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MSK CAT > pain > Flashcards

pain Flashcards

1
Q

nociceptive pain

A

Pain from actual or threatened damage to non-neural issue - due to the activation of nociceptors

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2
Q

Nociplastic Pain

A

Pain that from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.

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3
Q

Neuropathic Pain

A

Pain caused by a lesion or disease of the somatosensory nervous system

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4
Q

Acute Pain

A

Pain that is temporarily related to injury and that resolves during the appropriate healing period. It is usually short-lived.

  • Easily described- sharp, stinging, pulling
  • Specific location
  • Specific aggravating and easing factors
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5
Q

Chronic Pain

A

Chronic pain is any pain that lasts beyond the expected period of healing or exists for more than three months.

  • Difficult to describe
  • May move locations
  • Difficult to pin point things that make it better and worse
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6
Q

maladaptive

A

serves no purpose
becomes a limiter to someones life

pain catastophising - pain related fear- hypervigilance avoidance - disuse, depression, disability

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7
Q

does pain reflect the state of the tissues?

A

the more acute the more likely pain experienced is a reflection of their tissues

chronic pain is more likely to not be a result of the tissues

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8
Q

noxious stimuli

A

Events that damage or threaten to damage tissues and that activate specialised sensory nerve endings called nociceptors.
Stimuli adequate to activate nociceptors are not the same for all tissues.

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9
Q

pheriphery- detectors- sensory

A

SKIN- Thermal, mechanical and chemical

JOINTS- Mechanical -rotation/torque beyond the joint’s normal range of motion and chemical

MUSCLES- Mechanical -blunt force, stretching, crushing and overuse and chemical

VISCERAL SYSTEM- Mechanical (distension, traction on the mesentery) and chemical (released from inflamed or ischemic organs, inhaled irritants).

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10
Q

brainstem

Rostral ventromedial medulla (RVM)

A

in the brainstem determines whether nociceptive information is prioritised in the dorsal horn of the spinal cord.

It can enhance nociception following injury but failure to resolve after tissue healing can lead to chronic pain ‘locked in’.

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11
Q

brainstem

Descending modulatory system

A

Antinociceptive (Good cop)
* Norepinephrine, serotonin

Pronociceptive (Bad cop)

A genetically driven imbalance in the antinociceptive and pronociceptive activity within the RVM probably involving 5-hydroxytryptaminergic and norepinephrinergic mechanisms may represent a possible pain endophenotype

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12
Q

Distraction

A

using a cognitive task, high working memory load (HWML) Vs low working memory load.

HWML showed significant less activity at the spinal cord and significantly less pain. (Sprenger et al 2012)

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13
Q

networks that link sensors to the hub, brain to the periphery

A

brain stem
spinal cord
centeral sensitisation

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14
Q

nociceptors

activation spinal cord

A

Nociceptors are continuously active in our everyday behavior (subconsciously and consciously) as a way of protecting us.

Activation must reach a threshold to travel to the brain and be interpreted as pain. This threshold may be equated to the “pain control theory” melzack & wall 1965

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15
Q

2

Central Sensitisation

A

Where nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways.’ (Woolf 2011 p1)

Seen in the short-term with tissue damage (hyperalgesia) and in the long-term with chronic pain conditions (Woolf and Salter 2000).

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16
Q

7

what info is added at the brain (hub)

A
  1. Past experience (Memory)
  2. Personality
  3. Beliefs
  4. Attention
  5. Fear/Worry
  6. Mood
  7. Thoughts
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17
Q

2

Neuromatrix Theory

A

Pain is a multi dimensional experience produced by a characteristic “neurosigniture” patterns of nerve impulses generated by a widely distributed neural network “neuromatrix” within the brain.

They can be triggered by sensory inputs but can be generated independently of them (Melzack 2005)

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18
Q

Protectometer
SIMS

A
  • SAFETY messages in me SIMs (DOWN- desensitise)
  • Supportive family and friends, useful knowledge, fitness and mobility, hope, positive attitude/expectation, positive past experience, resilience, acceptance, healthy and balanced diet, love and friendship.
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19
Q

Protectometer
DIMS

A
  • DANGER message in me DIMs (UP- sensitise)
  • Low expectation, poor sleep, reducing movement and activity, negative attitude, worry, perceived injustice, bad past experiences, no hope, fear, low mood, lack of support, lack of knowledge or incorrect messages, loss of identify or role (job, family role), poor health of tissues, poor diet, loneliness and isolation
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20
Q

neurosigniture 1
Pain perception

A

needs to be routine activation often bilaterally of
* Primary and secondary somatosensory cortices
* The posterior, mid and anterior insula
* Anterior cingulate
* Pre frontal cortices

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21
Q

neurosigniture 2
Activation of subcortical areas such as

A
  • Hypothalamus
  • Amygdala
  • Hippocampus
  • cerebellum
22
Q

neurosigniture 3

A

COGNITIVE, EMOTIONAL AND CONTEXTUAL INFLUENCE

23
Q

neurosigniture 4
pain experience

A

PAIN EXPERIENCE – ‘Cerebral Signature’ of pain that is bespoke for an individual and requires activity within multiple brain regions

24
Q

insula cortex

A

INSULA CORTEX is the most consistently activated region during painful experiences (Tracey 2011).

25
Q

pain gate theory by melzack and wall (1965)

A
  • non-painful input closes the nerve gate to painful input
  • and prevents pain sensation from reaching the CNS.
26
Q

6

Descending pain inhibition

A
  1. The non-nociceptive myelin neurones pass up and connect to the somatosensory cortex of the brain.
  2. The SSC stimulates neurones in the periaqueductal gray area of the mid brain
  3. which stimulates cells in the medulla, such as the nucleus raphe magnus.
  4. Pain is then supressed through the release of serotonin and nor-adrenalin,
  5. this stimulates the inhibitory neurone in the posterior horn
  6. and blocks ascending pain impulses
27
Q

types of pain

A
  1. somatic superficial - skin - sharp fast pain - localised brief
  2. somatic deep - deep layers of skin/ muscles - burning aching slow pain- diffuse long lasting
  3. visceral - caused by lack of o2, inflammation - organs - dull ache slow pain - can cause nausea sweating/reffered
28
Q

detection of pain

A
  1. free nerve endings register damage
  2. 1st order neurons synapse with 2nd order neurons
29
Q

2 main nerve fibre types

A

Aδ fibre
1. mechanical - sharp pricking, fast pain
2. thermal and mechanothermal - slow burning, cold sharp, pricking

B fibre
polymodal - hot and burning sensation, cold, slow deep pain

30
Q

differences between peripheral and centeral sensitisation

A

peripheral
* substance P feedback loop
* presynaptic 1st order neurons sensitised

centeral sensitisation
* post synaptic neurons 2nd order sensory neurons sensitised
* many other factors involved in spinal hyperactivity

31
Q

how does info ascend the spine

A

spinothalamic tract decusses

32
Q

Sensory pathways

A

lead into the spinal cord then up the spinal cord through the brain stem up into the brain.

33
Q

Motor pathways

A

bundles of axons in a consecutive array of neurons creating a pathway of motor information to move in the other direction

34
Q

concious vs unconcious sensory receptors

A

Conscious: reach cerebral cortex
* Conciously aware of things that arrive at the somatosensory cortex

Unconscious: does not reach cerebral cortex
* Proprioceptive information goes to brain stem, cerebellum ect.

35
Q

1st, 2nd, 3rd order neurons

A
  1. First order neuron
    ○ Sensory cell body in dorsal route ganglion
  2. Second order neuron
    ○ Cell body in dorsal horn or brain stem
  3. Third order neuron
    ○ Cell body in the thalamus projecting to the somatosensory cortex
36
Q

sensory homunculous where is it found

A
  1. Somatosensory cortex
  2. Post-central gyrus
  3. Parietal lobe
37
Q

sensory homunculous what is it?

A

a map along the cerebral cortex of where each part of the body is processed

38
Q

LHS spinal cord injury - sensation loss?

A

(If the spinal cord injury is LHS, the loss of sense would be felt on the RHS due to the cross/dessecation)

39
Q

spinothalamic

A

info
* pain, temp, touch, pressure

2nd neuron crossover point
* spinal cord

projection to somatosensory cortex?
* yes

effect of injury in spinal cord
* loss of function opposite side

40
Q

dorsal column

A

info
* fine touch, vibration, concious proprio

2nd neuron crossover point
* medulla

projection to somatosensory cortex?
* yes

effect of injury in spinal cord
* loss of function same side

41
Q

spinocerebellar

A

info
* unconcious proprio

2nd neuron crossover point
* it doesnt

projection to somatosensory cortex?
* no

effect of injury in spinal cord
* loss of function

42
Q

concious

A

pyramidal - direct

43
Q

unconcious

A

extrapyramidal - indirect

44
Q

pyramidal motor pathway

A
  1. Interneurons at spinal level but upper neurons project down the spine and control motor neurons at the spinal level
    • Direct
    • Conscious
45
Q

extrapyrimidal

A

Extrapyramidal
1. Upper motor neurons are in the brain stems nuclei no (higher control aswell)
2. No well defined direct connection from motor cortex to lower motor neurons
* Indirect
* Mostly subconscious

46
Q

pyramidal direct pathway

A
  1. UMN- cortical cell body of the motor cortex (some will decussate and descend the spine)
  2. Often an interneuron
  3. Lower motor neuron- sends info out through the ventral root
47
Q
A

Extrapyramidal pathways unconscious
- Modifies movements: Modulatory actions on LMN

  • Rubrospinal- fine motor control upper limb
    - the start of the tract are in the red nucleus in the brain
  • Tectospinal- control neck muscles, head&eye coordination, visual/auditory feedback
  • Vestibulospinal- balance
  • Reticulospinal- motor functions, autonomic functions, pain modulation
48
Q

6

pain gate

A
  • Neural gate (spinal cord level – Substantia gelatinosa) modifies pain perception
  • Gate receives input from Peripheral nerve fibres
  • Descending central influences from the brain mediated by behavioural state (attention), emotional state (anxiety), past experiences and self-efficacy
  • Large and small fibres
  • Output from the gate sends information to an action system resulting in pain perception
  • The more the gate is open, the greater perception of pain
49
Q

3

factors responsible for opening the gate

A
  1. Physical factors (injury, activation of large fibres)
  2. Emotional factors (anxiety, worry, tension, depression
  3. Behavioural factors (focus on pain, boredom)
50
Q

3

Factors Responsible for closing the gate

A
  1. Physical factors (medication, stimulation of small fibres)
  2. Emotional factors (positive mood - happiness, optimism, relaxation)
  3. Behavioural factors (distraction, engagement in other activities)

MSK CAT (14 decks)

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