Pain science and theories

Question 1

Nociceptive pain defintions

Answer 1

pain due to activation of nociceptors in cutaneous, somatic or visceral structures and is the tissue injury pain of the classical physiological alarm system and is therefore usually adaptive.

Question 2

Cacner pain definition

Answer 2

Pain associated with the neoplastic process or its treatment (e.g. radiotherapy) which is pathologically speaking, may be nociceptive or neuropathic in nature or both.

Question 3

3 dimensions of pain

Answer 3

Melzack and Casey 1968-
Sensory discrimintative- localisation and description of ppain, physical experiences, limbic lobe, 1 somatosesnory cortex,
Motivational affective- emotional reponse to pain, feelings of unpleasantness, anterior insular, cinulate cortex
Cognitive evaluative- thinking about your pain adn making decisions

Question 4

Intensity theory

Answer 4

Erb 1874, pain is an emotion when a stimulus is stronger than usual, not a sensory experience

Question 5

Specificity theory

Answer 5

Von frey, 1895,
dedicated pathways for each somatosensory modality. all have their own receptor, fibre, stimulus. Pain is its own thing and has its own pathways

Question 6

Strongs theory

Answer 6

Strong

Pain is based on both the noxious stimuli and the psychic reaction to its unpleasantness

Question 7

Pattern theory

Answer 7

no unique circuits for pain and different somatosensory modalities, pain is an interpretation of a pattern of afferents

Question 8

Gate control theory

Answer 8

by rubbing you are activating a-alpha and a-beta you are closing the gate to larger C fibre and A-delta fibres (pain) to transmit to secod order neuron via t-cells

Question 9

Neuromatrix theory

Answer 9

network of neurons that integrate the thalamus, cortex and limbic system (genetic) and is shaped by external experienes. The neurosignature is is our awareness of pain, motor output and movement. It is a plastic system that results in an individualised response to noxious stimul. • S1, S2 and posterior insula: sensory discriminative aspect of pain (e.g. what it feels like, where it is, how intense)
• ACC, prefrontal cortex and anterior insula: affective emotional
• ACC: suffering, fear and taking action
• Insula: entire centre for overall well-being and homeostasis

Question 10

Nociceptors

Answer 10

unencapsulated, free nerve endings
A-delta (III)- thinly myleinated, larger, sharper local pain
C (Iv)unmyelinated, slower, diffuse pain, burny or achy

Question 11

Adequate stimuli

Answer 11

The stimuli that is required to activate it. Nociceptors adequate stimuli is potential tissue damaging stimuli that is unique to the tissue.

• Silent nocieptors is inflammatory mediators
• Muscles and joints- II, III and IV fibres, joints is end range stretching capsular tissue or pressure
• Muscle is ischaemia or pressure

Question 12

Bradykinin,

Answer 12

released by plasma after tissue inury, sensitises nocicpetiors, produces pain and heat

Question 13

Prostaglandin

Answer 13

directly excite and sensitise nociceptors of primary aferetns

Question 14

Cytokines

Answer 14

released by macrophaeges (e.g. interleukin, TNFa) sensitise primary afferent

Question 15

Nerve growth factor

Answer 15

neurtrophic factor released by muscles after tissue injury, activates and sensitises nocicpetors

Question 16

Peripheral sensitisation

Answer 16

express more receptors for inflammatory mediators, coupled onto ion channels to activate second messenger systems and influence more ion chnnels, induced within a few misn

Question 17

Neuropeptides

Answer 17

Substance P and calcintoni-g-related peptide (CGRP), small diameter afferents (III, IV) involved in neurogenic inflammation
also foind in lamina I (muscles and joints), lamina II of dorsal horn

Question 18

Opiods

Answer 18

After inflammation there is upregulation of opioid receptors (increased #) on the peripheral terminals of primary afferent fibres

Question 19

Glutamate

Answer 19

excitatory neurotransmitter, primary afferent fibres and CNS (b/x primarry afferent and dorsal horn interneuron)

Question 20

Glial cells

Answer 20

has receptors for substance P and glutamate

involved in central sensitisation

Question 21

GABA

Answer 21

CNS inhibitory cell bodies of dorsal horns

Question 22

Serotonin, norepinephrine and opiods

Answer 22

CNS inhibbitory pathways

Question 23

Spinoreticular tract

Answer 23

Is involved in the autonomic response to pain. It originates from neurons in lamina 7,8, lateral 5 and 10. Majority of cells are in upper cervical segments

Question 24

Spinomesencephallic trac

Answer 24

Can inhibit or control pain sensations, travels between spinal cord to midbrain nuclei. Cells originate from lamina 1, 4, 5 (7,10?) and project to the midbrain, PAG and nucleus cuneiformis. Has connections to lamina 1 and therefore may be influenced by central sensitisation emotion

Question 25

Thalamus

Answer 25

Processes almost all of the sensory and motor information before directing signals to other cortical areas.

Perceives, describes and localises pain

Question 26

Limbic system

Answer 26

Deals with emotion, memory and arousal

Control the emotional affective response to pain

Question 27

Anterior cingulate cortex

Answer 27

Anterior cingulate cortex is involved in the escape and avoidance of noxious stimuli

Question 28

Descending pain pathways

Answer 28

PAG and Rostro ventromedial medulla
Nocicpetive stimulation activates PAG, the n RVM, then
down to dorsal horn, release serotonin, inhibit firiin of neurosn in lamina I, II and V

Question 29

Pain adaptation theory

Answer 29

Activity of an injured/ painful muscles will be inhibied and the opposing muscle will be facilitated

Question 30

Vicious cycle theory

Answer 30

: increase in activity of muscles that are painful/move through a painful region → induced ischaemia from vascular compromise → further pain due to accumulation of metabolites.

Question 31

Hodge’s protection theory (2011

Answer 31

• Adapatation to pain inolves redistriubtion of activity within and between muscles
• Adaptation to pain changes mechanical behaviours
• Adaptation to pain leads to protection from pain, injury, or threatened pain
• Adaptation to pain involves chnages at multiple levels of the motor system
• Adaptation to pain has short term benefit but potential long term conseqences

Question 32

Sub-optimal tissue loading hypothesis

Answer 32

poor loading of tissues pre-disposes injury

Question 33

Impaired movement or motor control as a consequence of interfereance

Answer 33

Pain and injury leads to changes in motor movement
1. relfex inihition
2. inflamation,
3. chronifiation
• Direct injury to a mechanoreceptor/ tissue within which a sensory receptor lies (joint capsule) → modified afferent input → compromise the awareness of position and movement
• Nociceptive input and local chemical changes can alter muscle spindle sensitivity

Question 34

Modification of movemeent for protection

Answer 34

e.g. change of force direction, redistribtuion of activity btween muscle, decrease force amplitude

Question 35

modified movement can be explained by a conditioned association with pain

Answer 35

e.g. pavlovs dog

Question 36

Peripheral mechanisms of neuropathic pain

Answer 36

injured afferents hypothesis-, altered sodium channel expression in injured nerve fibres leads to spontaneous action potential generation at either side of the damaged nerve or in the DRG.
Intact nocicpetor hypothesis- intact nociceptors that survive injury and innervate the region subserved by the injured nerve or root are sensitised by the local degenerating nerve fibres and partly dennervated target tissues