Introduction
Pain is usually part of a protective mechanism that warns about factors in the immediate environment that could cause physical injury, or about functions within the body that might require attention. The response to pain is variable and depends on the intensity, character and location of the stimulus. Input from pain receptors (nociceptors) generally triggers arousal, initiates reflex and higher level withdrawal behaviour, and stimulates autonomic and endocrine stress responses. At a higher level, cognitive and emotional responses are manifest as part of the conscious response to pain. Importantly, because pain is a subjective experience, cognitive and emotional factors alter the individual’s perception of pain intensity and its significance. Knowledge of normal pain physiology allows appreciation of analgesic strategies and an understanding of persistent (chronic) pain, which is often neuropathic.
As a subjective experience, in the absence of nerve injury, pain is the conscious interpretation of noxious stimuli entering the central nervous system secondary to activation of nociceptors throughout the body. However, it is a considerably more complex process than a simple ‘stimulus and response’; it involves dozens of neurotransmitters in multiple pathways that induce a number of central responses, including positive and negative feedback mechanisms.
Pain responses can go wrong in a number of ways. Sustained nociceptive input (eg from injured nerves) will cause the central nervous system to become sensitised and ‘wound-up’, resulting in the amplification and perpetuation of pain responses. Also, it is now recognised that ‘pain memory’ occurs within the CNS, even at spinal cord levels, and contributes to many chronic painful conditions including phantom pain.
Nociceptive pain
Nociceptive (‘physiological’) pain, the ‘usual’ type of ‘everyday’ pain, is the most common type of pain; it can be either somatic or visceral in origin, or both.
Visceral pain is often described in vague terms such as dull aching, cramping or tightness. The pain from noxious visceral nociceptor stimulation arises from visceral distension, muscle spasm, or inflammation. It is often conducted by autonomic afferents (small unmyelinated C-type nerve fibres) and is associated with imprecise localisation or referral to somatic regions sharing the same spinal level(s) of input. This is the underlying mechanism for referred pain (eg pain due to myocardial ischemia being felt in the neck and arms).
Autonomic pathways to the brain involve more primitive pathways, and invoke brainstem-level responses such as nausea and sweating.
Somatic pain is well localised and often more precisely described than is visceral pain. It is conducted by both unmyelinated C fibres and small myelinated A-delta fibres. Localisation of somatic pain is much more accurate, due to a higher number of spinal second-order connections and detailed projection to the post-central gyrus of the parietal lobe of the brain. The quality of somatic pain is much more diverse, and is described with more precision, often using terms which presume the aetiology—such as hot, cutting, sharp, or stinging. Some nociceptors evoke the same response for vastly different noxious stimuli (eg extreme heat and extreme cold, which are both perceived as ‘heat’). The response to somatic pain tends to be more sophisticated, resulting in an integrated and purposeful attempt to avoid further exposure to the noxious stimulus.
Neuropathic pain
Neuropathic pain arises from a disturbance of neural pathways at any point from the primary afferent conducting system to receptive centres in the central nervous system. This can be the result of nerve cell body or axonal dysfunction due to compression, inflammation, trauma, metabolic insult or degenerative disease. Examples of neuropathic pain are postherpetic neuralgia, diabetic neuropathy, and nerve plexus avulsion. When the primary lesion is in the central nervous system, the resultant pain is known as ‘central neuropathic pain’ (eg following spinal cord injury or stroke). See Nerve injury or dysfunction and neuropathic pain , Acute neuropathic pain and Neuropathic pain for further information about neuropathic pain.
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