What is pain?
According to the Oxford dictionary pain can be described as “A strongly unpleasant physical sensation caused by illness or injury”(Oxford dictionary,2007,9ed). From a scientific perspective however, the definition of pain is more complicated. The purpose of pain is to make us aware of something in our body/ environment that is injurious to our health, and to generate avoidance behaviour through an aversive emotional response. From a physiological perspective, pain can be seen to have 2 components:
1) a nociceptive (“sensing of pain”) component: the basic sensation of pain, just like the sensation of touch or heat
2) an affective component: the emotional response to pain, causing us to perceive the nociceptive signals as unpleasant
Whenever we “feel” pain, it results from a combination of both of these components. The perceived intensity of pain is thus dependent both on the frequency of nociceptive neuronal firing AND our own feelings towards the pain- this has important implications to the treatment of pain.
There are 2 main types of pain: acute and chronic. Acute pain tends to be sharp and alerts us that we are, for example, exerting a body part too much. Chronic pain tends to be dull and throbbing and lasts for long periods of time, and is present where there is inflammation around, for example, a broken limb.
A third type of pain, of which little is known is neuropathic pain. This is pain that results from damage to nerves, by degenerative diseases such as multiple sclerosis. In this case, the pain is thought to be generated by spontaneous neuronal firing as a result of disintegration of sensory neurons.
Neural pain pathways
For now, we will focus primarily on the basic neural pathways that result in the detection and sensation of pain (nociception).
In the presence of a noxious stimulus such as excess heat, excess acidity, toxins, poisons or excess strain/ stretch, the dendritic processes of distinct neurons are triggered to fire action potentials which travel along the nerve processes to cell bodies in the spinal cord. There are 2 neuronal subtypes responsible for this initial detection of a pain stimulus: small diameter Aδ fibres and larger C fibres. Aδ fibres tend to fire when the stimulus is strong and acute, and thus are known to produce the sensation of “sharp”, but rapidly dissipating, pain. C fibres are fired when an area is continually subject to noxious stimuli, such as when inflammation occurs in a fractured limb, and so these fibres are most associated with chronic, “dull” pain.
The processes of both fibre types travel from the peripheral sensory zone (the skin or viscera) to their respective cell bodies in the centrally-located spinal cord, and enter via the dorsal horn. The dorsal horn appears to consist of several layers or “laminae”; C fibres terminate in laminae I and II, while Aδ fibres terminate in laminae I, III and V. The cell bodies of the fibres then synapse onto transmission neurons in layers I and V, which themselves project to the medial thalamus (an area of the diencephalon). From the thalamus, projections go to the cerebral somatosensory cortex (area responsible for associating pain with the correct area of the body/ at the correct intensity), and other areas such as the cingulated cortex and limbic lobe (the areas responsible for the emotional response to pain).
Regulation of neural pain pathways
The pain pathways detailed above are not however unilateral; they are modulated both by other nerves that descend from the mid/hindbrain down the spine, and also by the substantia gelatinosa (SG), a bundle of neurons found in lamina II. Together, these regulatory pathways allow the pain system to be gated- this ensures that pain is a novel sensation and not easily generated.
The substantia gelatinosa projects inhibitory neurons into laminae I and V. In the absence of pain, the SG fires continually, which inhibits the firing of transmission neurons- this prevents us feeling pain when we shouldn’t. In the presence of pain, the activated Aδ/C fibres inhibit the SG, allowing transmission of pain signals to the thalamus.
The descending spinal pathways work to modulate pain signals once they’ve already started. The periaqueductal gray (PAG) (in the midbrain) sends stimulatory projections to the nucleus raphe magnus (NRM) (medial medulla), which then goes on to inhibit transmission neurons in the dorsal horn. It also sends stimulatory projections to the SG, increasing its ability to inhibit transmission neurons. The NRM is also further stimulated by the nucleus reticularis paragigantocellularis (NRPG), an area activated by transmission neurones themselves, travelling up the spinothalamic tract. The result of all these inputs is a highly effective negative feedback system, where pain sensation is kept to the appropriate levels. It should be noted that the PAG is itself modulated by the cerebral cortex, thalamus and hypothalamus- this may be the route by which the perceived intensity of pain is controlled.
Notice: diagrams
All diagrams on this website are my own, generated using Microsoft Powerpoint and Paint.
Notice: diagrams
All diagrams on this website are my own, generated using Microsoft Powerpoint and Paint.