Pain Flashcards

1
Q

Gate Control Theory

A

Pain is the product of imbalance of small and large fiber input

Combination of:
-central control system (ascending) +
-processing (descending) control of sensory input

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2
Q

Neuromatrix Thoery of Pain

A

-Brain and spinal cord producers of pain (not tissue damage)

-CNS parts work together to produce pain

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3
Q

Neuromatrix Theory inputs

A

Cognitive:
-tonic input from brain (ie. cultural learning, past experience)
-panic input from brain (ie. expectation, anxiety, depression)

Sensory:
-phasic cutaneous sensory input
-tonic somatic input (ie. trigger points,deformity)
-visceral input (visual/vestibular)

Motivational-Affective:
-hypothalamic pituitary adrenal system
-noradrenaline sympathetic system
-immune system
-cytokines
-opiates

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4
Q

Neuromatrix Theory Outputs

A

Pain Perception:
-cognitive
-sensory
-motivational

Action Programs:
-involuntary
-voluntary
-social communication
-coping strategies

Stress-Regulation Program:
-cortisol
-NE
-cytokines
-immune system
-endorphins

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5
Q

Neuromatrix View of Pain (equation)

A

Nociception + threat = pain

-sometimes threat alone can cause pain
-focus on reducing the threat

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6
Q

Fear Avoiding Model

A

Perception of threat effects pain perception leading to positive or negative affects (fear/avoidance)

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7
Q

Pain Catastrophizing

A

Explain pain experience in exaggeration
Increases pain thru altered attention, anticipation, and emotional response

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8
Q

Stress Response to Pain

A

Receive sensory stimuli

Amygdala processes stimuli and perceives as stressful (w/ hippocampus -memories)

Long Term Response:
-signal pituitary -> adrenocorticotrophic hormone -> stimulate adrenal cortex -> cortisol -> maintain blood sugar thru stress response

Short Term Response:
-signal adrenal medulla -> NE/E released

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9
Q

Chronic stress

A

Negative feedback loop:
-Cortisol inhibits hypothalamus and pituitary

-Eventually lowers cortisol level which inhibits ability to control inflammation (immunosuppression)

-reduced BDNF in brain (repair and make new neurons)

-decreased function/size of hippocampus (mood/memory)

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10
Q

Effects of Sleep on Pain

A

Impairments stronger predictor of pain than vice versa

Dysregulation of endogenous opioids

Restorative/reparative function decreases (BDNF)

Memory consolidation

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11
Q

Cortical Changes (Homunculus) in Response to Pain

A

Size changes: body part representation grows

Laterality Recognition: difficult differentiating R/L

Smudge: representation blurs b/w parts in cortex; hard to tell borders of pain/sensation

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12
Q

Nociceptive pain dominant (cause and presentation)

A

Causes:
-stimulation of peripheral nociceptive fibers
-chemical, mechanical, thermal noxious stimulus

Presentation:
-pain localized and proportionate to injury
-response to aggravating/alleviating predictable
-intermittent/sharp w/ movement/provocation
-constant/dull ache at rest

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13
Q

Peripheral Neuropathic Pain Dominant (cause and presentation)

A

Cause:
-altered structure and function of peripheral nerve

Presentation:
-referred in dermatomal or cutaneous distribution
-provocation w/ tests that load neural tissue

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14
Q

Nociplastic/Central Sensitization (cause and presentation)

A

Cause:
-amplification of neural signaling in CNS that elicits pain hypersensitivity
-inhibition of descending inhibitory pain pathways
-> skews inhibitory/excitatory inputs that contribute to intensity, change in pain threshold, and spreading/radiation

Presentation:
-disproportionate pain (allodynia, hyperalgesia)
-diffuse pain

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15
Q

Pain Assessment (Severity)

A

Pain in expected proportion and distribution

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16
Q

Pain Assessment (Irritability)

A

Expected provoking and alleviating factors

17
Q

Pain Asessment (Nature)

A

Pain symptoms match the nature of the condition ?

18
Q

Pain Assessment (Stage)

A

Pain match the stages of healing and stage of injury?

19
Q

Pain Assessment (Stability)

20
Q

Good prognosis

A

Positive affect
High self efficacy

21
Q

Bad Prognosis

A

Negative affect
Low self efficacy

22
Q

Biopsychosocial Assessment

A
  1. Type - mechanistic categorization
  2. Somatic factors - general constitution, other conditions
  3. Cognitive factors - understanding; learning level
  4. Emotional factors - distress/anxiety/depression
  5. Behavioral factors - contribution
  6. Social factors - contribution (stress sources)
  7. Motivation - self efficacy, affect
23
Q

Quantity and Quality Assessment

A

Quantity: (not best option)
-VAS
-NPRS

Quality: better option
-patient characteristics
-location
-frequency/duration
-time of day
-activity and rest response

24
Q

Goals w/ pain experience and beliefs

A

Understand pt unique suffering/experience
Motivate pt in goal setting
Establish therapeutic alliance

25
What to watch for with manual assessment
Sensitivity at remote locations Hypersensitivity or allodynia
26
Neurological testing
Sensory Laterality discrimination 2 point discrimination Sensation location Graphestesia
27
Cortical changes in persistent pain states
Diminished ability to discriminate 2 points Decreased ability to localize pain Decreased ability to recognize common symbols on body Decreased Laterality recognition
28
29
Goals with persistent pain
Focus on functional abilities and validated measurement instruments that incorporate pain and are descriptive of dysfunction and disability
30
Communication of pain assessment findings
Promote safety Avoid fear inducing words Focus on functional limitations