IIS 2021 Tuckey et al article -Intro./Background Flashcards
What is the leading cause of disability (choose one):
A. Low back pain
B. Work-related injury
C. Chronic pain
D. Whiplash injury
C. Chronic pain
True or False: Myofascial pain syndrome also includes non-musculoskeletal symptoms.
True - eg, fatigue, sleep disturbance, visceral pain syndromes
What is retrograde inflammation & where is it produced?
Inflammation that is produced centrally (i.e.- at the DRGs) and then extends back out to the periphery
True or False: Persistent, peripheral nociceptive sources (eg-PANs) can perpetuate chronic pain states.
True.
Why do some people with active tender points not feel pain?
Because there is not enough of a stimulus to override the inhibitory system, in contrast to those who do feel pain
What is the main hypothesis of the IIS article? (state in 3 phases)
1) Elevated pro-inflammatory cytokine levels adversely impact vascular hemodynamics & lymphatic function (eg-drainage) in the extra cellular compartment, 2) which can then create a state of inflammatory interstitial stasis, 3) resultant ongoing nociceptive (eg-PANs) bombardment of dorsal horn (centralized sensitization)
In the IIS article hypothesis, what potentially are the specific pathophysiological mechanisms/factors (associated with the elevated cytokines) involved in the process?
-IL-1B, IL-6, TNF-a deactivate the local lymphatic pump (lymphangion) & stimulate differentiation of fibroblasts into myofibroblasts
-TGF-b1 released by fibro-/myofibro-blasts cause contraction of Fascial tissues which can then (hypothetically) cause compression of pre-lymphatic /lymphatic pathways, contraction, &/or fibrosis
Tissue injury &/or inflammation leads to release of (name at least 5 substances):
-glutamate
-serotonin
-bradykinin
-adenosine triphosphate
-protons (low pH)
-substance P
-nerve growth factor (NGF)
-Norepinephrine (NE)
________________ are unmyelinated free nerve endings that terminate peripherally in the ECM (of virtually all tissues) & respond to both inflammatory & mechanical stimuli.
Primary afferent nociceptors (simply called nociceptors, or PANs)
True or False: Primary afferent nociceptors enter the DRG & solely influence the segmental level at which they enter.
False - they trifurcate & thus influence ascending, descending, & segmental levels (eg -singular activated nociceptors can have heterosegmental nociceptive & reflexive impact)
What are 3 primary impacts of inflammation coming into the DRG from the PANs?
1) Neurogenic or Retrograde inflamm. out to the periphery & into the tissues convergent upon the DRG
2) a. Stimulation of Symp. reflexes (SNA) - both somato- & visceral guarding reflexes
b. Muscle guarding reflexes
3) Glial cell neural inflamm. - ie. in the cord [this is CSS]
______________________ can initiate the transition from acute to chronic pain states following Central sensitization
Glial cell neuroinflammation
True or False: Pro-inflammatory cytokines generated from trauma or immune responses can be transported from the periphery to the DRG & Dorsal Horn & facilitate the induction of central sensitization.
True (quote from p.5 of IIS article)
IL-1B, IL-6, and TNF-a are particularly associated with _______________ and _______________ (choose two):
A. Glial cell neuroinflammation
B. Primary afferent nociceptors
C. Secondary hyperalgesia
D. Chronic pain
E. Lymphangions
A. & D.
Define and describe a primary role of muscle guarding reflexes.
Body’s protective, involuntary motor response to reduce nociception (p. 5 IIS article)
Define Myofascial Trigger Points (MTrPs).
Hyper irritable nodules in a taut band of skeletal muscle; a principle cause of musculoskeletal pain, can be latent or active
Define Tender Points (TPs).
Areas of tenderness occurring in muscle, the muscle-tendon junction, bursa, or fat pad; considered part of Fibromyalgia
True or false: most fibromyalgia TPs lie within known MTrPs locations
True - implicates a degree of shared pathophysiology
Name 3 preceding Myofascial Pain hypotheses mentioned in the IIS article before the inception of the hypothesis.
-Simons’ Integrated hypothesis (described by Gerwin et al, 2004)
-Neurogenic Hypothesis (Srbely, 2010)
-Neuro-Fasciagenic Model of Somatic Dysfunction (Tozzi, 2014)
Summarize the Integrated Hypothesis
MTrPs formed by acute/chronic myotendinous injury… leads to…. hypoxia (possibly from high pressures in the muscle)…lower tissue pH, with resultant increased acetylcholine release could explain increased motor end plate activity & focal hypertonicity; if combined with SNS involvement could perpetuate this cycle.
In what ways does the Neurogenic Hypothesis (NH) expand upon the Integrated Hypothesis (IH)?
NH points out there can be:
-non-musculoskeletal contexts for MTrPs (eg- urogenital syndromes)
-infectious, psychogenic, & endocrine causes for MTrPs, inadequately explained by IH theory
What did Srbely hypothesize in the Neorogenic Hypothesis?
-MTrPs are neurogenic expressions of centralized sensitization (CSS) potentially evoked/maintained by an underlying primary pathology (OA or visc. disease) within the common neurological segment of the MTrP.
-CSS triggers neurogenic inflamm. that then can cause local changes observed at MTrP site interstitium
-CSS also responsible for ANS related effects of MTrP
Summarize the Neuro-Fasciagenic Model (Hypothesis) of Somatic Dysfunction:
A purely Fascial-based rationale can explain palpable features of somatic dysfunction via combined effects of >50 Fascial based factors; fascia may be involved in development of somatic dysfunction & chronic pain states.
True or False: A primary strength of the Neuro-Fasciagenic Model (Hypothesis) of Somatic Dysfunction is how it describes specific mechanisms of how fascia can create a continual nociceptive source for ongoing somatic dysfunction.
False - its weakness is that it does NOT provide a specific mechanism
Name 4 palpable features of somatic dysfunction:
-Tissue texture changes
-Asymmetry
-Restriction of motion
-Tenderness
