Pain and descending control mechanisms 2: The gate control theory of pain Flashcards
Define pain
An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,”
What is the purpose of pain?
- The initial pain experience prompts avoidance to remove the source of potential further damage.
- As pain limits activity, it forces the person/animal to rest if an injury has occurred, thereby helping the healing process. This can be useful for example in the case of a broken bone or damage to the skin.
- The experience of pain also modifies behaviour so that the person/animal will learn to avoid similar dangers in the future.
What was the 1644 - Descartes; The sensation intensity theory of pain?
This theory posits the existence of a direct connection from a location in the body to a pain centre in the brain. The intensity of pain felt would be proportional to the injury, a bit like ringing a bell by pulling a rope: the stronger one pulls, the more loudly the bell will ring.
What was one of the biggest weaknesses of the 1644; The sensation intensity theory of pain?
Could not account for a range of situations. They could not account for the presence of pain in certain situations, for example for pain without damage (e.g. phantom limb pain), or on the contrary damage with limited pain, such as that observed by the anaesthesiologist Beecher in WWII soldiers.
What is the 1965: Gate control theory of pain (Melzack and Wall)
They suggested that there is a mechanism in the spinal cord, which they defined as a gate, which can be open or closed. This gate acts to control the amount of nociceptive input which can reach the brain from the periphery. (Via C-fibres afferent, the nociceptors. )
What factors control the gate in the Gate control theory of pain?
- Amount of activity in nociceptive fibres
- Amount of activity in other peripheral fibres (Aβ fibres)
- Messages descending from brain, e.g. emotions (anxiety, relaxation), mental conditions (boredom, learning)
(Thus: psychological factors influence pain perception by regulating the gate mechanism.)
How do C and Aβ fibres control the gate?
- Aβ fibres: Can activate, if stimulated, inhibitory neurons in the substantia gelatinosa. These neurons inhibit the activation of projection neurons, either by inhibiting them directly as shown here, or by inhibiting pre-synaptically the nociceptive neurons
- C fibres neurons: Activate the projection neurons and inhibit the inhibitory interneurons, thus opening the gate.
What is the difference between the 1965 control gate theory and the modified gate control theory (1982) by Melzack and Wall?
- This modified theory did not just include inhibitory interneurons but also included excitatory links from substantia gelatinosa to the transmission cells (T) in the dorsal horn of the spinal cord.
- Importantly this modified theory included the influence of the descending inhibitory control systems and the system of cognitive control over the spinal gate-control system
Reminder
Attempt to understand slide 22
How do these descending inhibitory pathways work in the spinal cord?
- Neurons in the descending system can express noradrenaline and 5-HT, as we have seen, or also GABA.
- Whilst GABA is an inhibitory neurotransmitter, both noradrenaline and 5-HT can be inhibitory or excitatory, depending on the receptors expressed in post-synaptic cells. The descending systems can therefore work by inhibiting the release of neurotransmitter (glutamate) from primary afferents
- They can also inhibit postsynaptic projection neurons. Alternatively, they can activate inhibitory interneurons, which again can act pre or postsynaptically.
What are facilitator descending pathways, and how do they work?
- They act in the opposite way to the inhibitory ones
- They often share anatomical substrate.
- A wide range of neurotransmitters can activate these pathways
- Their anatomy and neurochemistry are less clearly understood than those of inhibitory pathways.
Why do we need to understand in detail the pathways and neurotransmitters involved in pain modulation?
There are a number of pharmacological and non pharmacological interventions which we could implement, to either stimulate descending inhibitory pathways, or to inhibit faciliatory ones, if we understood better their functioning.
Summarise the gate theory of pain.
If a pain input of e.g. +6 comes from pain fibres into the “gate” (in the dorsal horn of the spinal chord I think, double check this) other factors will determine if it is increased or decreased to e.g. +10 or +1.
What are some clinical applications of the gate theory of pain?
- The gate control theory is applied in clinical practice: stimulation of large A beta fibres to close the gate can be performed with TENS
- Or interferential current stimulation and can be used for localized pain, such as low back pain or labour pain.
- Counter irritants, and probably also acupuncture, would act by activating the descending pain inhibition, as seen in the studies of CPM.
