Chronic Pain 1 and 2

Question 1

What is pain?

Answer 1

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

Pain does not have to be associated with observable tissue damage or have a detectable underlying cause

Question 2

What is VOMIT

Answer 2

victim of medical imaging technology

happens when physicians (or others) anchor onto pain only being associated with actual tissue damage, but it is important to keep in mind that someone can be in pain with even just the potential of tissue damage (so imaging wouldn’t necessarily show it)

Question 3

Pain - danger

Answer 3

We are protected by neurophysiologic alarm system - pain can be seen as body’s alarm system to alert us of danger – it is a necessary and protective thing

Brain decides “how dangerous is this really” – how dangerous it is and what action needs to be taken - takes lots of factors into consideration

Question 4

Acute vs. Chronic pain - ACUTE

Answer 4

Direct result of tissue damage or potential tissue damage (injury/trauma or surgery)
Protective function

Question 5

Acute vs. Chronic pain - CHRONIC

Answer 5

Pain that lasts longer than normal tissue healing time
Impairment is greater than expected from physical findings or injury
Debatable that chronic pain is solely based on a time frame - is more about that it is longer than what you would expect based on specific injury

Question 6

Hyperalgesia

Answer 6

Increased pain sensitivity (more internal – like turning head)

Question 7

Allodynia

Answer 7

Painful response to a non-nociceptive stimulus (typically external)

Question 8

Nociception

Answer 8

The neural process of encoding and processing noxious stimuli

Question 9

Theoretical concepts - Specificity theory

Answer 9

Separate nerve endings for each sensory experience (touch, heat, cold, pain)
Often what patients think when they come in to see you – this is incorrect and incomplete though! We do NOT have separate nerve endings for each sensory input

Question 10

Theoretical concepts - Gate control

Answer 10

There is gating at the level of the spinal cord – this contributed to our understanding of pain that there is some regulation that happens at periphery and level of spinal cord and that decides what goes to brain to be determined as a sensory experience

Question 11

Theoretical concepts - Neuromatrix

Answer 11

Network of neurons that integrates the thalamus, cortex, and limbic system
Sculpted by sensory input
Neurosignature - unique

Question 12

Theoretical concepts - Neuromatrix - 3 main inputs

Answer 12

Cognitive-evaluative (past experiences, personality variables)
Sensory-discriminative (visceral, somatic, trigger points)
Motivational-affective (endocrine, immune systems)

Question 13

Theoretical concepts - Neuromatrix - 3 main outputs

Answer 13

Pain perception (all 3 inputs)
Action programs - could be tension for ex (coping strategy)
Stress regulation programs (hormone release)

Question 14

Theoretical concepts - mature organism model

Answer 14

A model designed to help explain pain to patients

Issues in the tissues – might be real or might be perceived
Provides input into the spinal cord
Brain needs to scrutinize and decide with this perception, assessing input and providing an output - will incorporate past experiences that will impact input and offer value to how they perceive the pain - get different output based on cognitive and affective domains

Cognitive - pain perception + altered thoughts
Affective - pain perception + altered feelings

Question 15

Theoretical concepts - Predictive coding

Answer 15

Recent theory that is a small conceptual shift in the mature organism model\
Mismatches between the brains predictions and sensory inputs leads to remodeling of the brains predictive outputs
Top down before bottom up

Question 16

Pain management models - Biomedical

Answer 16

Idea that based on pathology we can correlate the level of symptoms and stuff
This model does not account for discrepancies we see in tissue injury and tissue pathology and the actual symptoms

Question 17

Pain management models - biopsychosocial

Answer 17

Biological
Psychological
Social

Question 18

Pain management models - ICF

Answer 18

Not only talks about their health condition (disease, disorder – body functions and structure – activity – participation), but it also says that all of these things are dependent on contextual factors (like we said earlier, the neurosignature is dependent on contextual factors) – such as environmental factors and personal factors as well

Question 19

Nocipceptive pain

Answer 19

Non neural tissues
Pain diminishes according to natural healing process
Pain is localized

Question 20

Neuropathic pain

Answer 20

Peripheral
Injury to nervous tissue
hx of lesion or disease of the nervous system or posttraumatic/postsurgical damage to the nervous system
Related to a medical or systemic cause such as stroke, herpes, diabetes, or some form of neurodegenerative disease

Question 21

Non neuropathic central sensitization pain

Answer 21

NEUROANATOMICAL and ILLOGICAL – DOES NOT MAKE SENSE WITH WHAT WE KNOW PATHO-ANATOMICALLY

No hx of lesion, damage, or disease of NS
Pain disproportionate to nature and extent of injury or pathology

Question 22

Sensitization

Answer 22

increased responsiveness of neurons to their normal input or recruitment of a response to normally subthreshold inputs

Question 23

Central sensitization

Answer 23

increased responsiveness of nociceptive neurons in the central nervous system to their normal subthreshold afferent input

Question 24

Peripheral sensitization

Answer 24

increased responsiveness and reduced threshold of nociceptors to stimulation of their receptive fields

Question 25

Sensitization - development of chronic pain (chronification)

Answer 25

Biological - persistent acute pain is big risk factor
Psychological - emotional state, neuroticism, emotional state
Social - support

Question 26

Sensitzation - Neuroplasticity

Answer 26

Physical remodeling of neuronal cytoarchitechture

Does not know the difference between positive and negative change – good for people who have had a stroke, but can be bad for people who go from acute to chronic pain because of the neuroplasticity ability

Question 27

Sensitization - peripheral mechanisms that contribute to chronic pain

Answer 27

Fibers/sensors
NTs/receptors
Non neuronal activitors/inflammatory mediators
Ion channels

Question 28

Sensitization - peripheral mechanisms that contribute to chronic pain - fibers

Answer 28

A beta (low threshold, pressure, vibration, mechanoreceptors)
A gamma (high and low threshold, mechanoreceptors, nociceptors (high)) 
C fibers (high threshold, mechanoreceptors, thermoreceptors, nociceptors)

Question 29

Sensitization - peripheral mechanisms that contribute to chronic pain - sensors

Answer 29

Mechanical, thermal, chemical/acid/ischemia (NO PAIN SENSORS)

Rate of sensory turnover is 2-3 days! This is empowering to teach pts

Question 30

Sensitization - peripheral mechanisms that contribute to chronic pain - NTs/Receptors

Answer 30

Persistence in the increase of NTs including cytokines which are part of the immune system – link between immune system and nervous system
inflammatory mediators hanging on way too long and in too big of quantity

Question 31

Sensitization - peripheral mechanisms that contribute to chronic pain - ion channels

Answer 31

Increased number of channels
Change in distribution (greater number of channels sensitive to thermal stim)
Spontaneous activity

Question 32

Sensitization - central mechanisms that contribute to chronic pain

Answer 32

Neurogenic inflammation 
Inappropriate synapsing
Expansion of receptive field 
Decrease in endogenous mechanisms
Spinal cord wind up 
Nonneuronal activators/inflammatory mediators

Question 33

Sensitization - central mechanisms that contribute to chronic pain - neurogenic inflammation

Answer 33

Neuroimmune response - blurred lines between immune and neurologic response to nociception

Question 34

Sensitization - central mechanisms that contribute to chronic pain - expansion of receptive field

Answer 34

Multiple inputs from receptive field to the same secondary neuron – with sensitization this secondary neuron becomes influenced by additional primary neurons

Question 35

Sensitization - central mechanisms that contribute to chronic pain - Dec in endogenous mechanisms

Answer 35

Opioids (endorphin, encephalin), 5HT, DA – less descending inhibition that would normally reduce intensity of CNS

Question 36

Sensitization - central mechanisms that contribute to chronic pain - spinal cord wind up

Answer 36

spinal cord adapts and magnifies tissue reality – can magnify things coming in from the periphery

Question 37

Sensitization - central mechanisms that contribute to chronic pain - Nonneuronal activators/inflammatory mediators

Answer 37

Glial cells!
Glial activation leads to cytokine activation - cytokines have immune function - more cytokines - more sensitivity to pain
Increased glial activity with stress

Question 38

Chronic pain and the brain - orchestra of the brain

Answer 38

Pain signature/neurotag
Thoughts/beliefs are impulses too
Conversation with the brain

Question 39

Chronic pain and the brain - cortical representation and smudging

Answer 39

Spreading of pain, inaccurate body image and inaccurate body movement/posture
Mapping is distorted and converges on other ideas - so central can contribute to spreading too (along with peripheral)

Smudging - cortical reorganzation - ex of ES and mult merged