The Convergence Theory Summary

There have been multiple theories considered to explain the process of referred pain. One theory discusses the branching of peripheral nociceptive afferent fibres that has a receptive field in both the local and referred pain area.1 The limitation for this theory is that these bifurcated fibres are rare, fibres don’t generally branch over such large distances, semi-directional nature of referred pain & the latency of onset.2 This theory implies that if one receptive field is stimulated it will lead to the nervous system being unable to differentiate between the two areas due to synapsing at the same point at the dorsal horn (DH).1
The convergence theory is based on separate afferents converging from local and distant areas onto the same neuron in the spinal cord.2 Limitations to this theory is that the pain should be bi-directional & should occur at the same time. Due to both of the afferents converging on the same neuron a noxious stimulus in one area should trigger pain in the other this is not the case for referred pain. Similar to the bifurcation theory due to both afferents synapsing with the same neuron the pain should occur at the same time.2
The final and most likely mechanism for referred pain in Mrs Randall is the central sensitization theory.
This theory is based on the increase activity that results from central sensitisation leading to the activation and unmasking of previous dormant synapses in the DH.2 Afferent fibres entering the spinal cord extend from the primary neuron to have collateral synaptic connections with multiple DH neurons.2 This connection to latent synapses in other neurons allow these neurons to become operational.2 Prolonged noxious input from the periphery leads to the sensitisation of the central DH neurons as well as the activation of these latent synapses surrounding, triggering referred pain.1 These latent synapses are enhanced due to the train of impulses and high levels of glutamate associated with central
sensitisation.
These adjacent neurons although close in the spinal cord, may be associated with distinct, separate areas in the periphery. Therefore in Mrs Randall’s case afferent impulses from her neck will be synapsing with direct neurons but also will have synaptic connections with adjacent neurons.
In response to the nociceptor stimulus arriving in the spinal cord we get the release of substance P from the primary afferent. This neuromodulator is capable of spreading outside the synapse and affecting adjacent neurons. When substance p binds to the more distant neurons it undergoes the same process of sensitisation that the primary neuron has already undergone. Substance p binds to Neurokinin 1 (NK1) receptors, which triggers second messenger systems to release stored calcium triggering an increase response to noxious stimuli. Mrs Randall has been having this process for a period of four months now meaning these latent synapses have become potentiated. With the adjacent neurons becoming sensitised normal non-noxious inputs from the neck will activate these neurons as well, leading to the perception of referred pain in Mr’s Randall’s arm.

Explain somatic referred pain: deep diffuse, no sensory or motor changes, non-dermatomal, linked to m/s or jt inflammation