Cervicothoracic spine pt. 4: Test 2 Flashcards
etiology of age related joint changes
gradual onset due to:
-prior trauma that changes structure/fxn
-sedentary lifestyle with underloading
-genetics
-other diseases (i.e. RA)
-age
pathogenesis of ARJC
** Pathogenesis is progressive
frays, blisters, fissuring/tearing of articular cartilage
subchondraln bone penetrated/overloaded
osteophyte or spur formation
what are the 2 pathogeneses of articular cartilage
degenerative: more common, typically in older, chondrocytes can’t keep up
acute tears: rare typically in young/active, involves high shear forces
structures involved with ARJC
synovial components
-articular cartilage things and joint space narrows
-fibrous capsule slackens and becomes more fibrotic and then stiffens with persistent inflammation
-synovial membrane produces less synovial fluid and nutrients so drying occurs and increases friction
structures involved in ARJC that pain is attributed to
subchondral bone and injury to bone marrow
increased interosseous tissue (capsular fibrosis)
synovial membrane inflammation
periarticular tissue inflammation (i.e. ligaments, capsule)
persistent inflammatory response
foraminal narrowing or spinal nerve
persistent inflammatory response with age related joint changes can be partly due to what factors
increased local nociceptor sensitivity for greater pain transmission fostering inflammation
local production of nitrous oxide leads to more interstitial inflammation and excess collagen (joint fibrosis)
cervical symptoms of age related joint changes
-gradual onset of neck pain
-P! with prolonged positions like FHP or sleeping (due to no refilling of cartilage with synovial fluid)
-moring stiffness after prolonged positions for >30 min
-P!/limit looking in one blind spot and with looking up
-possible paresthesias (compression of spinal N b/c of thin cartilage/narrowing foramen)
-some movement helps but some makes it worse
what would limitations be with R sided ARJC
P! with R SB, R RT, and ext
anything that will compress the joint and increase congruency
ROM and combined motion scan findings with ARJC
ROM painful and limited; specifically with ext and ipsilateral SB/RT
typically worse on one side, but could be bilateral
capsular pattern of restriction
CM = consistent block often into an ext quadrant OR opposing quadrants consistently blocked
Restisted/MMT for ARJC
depends on acuity
typical stress test findings for ARJC
likely pain with compression, particularly if added while in ext, SB, and/or RT
PA glides likely painful at involved level
likely + distraction for relief if symptoms are present
typical neuro tests results for ARJC
often negative bit could be positive for radiculopathy if spurring creates stenosis on spinal nerve
cervical signs in the biomechanical exam for ARJC
accessory motion = hypo mobility
special tests = spurlings may be positive for radiculopathy
for early ARJC describe what findings might be present
capsular pattern if there is a past trauma
hyper mobility die to narrowing if no past trauma
Rx = POLICED, JM, CPP, and MET
describe the possible findings for intermediate ARJC
capsular pattern with firm end feels
hypo mobility
Rx = JM, MET, and involved AND adj joints for ROM
describe the findings for late/advanced ARJC
no capsular pattern; body end feels due to osteophytes
hypo mobility
Rx: JM and MET with greater focus on adj jt motion
PT Rx for degeneration
focus on improving integrity of cartilage and mobility
POLICED (pt ed on weight/avoiding provocation and assistive devices to unload involved cartilage)
JM for pain, tissue integrity, and mobility
what type of MET would you do for PT Rx for degeneration
ultimate focus on improving motion, cartilage integrity, and neuromuscular benefits
pure strengthening parameters = possible problem
efficiency of supplements for articular cartilage issues
glucosamine and chondroitin sulfate have no evidence of minimum clinically important outcomes compared to placebo in knee
how might deeper defects in articular cartilage be beneficial
deeper stimulates bleeding by penetrating bone (crossing tide mark) and heal better than superficial lesions (b/c bone is highly vascular)
how might deeper defects stimulate a problem with articular cartilage injuries
may fill with a lesser type I collagen instead of original type II
type I collagen resists tension > compression
insufficient patch; lasts about 6 months
limited healing capacity if any with poor conservative outcomes
where is RA primarily
primarily in C-spine
possible AA sublux/instability (40-85% prevalence; neuro symptoms may not be present with up to 10 mm sublux)
possible low cervical dislocations
prevalence of stenosis
unknown
most common dx for spinal sx in adults > 60
population = typically > 65, younger pts are generally due to instability
30% of asymptomatic individuals had canal narrowing
pathogenesis of stenosis ( 2 causes)
narrowing of spinal canal
fibrotic spinal nerve die to persistent inflammation associated with instability
