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MBCHB3: Nervous system module. > Lecture 33: Pain physiology > Flashcards

Lecture 33: Pain physiology Flashcards

1
Q

Define Pain:

A

Pain is an unpleasant SENSORY and EMOTIONAL experience associated with actual or potential tissue damage, or described in terms of such damage.

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2
Q

What are the four pillars of pain?

A

Autonomic: HR, BP, RR, Sweating
Motor: Withdrawl, immobil, vocal
Sensory: Where, type etc
Affective: Mood, emotion, Anx, distress

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3
Q

What is the physiological response to pain:

A
  • Inc HR, BP, RR, Blood sugar
  • Decrease GI motility, blood flow to viscera, renal, skin
  • Nausea, pallor, dilated pupils
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4
Q

What is pain threshold and what is it determined by?

A

A point at which a stimulus is perceived as pain OR DURATION or INTENSITY of pain that an individual will tolerate before initiation of overt pain response.

  • Stress, mood, anxiety, culture, prev exp, activity level, emotion, personality
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5
Q

What can decrease a persons tolerance to pain?

A
  • Repeated exposure
  • Fatigue, anger, boredom, apprehension
  • Sleep depreivation
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6
Q

What can increase a persons tolerance to pain?

A
  • Alcohol
  • Meds, hypnosis
  • Warmth, distracting activities
  • Strong beliefs or faith
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7
Q

How does age change a person tolerance to pain?

A

Newborns less sensitive (or cant vocalize)
Children (15-18): Lower than adults
Adults: Pain thresholds tends to increase with age, potentially thanks to neuropathies or thickness of skin

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8
Q

Define analgesia

A

Absence of pain in response to a stimulus that would

normally be painful

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9
Q

Define anaesthesia

A

Absence of all sensory modalities

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10
Q

Define hyperalgesia

A

An increased response to a stimulus that is normally painful

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11
Q

Define allodynia

A

Pain due to a stimulus that is not normally painful

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12
Q

Define parathesia

A

An abnormal sensation of burning, numbness, tingling,
itching, prickling -
(usually caused by nerve compression or damage)

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13
Q

Define causalgia

A

A syndrome of sustained burning pain, and allodynia

after a traumatic nerve lesion.

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14
Q

Define central pain

A

Pain associated with a lesion of the central nervous system.

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15
Q

What are nocioceptors?

A

Free nerve endings; Primarily Adelta and C fibers. Respond to mechanical, thermal or chemical stimuli

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16
Q

What are the characteristics of the C fibres?

A
  • Primary afferent fibers
  • Small diameter
  • Unmyelinated
  • Slow conducting (0.5-2ms)
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17
Q

What are the characteristics of A-delta fibers?

A
  • Primary afferent fibres
  • Medium diameter
  • Myelinated
  • Fast conducting (4-30m/s)
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18
Q

What is the pain quality of c fibers?

A 
Diffuse
Dull
Burning
Aching
Referred to as 'slow' or second pain

Throbbing, chronic pain

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19
Q

What is the pain quality of A-delta fibers?

A 
Well-localised
Sharp
Stinging
Pricking
Referred to as 'fast' or 'first' pain

Quick and intense, beginning of pain

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20
Q

What do c fibers free nerve endings detect?

A

Mechanical
Thermal
Chemical stimuli.

Polymodal

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21
Q

What do a-delta free nerve endings respond to?

A

Responds to noxious mechanothermal stimuli over a certain intensity

22
Q

What are the four processes involved in nocioception?

A

Transduction
Transmission
Perception (Brain)
Modulation (SC)

23
Q

Describe transduction:

A

Noxious stimuli cause cells to release chemicals i.e PG, Bradykinin, Serotonin, Substance P, Histamine -> Activate nocioceptors -> Generation of action potentials

24
Q

Describe the transmission process:

A

Nocioceptor excitation is conducted to the sensory cortex via a combination of electric (Action potentials) and chemical (neurotransmitters)

25
Q

Describe the location of C and Adelta fibre synapses in the dorsal horn… Watch lecture

A

…

26
Q

What are the two subdivisions of the spinothalamic tract for pain? and what do they do?

A

Neo spinothalamic - Lamina 1 -> Post central gyrus (Runs laterally)

Paleospinothalamic - Lamina 2 and 3 -> Reticular formation and limbic system (runs medially) (EMOTION)

27
Q

Where is pain perceived? and whats the implication of the where?

A

The reticular system: Autonomic and motor response to pain.

Limbic system: Emotional and behavioural responses

Somatosensory cortex: Perception and interpretation

28
Q

What are the two ways pain can be modulated?

A

Dampening

Amplification

29
Q

What methods dampen/down regulate pain?

A
  1. Segmental inhibition

2. Descending inhibitory nerve system

30
Q

Write some notes on segmental inhibition:

A

Is based on the premise that a gate, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses

Implies that a non-painful stimulus can block the transmission of a noxious stimulus

31
Q

Variables that affect the gate theory of pain down regulation:

A
  1. A-delta and c fibers - ‘open the gate’

2. A beta fibers that carry messages of light touch “closes the gate”

32
Q

What are conditions that open and close the gate?

A

Open:
Physical: Extent of injury
Emotional: Anxiety, worry, tension
Mental: Focusing on pain, boredom

Close:
Physical: Meds
Emotional: Postive emotions, relaxation
Mental conditions: Intense concentration or distraction, life activities

33
Q

Describe descending modulatory pain pathways:

A

Brainstem -> Spinal cord pathways i.e

  1. Periaqueductal gray area in midbrain by ascending pathways of pain signal, activates neurons that project to locus ceru leus (PONS) and Nucleus Raphe magnus in medulla.
  2. These have descending neurons that release nor adrenalin and serotonin respectively, that stimulate inhibitory interneurons in the dorsal horn that release enkephalin
34
Q

Pain amplification is caused by wind-up, what is wind up?

A

Windup is a term used to describe the process of increased AP output from the dorsal horn cells (second order) in response to SUSTAINED low Hz input from nociceptive afferents via C fibers

i.e sensation of pain is heightened (Hyperalgesia, Allodynia)

35
Q

What is the mechanism of windup?

A

Receptors (NMDA, AMPA, NK1) on the DH neurons are stimulated by GLUTAMATE and SUSBTANCE P from the c fibers terminals due to their continuous activation for an extended period of time. This leads to increased Ca influx in the DH neurons.

Consequently, pathophysiological changes take place in the DH neurons LEADING TO LOWERING OF RECEPTORS THRESHOLDS thus becoming MORE RESPONSIVE to all of its inputs. -> Central sensitisation -> hyperalgesia -> Allodynia

36
Q

What drugs target NMDA and NK1?

A

NMDA receptor inhibitors ketamine and methadone, KN-1 receptor blocking agents, or calcium channel modulators, prevent windup and may play a central role in managing chronic pain.

37
Q

What are the types of pain?

A
  1. Nocioceptive pain
  2. Inflammatory pain
  3. Neuropathic pain
  4. Referred pain
38
Q

What is nocioceptive pain?

A

Due to stimuli from somatic and visceral structures after tissue damage

i.e Chemical, intense heat, mechanical forces

Usually opioid sensitive

39
Q

What are some algesic substances? and what releases them?

A 
K -> Damaged cells
Serotonin -> Platelets
Bradykinin -> Plasma
Histamine -> Mast cells
PGs -> Damaged cells
Leukotrienes -> Damaged cells
Substance P -> Primary nerve afferents
40
Q

What causes neuropathic pain? how can it be treated?

A

Due to damage of neuronal structures

  • Usually opioid resistant
  • > But sensitive to;
  • Membrane stabilizers (gabapentin, carbamzepine)
  • Tricyclics (amitriptyline)
  • Spinal cord stimulator
41
Q

What are the types of neuropathic pain?

A
  1. Peripheral
  2. Central
  3. Complex regional pain syndrome
42
Q

What are some examples of peripheral neuropathy:

A
  1. peripheral (outside CNS)
    - Diabetic neuropathy
    - Trigeminal neuralgia
    - Post herpetic zoster pain

Burning, tingling, shooting, stining, or ‘pins and needles’ sensations

43
Q

Whats some examples of central neuropathic pain:

A
  • Thalamic pain syndrome (After stroke)

- Damage to spinal cord

44
Q

What is complex regional pain syndrome?

A
  • AKA Causalgia
    Following major injury, pt has severe debilitating pain after recovery.

Signs in affected limb include: Abnormal circulation, temperature, sweating, loss of function, atrophy of muscles, changes in the hair and skin (RELATED TO SNS)

45
Q

What is the management of neuropathic pain?

A

Physical therapy
SNS blocks
Medication

The longer it remains untreated, the less chances of reversing the symptoms.

Neuropathic pain frequently coexists with nociceptive pain

46
Q

What types of inflammation lead to neuropathic pain?

A
  1. Non-neurogenic inflammation; Release of inflam substances i.e histamine, PG, Cytokines, Leukotrienes, bradykinin from blood vessels and CT in response to tissue damage.
  2. Neurogenic inflammation (INCLUDES THE RELEASE OF NEUROPEPTIDES I.E SUBSTANCE P, NORADREALIN) from c fibers terminals.

Both processes lead to lowering the threshold of the receptors leading to hyperalgesia

47
Q

What is primary vs secondary hyperalgesia?

A

Secondary is the tissue surrounding the site of damage that becomes inflammed / enhanced sensitisation to pain.

48
Q

Write some notes on acute pain:

A
  • biologic function
  • Acts as a warning system indicating tissue injury
  • Recent onset
  • Finite duration
  • Remits when underlying pathology is resolved
49
Q

Write some notes on chronic pain:

A
  • No biologic value
  • Detrimental effect
  • Persists beyond usual course of acute illness or injury
  • Chronic pathologic process; can recur at intervals
50
Q

What is the mechanism of chronic pain?

A

Neuroplasticity: Changes to the neuronal anatomy and physiology in the dorsal horn

Behavioural and psychological changes

51
Q

How is pain assessed?

A
  • Verbal scale
  • Visual analogue scale
  • Numerical
  • Wong-baker faces scale
  • Objective: McHIll pain questionnaire
52
Q

Describe the numeric scale of pain:

A 
<4/10 = mild
5-6 = moderate
>7/10 = Severe

MBCHB3: Nervous system module. (39 decks)

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