Pain and pain management
Introduction
Pain is a primitive, multi-dimensional experience with physiological, psychological, social and emotional components. The International Association for the Study of Pain (IASP) Subcommittee on Taxonomy (Merskey & Bogduk 1994) describes pain as ‘an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’. Pain is also a valuable and necessary part of the body’s defence mechanism and usually indicates that something is wrong, for example, physical damage or disease (Scholz & Woolf 2002). Pain management meanwhile is a fundamental feature of healthcare with the aim to achieve comfort through some form of analgesia – taken from the Greek word for painlessness.
Feeling pain – transmission anatomy and physiology
Pain is felt when sensory nerve endings are stimulated and neurones relay information to the brain. Specialized pain receptors, known as nociceptors, are found in free nerve endings close to mast cells and small blood vessels that all work together to respond to pain (McHugh & McHugh 2000). Nociceptors are found in large numbers in the skin, arterial walls, periosteum and joint surfaces and in smaller numbers in all of the deep tissues of the body (Marieb & Hoehn 2007).
There appear to be two distinct types of nociceptors: high-threshold mechanoreceptors that respond to strong mechanical stimuli, and polymodal nociceptors that respond to mechanical, thermal and chemical stimuli (McHugh & McHugh 2000). Mechanical stimuli, e.g., compressing or stretching tissues and thermal stimuli, e.g., excess heat or cold, appear to stimulate the nociceptors through chemical mediator release (Allan 2005). Chemical stimuli occur as a result of the substances that are released from damaged tissues, e.g., prostaglandins, serotonin, bradykinin and histamine (McHugh & McHugh 2000). Examples of tissue damage when such chemicals are released are infection, ischaemia, inflammation, ulceration and nerve damage (Godfrey 2005).
• A-delta fibres respond to stimulation of the high-threshold mechanoreceptors. The fibres are large diameter and thinly myelinated. They transmit pain impulses rapidly (about 5–30 m/s) and are known as ‘first’ or ‘fast’ fibres. Pain sensation is usually sharp pricking, well-localized or stinging (Hudspith et al. 2006).
• C fibres connect to the polymodal receptors. They are smaller, unmyelinated fibres that conduct at 0.5–2 m/s and are known as ‘second’ or ‘slow’ pain fibres. Pain sensation may be burning, dull and poorly localized or aching.
Other fibres and receptors involved are:
• A-beta fibres are thicker and heavily myelinated, conducting information such as touch, pressure and temperature very rapidly (30–100 m/s) but not pain.
• opioid receptors are found throughout the brain and spinal cord and respond to naturally occurring endogenous opioids and to synthetic exogenous opioids.
A-delta fibres, C fibres and T (transmitter) neurones in the spinal cord
Information carried by the A-delta fibres and C fibres is relayed to the substantia gelatinosa in the dorsal horn of the spine where the neurones terminate and synapse with T (transmitter) neurones (Fig. 25.1). For the transfer of this information between the A-delta and C fibres to the T neurones excitatory neurochemical transmitters need to be released, since there is a synaptic cleft between the two (Strøma et al. 2012). These transmitters include adenosine triphosphate, glutamate, calcitonin gene-related peptide, bradykinin, nitrous oxide and substance P. The T neurones cross the spinal cord and ascend on the opposite side of the spino-thalmic tract carrying pain information to the medulla where they re-cross to the original side and synapse with secondary sensory neurones that transmit the sensation onto the thalamus in the brain. It is at this point that the sensation is experienced in a general manner without detail. From the thalmus a third group of neurones relay the information to the cerebral cortex and the somatosensory cortex to allow pain localization and stimulus interpretation. This perception of pain in the brain is vital as it allows us to act to relieve or alleviate the situation. Fibres from the thalamus also connect with the hypothalamus and reticular system, accounting for the changes in the autonomic nervous system outlined below and the motor response, and to the limbic system where emotional and behavioural responses are generated (Godfrey 2005).
Figure 25.1 The pain pathway.
Opioids and opioid receptors
While substance P and glutamate have been implicated in the transmission of pain, other neurochemicals appear to possess analgesic properties. These include endorphins, enkephalins and dynorphins, which are produced by the body and have an analgesic action similar to that of morphine. Further research is required, but the existence and action of these chemicals help to explain phenomena such as the placebo response, where an individual perceives pain relief even though no analgesic agent has been given. It appears that, in such cases, the mere expectation of pain relief is sufficient to release psychogenically the endogenous opiates, which would then cause a genuine analgesia even without the administration of an analgesic drug (Allan 2005).
Pain theories
Specificity theory
The traditional specificity theory was developed by Descartes in 1644 (Godfrey 2005). Descartes thought there was a direct link from the point of pain to the brain, suggesting that pain is a specific sensation and that pain intensity is proportional to the extent of the tissue damage (Watt-Watson & Ivers Donovan 1992). According to this theory, pain associated with a minor cut gives minimal discomfort, whereas pain associated with major trauma hurts far more. It is now known that pain is not simply a function of the amount of bodily damage, but is influenced by attention, anxiety, suggestion, experience and other psychological variables (Melzack & Wall 1982). However, current research indicates that conduction of pain impulses is more complex than was originally proposed. The recognition of the pain pathways inherent in the specificity theory provides the basis for surgery of intractable pain where the pain pathway is interrupted so impulses cannot reach consciousness (Hallet 1992).
Gate control theory
The gate control theory of pain proposed by Melzack & Wall (1965) revolutionized the understanding of pain. They proposed the idea of a ‘gate’ in the substantia gelatinosa in the dorsal (or posterior) horn of the spinal cord through which pain information must pass on its way to the brain. The substantia gelatinosa is an area of special neurones located close to each posterior column of grey matter and extending the length of the spinal cord. A number of factors can block or close the ‘gate’ to pain messages, but equally other factors will open the gate and allow pain to be experienced by the individual. When nerve impulses from the nociceptors are brought to the dorsal horn by A-delta and C fibres and relayed to the T neurones, the gate is opened.
The T neurones can be inhibited by neurochemical transmitters released by tiny interneurones in the substantia gelatinosa. The A-beta fibres synapse with these interneurones and inhibit transmission of information to the T neurone (Fig. 25.2).
Figure 25.2 Inhibitory interneurone and pain transmission.
Inhibition of the T neurone reduces the flow of pain information to the brain, effectively ‘closing’ the pain gate. Increasing activity in the A-beta fibres (touch, pressure, temperature) lessens the pain felt, while an increase in activity in the small-diameter A-delta and C fibres means that more pain is perceived (Barasi 1991). This is the basis for many of the non-pharmacological pain-relieving measures, including ‘rubbing it better’, the application of heat or cold, electrical stimulation and counter-current irritation, all of which stimulate the A-beta fibres and so reduce the pain messages being relayed to the brain.
The gating mechanism is affected by information flowing from the brain through the descending inhibitory pathways. These pathways originate in a number of areas of the brain (i.e., reticular formation, periaqueductal grey matter, raphe nuclei) and synapse with the inhibitory neurones in the substantia gelatinosa, releasing the neurotransmitters serotonin and noradrenaline norepinephrine (Barasi 1991). These inhibitory neurotransmitters excite the interneurones in the dorsal horn of the spine secreting the body’s natural endogenous opioids (endorphins, enkephalins and dynorphins) that inhibit the T neurones suppressing pain transmission. They also block the release of substance P from the A-delta and C fibres and block the receptors for substance P on the T neurones (Sherwood 2010). Allowing the brain to release endogenous opiates is a key factor in pain relief and several methods can be employed in emergency settings to try to achieve this:
• use of sensory input, such as distraction, guided imagery and hypnotism
If the inhibitory interneurones are stimulated, either by the A-beta fibres or by input from descending brain pathways, fewer pain impulses will be relayed to the T fibres and so less pain information will be carried to the brain. Melzack & Wall (1965) felt that this theory explains why the relationship between pain and injury is so variable and why the location of pain can differ from the site of injury. It also explains how pain can persist in the absence of injury or after healing and why the nature and location of pain can change over time. Hallet (1992) suggested that the gate control theory expands the role of the spinal cord; it is not just a relay station, but a centre for filtering and integrating incoming sensory information.
Effects of pain
The physiological responses that occur when the nociceptors are stimulated are similar to those of the acute stress (‘flight-or-fight’) response as first described by Cannon (1915) also known as the freeze, fight, or flight response (Bracha et al. 2004). The sympathetic nervous system is activated causing general vasoconstriction, while dilating the arteries supplying vital organs such as the muscles (McArdle et al. 2006). This results in tachycardia, tachypnoea, hypertension, sweating and pallor. Tidal volume and alveolar ventilation may be reduced, as is gastric motility. Skeletal muscle spasm may occur and hormonal changes may cause electrolyte imbalances and hyperglycaemia (Sutcliffe 1993).
