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Dr. Worst Exam 1 > Chronic Pain & Central Sensitization > Flashcards

Chronic Pain & Central Sensitization Flashcards

1
Q

Number of people worldwide who suffer from chronic pain.

A

More than 1.5 billion

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2
Q

Hours of productive time workers lose on average due to a pain condition

A

4.6 hours

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3
Q

International Association on the Study of Pain defines pain as:

(plus 3 things about pain)

A

“An unpleasant sensory and emotional experience which follows actual or potential tissue damage or is described in terms of such damage.”

■ Pain is complex and poorly understood.

■ Physical pain is equal to emotional pain

■Threat or potential for injury can cause pain

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4
Q

Moseley defines pain as:

A

“A multiple system output that is activated by an individual’s specific neural signature. This neural signature is activated whenever the person perceives a threat.”

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5
Q

Pain is the end result of

A

Central processing of sensory stimuli.

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6
Q

Description of Chronic pain:

A

Pain that persists for more than 3 months or pain that persists after the ‘usual’ time for tissue healing or pain in the absence of obvious nociception.”

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7
Q

4 types of acute pain: FINN

A
  • Functional
  • Inflammatory
  • Nociceptive
  • Neuropathic

All 4 types of pain typically contribute to chronic pain syndromes.

Peripheral or central sensitization

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8
Q

Mechanism of Pain: Neuroplasticity- How does a chronic pain state develop?

A

Peripheral Sensitization

  • Injury causes release of “sensitizing soup”
  • Reduction in threshold and increase response of nocioceptors

Central Sentisization

  • Membrane excitability, synaptic recruitment and decreased inhibition.
  • Uncoupling of pain from peripheral stimuli
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9
Q

2 ways that the brain controls pain

A
  • Facilitatory System- “Accelerator”
  • Inhibitory System

“Brake”

Malfunctioning in people with chronic pain

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10
Q

How is pain processed by the brain? (5)

A
  • Entire brain is active during pain- No specific “pain areas”
  • Brain has a particular “Pain Map” that occurs regardless of the specific tissues injured
  • “Smudging” in the cortex with distorted pain maps
  • A representation of pain can be caused in the brain by anticipating pain or giving the illusion of pain- Distraction or anxiety can contribute
  • Emotional Pain uses similar brain areas to physical pain- Why we use a Biopsychosocial approach to pain
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11
Q

When does sensitization occur?

A

after repeated or intense noxious stimulus

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12
Q

Sensitization Lowers threshold for activation. True / False

A

True

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13
Q

Types of Sensitization

A

Peripheral

  • Increased responsiveness nociceptors

Central

  • Changes to the synaptic transmission to the spinal cord
  • With or without real tissue damage
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14
Q

Sensitization Produces: ASH

A
  • Allyodynia- Pain produced by a normally innocuous stimuli
  • Hyperalgesia or hypersensitization- Exaggerated and prolonged response
  • Secondary Hyperalgesia- Spread beyond site of stimulation or injury. Also known as “referred pain”
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15
Q

Allyodynia

A

Pain produced by a normally innocuous stimuli

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16
Q

Hyperalgesia or hypersensitization

A

Exaggerated and prolonged response

17
Q

Secondary Hyperalgesia

A

Spread beyond site of stimulation or injury. Also known as “referred pain”

18
Q

Mechanisms of peripheral sensitization

(4-5ish)

A

Brief (lasting days) muscle hyperalgesia

  • Induced after eccentric exercise
  • Soreness after 1-2 days (DOMS)
  • Occurs at different sites among subjects
  • Model for hyperalgesic trigger points in MPS
19
Q

Central Sensitization (4)

A
  • Amplification of response
  • Novel inputs to nociceptive pathways- Actives A-beta large low-threshold mechanoreceptor pathways
  • Pain in non-inflamed tissues- Central pain in absence of peripheral injury
  • Functional shift- High threshold mechanoreceptors now respond to low threshold inp
20
Q

Conceptual framework for Understanding pain in the Human:

A

Inputs to body-self matrix from:

  • Cognitive-relatied brain areas- memories from past experiences, attention, meaning & anxiety
  • Sensory signalling systems- Cutaneous, Visceral & MSK inputs
  • Emotion-related brain areas- Limbic system and associated homeostatic/stress mechanisms

Outputs to brain areas that produce:

  • Pain perception- Sensory, Affective & Cognitive dimensions
  • Action programs- Involuntary & voluntary action patterns
  • Stress-regulation programs- Cortisol, Noradrenalin, and endorphin levels immune system activity
21
Q

Facts about sensitization (6)

A
  1. Occurs after repeated or intense noxious stimulus
  2. Lowers threshold for activation
  3. Amplifies subsequent inputs
  4. Nervous system adapts and becomes over effective where anything can cause a big reaction
  5. Adaptive
  6. Hyperalert to potentially damaging conditions

NO LONGER ABOUT PROTECTION!

22
Q

What happens during normal sensation?

A
23
Q

Central sensitization? Receptive Field Expansion

A
  • Sleeping neurons become activated
  • Over efficiency of all neurons

Conclusion

  • Somatosensory Neuron Receptive Fields are Malleable (Plastic)
  • Plasticity is the basis for the effects of central sensitization
24
Q

Mechanisms of Central Sensitization: SIR

A

ENHANCEMENT

Synaptic efficacy

  • Neuronal plasticity
  • Nervous system becomes too efficient and responds to things it normally doesn’t respond

Increase in membrane excitability at the dorsal horn

Reduced inhibition of descending system

  • Periaquaductal grey matter doesn’t inhibit pain as it should (Blocks unnecessary information & If not working, all information ends up in cortex)
  • Some studies show PAG is smaller in individuals with chronic pain- Also linked with depression in chronic pain
25
Q

Changes that occur in the brain from sensitization

(2 things they do)

A

● Decrease in grey matter

● Impaired motor control of spinal muscles

26
Q

What is the basis for the effects of central sensitization?

A

Plasticity

27
Q

Effect of central sensitization on dorsal horn neurons in SC (4)

A
  • Lowered threshold of activity
  • Increased response to stimulation
  • Increase in spontaneous activity
  • Enlargement of receptive field
28
Q

Central Sensitization- Activity Dependent

(how does it happen?)

A

Induction by c-nociceptor

  • Tissue injury is not necessary
  • Noxious stimulus is:

Sustained

Intense

Repeated

29
Q

Key points about chronic pain with patients (3)

A
  • You can have tissue damage with no pain, and vice versa: you can have no damage, yet still have pain!
  • Chronic Pain’, is pain that persists even after tissue damage has had plenty of time to heal (about 3-6 months).
  • There are many factors that contribute to your perception of pain. Biological, psychological, social & cultural
30
Q

Degeneration doesn’t mean pain

Explain (2 points)

A
  • Just because you have pain, it doesn’t mean there is any significant damage or degeneration occurring in your body.
  • Learning this can be very relieving for people who are afraid they might have a serious problem.
31
Q

Strengthening vs. Conditioning- results from study

regarding pain

A
  • Strengthening group initially had increased pain, but after 5 weeks of strength training, had the greatest decrease in pain
  • Conditioning group reported decreased pain while performing aerobic exercise, but then pain increased for 2 hours, then returned to baseline.
  • However, after 5 weeks of conditioning, there was no increase in pain afterwards.
32
Q

Chronic neck pain- Results from study

(3points)

A
  • Poor cervical extensor endurance was related to the development of chronic neck pain
  • Weakness and fatigue caused increased metabolites to travel to the brain, contributing to development of chronic pain
  • At baseline, patients had impaired ability to block nocioceptive input and tended to have higher depression and anxiety
33
Q

Risk factors for progression from acute to chronic pain- study results

3

A
  • Sedentary behavior was the 4th greatest risk factor for chronic pain
  • Only 40% of primary care physicians meet the U.S. minimum standard for physical activity
  • Exercise can target both central and peripheral triggers by affecting the nocioceptive inhibition and targeting depression

Dr. Worst Exam 1 (5 decks)

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