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Pain science > neuroscience of pain and PNE > Flashcards

neuroscience of pain and PNE Flashcards

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1
Q

is avoidance a long term solution for chronic pain ?

A

no
“avoiding the fire” is not a good solution becase is may lead to disability disuse and depression
- leads to fear avoidance, fear of movement

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2
Q

according to the cartesian model, what does putting out the fire mean?

A

dealing with pain by meds or injections

  • not a good way to mgmt chronic pain
  • docs try to find the pain generator and deal with it
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3
Q

what is the gate control theory ?

A

small nerve fibers will convey pain to an inhibitory neurons via the spinothalamic tract. When large nerve fibers are activated, the stimulate an inhibitory neuron that which “closes the gait” and pain is not percieved by the brain.
- large fibers are activated by pressure: massage, walking it off, rubbing

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4
Q

what are limitations of the gate theory ?

A

cant explain:

  • phantom limb pain
  • complete SC injuries
  • complex immune and inflamatry conditions
  • emotion/ physcosocail factors with pain
  • only shows that pain can go to the brain, and does not show what endogenous mechanisms can do
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5
Q

what are input mechanisms ?

A

various forms if info sent to SC and brain to be processed

includes: info form tissues (nociception)enviromental influces and peripheral nervous system (outside of dorsal horn)

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6
Q

what are processing mechanisms ?

A

stxs and processes in the CNS that analyze inputs

  • processing mechanisms include processing sensory, cognitive, and emotional aspects
  • place value on input information which leads to a conclusion about the recived info
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7
Q

what are output mechanisms ?

A

a response to a input and the brain interpretation

  • driven by survival instincts and not pain experince
  • pain, action programs and stree regulation are outputs
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8
Q

are A-delta and C-fibers pain fibers?

A

Yes, but they really shoudl be thought of as “nociceptive fibers” because if they were truly pain fibers, then everytime they were stimulated/ damaged we would experince pain

  • this isnt the case
  • damaged fibers with a sprained ankle and the associated pain quickly dissapear if your life is in danger (about to be hit by a bus).
  • if they were truly pain fibers, there would always be pain no matter what
  • this shows that pain is a construct of the brain
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9
Q

what kinds of stimuli can cause an action potential

A

not just pain

receptors responds to mechanical, thermal or chemical stimulation

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10
Q

what determines what ion channels are on axons and in which amount?

A

genetic coding

brains guess at what is important for survival

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11
Q

what is the link btwn ion channels and pain perception

A

the opening/ activation of receptor specific ion channels can be activated with nociception channels
mechanical, thermal, chemical

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12
Q

what can cause demylination and what is the consequnce

A

mechanical, immune or chemical process can strip mylin off a nerve

  • these allows for ion channels to deposit themselves in these newly “created” spaces
  • chemicals like inflammatory mediators can strip mylin, disease (MS) or trauma can demyliante too
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13
Q

how can an axon generate an impulse ?

A

abnormal concentration of ion channels in axonlema can generate an AP

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14
Q

is pain an input or an output

A

multiple system output

- pain is a perception

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15
Q

when is the nueral signature activated ?

A

whenever the brain perceives a threat

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16
Q

what are input types of tissues?

A

mechanical. cheical and thermal

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17
Q

what can retrograda firing cause

A

retrograde firring = antidromic

- results in increased inflammation, swelling and immune responses

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18
Q

What anatomical part does info enter the spine?

A

dorsal horn

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19
Q

how does frequent firring of c-fibers effect the dorsal horn ?

A

destroys internueron due to increase of amino acids

  • therfore, the gatekeeper of info is gone and Bombardment of C-fiber activity into the CNS dorsal horn resulting in permanent changes over time
  • excess info enters
  • essence of centralization; light touch can cause pain
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20
Q

Decreased endogenous mechanisms = _____

A

Increased sensitization/pain experience

  • normally our brain is “wet” and can calm pain down with good chemicals like endogneous opiods, enkphalins, serotonin ect
  • this mechanism dries up. The brain wants us to recognize pain as a protective mechanism and takes away wetness
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21
Q

How does the brain process info?

A

memories activate several parts of the brain; vision, emotion, moves, memory, smell,

“grandma”

22
Q

what is the pain neural signature?

A

common areas that are frequently ignited
- areas are ignited via connections, backfiring neurons, and
neurotransmitters, pain is perceived

23
Q

what does the PREMOTOR/ MOTOR CORTex do ?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

  • organize and prepare movements
  • PT cant do pelvic tilt
24
Q

WHAT DOES THE 2. CINGULATE CORTEX DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

  • concentration, focusing
  • pt in a fog
25
Q

WHAT DOES THE PREFRONTAL CORTEX DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

-problem solving, memory

26
Q

WHAT DOES THE AMYGDALA DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

-fear, fear conditioning, addiction

27
Q

WHAT DOES THE SENSORY CORTEX DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

-sensory discrimination

28
Q

WHAT DOES THE HYPOTHALAMUS/ THALAMUS DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE
-stress responses, autonomic regulation,
motivation
- affects our sleep, hot flashes, the way food tastes

29
Q

WHAT DOES THE CEREBELLUM DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE

-movement and cognition

30
Q

WHAT DOES THE HIPPOCAMPUS DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE
-memory, spacial recognition, fear
conditioning

31
Q

WHAT DOES THE SPINAL CORD DO?

A

involved in TYPICAL PAIN NEURAL SIGNATURE
-SPINAL CORD
gating from the periphery

32
Q

when we have pain, a “map” is formed in our brain, why

A

interaction of areas of brain that are ignited (synaptic modulation) that are specific to individual and the interaction of belifs, knowledge, socail context, anticipated consequences, sensory cues and physical therapy

33
Q

Why is my pain not the same as your pain ?

A

interaction of areas of brain that are ignited (synaptic modulation) that are specific to individual and the interaction of belifs, knowledge, socail context, anticipated consequences, sensory cues and physical therapy

34
Q

how does the brain respond to facilitation of neural adaptation ?

A

The brain asks “how dangerous is this” and brain responds by saying:
“this is dangerous, more info please”
- then neural adaptation occurs

35
Q

how does the brain respond to inhibition ?

A

The brain asks “how dangerous is this” and brain responds by saying :
this isnt dangerous
- then engogenous things occur

36
Q

How do we react to facilitation of neural adaptation ?

A

Homeostatic shift for survival

- increased levels of Adrenaline and cortisol

37
Q

increased levels of cortisol will cause:

A 
issues with tissue and brain, commonly seen in chronic disorders:
Tissues
• Sore
• Tired
• Sensitive
• Fatigued
 Brain
• Memory
• Sleep
• Concentration
• Blood pressure
• Reproduction

persistent pain, sensitivity, inflammation

38
Q

in a nut shell, what is a the roadmap for how can we use PNE to decrease fear

A 
Pain neuroscience education
>
Reconceptualization of ‘pain’
>
Reduced threat value of pain
>
Less fear
39
Q

how does stress effect the pain matrix

A

stress effects excitatory synapses in the brain
- stress will increase cortisol and noradrenaline in the brain
-increase excitatory synapses in hippocampus,
amygdala, prefrontal cortex

40
Q

what is Central sensitization?

A

s increased synaptic efficiency /

excitatory synapses ~ learning / memory (hippocampus)

41
Q

can mindfulness, meditation & Schultz relaxation decrease pain?

A

yes, by altering the pain matrix

42
Q

Besides mindfulness, how else can we decrease activity of the pain matrix?

A

walk more, increase activity

- achieve a cognitive change to get pts to move. Pt is prolly afraid to move which can lead to isolation and disability

43
Q

what are 2 methoods of contingency for changing the perspective of pain?

A

• Pain contingent
• “I stop gardening once the pain gets worse”
• “Please say when the exercise hurts, then we will adapt the
exercise accordingly”
• Time contingent
• “I garden for 20 minutes. That we have agreed. If after 20 minutes I
feel that I can still continue, I stop anyway. If the pain worsens
after 15 minutes, I continue anyway.”

44
Q

what are considerations for exercise for someone with central sensitization?

A
  • get an idea of what baseline is
  • set goals
  • be careful with isometric and eccentric exercises
  • pace activities
45
Q

overall, what does a tx program include for someoen with chronic pain

A 
1 PNE 
2 stress mgmt 
3 activity self mgmt (baseline)
4 grading
5. recovery
46
Q

What is long term potentiation

A
  • LTP in part regulated by cortisol & noradrenaline in the brain
    (stress!)
  • pain can create memories that cause central and peripheral effects
  • results in, for example, revisiting a place or going into a certain position, re-experincing that pain, maybe even after 10 years!
47
Q

What roel does anger play in PNE?

A

Perceived injustice, anger & chronic pain.

  • anger can trigger chemical which can effect pn nuero matirx
  • prefrontal cortex and amygala have to do with memory of fear and safety
48
Q

How can you redirect a patient who anticipates pain with activity/movement

A
  • challenge pain
  • challenge thoughts
  • “whats the worst that could happen” then rationalize it
  • combat fear with graded exposure, watching, thinking doing activity.
49
Q

what is Desensitization?

A
  • Retraining pain memories
  • Desensitization by exposure
  • Repeated exposure generates a new memory for safety
50
Q

how do you retrain the memory

A

• What kind of movements will damage your
back? Please indicate the threat value on a scale ranging from 0 to
100.
• Thorough questioning of perceptions about these movements:
anticipated body response etc.
• Discussion of movements’ perceptions – challenge the patient’s
cognitions prior to executing the movement / exercise

51
Q

Treatment of central sensitization pain:

take home messages

A

Pain neuroscience education is the first (effective) step
• Long-term stress accelerates the mechanism of central
sensitization: stress management is often a cardinal part of
treatment
• Graded activity & exercise therapy should account for cognitive emotional sensitization
• Exercise therapy implies desensitization by retraining pain

Pain science (4 decks)

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