There are several other aspects of pain that distinguish it from other sensory modalities. First, unlike other sensory modalities such as taste, vision, or audition, pain is a submodality of somatosensory processing. Somatosensation involves the detection of mechanical, thermal, and chemical stimuli impinging on structures outside the CNS. At low intensities, these stimuli are not perceived as painful. At higher intensities, each of these stimuli may result in tissue damage. Such intense stimuli are referred to as noxious and are generally perceived as painful. For somatic structures such as skin and muscle distinct afferent populations are involved in encoding non-noxious and noxious stimuli (13). Low-threshold mechanoreceptors and warm and cool fibers encode non-noxious stimuli, and nociceptors encode noxious stimuli. However, because many noxious stimuli will activate both low-threshold and nocicep-tive afferents, the quality of pain associated with these stimuli is often influenced by activity in low-threshold afferents. Visceral structures such as the colon (14) and the esophagus (15) are innervated by both low-threshold and high-threshold afferents. However, even the
Three major theories have dominated views about how noxious stimulation of peripheral tissue may ultimately be perceived as pain. One is the labeled line theory. The idea here is that like other sensory modalities, such as vision and audition, there are specialized neural pathways dedicated to the perception of pain. The result would be a dedicated neural pathway, or labeled line, from the periphery to the brain, activity in which would result in the perception of pain. A second is the frequency-encoding theory. This theory is based on the observation that for other sensory modalities, the amount of neural activity encodes the intensity of a stimulus. The prediction of this theory was that there would be neurons that could encode stimulus intensity over a wide range, and at some level of activity, the perception of the stimulus would change from nonpainful to painful. The Gate Control Theory by Melzack and Wall (12) was an alternative to both of these theories, incorporating aspects of both, but formally proposing a third mechanism for the perception of pain that depended on neural circuitry. Melzack and Wall proposed that the perception of pain depended on the relative activity in a number of different neurons that were interconnected in ways that enabled these neurons to influence, either directly or indirectly, the activity of other neurons in the circuit. Data from studies designed to elucidate the complexity of the neural circuitry underlying the perception of pain, particularly that arising from visceral structures, indicates that fundamental aspects of each of these theories are correct.
low-threshold afferents appear to encode stimulus intensity into the noxious range. This difference between visceral and other somatic structures may contribute to the observation that the ability to distinguish the modality of noxious stimuli impinging on the viscera is relatively poor.
A second, unique aspect of pain is that it demands attention and, more importantly, action. From an evolutionary perspective, this makes intuitive sense, as tissue integrity, and, ultimately, survival may depend on escape from noxious stimuli. Consequently, noxious stimuli result in the activation of neural circuits that enable not only rapid escape from the stimulus, as is observed in a withdrawal reflex, but also cardiovascular changes that facilitate whole body "fight or flight'' responses (16). Thus, again in contrast to other sensory modalities, the response to acute noxious stimuli can be measured with changes in a host of autonomic measures such as heart rate and blood pressure. These responses may change in the face of tissue injury or prolonged noxious stimulation where behavioral changes conducive to wound healing, such as inactivity, may come to predominate (6).
A third unique aspect of pain is that application of the same stimulus, for example, a contact probe at 48°C, does not always produce the same perception. This dynamic nature of pain appears to reflect a number of mechanisms. As mentioned above, cognitive factors are but one class of mechanisms that influence the perception of pain. The impact of cognitive factors has been eloquently demonstrated in studies employing distraction (17) and/or hypnotic suggestion (9) to alter the perception of pain. Other factors include (i) the state of the organism, which is influenced by variables such as nutritional status (18,19) and diurnal fluctuations of physiological processes (20); (ii) the age of the organism (21), and (iii) the history of the organism (22,23). The history of the organism, particularly, that associated with previous noxious stimulation may have a particularly profound impact on the perception of pain. This impact may be observed within seconds (24) as well as over the lifetime of the organism (23).
Following tissue injury or in the presence of disease, there may be changes in pain perception that are the most clinically relevant. These changes in pain signal the presence of injury and disease and serve as a primary motivation for patients to seek medical attention. Undertreated, this pain may have serious deleterious consequences, as pain has been shown to suppress immune function (25), thereby slowing recovery or worsening the progression of a disease (26). Furthermore, persistent pain may develop into a disease in its own right as it may persist following resolution of initiating causes or in the absence of any apparent underlying pathology.
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