPT 730/1: MSK (11 decks)

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