13 - Pain Flashcards
Example of a definition of pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Different types of pain 1 2 3
1) Nociceptive pain 2) Inflammatory pain 3) Neuropathic pain
Chronic pain
Pain for three of the past six months. A large proportion of people with chronic pain don’t respond to treatment.
Relationship between pain and nociception.
Not synonymous. Nociception is nerve detection of noxious stimulus. Pain is cortical recognition thereof.
Stages of nociception 1 2 3 4
1) Transduction (receptor detection of H+. heat. noxious cold, pressure, chemicals, etc) 2) Transmission (peripheral and central) 3) Perception (sensory/discriminative, emotional) 4) Modulation
Sensory/discriminative pain
How intense pain is, where it is. Carried through lateral spinothalamic tract to the lateral thalamus.
Spinal tract through which nociceptive information travels to brain
Spino-parabrachial tract, lateral spinothalamic tract. Travel to the lateral thalamus, limbic centres.
Emotional/aversive pain
Emotional perception of pain. Travels through spinoparabrachial tract to limbic centres.
Responses to nociceptive pain 1 2 3
1) Pain 2) Autonomic reflexes 3) Withdrawal reflex
Nociceptor nerve endings
C-fibres, A-delta fibres.
Location of nociceptive neuron cell bodies
In dorsal root ganglia, trigeminal ganglia (for pain of head and face)
C-fibre morphology
Unmyelinated. Thin (under 1.5 micromete) Slow transmission (under 3m/s)
A-delta fibre morphology
Myelinated. Thin (1.5 - 4 micrometes) Medium-fast transmission (3-30m/s)
Temperature around which a heat nociceptor will start being stimulated
~42 degrees. High-threshold.
Difference in type of pain from C-fibres and A-delta fibres
C-fibres give slow, burning pain. A-delta give sharp pain.
*First and second pain
FIRSTSECONDPAIN
*Projection of second-order neurons to brain via anterolateral tract
Nociceptor afferents synapse ipsilaterally with a spinal interneuron, which crosses contralaterally and ascends to brain in anterolateral system.
Inflammatory pain
Similar to nociceptive pain, but system is modulated by inflammatory mediators released by immune cells (hyperalgesia). System evolved to protect damaged tissues (eg: with behaviour).
‘Inflammatory soup’
Inflamed or damaged tissues release nociceptor sensitisers.
*TRP channel
Transient receptor potential channel. TRPV1 is a nociceptive transducer.
Stimuli that TRPV1 often responds to
Noxious heat, acid, reactive chemicals.
TRP channel responsible for detecting environmental cold
TRVM8 (EG activated by menthol)
What causes secondary allodynia to come about?
Central sensitisation by inflammation. An innocuous stimulus of a low-threshold neuron leads to stimulation of sensitised central pathway, leading to secondary allodynia.
Difference between hyperalgesia and allodynia
Hyperalgesia is an increased response to a normally painful stimulus. Allodynia is a painful response to a normally innocuous stimulus.
Secondary hyperalgesia
Expansion of an area that feels painful from area of initial injury. Sensitisation of adjacent spinal segments, leading to hyperalgesia of area surrounding initial injury.
Types of maladaptive pain 1 2
1) Neuropathic pain (neural lesion, positive and negative symptoms. 2) Dysfunctional pain (no neural lesion, no inflammation, positive symptoms). EG migraine (no identifiable pathology apart form the pain itself)
*Ways in which peripheral neuropathic pain can airse
Parts of the brain involved in pain
Somatosensory cortex, insular cortex, cingulate cortex, amygdala, parabrachial nucleus.
*Brain pathways of pain
Parts of brain that can modulate pain
Periaqueductal grey matter, rostral ventral medulla
Drugs that can act on the periaqueductal grey matter for analgesia
Opioids, NSAIDS (mimic molecules in descending pain pathway)
Descending pain pathway
From amygdala, engages in descending pain modulation. Can be modulated by inflammation, analgesic drugs.
Effects of anxiety and fear on pain perception
Hypoalgesia.
Human cortical areas involved in top-down psychological modulation of pain 1 2 3
1) Anterior cingulate cortex 2) Prefrontal cortex 3) Insula cortex These interact with the periaqueductal grey matter to modulate descending pain pathway
Can placebo effect be pharmaceutically reversed?
Yes. Can reverse/prevent with opioid antagonists (EG loxone).
Endogenous molecules involved in pain inhibition
Encephalins.
Nocebo
Anticipation of pain can lead to hyperalgesia.
