Pain final

Med for muscle issue

muscle relaxant

psychosocial meds

SNRI, tricyclic antidepressant

meds for neuropathic pain

gabapetenoid

gabapentinoid can’t be taken

prn

pregabalin has lower dosage than

gabapentin

nociplastic pain meds

SNRI, tricyclic antidepressant (also maybe gabapentinoids, acetaminophen, and NSAIDS?)

nociceptive pain meds

topical analgesic, NSAIDs, opioid, channel blockers

time to fall asleep

sleep latency

ideal sleep latency

0-30 min

desired sleep efficiency

>85%

graded exposure

progression of engagement along fear hierarchy, psychological

graded activity

progressive increase

isometrics are used early in rehab to produce analgesia with

certain tendon pains

aerobic exercise is appropriate for

all pain mechanisms

exercise impact on central inhibition

increases central inhibition (opioidergic and serotonergic)

exercise impact on central facilitation

reduces central facilitation (NMDA receptors not active)

exercise impacts

systemic inflammation and the immune system

sedentary lifestyle and chronic pain have a

bidirectional relationship

proposed mechanisms of neurodynamics

• reduce immune response/inflammation from n. injury

• reduce local perineurial and intramural edema

• reduce hyperalgesia (mechanical and thermal(

• reduce neural adhesions

neurodynamics could have

systemic effects

types of manual therapy

• soft tissue based

• nerve biased

• joint based

  • mobs (low velocity)

  • manipulations (high velocity)

velocity of mobs

low

velocity of manipulations

high

STAR shoulder classification

screen flags, assign pathoanatomical diagnosis, assign rehab classification

LBP you should

screen for red flags, clarify symptom irritability, classify into treatment classification (manipulation, stabilization, special exercises, traction)

with low irritability, you can push

into resistance

with medium irritability, use

caution against high force mobs

with high irritability, push not

into tissue resistance

nerve treatment dosage

less is more, touch into symptoms, keep it low to avoid flareups

tendon/muscle exercise should not cause pain to be

≥4/10 before or after exercise

exercise for bone should have

no pain before/after

for nociplastic pain, address

neuroplasticity

top-down drivers

• bad childhood experiences

• depression

• anxiety

• stress

• fear avoidance beliefs

bottom-up/peripheral drivers

• tissue injury

• muscle weakness

• medical co-morbidities

Stages of GMI

L/R discrimination, explicit motor imagery, mirror therapy

SINSS model

Severity, irritability, nature, stage, stability

“why did things that were fine now cause pain?”

envelope of function (preventing boom/bust)

“will it ever go away?”

pain vs function

“why am I still in pain?”

alarm system

Cellular processes that can contribute to central sensitization

increase of membrane excitability, synaptic facilitation, disinhibition

nervous system changes resulting from central sensitization

development or increase in spontaneous activity, reduction in threshold for activation by peripheral stimuli, enlargement of receptive fields

enlargement of receptive fields refers to

conversion of nociceptive-specific neurons to wide dynamic neurons that now respond to both innocuous and noxious stimuli

sensitization can occur at

any point along the neural axis

maladaptive neuroplasticity

subcortical and cortical reorganization

central sensitization changes at

secondary nociceptive neuron

peripheral sensitization changes at

primary nociceptive neuron

peripheral sensitization cell body

in DRG

central sensitization cell body

in spinal cord

CSI is a… outcome measure

nociplastic

CSI>40 indicates

likely central sensitization

OA can cause

chronic pain, brain changes

ACL-R can cause

maladaptive neuroplasticity

chronic LBP can cause

tactile dysfunction, body image distortion

tendinopathy can cause

sensitization

MSK dx can cause

altered pain processing, impairments to CNS

central sensitization in neuropathic pain

neuroinflammation and glial cell activity, increased responsiveness of dorsal horn neurons (wind-up or temporal summation) likely cause and/or reduction in descending inhibition/cortical reorganization, unregulated NK1-R, decreased threshold for substance P to activate SC neuron, pro-inflammatory cytokines released from microglia

peripheral sensitization in neuropathic pain

up regulation of receptor channels at 1° afferent nociceptor (a delta), reduced threshold to responsiveness

c fiber cell bodies live in

DRG

NK1-R is a receptor for

substance P

possible causes of neuropathic pain

ectopic impulse generation at site of nerve injury or DRG (phantom limb pain), compression of nerve (vascular compromise), up regulation of TRPV1 and/or acid sensing channels @ 1° sensory afferent (peripheral sensitization)

neuropathic pain possible lesion sites/types

genetic disease affecting receptors and/or ion channels of peripheral nociceptive neuron, damage to peripheral nociceptive axon or myelin, SC lesion affecting spinothalamic tract, thalamic lesion

nerves need

blood, movement, and space

neuropathic pain is caused by

lesion or disease of somatosensory system

cerebellar lesions can/cannot cause neuropathic pain

CANNOT

somatosensory lesion can be in the

PNS or CNS

pain DETECT <12 indicates

unlikely neuropathic component to pain

pain DETECT ≥19 indicates

likely neuropathic component

S_LANSS <12 indicates

unlikely neuropathic component

S-LANSS ≥12 indicates

likely neuropathic component

spinothalamic tract, aka

anterolateral system

MCID on NPRS

2 points

NPRS

numeric pain rating scale

VAS MCID

20mm

nociceptive pain outcomes

VAS, NPRS

4 D’s of nociplastic pain

disproportionate pain, disproportionate aggravating/easing factors, diffuse pain/palpation tenderness, distress

3 S’s of neuropathic pain

subjective hx of nerve pathology, sensory deficits in dermatomal pattern, stretching nerve provokes

4 P’s of nociceptive pain

proportional, provokable, periodic, predictable

exercise therapy for neuropathic and nociplastic pain should take this approach

cognitive behavioral (including time-contingent approach)

exercise therapy for nociceptive pain should take this approach

pain contingent approach

pt ed for nociceptive

explain presumed source of nociception

pt ed for neuropathic

explain lesion or disease of nervous system and central sensitization

nociplastic pt ed

explain central sensitization

neuropathic is limited to

neuroanatomically plausible distributions

nociplastic outcome measures

CSI

neuropathic outcome measures

S-LANSS, painDETECT

nociceptive outcome measures

NPRS, VAS

CPM

ability of descending pain inhibitory mechanisms (central) to effectively inhibit pain following a painful stimulus (e.g. increased PPT after cold water bath)

wind-up

progressively increasing activity in dorsal horn cells following repetitive activation of primary afferent c fibers

temporal summation

increased pain response to repetitive noxious stimuli to C/A delta fibers at <3Hz, central sensitization results in steeper ramp up in responsiveness

neurogenic inflammation

nociceptors acting on adjacent tissues by releasing inflammatory mediators (can vasodilate and increase permeability)

process proposed to contribute to 2° hyperalgesia

heterosynaptic facilitation

heterosynaptic faciliation

interneuronal facilitation of adjacent spinal projection pathways, may explain expansion of pain beyond area of insult (nosy neighbors)

process proposed to contribute to primary hyperalgesia

homosynpatic facilitation

homosynaptic facilitation

repeated peripheral input sensitizes dorsal horn projection neurons in nociceptive pathway

central sensitization

increased responsiveness of dorsal horn (spinal cord) neurons (wind up or temporal summation) and/or reduction in descending inhibition

central sensitization has increase in activity of

microglia and astrocytes at dorsal horn

peripheral sensitization

reduced threshold of peripheral nociceptive neurons (A delta, C fibers) and/or increased responsiveness

TRP

transient receptor potential

in peripheral sensitization, channels

TRP and sodium/calcium channels may have increased expression and/or responsiveness, this makes it easier to activate neurons (which increase peripheral nociceptive input to nervous system)

C fibers

slow, small diameter, unmyelinated, nociception, cell body in DRG, associated with dull, subacute, longer lasting pain, poorly localizezd