Exam 1- LBP- Facet jt Impingement Flashcards
what components of a thorcaolumbar scan are done in standing
A/PROM with overpressure
combined motion
myotome- L4/5 heel walk and S1/2 toe walks
what components of a thorcaolumbar scan are done in sitting
stress test - stress fractures
dural mobility - SLR and slump test
DTR - L2/3 patella and S1/2 achilles
dermatome
what are the dermatome pattern for the thoracolumbar scan
L1/2 - antlat hip, upper antlat hip
L3- medial knee
L4- ant knee, medial malleolus
L5- fibular head
S1- lateral malleolus
S2- heel
what components of a thorcaolumbar scan are done in supine
dural mobility - SLR
stress test - lumbar and sacroiliac
myotome
what is the myotome pattern in the thoracolumbar scan that is done in supine
L1/2- hip FLX
L3/4- knee EXT
L4/5- dorsiflexion
L5/S1- eversion
S1- knee FLX
S2- curl toes
what are the stress tests done for the lumbar region in the thoracolumbar scan in supine
- compression- gather legs and push towards head or strike ischial tuberosity
- distraction- trap feet and pull calves
what are the stress tests done for the sacroiliac region in the thoracolumbar scan in supine
- compression - press ASIS
- distraction - push ASIS outward
- thigh thrust - place hand under sacrum, hip in flexion, push through long axis
- Gains Levenes test - drop one leg off table into EXT and lift other leg into hip FLX, push each respectively
- PRONE, press sacrum on posterior aspect
what components of a thorcaolumbar scan are done in sidelying
myotome- L3 ADD hip, L5 ABD hip, L5-S2 hyperext
dural mobility- femoral nerve
what components of a thorcaolumbar scan are done in prone
dural mobility- femoral nerve
stress test - PA pressure lumbar and torsional stress
DTR- semitendinosis
What are the variables for stabilization
Jt integrity
Passive stiffness
Neural input
Muscle function
What muscles increase contraction of multifidus
Pelvic floor and transverse abdominus
what are the S&S of spondylogenic pain
non segmental pain
vague, deep, achy, boring pain
referred pain- not specific
neuro scans normal
can’t reproduce pattern with motion
what is viscerogenic pain S&S
cannot produce mechanically
neuro scan normal
what are the S&S of radicular pain
electrical shock pain
derm/myotomes, DTRs=normal
dural mobility= ++++
imaging helpful
what are the S&S of radiculopathy pain
segmental paresthesia- constant/long duration, slow progression
possible weakness
neuro scan ++++
imaging helpful
what are the S&S of peripheral pain
non segmental paresthesia- short/intermittent, fast progression of numbness
possible weakness
derm/myotomes, DTRs,= normal
dural momility= ++++
Name the pain:
referred pain
sensory, DTR, dural= normal
can’t reproduce pain with motion
what is the source/description
viscerogenic
referred pain from organ
name the pain:
Sensory, DTR= normal
can’t reproduce pain with motion
dural mobility= ++++
quick pain
what is the source/description
radicular
highly inflammed spinal n
name the pain:
Sensory, DTR, dural= ++++
possible weakness
slow progression
what is the source/description
radiculopathy
spinal n, blocked conduction
name the pain:
Sensory, DTR, dural= normal
can’t reproduce entire pain with motion
what is the source/ description
spondylogenic
local/referred spinal pain
name the pain:
Sensory, DTR= normal
dural= +++
possible weakness
short, intermittent pain
what is the source/description
peripheral
peripheral n, decreased conduction in extremity
Why does pain, swelling, inflammation, and disuse cause increase stress on non contractile tissues
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
Once a passive, non contractile tissue has healed, how do we make the jt more stable
By improving muscle function and creating more control of the smaller/deeper muscles
what is the peripheral patho of nociplastic pain
thinning myelin sheaths
a delta and c fibers get excited easily making it hard to override pain with motion
what is the central patho for nociplastic pain
increased excitability of dorsal horn
loss of descending anti-nociceptive mechanism- less pain control - no endogenous opiate released
what are the S&S for possible nociplastic pain
less than or equal to 3 months of pain
regional or spreading
Pain can not be explained
pain is hypersensitive or allodynia
what criteria if present can be probable nociplastic pain
sensitivity to light, sound, or odor
sleep disturbance
fatigue
cognitive problems
what are ANS S&S for nociplastic pain
pitting edma
decrease sebaceous gland
sweaty hands/feet
coldness/clamminess- decrease peripheral arterial shunting
loss of laterality
increased erector pili muscles
what is the general Rx for nociplastic pain
JM
MET
neuroscience education/behavioral therapy
why is JM the best treatment in CNS
stimulates descending inhibitory pain mechanisms- release endorphins
induce presynaptic inhibition
reduce dorsal horn excitability
decrease inflammatory mediators
what is the MET parameters for nociplastic pain
low to moderate intensity global aerobic and resistance
2-3x/wk
30-90 minute sessions
7 weeks duration
what are the benefits of MET with nociplastic pain
endogenous analgesia
helps pt to interpret pain and motion as non threatening
reorganize homunculus
why is neuroscience education/behavioral counseling beneficial for nociplastic pain pts
explain increased sensitivity and misinterpretation to reduce stress and anxiety
transition to adaptive pain coping
what are risk factors for LBP
previous LBP
co morbidities
poor mental health
smoking, obesity, low activity levels
awkward posture
what ROM is required for sit to stand
35-42 deg flexion
what ROM is required for picking up objects from the floor
60 deg flexion
what abnormal findings can be found with MRI with a chief complaint of LBP
IDD
age related disc changes
N compression
facet hypertrophy
who should get imaging with LBP
> 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
what are preventative measures for adults with LBP
exercise
what are preventative measures for children with LBP
ergonomic furniture
what is the first line Rx for LBP
education, cognitive behavioral therapy, stabiization
what do we need to educate the pt on that has LBP
spinal structure ad structural strength
neuroscience explanation
overall favorable prognosis
active coping mechanism
stay active with early resumptions of ADL
emphasis on function
why is education important for prognosis of LBP
greater emotion = greater pain
improve emotion = less pain
what treatments give short term benefits at best for LBP
modalities- heat, electrical stimulation, ultrasound
soft tissue mobilization
when are treatments with only short term benefits best used
used for opening a window for MET or MT
what can we do as providers to better our practice for LBP
increase consultation time and follow up
reward quality and not volume with reimbursement
increased provider knowledge of evidence and guidelines
what is centralization
abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motion
when is intermittent traction the most beneficial for pt with LBP
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
what factors favor stabilization to confirm treatment
younger age
postitive prone instability test
aberrant motion
greater SLR ROM
hypermobility with spring testing
increasing episodes
what factors favor directional preference to confirm treatment
strong preference for sitting or walking
centralization with motion testing
peripheralization in oppositie direction
what classifies the patient for directional preference
centralize with 2 or more movements in the same direction
centralize in one direction and peripherilize in the opposite direction
what classifies the patient for manipulation
have recent onset of symptoms <16 days
AND
no symptoms distal to the knee
what classifies the patient for stabilization
average SLR ROM >90 deg
positive prone instability test
positive aberrant motion
less than 40 years of age
what is directional preference
a position, motion, and factor that alleviates symptoms
what subgroup is most effective for LBP
mobilization/manipulation
what are the predicators for a manipulation of LBP
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
what is the most effective treatment for stabilization of LBP
motor activation/coordination and stabilization
aquatic therapy, pilates, yoga
trunk balance
progressive aerobic endurance exercise
explain williams flexion exercise/protocol
deforming the spine by forcing ourselves to stand
reduce lordosis
involved posterior pelvic tilt and trunk and hip flexion
weak evidence
what is cognitive behavioral therapy
helping patients understand and manage all biopsychosocial elements contributing to their symptoms
what is the prognosis of LBP
rapid improvements in one month
most improve substantially in 6 wks
how should medications be used with LBP
recommend only with an inadequate response to exercise and cognitive behavioral therapy
how does epidural injections affect LBP
recommend only for radicular pain
if no benefit by 4 weeks
what is acute IDD
annulus and end plate tear
least common is acute herniations
where is IDD most common
lumbar region
95% at L4-S1
what part of the disc is most common for IDD and why
posteriorlateral
weaker, thinner, with more vertical and less oblique annular fibers
how can acute IDD occur in the lumbar spine
FB with or without twisting cause:
non- symmetrical tension
limited stabilization
more anterior shearing
increase stress on weaker structures
what is the immunoreactive response once the disc is injured
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
what are typical postlat IDD symptoms
dull/achy spinal pain
radiculopathy- segmental paresthesia in the first 24 hours into distal extremity
referred pain into glutes and groin due to swelling
why is there more swelling with lumbar IDD than cervical
more GAGs so there is more significant swelling
what pain behaviors would the patient describe about lumbar postlat IDD
increase pain with FB, sitting, coughing, lifting
decrease pain with unloading, standing, walking
increase pain in the AM
what would we observe with postlat IDD in the lumbar region
lateral shift of shoulders on pelvis
smaller calf girth not until 4-6 weeks after injury - spinal n compression 80% conduction loss
what would we find in a scan for ROM for acute postlat IDD
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
why might spinal pain increase with EXT, but nerve symptoms centralize for a patient with postlat IDD
due to increase of hydrostatic pressure on disc with high osmotic pressure due to swelling. this is squeezing the inflammation out.
what other things can be found in a scan for acute postlat IDD
ST- + for compression, distraction, PA, torsion
neuro- fatiguing, hyporeflexive, diminished dermatome, + dural
BE- + stability test
what are the classification syndromes with Mckenzie method
postural- correct posture
dysfunction- stretch to improve ROM
derangement- use end range ROM to improve theoretical nucleus migration in disc
what is the treatment priority for acute IDD
get n pain and LE symptoms under control to prevent n damage
what is the PT Rx for acute postlat IDD
POLICED
directional preference
intermittent traction
postural/ergonomic edu
neural mob
MET
how should we prescribe for directional preference
10-20 reps every 1-2 hours as needed
what is our posture edu for acute IDD patients
limited to no sitting
limited to no driving/FB
what is our MET for acute IDD patients
tissue proliferation and stabilization
unweighted walking
what can cause persistent IDD
acute IDD
mixed findings with age
lower strength
sedentary lifestyle
heavier occupational lifting
smoking
genetics
how can persistent IDD occur from persistent inflammation
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
what does persistent inflammation limit
limits proliferation
what is the patho for persistent IDD
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
what is protrusion
bulge
nucleus migrates but remains in annulus
what is extrusion
nucleus migrates thru the outer annulus
what is free sequestration
nucleus migrates and breaks away from annulus
what is schmorl’s nodes
where nucleus migrates into the vertebral body
why is the disc not white in a T2 MRI when the patient has persistent IDD
low grade inflammation is black
acute (high grade) inflammation is white
how might persistent IDD due to narrowing affect the spine
loss of disc height/integrity
jt hypermobility during sagittal/frontal plane
foramen narrowing = stenosis
why might the patient not have symptoms with RT if they are presenting with persistent IDD due to narrowing
the lumbar spine does not have much RT so there isnt as much stress on the spine like EXT or SB
what 3 conditions can be caused by persistent IDD when disc height and integrity are lost
hypermobility
ARJC
stenosis
how do persistent IDD symptoms compare to acute IDD
slow change allows tissues to adapt without symptoms
how do you treat persistent IDD
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
what is the prognosis of IDD
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
what are negative predictors for prognosis with IDD
perpheralization
mental depression
pain behaviors
fear of work
why might antibiotics be prescribed for IDD
potential infection with persistent IDD due to chronic inflammation
when would a steroid pack be given for IDD
for a large inflammatory response
when is spinal decompression sx indicated for a pt with IDD
persistent or worsening radiculopathy
use when symptoms are unresponsive to non-sx treatments
why is TDR a better option with persistent IDD
better load distribution
preserves facets, foramen, and stability
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
annular disorganization
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
radiculopathy
Once a herniation occurs, which of the following categories indicates the nucleus migrates through the annulus?
Bulge
Protrusion
Extrusion
Sequestration
extrusion
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
outer annular and end plate tearing
Which direction preference is the MOST common with an acute internal disc derangement?
Extension
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
causa equina syndrome
Which of the following are risk factors for low back pain?
Regular exercise
Previous neck pain
Awkward postures
Light lifting
awkward posture
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
most will improve within 4-6 weeks of onset
what changes IAR
abnormal movement of spinal segment under loaded conditions, resulting in pain or disability
what can cause hypermobility
trauma
ARDC
repetitive activities
creep
adjacent jt hypo
connective tissue disorder
what is the most common place for hypermobility in the lumbar region
L4-S1
why is L4-S1 the most common region for hypermobility
L4/5 are more sagittal plane but L5/S1 transition to more frontal plane to limit ant shear
what are symptoms of functional instability in the low back
predictable pain
spine and referred pain
decrease pain with positional changes
increase pain with prolong position
catching
self manipulation
what can be seen with ROM from a pt with functional instability if acute
limited with aberrant motion
EXT due to increase of ant shearing
FLX with Gowers sign
what can be seen with ROM from a pt with functional instability if persistent
PROM > AROM when NWB vs WB
WNL or excessive, EXT still could be limited plus creasing
What can be found in a SCAN for functional instability
CM- inconsistent block
ST- + PA, mixed distraction
neuro- neg, possible hyperesthesia
what is aberrant motion
painful arc
uncoordinated motion
Gowers sign - UE assistance from FB
LE/pelvis compensation
what would show in accessory motion with functional instability
possible hypomobility (stuck drawer)
adjacent jt hypo from T10-12 RT, SI jt motion, hip hyperextension
what would show in stability test with functional instability
+ possible prone LE ext test
+ linear stability - most likely ant shearing
+ ASLR
inhibited local m
how can the LBP lead to an over recruited psoas m
psoas maintains lordosis
excessive recruitment can lead to lumbar hyperext and ant shearing most often occuring with instability
what are the symptoms for mechanical instability
unpredictable pattern
worsening symptoms with more frequent episodes
increased pain with trivial or lesser ADLs
how does mechanical instability differ in a SCAN
+ stability test wont stabilize in closed pack postion
what can show on a radiograph for mechanical instability
vertebral position in various position
spondylolisthesis
how do we treat functional and mechanical instability
rx for lig
POLICED
postural activities to activate local m
JM - adjacent hypo
bracing/taping
MET
what should MET emphasize on with instability
stabilization, local m (neutral or FLX and progress into EXT)
hip exercise - EXT, ER, IR decrease LBP
hyperextension is contraindicated
what can cause ARJC
prior trauma
age
genetics
other disease
sedentary lifestyle with underloading
what happens to synovial jt structures in ARJC
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
what are symptoms a pt may tell you when experiencing ARJC in lumbar spine
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
what can be in the SCAN for a pt with ARJC in lumbar spine
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
how can we treat ARJC in lumbar spine
improve integrity and mobility
POLICED- edu and orthotics
JM for pain, integrity and mobility
MET improve motion, integrity and neuromuscular
why could pure strengthening parameters be a problem for LBP early on in PT
cant overload the jt
too much stress all at once
work up MET parameters as jt integrity increases
what can compression of a nerve from outside in be due to
ARD/JC
instability
enfolding of lig flavum
What can compression of a nerve from inside out be due to
sheath around n is fibrotic due to persistent inflammation
increased blood supply to nerve with activity, particularly walking, causes n to enlarge
what are stenosis symptoms
unilateral LE
decrease pain in LE with FB/sitting/AM
increase pain in LE with standing/walking
what can you observe with a patient with stenosis
slouched
possible scoliosis
what can you find in a SCAN for stenosis
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
what can you find with accessory motion if a patient has stenosis
hypomobility- FLX/contra SB
possible adjacent jt
what can you find in special test if a patient has stenosis
stability test- shearing
LE discrepancies
balance deficits
how do you differentiate whether stenosis is due to neural or vascular disease
Ankle brachial index test for possible peripheral arterial disease
bicycle test
how can the bicycle test indicate stenosis or PAD
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
how do we treat stenosis
pt education
directional preference - flx
intermittent traction
manual therapy
neural mob
MET
corsets
how can manual therapy be effective for stenosis
jt mob in FLX and contra SB direction
manipulation - most effective with exercise
how is MET directed for a patient with stenosis
aerobic- repetitive stress gains integrity and circulation
balance training
local m stabilization
what are indications for sx with stenosis
presence of constant and or worsening symptoms
failure to obtain relief with 3-6 months of non sx treatment
what is spondylolysis
bony defect or fx of pars interarticularis unilateral or bilateral
what can cause spondylolysis
congenital
repetitive stress, EXT and RT
direct trauma
what structures are most common with spondylolysis
L5-S1
what are S&S of spondylolysis
acute- fx S&S plus + bilateral torsion test
persistent- asymptomatic or instability S&S
what is spondylolisthesis
anterior vertebral seg slippage due to mechanical instability
what are 2 most common types of spondylolisthesis
isthmic or adolescent with spondylolysis
degenerative
what is isthmic or adolescent with spondylolysis spondylolisthesis
most common
most rapid slipping
repetitive or traumatic EXT
what is degenerative spondylolisthesis
due to ARDC
no fx
what are S&S of spondylolisthesis
worst case instability
possible lateral or central stenosis S&S with slippage
no correlation with slippage and degree of symptoms
how do we treat spondylolysis/listhesis
worst case instability
MET- local m stabilization
what is a meniscoid
facilitate the spread of synovial fluid
what is facet jt impingement
meniscoid becomes wedged due to prolong position or quick movement
what are S&S of facet jt impingement
woke up or made a quick movement and couldn’t move
acuity with ARJD S&S
instability S&S
how do we treat facet jt impingement
isometrics to pull meniscoid out of the way
gapping manip
