Nociplastic P!, Neck P! and Bone healing - Exam 2 Flashcards
describe nociplastic p!
altered P! perception without complete evidence of actual or threatened tissue compromise
S&S of sensitization are present - an underlying mechanism of nociplastic P!
how does nociplastic P! happen?
thinning of myelin sheath in spots (PNS)
–nerves lose their protection (aka loose wires)
Nociplastic pain happens to increased sensitivity and misinterpretation
- -peripheral nociceptors (a-delta and c-fibers) (PNS)
- -central structures (CNS)
what’s happening with increased sensitivity and misinterpretation by peripheral nociceptors? (PNS)
persistent excitation of A-delta and C fibers inhibits A-beta fibers pre-synaptically so it is also harder to override P! with motion
- carrying P! more frequently and more intensely
what is happening with increased sensitivity and misinterpretation by central structures? (CNS)
-increased excitability of:
-lowered synaptic resistance so:
-loss of descending anti-nociceptive mechanisms so
-segmental dorsal horn neurons
-P! sensations occur easier
-less P! control with typical endogenous opiate release in the body
what happens to the C-fibers in somatic convergence (referred P!)?
give example
C-fibers split and travel at least 2 spinal segments superiorly and inferiorly
example: persistent symptoms with C5,6 hypermobility/instability can eventually spread and create symptoms through the entire UQ (C3-T1)
–(2 levels up and 2 down)
– domino effect
explain how the brain perceives somatic convergence?
brain perceives pain as coming from even more areas with persistent symptoms
- downward spiral
what happens to the homunculus with somatic convergence?
it gets smudged
small parts of the body can get perceived as large pain areas
persistent fatigue syndrome
fibromyalgia
LBP
age-related joint changes
lateral elbow pain
shoulder pain
migraine
neck pain - traumatic & non-traumatic
prevalence of conditions (growing number of conditions) related to nociplastic pain
what are “possible” nociplastic p! S&S/criteria?
> 3 months of P!
regional or spreading symptoms
P! that cannot be entirely explained by nociceptive or neuropathic pathways
P! hypersensitivity or allodynia (nonpainful stimuli causing P!)
what are “probable” nociplastic P! S&S/criteria?
(in addition to “possible” criteria)
sensitivity to sound, light and/or odor (picks up sensitivity to other sensations)
sleep disturbances
fatigue
cognitive problems
** can seem unrelated
-sweaty hands/feet
-pitting edema with lymph compromise
-decreased skin mobility and sensitivity
-scratch test (+) excessive reddening
ANS S&S of nociplastic P!
decreased sebaceous (oil) gland and hair follicle activity
– skin appears scaly and fragile
– decreased skin mobility/rolling and increased sensitivity
– + scratch test - excessive reddening response
ANS S&S of nociplastic pain
sweaty hands/feet
ANS S&S of nociplastic pain
decreased peripheral arterial shunting leading to coldness/clamminess
ANS S&S of nociplastic P!
loss of laterality - can’t differentiate sides, particularly around spine
ANS S&S of nociplastic P!
increased erector pili muscle activity (goose bumps)
ANS S&S of nociplastic P!
+ graphesthesia - can’t differentiate drawn letters/numbers on skin
ANS S&S of nociplastic P!
what are the reasons for prescribing JM, including manipulation for nociplastic P!
most accepted!
stimulates descending inhibitory P! mechanisms (more endorphins)
includes presynaptic inhibition
– limit P! transmission by A-delta and C fibers
– better overriding of P! by A-beta stimulation
reduces dorsal horn excitability
decreases inflammatory mediators
What MET parameters would you prescribe a patient with nociplastic P!
low to moderate intensity global aerobic and resistance activities
2-3 x/wk
30-90 minutes per session
at least 7 weeks duration
what benefits does MET provide to a patient with nociplastic P!
endogenous/opiate analgesia (inhibits spinal nociceptive processing)
helps pt to interpret P! and motion as non-threatening
reorganize homunculus
why would you “prescribe” neuroscience education/behavioral therapy to a patient with nociplastic P!
not just mind over matter
explains increased sensitivity and misinterpretation to reduce stress/anxiety of misperceived tissue injury
– challenge’s patient’s reasoning of fears and P!
– ensure safety of exercise
transition to adaptive pain coping
what is the prognosis for nociplastic p!
varying degrees of improvement - lots of variables
longer recovery (at least 7 weeks)
likely not full resolution of symptoms
True or false. Most of the population experiences neck P!, with almost half having persistent neck P!
true
true or false. younger males are more likely to experience cervical neck P!
false - older females experience more C neck P!
what are two of the strongest risk factors for neck P!
female (specifically > 40)
history of neck P!
if a patient with LBP complains about neck P!, are they making it up? why or why not?
no - LBP can cause neck P! because “one breaker controls lots of muscles” therefore the pain in the low back can shoot up the back
what is the etiology for neck P!
most often unidentified
typically classified as mechanical neck disorder (MND) or nerve root compromise
are we looking to get the patient back to more normal ROM or more functional ROM?
functional ROM
what degree range is full extension to look up?
40-50 degrees
what degree range is functional ROM for driving?
60-70 degrees
what are S&S for neck P!
varied in the cervical spine and possibly into the upper extremity
impaired scapular mechanics (don’t just address the painful area)
Is imaging good for identifying related structures with neck P!?
no, fails to find related structures
- most patients don’t have a pathoanatomical cause or known tissue producing symptoms