Acute and Chronic Pain

Question 1

analgesia

Answer 1

absence of spontaneous report of pain or pain behaviors in response to stimulus normally expected to be painful

Question 2

dysesthesia

Answer 2

and unpleasant abnormal sensation, whether spontaneous or evoked

Question 3

hyperesthesia

Answer 3

increased sensitivity to stimulation, excluding special senses

Question 4

hypoalgesia

Answer 4

diminished pain in response to a normally painful stimulus

Question 5

neuropathic pain

Answer 5

pain arising as a direct consequence of a lesion or disease affecting the somatosensory system

Question 6

nociceptor

Answer 6

a receptor preferentially sensitive to tissue or trauma or to a stimulus that would damage tissue if prolonged

Question 7

nocioception

Answer 7

activation of sensory transduction in nerves by thermal, mechanical, or chemical energy impinging on specialized nerve endings

Question 8

plasticity

Answer 8

nociceptive input leading to structural and functional changes that may cause altered perceptual processing and contribute to pain chronicity

Question 9

What is the gate control theory?

Answer 9

an modulate pain at the spinal chord

Rubbing of large fibers will gate pain fibers at the spinal cord

highlights the importance of the spinal cord dorsal horn in modulating increasing pain signals, can be gated to eliminate pain signal from C-fibers

Descending pathways are also involved

three components: sensory, affective, evaluative

Question 10

What is the neuromatrix theory?

Answer 10

individuals develop their own “neurosignature” as part of a neural netowrk which is influenced by a number of inputs (previous physical or psychological trauma), genetic susceptibility, cognitive and evaluative, that feed into a network of brain structures in creatin g”outputs” over time in one’s life manifesting as pain, one’s action program, and long term effects on the stress regulation or endocrine system

updated Gate Control Theory

Question 11

transduction

Answer 11

detection of noxious or damaging stimuli

this signal is transduced into electrical activity by various types of nociceptors

thermal nociceptors detect extreme temperatures, chemical nociceptors detect noxious substances, and mechanical nociceptors detect high-intensity pressure

Question 12

conduction

Answer 12

detection of noxious or damaging stimuli

resulting electrical signals are conducted via primary afferent nociceptive neurons to the dorsal horn of the spinal cord

Question 13

transmission

Answer 13

synaptic transfer of input to neurons with specific laminae of DH

two ascending pathways - spinothalamic and spinoparabrachial tracts

spinothalamic tract relays through the thalamus to the somatosensory cortex and related areas

Question 14

modulation

Answer 14

the sensation of pain and the response to pain are affected not only by pain transmission from affected neurons (via ascending pathways) but also by the brain’s response to that transmission (via the descending pathways)

inhibitory spinal interneurons and projections from the brainstem to the dorsal horn of the spinal cord modulate pain signaling by limiting the transfer of incoming snesory input to the brain

Question 15

perception

Answer 15

the spinothalamic tract relays pain information through the thalamus to th esomatosensory cortex and associated areas, allowing for localization of pain, avoidance behavior, and cognitive processing of pain

Question 16

affective response

Answer 16

the spinoparabrachial tract relays the pain stimulus to the parabrachial nucleus of the brainstem, continuing on to the ventral medial nucleus of the hippocampus and the central nucleus of the amyglada, brain regions involved in the affective response to pain

Question 17

allodynia

Answer 17

a pain due to astimulus which does not normally provoke pain.

Temperature or physical stimuli can provoke allodynia, (which may feel like a burning sensation), and it often occurs after injury to a site.

Question 18

hyperalgesia

Answer 18

an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves

what is normally painful becomes much more painful

Question 19

What are the outcomes of healing to injury with plasticity?

Answer 19

hyperalgesia and allodynia

will lead to chronic pain

Question 20

What are Abeta fibers?

Answer 20

large, thickly myelinated fibers that are non-nocioceptive

• normally responds to non-painful (mechanical) stimuli
• can be recruited into pain processing over time

Question 21

What are Adelta fibers?

Answer 21

small, thinly myelinated nociceptive fibers

• respond to heat, cold, and high-intensity mechanical stimuli

Question 22

What are C fibers?

Answer 22

unmyelinated, nociceptive fibers

responds to head, mechanical, and chemical stimuli

Question 23

What is the response for non-painful stimuli?

Answer 23

specificity for a particular stimulus

high degree of gain to amplify weak signals

rapid adaptation to increasing intensities

Question 24

What is the response for painful stimuli?

Answer 24

specificity is less important

high threshold receptors - thermal, chemical, and mechanical stimuli (polymodal)

threshold for firing may decrease

Question 25

What is the framework for acute/subacute injuries?

Answer 25

clinical alterations - symptoms anatomical alterations - tissue injuries and overload functional alterations - biomechanical deficits and subclinical adaptations

Question 26

What are the clinical symptoms of musculotendinous overload?

Answer 26

pain instability dysfunction

Question 27

What are functional biomechanical deficits of musculotendinous overload?

Answer 27

muscular weakness inflexibility scar tissue muscle strength imbalance

Question 28

What is the signaling cascade in peripheral nerve terminals?

Answer 28

chemical, mechanical, or thermal activation of peripheral nociceptors via nonselective cation or Na+ channels influx of calcium and sodium ions depolarizes the membrane voltage-gated sodium channels open and further depolarize the membrane burst of action potentials

Question 29

What are the key neurotransmitters and modulators involved in pain processing?

Answer 29

**increased processing**: glutamate and substance P **decreased processing**: norepinephrine, serotonin, GABA, glycine, endocannabinoids, endorphins, monoamines

Question 30

What are the features of central sensitization?

Answer 30

development of or increases in spontaneous neural activity reduced threshold for activation by peripheral stimuli or for dorsal horn neural activation increased receptive field of nociceptive afferents or dorsal horn neurons increased response of dorsal horn neurons to painful stimuli

Question 31

What are the potential mechanisms for central sensitization?

Answer 31

cellular processes such as decreased inhibition, increased membrane excitability, and synaptic facilitation microglial activation

Question 32

What are some of the effectors altered in central sensitization?

Answer 32

changes in threshold and activation kinetics of NMDA and AMPA receptors changes in AMPA receptor membrane trafficking alterations in ion channels to increase inward currents and reduce outward currents reductions in the release or activity of GABA and glycine altered gene expression in dorsal horn neurons

Question 33

What is the function of calcium channels in the nervous system? What are drugs that modify its function?

Answer 33

inward channel, primary driver for most intracellular responses to stimulation **drugs**: pregabalin, gabapentin, ziconotide

Question 34

What is the function of potassium channels in the nervous system? What are drugs that modify its function?

Answer 34

outward channels - efflux of potassium makes the membrane potential more negative (hyperpolarized) **drugs**: baclofen, clonidine, opioids

Question 35

What is the function of sodium channels in the nervous system? What are drugs that modify its function?

Answer 35

inward channel - influx of sodium through open channels makes membrane potential less negative, bringing it closer to the threshold potential necessary to initiate an action potential **drugs**: local anesthetics, carbamazepine, phenytoin

Question 36

What is the function of chloride channels in the nervous system? What are drugs that modify its function?

Answer 36

inward channel: influx of chloride makes the membrane potential more negative (hyperpolarized) **drugs**: benzodiazepines (amplify GABA, induced opening of channel)

Question 37

What are the key steps in pain mechanisms?

Answer 37

sensitization and abnormal peripheral input leads to... sensitization and amplification of peripheral input in the dorsal horn leads to... sensitization of neuron in the brain

Question 38

What are the mechanisms of nocioceptive central pain?

Answer 38

autosensitization of receptors ectopic firing of dorsal root ganglion cell calcium-induced molecular cascades from excess glutamate phenotypic change of A-ß cells and DRG changes in gene expression of sodium channels and neuropeptides anatomic changse at dorsal horn

Question 39

Where is pain processed?

Answer 39

center just for pain: thalamus center for pain and emotion: somatosensory cortex, insular cortex, hippocampus, amyglada, anterior cingulate cortex

Question 40

What is catastrophizing?

Answer 40

**definition**: exaggerated negative orientation toward a noxious stimulus **rumination** - "I can't seem to get it out of my mind" **magnification** - "I become afraid that the pain will get worse" **helplessnes**s - "I feel I can't stand it anymore"

Question 41

What is Gatchel's 3-stage model for acute to chronic pain?

Answer 41

state I - normal emotional reaction during acute phase stage II - behavioral and psychological reactions and problems stage III - acceptance or habituation to "sick role"

Question 42

What are the symptoms of central sensitization?

Answer 42

hyperalgesia spontaneous pain allodynia decreased threshold to peripheral stimuli expansion of receptive field increased spontaneous activity

Question 43

What are the features of muscle pain?

Answer 43

aching and cramping difficult to localize and refers to other deep somatice tissues (fascia, muscles, joints) muscle nocioceptive activity is processed differently in the CNS inhibited more strongly by descending pain-modulating pathways than cutaneous pain

Question 44

What is myofascial pain?

Answer 44

characterized by regional areas of muscle weakness or dysfunction many times associated with an area of acute or chronic injury that has characteristic referral patterns of pain, many times mimicking a "pinched nerve" or radicular spine syndrome

Question 45

symptoms of myofascial pain

Answer 45

local and referred pain pain with iso contraction stiffness, limited ROM muscle weakness paresthesia and numbness propioceptive disturbance autonomic dysfunction

Question 46

What are the physical findings of myofascial pain?

Answer 46

local tenderness single or multiple muscles palpable nodules firm or taut bands "twitch response" (LTR) jump sign muscle shortening limited joint motion muscle weakness

Question 47

What are some causes of chronic pain?

Answer 47

trauma congenital or familial abnormalities nerve or nervous system injury osteoarthritis muscle or visceral injury other systemic disorders where pain continues to persist for at least 3 to 6 months with characteristic central or peripheral nervous system changes

Question 48

What is the treatment for chronic pain?

Answer 48

relies on pharmacologic therapies to help reduce pain, improve mood, improve sleep quality, and return patients to previous lesure activities and work

Question 49

What are teh characteristics of organ pain?

Answer 49

the viscera have lower densities of sensory nerve innervation and share sympathetic and parasympathetic convergence in the central nervous system visceral or organ pain is usually more poorly localized