Class 3-4: LBP-IDD Flashcards
why is the general classification non specific LBP
nearly all cases have an unidentified nociceptive source
what does the STarT back tool do
determines risk of persistent diabling pain and matches treatment
prevalence of lumbar LBP
leading cause of worldwide disability and activity limitation/work absence
half of people over 65 will have it
80% of people will experience in their life
prevalence factors for LBP
women
older
lower edu status
higher physical work demands
risk factors for LBP
previous LBP
co-morbidities
poor mental health
smoking
obesity
low activity level
awkward posture
heavy lifting
fatigue
genetics with ARDC ONLY
functional lumbar flexion ROM for sit to stand
35-42 degrees lumbar flexion
functional lumbar flexion ROM for picking up objects on floor
60 degrees lumbar flexion
how many asymptomatic individuals will have positive findings on imaging
1/3
i.e. IDD, ARDC, N compression, or facet hypertrophy
2/3 had disc changes from 30-80 years old
how many symptomatic individuals had positive scan findings
1/2 had an abnormality
who should get imaging with LBP
over 50 years old AND hx of cancer
saddle paresthesias
bowel/bladder dysfunction
specific neuro deficits
progressive/disabling symptoms
NO improvement after 6 wks
problems that are presented with over-utilization of unsupported and ineffective PT Rx for LBP
higher costs
greater opioid addiction
greater imaging/radiation exposure
more likely to have invasive procedures/side effects
more absences from work
fear avoidance behaviors are promoted with passive interventions like modalities and even some manual therapies
things to keep in mind for the prevention component of LBP RX
inadequate research
most promoted preventions lack evidence
exercise is largely effective in adults
children = ergonomic furniture is effective but exercise is not evaluated
benefits of early PT with LBP
2% developed persistent LBP vs 15% with later PT
significant reduction in work absence
supported in many studies
what edu and advice should be given to LBP pts as a first line Rx
advise against bed rest and in-depth explanations of what is causing LBP
advise for:
-Spinal anatomical and structural strength
-neuroscience explanation
-overall good prognosis
-active P! coping mechanisms that decrease catastrophizing
-stay active and resume ADLs early
-emphasis on function
importance of edu in PT Rx for LBP
greater emotion = greater pain and persistence
improve emotions = less pain and persistence
validity of dry needling for any MSK condition
low/mod evidence of benefit on pain vs no treatment or placebo
no functional benefit
no support to use over exercise and manual therapy
effectiveness of modalities for LBP
generally ineffective/non reccomended
short term results at best; often no better than placebo
STM/massage effectiveness for LBP
only short term benefit
ways to overcome barriers to best practice in PT
increase consultation time and follow up
decrease lawsuits based on evidence
better incentives to return to work
public service announcements
reward quality and not quantity with reimbursement
increased provider knowledge of evidence and guidelines for use in clinical reasoning and decision makinh
what are the 4 LBP Rx subgroups
mechanical traction
directional preference
mobilization/manipulaiton
stabilization
effectiveness of intermittent traction with LBP
preliminary support for LBP when symptoms peripheralize during repetitive ext and when there is a positive SLR special test
intermittent traction is more supported in prone and when..
18-60 yrs
paresthesias in last 24 hrs distal to knee
oswestry questionnaire > 30
+ n root compression, crossed SLR, and/or centralization
there is moderate evidence against all types of tx when used alone in patients with…
acute, subacute, and persistent LBP
non-radicular LBP
varying symptom pattern
how can you tell if a patients LBP has directional preference
pt centralizes with 2 or more movements in the same direction (i.e. flex or ext)
or
pt centralizes with movement in one direction and peripheralizes with an opposite movement
effectiveness of mckenzie exercises for acute LBP
nor superior to other treatments for pain/disability
often utilized well with acute IDD in short term
effectiveness of mckenzie exercises for persistent LBP
no difference in pain/function vs no intervention at all
what classifies a LBP pt as a manipulation classification
recent onset of symptoms (<16 days)
no symptoms distal to knee
least common IDD
acute herniations- nuclear migrations
most prevalent IDD
disc changes due to variables that allow herniations that gradually develop over time
persistent IDD
what region are IDD injuries most common
most common in lumbar
only 1-3% IDDs are symptomatic
95% at L4-S1
most common portion of the disc to tear
posterolateral
weaker, thinner
has more vertical and less oblique fibers
just lateral to posterior longitudinal ligament
how does the acute disc injury usually happen
forward bending at waist with or without twisting/lifting
describe how the lumbar spine is not flexing like you think
b/c of pelvic tilt
less circumferential disc compression/uneven annular tension with lumbar flattening and pelvic tilt
less fixated end plate
more anterior shearing and possible rotating stresses with additional influence of gravity
increased and asymmetrical stress on weaker and thinner posterolateral annular and end plate fibers
best way to squat
not holding lordosis; avoid excessive arch
let body move the way it wants
let lumbar region curve and pelvic tilt
allows symettrical compression
are outer or inner annulus tears more common
outer + end plate avulsion more common
once damaged how do disc structures act
immunoreactive
what happens as a result of the large inflammatory response of the disc when injured
excessive osmotic pressure OR increased static fluid pressure and around disc and spinal nerve
static fluid has more inflammatory chemicals that sensitize nerves and cause pressure/tension
no lymph drainage
extended inflammatory phase
typical posterolateral IDD symptims
dull achy pain
radiculopathy
referred pain into glutes and groin
decreased pain when unloading or lying/supported/walking
increased pain with FB/sitting/coughing/lifting
24 hr behavior: increased pain in the morning
why does IDD cause dull/achy pain
annulus is highly innervated and very painful
significantly more swelling than cervical disc due to higher number of gags
why might there be radiculopathy with IDD
possible segmental paresthesias within 24 hours
worse situations = radiculopathy + coldness bc vv have rich routes and high degree of resistance to ischemia
observation of someone with posterolateral IDD
lateral shift of shoulders on pelvis common
SB away from pain
counter contralateral SB to levels
rare = smaller calf growth
-wasting likely at 4-6 wks of severe spinal n compression
-more a sign of persistent radiculopathy
ROM findings for posterolateral IDD
all may cause pain
flx + SB away from injured side = limit/P!; pushes swelling toward n and puts tension on area of injury
ext + SB towards injury = less limited; often centralizes extremity pain BUT may increase spine pain from high osmotic pressure on disc (squeezing out swelling from pressure needed to relive leg pain)
scan findings for posterolateral IDD
resisted and MMT = variable
possible + stress test with compression/distraction/PA pressures/torsion
neuro = possibly + depending on severity/timing
possibly + stability tests
rare central IDD signs
cord or cauda equina S&S depending on level
immobilize and emergency referral
mckenzie method based on what
belief that most of the spinal pain comes from injuries to the disc
classifies symptoms based on location of symptoms and positions/motions that decrease symptoms
research says this is NOT the case
3 classification syndromes of the mckenzie method
postural = essential to correct posture
dysfunctional = essentially stretches to improve end ROM
derangement = essentially using end range motion to improve the theoretical nucleus migration in the disc
effectiveness of mckenzie method
evidence suggests NOT superior to the other treatments for pain/disability
overall long term treatment effect is small; more needs to be done
strong evidence for mckenzie method when
benefit with LE symptoms and when centralization occurs with acute IDD
possible mechnisms of action for the mckenzie method
dynamic disc theory (nucleus repositions centrally) = unproven
fluid dynamics with or without herniations (squeezing swelling away with repetitive motion)
PT Rx for acute IDD
POLICED
directional preference = 10-20 reps every 1-2 hours
intermittient traction if radiculopathy
posture/ergonomic edu
limited sitting
neural mobilizations
HEP for 1-2 weeks possible to avoid sitting while driving
unweighted walking lessening over time
for acute IDD MET is ultimately for what purpose
tissue proliferation and stabilization
why should we squat “like a toddler”
more circumferential disc compression
even annular tension with lumbar flexion/posterior pelvic tilt
more fixated end plate
less anterior segmental shearing and possible rotational stresses with additional influence of gravity
