Physiology of pain Flashcards

1
Q

List and describe the three dimensions of pain

A

Sensory: discriminative
• Relates to the location, intensity, duration and quality of pain

Motivation: affective:
• Conscious or unconscious drive for a person to initiate, sustain or direct behaviour
• Related to the unpleasant feeling associated with pain, e.g., feel unwell, depressed, etc
• You want to escape from the pain

Cognitive: evaluative:
• Pain is evaluated in terms of current and past experience
• Interpreted in relation to the actual situation, e.g. fearful dental patient – everything is painful!

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2
Q

What are the three entities that may cause pain in the head and neck area?

A
  • Intraoral pain conditions: e.g. tooth, periodontal tissues, tongue, salivary glands, may refer to other teeth and distant areas in head, neck and mandible – diagnostic dilemma
  • Musculoskeletal pain disorders: Includes cervical spine disorders and TMDs – the most common non-dental orofacial pains

• Medical conditions masquerading as orofacial pain disorders: Pain source may not be the same as the pain site; differential diagnosis very difficult:
○ Intracranial disorders (e.g. neoplasia, haematoma)
○ Neurovascular disorders (e.g. primary headache, migraine)
○ Neuropathic pain disorders (e.g. trigeminal neuralgia, burning mouth syndrome)
○ Extracranial disorders (e.g. sinuses, eyes, ears, neck)

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3
Q

What are the peripheral mechanisms of nociception and pain?

A
  • Nociceptionis the neural processes of encoding and processing noxious stimuli
  • Activation of nociceptors does not necessarily lead to pain
  • Nociceptors are present as free-nerve endings. They are widely distributed in the skin, mucosa, and deep tissues
  • Aβ fibres: touch and pressure fibres
  • Aδ and C fibres: convey nociceptive information
  • They convert a noxious stimulus into action potentials
  • Nociceptors provide information about the location, intensity and duration of a noxious stimulus (sensory- discriminative dimension of pain)
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4
Q

How do nociceptors work in physiological pain?

A
  • Acute mildly tissue-damaging stimuli (heat, cold)

* Acts on ion channels, and the action potentials travel to the brain

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5
Q

How do nociceptors work in inflammatory pain?

A
  • Involves immune cells (mast cells, macrophages)
  • These cells release chemicals like H+, interleukins and pro-inflammatory cytokines
  • These chemicals bind to receptors which leads to the generation of action potentials, and 2nd messenger cascades
  • These 2nd messenger cascades activate nociceptors (peripheral sensitisation)
  • The nociceptors are now very active (more likely to fire off action potentials)
  • Once activated, they respond to light touches where pain is generated from a non-painful stimulus (allodynia)
  • They’ll also experience increased pain to a painful stimulus (hyperalgesia)
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6
Q

What are the action of NSAID analgesics in pain

A
  • NSAID analgesics are said to block the peripheral transmission of pain
  • Aspirin and other NSAIDs have good analgesic effects in inflammatory pain
  • Decrease peripheral sensitization process – reduce allodynia and hyperalgesia
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7
Q

Describe the process of nociception and pain

A
  • There are two types of afferent nociceptive nerve fibres
    • Aδ fibres: myelinated thus sharp, pricking pain that’s well localised
    • C fibres: unmyelinated, thus dull pain that is poorly localised. It is a secondary or slow pain
  • The first order neurons travel from the trigeminal nerves to the brain stem to a place called “subnucleus caudalis”
  • Here, these trigeminal neurones synapse with second order neurons which ascend to the thalamus
  • Second order neurons synapse with third order neurons called Ventroposteromedial (VPM). * It is in the nucleus of the thalamus, which will discriminate where the pain is coming from in the body
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8
Q

What is central sensitisation?

A
  • Refers to changes in the excitability of 2nd order (and higher) neurones in the Trigeminal Brainstem Sensory Nuclear Complex
  • This can occur because an intense barrage of action potentials come from the first order neurons
  • This intensely depolarises the second order neurones, and so they may continuously fire action potential after actional potential
  • May explain allodynia and hyperalgesia
  • Continued central sensitisation may partly contribute to chronic pain
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9
Q

What is referred pain?

A
  • Referred pain is pain felt at a site distant from the site of injury
  • Nociceptive afferents from different orofacial regions converge onto the same 2nd order neurone
  • The brain gets confused as to which nociceptive afferent is the source of the problem
  • Thus, pain source may not be the pain site
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10
Q

Describe the modulation of pain

A
  • Pain can be made to become more or less intense; modulated
  • The nociceptive pathway can be turned off partly/ completely or opened up further
  • Descending inhibitory pathways: PAG/ GABA will dampen the transmission of pain from the brain stem complex. OR, this can be amped up
  • Also, when you get hurt, you rub that area. This activates the Aβ fibers, which will inhibit the pathways of the Aδ and C fibers, alleviating the pain a little
  • Gate control theory
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