Exam 1 - Thoracolumbar spine Flashcards
___ of facets determines direction and amount of motion
orientation
what plane are thoracic facets oriented and what motion do they favor
frontal plane
favors side bending but are limited by ribs
what plane are lumbar facets oriented and what motion do they favor
sagittal plane
favors flexion and extension
t/f
lumbar spine has the most degrees of motion with flx/ext and rotation
false
lumbar spine has most degrees of motion in flexion and extension
least amount of motion with rotation
what are the 4 variables of stabilization
joint integrity
muscle function
neuro input
passive stiffness
give examples of local muscles in the thoracolumbosacral region
psoas
pelvic floor
transversus abdominis
quadratus lumborum
transversospinalis
t/f
if one muscle of the thoracolumbar region fires, all local muscles should fire
true
bc all of the muscles are around the spine and work to stabilize
pain, swelling, joint laxity, and disuse can cause…
decreased and delayed motor performance/control of local muscles
inhibition preferential to type I muscles
local muscle atrophy (multifidus) leading to fat infiltration
increased stress on non-contractile tissues
increased demand of global muscles
fiber transformation from type 1 to type 2
what are examples of non contractile tissues
why is there increased stress on the non contractile tissues when local muscles are inhibited
ligaments, cartilage
increased stress is d/t stress being placed on non contractile structures because the local muscles are unable to stabilize
muscle activation of __% is sufficient to keep stability and can improve muscular endurance
30%
does muscle activity return spontaneously because the pain is gone
no
what is nociceptive pain
non-nervous tissue compromise
MSK and viscerogenic
what is neuropathic pain
nervous tissue compromise
radicular, radiculopathy, peripheral
what is nociplastic pain
altered pain perception without complete evidence of actual/threatened tissue compromise
how would a patient report spondylotic pain
what is spindylogenic pain
common
local/referred spinal pain from noxious stimulation of spine structures
can spondylogenic pain cause visceral dysfunction
no
the spine cannot affect organ function
what are S&S of spondylogenic pain
non-segmental pain
rare paresthesia’s
vague, deep, achy, boring pain
neuro - WNL
can’t reproduce symtoms
describe somatic convergence or referred pain
sensory afferents converge and share same innervation
greater referral of proximal and deep structure than distal and superficial
what area is the most often area of referred sponylogenic pain in the lumbar region
gluteal region and proximal thigh
what is viscerogenic pain
referred pain from an organ
what is viscerosomatic convergence
viscera and somatic sensory afferents converge on and share the same innervation
can viscerogenic pain be mechanically reproduced
no
what is radicular pain
extopic or abnormal discharge form highly inflammed spinal nerve
what are radicular pain symptoms
lancing, electrical shock like pain in a 2-3 inch band down an extremity
what are the signs of radicular pain
dermatomes, DTRs, mytomes - WNL
dural mobilty test - +
what is radiculopathy pain
blocked conduction of spinal nerve due to compression and/or inflammation
what are the signs of radiculopathy pain
segmental paresthesia’s
slow progression to ill defined area
possible weakness (with 80%) loss of conduction
what are the signs of radiculopathy pain
neuro scan - + for spinal nerve hypoactivity
what is peripheral nerve pain
decreased condition of nerve brance
what are the symptoms of peripheral nerve pain
non-segmental
intermittent and short duration
fast progression to well-defined area
possible weakness
what are the signs of peripheral nerve pain
dermatomes, DTR, mytomes - WNL
non segmental peripheral nerve hypoactivity
dural mobility - +
what is the pathogenesis of nociplastic pain
thinning of myelin sheath
increased sensitivity and misinterpretation by peripheral nociceptors
persistent excitation of alpha-delta and C fibers
increased sensitivity and misinterpretation by central structures
loss of descending anti-nociceptive mechanisms
why can symptoms of nociplastic pain spread
somatic convergence
describe somatic convergence
shared areas of innervation share symptoms
brain perceives the pain as coming from even more areas with persistent symptoms
how do c fibers contribute to nociplastic pain
c fibers transmit pain
split and travel at least 2 spinal segments superiorly and inferiorly
what are the S&S/criteria for possible nociplastic pain
> /= 3 months pain
regional/spreading symptoms
pain that cannot be entirely explained
pain hypersensitivity or allodynia
what are the S&S/criteria for probably nociplastic pain
sensitivity to sound, light, odor
sleep disturbances
fatigue
cognitive problems
what are the S&S of autonomic nervous system nociplastic pain
pitting edema with lymph compromise
decreased sebaceous gland and hair follicle activity
sweaty hands/feet
what are the indicated S&S of autonomic nervous system nociplastic pain
decreased peripheral arterial shunting leading to coldness/clamminess
loss of laterality
increased erector pili muscle activity
+ graphesthesia
what are the indicated interventions for nociplastic pain
joint mobilizations/manipulations
patient education
MET
what is the MET prescription for nociplastic pain
low-moderate global aerobic and resistance activities
2-3x/week
30-90 minutes per session
at least 7 weeks duration
how does MET improve nociplastic pain
endogenous/opiate analgesua
helps pt interpret pain as nonthreating
reorganizes homunculus
what is the prognosis of nociplastic pain
varying degrees of improment
longer recovery
likely not full resolution of symptoms
you are assessing the functional motion and A/PROM of the thoracolumosacral region
you find a fulcrum/sharp angle in the lower thoracic region. what should you do next
assess in flexion and extension to see if the fulcrum is still present
you are assessing the functional motion and A/PROM of the thoracolumbosacral region
you find a fulcrum in SB and in FLX. what is indicated
contralateral z joint
you are assessing the functional motion and A/PROM of the thoracolumosacral region
you find a fulcrum in SB and in EXT. what is indicated
ipsilateral Z joint
you are assessing the functional motions and A/PROM of the throacolumbosacral region
what curve of the spine is considered normal for rotation
what curve of the spine is considered abnormal
S curve
C curve
what is considered abnormal during thoracolumbosacral extension
what is indicated
skin crease
hypermobility or instability
creasing that is asymmetrical during thoracolumbosacral extension indicates…
excessive anterior shearing
the lumbar spine is the leading cause of
worldwide disability
activity limitation and work absence
what is the prevalence of LBP
(sex, age, education)
women > men
older > younger
lower educational status
higher physical work demands
what are the risk factors of developing LBP
previous LBP
co-morbidities
poor mental health
smoking, obesity, low activity levels
awkward postures, heavy lifting, fatigue
genetics with ARD changes only
what is the functional ROM of the lumbar spine for sit to stand
35 to 42 flexion
what is the functional range of motion to pick up an object from the floor
60 flexion
___% of asymptomatic individuals had abnormal findings with MRI
33%
___% of symptomatic individuals had an abnormality with MRI
50
what characteristics would indicate a pt with LBP should get an MRI
> 50 years with hx of cancer
saddle paresthesias
bowel and bladder dysfunction
specific neurological deficits
progressive/disabling symtpms
no improvement after 6 weeks of conservative Rx
t/f
imaging improves outcomes and guidelines consistently recommend routine imaging
false
imaging does not improve outcomes and guidelines consistently recommended against routine imaging
nearly all cases have an unidentified ____ source of LBP
nociceptive
what can occur with overutilization of unsupported and ineffective Rx for LBP
higher costs
contributes to greater opioid addiction
greater imaging and radiation exposure
more likely to have invasive procedures
fear avoidance behaviors promoted with passive interventions
what education and advice would you give a pt with LBP to not do
against bed rest and in-depth explanation of the cause
what education and advice would you give a pt with LBP to do
spinal anatomical and structural strength
neuroscience explaintion
overall favorable prognosis
staying active with ADLs
emphasis on functional improvements
how does one’s emotions about/towards LBP affect pain/persistence of symptoms
greater emotion leads to greater pain and persistence
what is the prognosis of dry needling with LBP
very low-moderate evidence of benefit
what is the prognosis of modalities for LBP
generally ineffective and not recommended
short term benefits only
what is the prognosis of soft tissue massage for LBP
only short term benefit
what are the 4 LBP Rx classification subgroups
mechanical traction
directional preference
mobilization/manipulation
stabilization
what is the prognosis of mechanical traction for LBP
no benefit with static traction
what pt characteristics show more support when mechanical traction is used
18-60 years
paresthesias in last 24 hours distal to knee
owestry questionnaire > 30
(+) n root compression, crossed SLR, centralization
what is centralization
abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motion or sustained positions
t/f
mechanical traction is not indicated when used alone in pts with acute/subacute/persistent LBP, non-radicular LBP, pts with varying symptom patterns
true
pt reports LBP with pain decreasing with repetitive back hyper/extension. the pain now is located into just the glute. what exercises would you include in the pt’s program
hyper/extension
lat pulldowns/rows in standing
what is directional preference
position, motion, and/or factor that alleviates symptoms
can help to choose positions and motions to avoid symptoms and promote exercise and activity
what pt characteristics indicate manipulation/mobilization
> /= 4 of 5
no symptoms distal to knee
symptoms < 16 days
lumbar joint hypomobility
fear avoidance behavior questionnaire at work < 19
are joint manipulations or joint mobilizations more effective for patients with LBP
joint manipulations are more effective
what is the purpose of joint mobilizations/manipulations
gets the pt back to exercise faster
short course at most
t/f
stabilization is safe and effective to do early with a pt with acute LBP
true
what is the order of treatments for functions with patients with sub-acute and persistent LBP
motor activation/coordination and stabilization
aquatic therapy, pilates, yoga
t/f
motor control is ineffective for non-specific LBP and functions in isolation or with other exercises
false
motor control is effective for non-specific LBP and functions in isolation or with other exercises
improves trunk control and creates earlier muscle activation
what exercises should be included with LBP to improve stabilization
trunk balance
progressive endurance exercises
what muscle function is commonly impaired with pts that have LBP
diaphragmatic breathing
what is the prognosis of stretching with LBP
no difference in pain and function
what is the purpose of cognitive behavioral therapy with patients that have LBP
first line rx with persistent LBP
helps patients understand and manage all biopsychosocial elements contributing to their symptoms
__% patients report pain at 3 and 12 months with persistent LBP
66%
__% of patients have reoccurrence of LBP within 1 year
33%
what pt factors influence the prognosis of LBP
mental status, lack of self-efficacy
fear avoidance behaviors
beliefs/behaviors
low education/income
high pain intensity and multiple painful areas
when are medications indicated for LBP
recommended only with inadequate response to exercise and cognitive behavioral therapy
mostly insufficient and not recommended
how should medication be used with low back pain
any utilization should be limited and very selective with the lowest effective dose
what is the prognosis of epidural and facet joint injections
not recommended for non-specific low back pain
when are epidural injections indicated for LBP
recommended for radicular pain
don’t reduce risk of surgery
create rare but serious side effects
what are the 2 methods acute IDD occurs
which is the least common
annular and end plate tear
acute herniations (nuclear migration) - least common
what is the most prevalent IDD
chronic or persistent
describe chronic or persistent IDD
disc changed due to numerous variables allowing herniations (nuclear migration) to gradually develop over time
most are not symptomatic
what region of the spine is IDD most common
lumbar region
persistent IDD is the cause of LBP in _% of patients
5%
what ages are most affected by IDD in the lumbar region
30-50 years
what spinal segments most commonly have IDD
L4-L5, L5-S1
t/f
IDD is common in the throacic region
false
<1% of all symptomatic disc herniations are in the thoracic region
what region of the spine has the greatest consequences of IDD, why
throacic region
area of the narrowest canal
more likely to press on the cord
very rare
what area of the disc is most commonly affected by IDD, why
posterolateral portion - just lateral to posterior longitudinal ligament
weaker, thinner, more vertical/less oblique annular fiber
what degrees is considered normal for resting lumbar lordosis
20-45
what is the etiology for acute IDD
forward bending at the waist with or without twisting/lifting
describe how the lumbar spine moves to result in a acute IDD
anterior pelvic tilt
less circumferential disc compression, uneven annular tension
less fixated end plate
more anterior segmental shearing, possible rotation stresses, gravity influence
increased asymmetrical stress on weaker and thinner posterolateral annular and end plate fibers
why would lumbar flexion increase pain with a patient with IDD
causes anterior shearing
most likely the method the injury was created
with acute IDD, more commonly __ annular tearing and end plate avulsion and less commonly __ annular tearing and NP herniation
outer, inner
describe the disc
shock absorber
long, large inflammatory pahse
resists compression d/t type 2 collagen
hydrophilic = lots of GAGs
no lymphatic drainage
avascular/aneural
what occurs when disc structures are injured
large and extended autoimmune inflammatory response
increased static fluid around disc and spinal nerve
static fluid has increased inflammatory chemicals that sensitize spinal nerve and structures to pressure/tension
no lymphatic drainage
what S&S would you expect with an injured disc
radiculopathy/radicular S&S
what are typical posterolateral IDD symptoms
Dull/achey spinal pain
radiculopathy
referred pain to glutes and groin
would you expect more or less swelling in the lumbar region vs the cervical with IDD, why
significantly more swelling than cervical discs
higher number of GAGs
what symptoms with IDD indicate a worse situation
presence of coldness
presence of radiculopathy
what would increase pain/symptoms with posterolateral IDD
forward bending
sitting
coughing
lifting
more pain in morning d/t pooling of swelling
*anything that increases tension on ligament
what would decrease pain/symptoms with posterolateral IDD
unloaded or lying supported/standing/walking
standing in lordotic position allow disc to slacken
*moving moves fluid around and away from spinal nerve
what would you expect to observe in a patient with postlateral IDD
lateral shift of shoulder on pelvis
- side bend away from pain
- counter contralateral side bend to level eyes
when would calf wasting occur and what does this indicate
4-6 weeks
indicative of severe spinal nerve compression, more of a sign of persistent radiculopathy
what ROM is expected with pt with posterolateral IDD signs
all motions may increase pain
FLX, possible SB away from injured area limited
EXT, possible SB toward injured area less limited
RT not consistent
why would flexion and side bending away from the injured area of IDD increase extremity and spinal pain
pressure placed on spinal nerve by pushing the swelling toward the spinal nerve
tension on annulus and end plate
why would extension and possible side bending toward injured areas of disc be less limted
repetitions cand push the swelling away from the affected area
what would you expect to find with repetitions of lumbar extension with IDD
centralization of pain with repetition
can increase spinal pain d/t increased hydrostatic pressure on disc with high osmotic pressure
what is centralization of symptoms
abolition of distal and/or spinal pain in a distal to proximal direction in response to repetitive motions or sustained positions
what woud you expect to find in a scan of a pt with acute IDD
RST and MMT - variable
ST- possible (+), torsion and PA pressures
neuro - possibly (+)
what are unique central S&S of acute IDD
cord or cauda equina S&S depending on the level
what is the basic belief of the McKenzie method
based on the belief that most of the spinal pain comes from injuries to the disc
research does not support the theory
classified based on symptom location and position/motion that decrease symptoms
what position is most commonly (~70% of cases) the directional preference
extension
what are the 3 classification syndromes of the McKenzie method
postural
dysfunction
derangement
what is the postural classification syndrome of the Mckenzie method
essentially correct poor posture
what is the dysfunction classification syndrome of the Mckenzie method
essentially stretches to improve end range motion
what is the derangement classification syndrome of the Mckenzie method
essentially using end range motion to improve theoretical nucleus migration in the disc
t/f
the Mckenzie method is supported by strong evidence that shows the benefit with LE symptoms and when centralization occurs with acute IDD
true
what are the mechanisms of action of the Mckenzie method
dynamic disc theory with herniations
fluid dynamics with or without herniations
what is the dynamic disc theory with herniations of the Mckenzie method
nucleus repositions centrally
unproven
what is are the fluid dynamics with or without herniations of the Mckenzie method
high osmotic pressure with large auto-immune swelling response
increased hydrostatic pressure through repetitive motion, most often extension
what symptoms might a patient with IDD report with repetitive extension
spine pain initially increases d/t resistance of high osmotic pressure being overcome by increased hydrostatic pressure
how does repetitive extension improve symptoms of acute IDD
swelling/fluid is squeezed away from spinal nerve into the nucleus and the end plates for drainage
centralizes pain, LE symptoms decrease
what is the effectiveness of the Mckenzie method
good evidence, but is not superior to other treatments for pain/disability
overall/long-term treatment effect is small to moderate
why is treatment needed beyond Mckenzie method
annulus and end plate are torn = loss of stability
stabilization still needed
what is the PT Rx for acute IDD
POLICED
directional preference for centralization - extension
intermittent traction can be helpful with radiculopathy
neural mobilizations
pt education - posture
HEP to avoid counter-productive sitting with driving
what would be included with pt education for acute IDD
postural/ergonomic education/taping/bracing for ext preference
limited to no sitting
limited to no driving
limited to no forward bending
what is the purpose of MET with acute IDD
tissue proliferation
stabilization
local muscle activation
unweighted walking
how should we properly squat
more circumferential disc compression, evenly distributed annular tension with lumbar flexion and posterior pelvic tilt
more fixated end plate
less anterior segmental shearing
what is the etiology of persistent IDD
acute IDD
mixed findings with age
lower strength
sedentary lifestyle
heavier occupational lifting
smoking
genetics
explain how genetics influence one’s likelihood of developing persistent IDD
lumbar IDD associated with age-related disc changes in cervical region
65-85% inheritance but can be modified by diet and lifestyle
how does routine loading and driving affect persistent IDD
not from routine loading and prolonged driving
routine loading was beneficial
what is the pathogenesis of the persistent IDD or how are the disc and adjacent structures changing
less GAGs = more fibrotic/dehydrated nucleus
more acidic disc = kills disc cells, limits proliferation
annular disorganization
thinning/loss of cartilage @ end plates
increased inflammation/fatty deposits in vertebra
how does persistent inflammation influence persistent IDD
in-growth of nociceptive fibers from acute IDD healing can lead to nociplastic pain
brings excessive and destructive proteins and low-grade infection to disc
what are the 3 categories of hernation per miller
protrusion
extrusion
free sequestrian
describe the protrusion category of herniation per miller
NP migrates but remains contained in annulus
what is the most common NP herniation
protrusion (buldge)
describe the extrusion category of hernation per miller
NP migrates thru the outer annulus
describe the free sequestrian herniation
NP migrates and breaks away from annulus
what is likely to develop where the NP migrates into the vertebral body
schmorl’s nodes
why would a herniated disc no be bright white on a T2 MRI
no fluid d/t no GAGs
no acute inflammation because of slow progression
what are the initial effects of decreased disc height and integrity
instability
joint hypermobility in sagittal and frontal plane motions only
joint space narrows
foramen narrows leading to stenosis
what are the later changes that will occur with decreased disc height and integrity
greater age-related joint changes
can lessen prior instability d/t stiffening of joint
what 3 conditions will affect the disc
stenosis
age-related joint changes
hypermobility/instability
how do S&S progress with persistent IDD
what would you expect with persistent IDD
slow changes allow tissues to adapt w/o symptoms
about how many people with persistent IDD have a lack of symptoms with changes in imaging
2/3
what symptoms would you expect with persistent IDD
gradual onset of symptoms
acute IDD S&S if inflamed
“mixed bag”
what PT Rx is effective with pt with persistent IDD
acute IDD Rx if inflamed
consider primary driver of symptoms
why is the Mckenzie method only effective with acute IDD and not as effective with persistent IDD
Mckenzie method works to move inflammation away from spinal nerve
with persistent IDD, there is no inflammation/fluid to be moved
Mckenzie method shows short term benefits
how does Mckenzie method compare to manual therapy and stabilization exercises with persistent IDD
Mckenzie method is not superior to exercise or manual therapy with persistent IDD
what is the prognosis for acute and persistent IDD
likely prolonged inflammatory phase
90% improve in 4-6 weeks, symptoms resolve in 12 weeks
what is the prognosis for surgery with acute and persistent IDD
most do not require surgery
PT is slower than surgery but results in the same outcome after 2 years
surgery could offer quicker short term results
waiting ~4 months on surgery did not minimize benefits of surgery
what is the negative outcome predictor for acute and persistent IDD
peripheralization
peripheralization of acute and persistent IDD has a significant association with..
mental distress/depression
pain behaviors
somatization - conversion of anxiety into bodily symptoms
fear of work
non-organic signs
worse outcomes with __ months prior to any treatment with acute/persistent IDD
> 6 months
what is the prognosis/muscle relaxants/acetaminophen of NSAIDS for acute/persistent IDD
conflicting and unclear
steroid dose pack is prescribed for large inflammatory response
what is the prognosis of epidural injection for acute/persistent IDD
short term but not long term relief/functional changes
what is teh prognosis of antibiotic treatment for acute/persistent IDD
benefits potential infection source
what is spinal decompression that could be performed by MD
what are the indications for spinal decompression
laminectomy, partial discectomy
persistent and/or worsenign radiculopathy
use when symptoms unresponsive to non surgical treatment
describe the risks/benefits of lumbar fusion
no difference vs PT in long term outcomes
not additive to laminectomy/discectomy
may lead to adjacent joint hypermobility
describe the pros/cons of total disc replacement with persistnet IDD
better load distribution across segments
safe/effective treatment >5 years post op
no difference vs PT @ 2 years post op
what are the 4 variables of stabilization
joint integrity
passive stiffness
neural input
muscle function
what is functional instability
instability that can be stabilized with muscle activity/positioning
what is mechanical instability
instability that cannot be completely stabilized with muscle activity/positioning
what sex is hypermobility more common
males
what are the etiologies of hypermobility/instability
traumatic/recurrent sprians
ARDC
repetitive extension activities
creep
adjacent joint hypomobility
connective tissue disorder
what segment is hypermobility most common
L4-S1
what are the symptoms of functional instability
predictable pain
spine and referred pain. possible paresthesia
decreased pain with positional changes/support
increased pain with prolonged positions, repetitive bending and arching, sudden motions, strenuous ADLs
catching
easy self manipulation
what are the signs of functional instability in the scan and CM
< 40 years of age
limited, aberrant motion if acute
limited, painful extension
PROM > AROM
greater flexibility overall
no acute - often WNL or excessive except for extension that can still be limited
inconsistent block
what AROM would you expect with functional instability
aberrant/ddeviating
painful arc
uncoordination
Gower’s sign
LE/pelvis compenations
what signs would you expect with RST and neuro in functional instability
acute = painful
strong, painless bc global muscles are not affected
neuro (-)
what would you expect to find during ST for functional instability
PA pressures (+)
mixed findings with distx
what would you expect to find in accessory motion testing with functional instability
possible hypomobility if hypermobility present
(T10-12 rotation, SI joint motion, hip hyperextension)
what special tests would you expect to be positive with functional instability
prone LE extension test
linear stability (most likely anterior shearing)
possibly active straight leg raise
what muscle is excessively recruited with LBP
what does this lead to
psoas
excessively recruited psoas can further add to the hyperextension and anterior shearing most often occurring with lumbar hypermobility
describe mechanical instability
unpredictable pattern of provoking activities
worsening symptoms with more frequent episodes
increased pain with lesser ADLs
t/f
(+) stability tests wont stabilize fully with repositioning and/or muscle activity
true
will mechanical instability show up on imaging
yes
shearing is so severe it will show up on imaging
what are the MD rx for severe shearing/slippage
prolotherapy for stbailization into iliolumbar ligaments along with PT
spinal fusion
what is the PT rx for functional and mechanical instability
rx - ligamentous laxity
POLICED
postural education to activate local muscles and for chair support
JM to increase adjacent joint hypomobility
bracing/taping
MET
what MET is efficient for functional and mechanical instability
emphasis on stabilization (local muscles)
hip exercises provided greater pain and disability improvements
hyperextension is contraindicated
what are other names for age-related joint changes
degenerative joint disease
osteoarthritis
spondylosis (if multiple spinal levels)
what are the most common regions for age related joint changes
L4-S1
progresses along with age related disc changes
are degenerative or acute tears more common with age related joint changes
degenerative is most common, older > younger
acute tears are rare, younger > older, involves high shear forces
what is the etiology of age related joint changes
prior trauma
age
genetics
other diseases (RA)
sedentary lifestyle with underloading
what are the 5 components of synovial joint and what happens to them with age related joint changes
articular cartilage - frays, blisters, thins
joint space - narrows
fibrous capsule - slackens then thickens/stiffens
synovial membrane - produces less synovial fluid
synovial fluid - decreases
persistent pain and inflammatory response with age related joint changes are partly d/t…
stress on other tissues like bone
increased local nociceptor sensitivity for greater pain transmission fostering inflammation
local production of nitrous oxide leads to more interstitial inflammation and excess collagen
bone being released from bone marrow
what are the lumbar symptoms of age related joint changes
gradual onset of LBP
P! with prolonged positions - standing, sleeping
morning stiffness or after prolonged positions >30 mins
possible paresthesias
movement can help but too much movement increases pain
why do pts experience pain with prolonged positions with age related joint changes
synovial fluid is squeezed out without ability to refill
what would you expect to observe and find in the scan with age related joint changes
observation - possibly forward head posture
ROM - pain with ext, ipsilateral SB, contralateral RT
- capsular pattern of restriction
CM - consistent block often in ext quadrant or opposing quadrants consistently blocked
RST - depends
ST - (+) compression, particularly in ext, ipsilateral SB, contralateral RT
- (+) PA and unilateral torsion
neuro - (-), could be (+) for radiculopathy
what would you expect to find with accessory motion tests with age related joint conditions
hypomobility
what is the PT rx for age related joint changes
greater focus on improving integrity of cartilage and mobility
POLICED
JM for pain, cartilage integrity and mobility
what is the focus of MET with age related joint changes
ultimate focus on improving motion, cartilage integrity, neuromuscular benefits
describe stenosis
narrowing around and compression of neurological structures
what is the prevalence of stenosis
most common dx for spinal sx in adults > 60 yrs
30% asymptomatic individuals had canal narrowing on imaging
what are the 2 ways compression of the spinal cord occurs with stenosis
inflammation of the sheath around the nerve and becomes fibrotic - nerve can’t expand
spurring/narrowing of spinal canal
compression from the outside in with stenosis is due to…
age related disck and joint changes - most common
instability - older and younger
enfolding of lig flavum
what are the typical symptoms of lateral stenosis
unilateral LE > LBP
segmental paresthesias
gripping type pain d/t ischemia
what will decrease symptoms with lateral stenosis
forward bending
sitting
in morning - disc is more hydrated = more space
incline walking
what will increase symptoms with lateral stenosis
standing and walking
what would you observe with a pt that has lateral stenosis
slouched
possible scoliosis
what ROM would increase pain with lateral stenosis
extension
ipsilateral SB
what ROM would decrease pain with lateral stenosis
flexion
contralateral SB
what would you expect to find with neuro and stress tests for lateral stensosis
(+) neuro for radiculopathy
ST (+) PA pressures/torsion when sustained
what would you expect to find with accessory motion with lateral stenosis
hypomobility in lumbar flexion and contralateral SB
adj joint hypermobility in lower throacic and LE (hip)
what would you expect to find with lateral stenosis with special tests
stability test - excessive shearing
LE discrepancies (LLD, impaired mechanics)
balance deficits with wide based gait
Cooks CPR
what tests would you use to differentiate stenosis vs vascular symptoms
ankle-brachial index test for peripheral arterial disease
bicycle test
what is the bicycle test used to differentiate stenosis vs vascular symptoms
cycle upright then bend to lean on handlebars for 3 min each
is stenosis, pain will decrease with bent position. if it doesn’t, PAD is indicated
what are the PT implications for stenosis
directed at foraminal opening
pt education of foramen and good prognosis
directional preference into flexion
intermittent traction may be helpful with radiculopathy
manual therapy
neural mobilizations
MET
what MET is benefical for stenosis
aerobic
balance training (physioball if unable to stand)
local muscle stabilization
when is surgery indicated for stenosis
presence of constant and/or worsening symptoms
failure to obtain relief within 3-6 months of nonsurgical treatments
what are the common surgeries that are utilized for LBP
laminectomy, partial discectomy
what is spondylolysis
bony defect or fracture of pars interarticularis unilaterally or bilaterally
what is the etiology of spondylolysis
congenital
repetitive stress (extension and rotation)
direct trauma
what spinal segments are most commonly involved with spondylolysis
L5-S1
what are the S&S of spondylolysis
acute - fracture S&S and (+) torsion test
persistent - asymptomatic, instability S&S if symptomatic
what are the 2 most common types of spondylolisthesis
isthmic or adolescent with spondylolysis
degenerative
describe isthmic or adolescent with spondylolysis
most common
age group with most rapid slipping
repetitive or traumatic extension
describe degenerative spondylolisthesis
d/t age related disc changes
>50 years old
no fracture
what are the S&S of spindylolisthesis
worse case of instability
possible lateral or central stenosis S&S with slippage
no correlation with lippage and degree of symptoms
what is the prognosis of surgery for spondylolisthesis
83% excellent to good outcomes with modified Scott technique
what structures are involved with facet joint impingement
meniscoid
facet joint
what are teh pathomechanics of facet joint impingement
meniscoid becomes wedged d/t prolonged position or quick movement
associated with instability
what are the S&S of facet joint impingement
woke up or made a quick movement and couldn’t move
acuity with age related joint diseases S&S
underlying instability S&S
what is the PT rx for facet joint impingement
isometrics to use attaching multifidi to pull meniscoid out of the way
gapping manipulation
stabilization to address cause
inflammation, symptoms, and function often improve on its own before PT pursued
describe scoliosis
what are the 2 types
> /= 10 degree curvature
SB and contralateral rotation
structural, functional/postural
describe structural scoliosis vs functional/postural
structural = doesnt go away with FB
functional = goes away with FB, able to modify with PT
describe sway back posture
increased lumbar lordosis
anterior pelvic tilt
flexible body type
describe flat back posture
straight spine
flattening of normal curves
greater proportion of persistent LBP d/t less dissipation of forces
posterior pelvic tilt
rigid body type
describe rounded or crouched body posture
increased throacic kyphosis
flattening of lumbar curve
posterior pelvic tilt
often associated with FHP
