Physiology of pain Flashcards
List and describe the three dimensions of pain
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!
What are the three entities that may cause pain in the head and neck area?
- 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)
What are the peripheral mechanisms of nociception and pain?
- 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)
How do nociceptors work in physiological pain?
- Acute mildly tissue-damaging stimuli (heat, cold)
* Acts on ion channels, and the action potentials travel to the brain
How do nociceptors work in inflammatory pain?
- 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)
What are the action of NSAID analgesics in pain
- 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
Describe the process of nociception and pain
- 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
What is central sensitisation?
- 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
What is referred pain?
- 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
Describe the modulation of pain
- 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