Pain

pain definition

a distressing experience associated with actual or potential tissue damage with sensory, cognitive, emotional, behavioral, and social components

because pain is an internal, private experience, what is the gold-standard for its measurement?

self-report

peak-end phenomenon

when asked to report pain over a recent period, pt recall is predominantly influenced by the worst pain experienced over that time (the peak) and most recent pain they experienced (the end)

pain scales

numeric

verbal

visual analog

faces

pain is a ___, not a ___

issue; tissue

nociception

neural process of encoding noxious (painful) stimuli

nociceptor

high-threshold sensory receptor of the peripheral somatosensory NS that is capable of transducing and encoding painful stimuli

noxious stimuli

stimulus that is damaging or threatens damage to normal tissues

afferent

conducting toward something (CNS)

efferent

conducting away from something (CNS)

pain matrix

when peripheral nociceptors are stimulated, the signal travels up the matrix

brain structures that process and regulate nociceptive info

brainstem

amygdala

hypothalamus

thalamus

areas of the cerebral cortex

lateral pain system

discriminative aspect

perceived location and intensity of tissue damage or potential tissue damage

lateral pain system travels

spinothalamic tract (sensory pathway)

lateral pain system processed in the

somatosensory cortex

medial pain system

motivational aspect

emotions and behavior

cognitive evaluative aspect

medial pain system travels

spinolimbic and spinoreticular

medial pain system processed

limbic system (emotional system of brain)

pain matrix generates a

top-down response to regulate afferent signals

pain matrix generation is dependent on

psychological

physiological

social

genetic factors

3 patterns of pain

acute pain

episodic pain

chronic pain

acute pain

starts suddenly, ends when its cause is treated/healed

usually sharp feeling (warning signal)

common causes: strained muscles, broken bones, dental work, surgery, childbirth, infections, and/or burns

episodic pain

time to time, irregular intervals

may be associated with long-term condition (ex. migraines)

can happen out of nowhere or may be caused by known triggers

chronic pain

lasts longer than 3 months, or expected healing time

acute pain might persist and become chronic pain

can happen for no reason

can experience chronic and acute at same time

2 types of chronic pain

chronic primary pain

chronic secondary pain

chronic secondary pain 2 subcategories

neuropathic pain

nociceptive pain

chronic primary pain

neural dysfunction creates pain in the absence of tissue damage

gain of function in the central nociceptive system

chronic secondary pain

pain that is initially experienced as a symptom of another medical condition

continued stimulation of nociceptors from injury

maintained signaling after injury has healed

damage to the somatosensory system

normal nociceptive processing (how it works)

nociceptive stimulus —> nociceptive afferent —> to pain matrix

peripheral sensitization (how it works)

nociceptive stimulus —> nociceptive afferent (increased response of nociceptor to same stimulus) —> to pain matrix

respond more vigorously

increased excitatory transmitter/receptor activity in nociceptive neurons eventually elicits…

long-term functional changes that lead to hyper-excitability, spontaneous activity, and structural changes in connections

respond normally, but more vigorous response of pain matrix

signs of central sensitization: “dysestheasis”

hyperalgesis

allodynia

spontaneous pain

temporal summation

secondary hyperalgesia

hyperalgesis

increased pain response to nociceptive stimulus

ex. pain amplified because already swollen toe after being stepped on later that same day

allodynia

perceiving innocuous (not harmful) stimuli as painful

ex. putting on shirt over sunburn when putting on shirt usually is not painful

spontaneous pain

temporally distinct from external stimulus, unprovoked

described as burning, shooting, electrical

ex. feeling like you hit your funny bone without hitting it

temporal summation

perception of increased pain as response to increased stimulus or continuous presence of stimulus

secondary hyperalgesia

spread of pain adjacent to uninjured areas

ex. paper cut localized to small portion, feel around whole pad of finger

structural reorganization in the cortex (rewiring)

nociceptive message —> cortical neuron —> formation of synapses with new neurons

how we feel more pain than we should

reduced descending inhibition

on the way back down, we can have different tracts in the same limbic systems that can dull our pain a little bit

cellular changes (neuroplasticity) that reflect central sensitization

increased spontaneous activity

increased responsiveness to afferent inputs

prolonged after-discharge in response to repeated stimuli

expansion of receptive fields

some evidence suggests as we move from acute to chronic

pain processing moves from the sensory areas of the brain to the emotional/interventional part

nociceptive pain

pain caused by tissue damage

sensation can be sharp, pricking, dull/aching

ex. pain, infection, broken bone, osteoarthritis

neuropathic pain

pain caused by nerve damage due to injury or disease

sensations are burning, tingling, shooting, electric

ex. diabetic neuropathy, shingles, sciatica

nociplastic pain

caused by changes in how the NS processes pain

not linked with clear injury, tissue damage, inflammation, or disease

sensations vary widely

ex. fibromyalgia, IBS, tension headaches

nociceptive chronic pain

due to continuing stimulation of nociceptive receptors

ex. chronic pain that results from a vertebral tumor pressing on nociceptors in the meninges surrounding the SC

primary hyperalgesia

chemical changes in the damaged tissue awaken sleeping peripheral nociceptors

chronic secondary pain can occur from

central sensitization

ectopic (abnormal location) foci

ephaptic (cross-talk, occurs in demyelinated regions) transmission

ectopic foci

a signal coming from a place it shouldn’t

ridiculopathy (nerve pinched in neck, feeling in fingers)

cross-talk

ephaptic transmission

occurs in demyelinated regions

occurs as a result of lack of insulation between neurons

neuropathic pain can arise from abnormal neural activity in the following:

periphery

CNS in response to deafferentation

dorsal horn

complete nerve resection

results in lack of sensation from that nerve’s receptive field

partial damage

can result in allodynia and sensations similar to an electric shock-pain

damaged area =

demyelinated

demyelinated =

chance for ectopic foci and/or ephaptic transmission

most common cause of neuropathic pain

periphery

A-alpha nerve fibers carry info

related to proprioception (muscle sense)

A-beta nerve fibers carry info

related to touch

A-delta fibers carry info

related to pain and temp

C-nerve fibers carry info

related to pain, temp, and itch

gate theory of pain

mechanism in SC

pain signals can be sent up to the brain to be processed to accentuate the possible perceived pain, or attenuate it at the SC itself

counterirritant theory

inhibition of nociceptive signals by stimulation of non-nociceptive receptors occurs in the dorsal horn of the spinal cord

enkephalin binding depresses

release of substance P (neuropeptide)

antinociceptive systems

suppression of nociception in response to stimulation that would normally be painful

serotonin and norepinephrine

inhibitory

endogenous opioids

chemicals produced by the body that activate the antinociceptive system

found throughout CNS

suppressor system made up of

endogenous opioids

serotonin

norepinephrine

does the antinociceptive system wait around and wait to be stimulated?

no, on in background

stress-induced antinociception

how many sites of antinociception?

5

level I

occurs in periphery

level II

occurs in dorsal horn

level III

fast-acting neuronal descending system

level IV

hormonal system

level V

amygdala and cortical level

pain neuroscience education

process to explain to a patient the neurobiology and neuroscience of their pain experience in a manner that is easily understandable and applicable

if a pt truly understands PNE, they will

have less pain

have less disability

move better

perform better with rehab

have better cognitions regarding their pain

negative pain experience

pain experience —> pain catastophizing —> pain-related fear —> avoidance —> disuse depression disability

pain knowledge

more activity in brain centers before PNE education

less activity in brain centers after PNE activity (can modulate their own pain)

4 pillars of focus

pain knowledge/education

exercise/aerobics

sleep/stress management

goals setting

pain inhibiting system occurs

throughout the NS

pain is always a

personal experience that is influenced to varying degrees of biological, psychological, and social factors

pain cannot be inferred

solely from activity in sensory neurons

through life experiences, individuals learn

the concept of pain

a person’s report of an experience as pain should be

respected

pain serves an

adaptive role

pain may have adverse effects on

function, social, and psychological well-being

inability to communicate does not

negate the possibility that a human or nonhuman animal experiences pain