The neurophysiology of pain

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Stimulation of a nociceptor produces impulses in peripheral nerves that enter the dorsal column of the spinal cord. Traditional physiology then described specific pain pathways in the spinal cord, leading to the sensory cortex. We might imagine it as a kind of giant telephone exchange. Pressing a peripheral button would ring a bell in the corresponding area of the cortex and bring the stimulus to conscious attention as pain. This oversimplification may seem attractive but it is inaccurate.

Modern neurophysiology provides a more complex but much better basis for understanding clinical pain. There are three fundamental ideas. First, pain signals do not pass unaltered into the central nervous system (CNS), but are filtered, selected, and modulated at every level. Second, pain is not a purely physical sensation that passes all the way up to consciousness and only then produces secondary emotional effects. Emotions are hardwired. The neurophysiology of pain and emotions are closely linked throughout the higher levels of the CNS. Sensory and emotional events occur simultaneously and influence each other. Third, pain does not depend only on conscious reaction to produce changed behavior. Rather, sensory and motor elements are also closely linked at every level of the CNS, so that pain behavior is an integral part of the pain experience.

Melzack & Wall's (1965) gate control theory of pain crystallized these ideas. Their graphic concept of a pain "gate" made it easy to understand and popularized the theory (Fig. 3.3). Stimulation of nociceptors produces impulses in peripheral nerves that enter the dorsal column of the spinal cord. Melzack & Wall suggested that the dorsal horn then acts as a gate control mechanism. Sensory information arrives in both large and small afferent fibers. Immediate, sharp pain is transmitted by large myelinated A fibers, and slow, diffuse, or aching pain by small unmyelinated C fibers. The balance of activity in different afferent fibers may stimulate or inhibit the next cells in the dorsal horn and so open or close the gate for transmission

Simple Gate Control Theory

Figure 3.3 Gate control theory I (GCT-I). L, the large diameter fibers. S, the small diameter fibers. The fibers project to the substantia gelatinosa (SG) and first central transmission (T) cells. The inhibitory effect exerted by the SG on the afferent fiber terminals is increased by activity in L fibers and decreased by activity in S fibers. The central control trigger is represented by a line running from the large fiber system to the central control mechanisms; these mechanisms, in turn, project back to the gate control system. The T cells project to the action system (+, excitation, -, inhibition.) From Melzack Et Wall 1965, p. 971, reproduced with permission.

Figure 3.3 Gate control theory I (GCT-I). L, the large diameter fibers. S, the small diameter fibers. The fibers project to the substantia gelatinosa (SG) and first central transmission (T) cells. The inhibitory effect exerted by the SG on the afferent fiber terminals is increased by activity in L fibers and decreased by activity in S fibers. The central control trigger is represented by a line running from the large fiber system to the central control mechanisms; these mechanisms, in turn, project back to the gate control system. The T cells project to the action system (+, excitation, -, inhibition.) From Melzack Et Wall 1965, p. 971, reproduced with permission.

of impulses higher up the nervous system. Thresholds to excitation depend on pre-existing levels of activity within the spinal cord. Higher CNS activity can also influence the gate, both by descending nerve impulses (Ren & Dubner 2002) and by the release of analgesic chemicals such as endorphins.

But filtering at the first synapse in the dorsal horn is only the start of a continuous process of selection and modulation of information. It was previously thought that different parts of the CNS might serve different aspects of the pain experience. For example, the spinothalamic tract might process information about the location and sensory qualities of the pain. The brainstem, reticular formation, and limbic system might be more concerned with the emotional or affective qualities of the pain. Fast dorsal column pathways and central control mechanisms at a cortical level might evaluate the sensory information, and relate it to other sensory information and past experience. That might then produce feedback to influence how all the other parts of the system deal with the incoming information. Now, we think instead that it all works as a complex, integrated, neural network or neuromatrix (Melzack 1999). It is genetically determined, but modified by earlier learning. It allows multiple stress, endocrine, autonomic and immune system inputs, and mental functions, as well as the traditional sensory inputs, to interact and modulate pain. Recent studies with functioned brain imaging confirm that many parts of the brain are active in pain states (Casey & Bushnell 2000). We are coming back to the holistic view that pain is a response of the whole human brain (Devor 2001).

There is also a close link between afferent and efferent activity at all levels in the nervous system. Segmental reflexes can produce reflex muscle spasm or autonomic activity. Multisegmental effer-ents from the spinal cord and medulla may produce coordinated motor withdrawal responses. Higher CNS motor activity forms the basis of all pain behavior.

Since 1965, there have been many attacks on the neurophysiologic detail of the gate control theory, but there is now general agreement on the main events (Melzack 19%, Wall 1996). Pain signals do not pass unaltered to the cerebral cortex, but are always and constantly modulated within the CNS before they reach consciousness. Pain, emotions, and pain behavior are all integral parts of the pain experience. The spinal cord and the brain are best seen as a neural matrix rather than as pain tracts. The CNS is not like some enormous telephone exchange, but more like a complex computer network that responds actively to incoming signals.

These concepts provide a physiologic basis for many clinical observations:

• Fundamental to all understanding of pain, they explain how the pain and suffering that we experience may diverge greatly from peripheral nociception.

• Other afferent inputs and neural activity in other parts of the CNS can greatly modify pain signals. This may explain the effects of counterirritation, acupuncture, and transcutaneous electrical nerve stimulation (TENS).

• Pain transmission may be modulated by endorphins. These are chemical substances in the cerebrospinal fluid that act as analgesics like opiates. Certain cells in the CNS produce these and a number of similar substances. The concentration rises in the cerebrospinal fluid after exercise.

• The complex neurophysiology of pain explains why surgical division of a nerve or pain tract is unlikely to give long-term relief of pain. Pain soon recurs and associated sensory disturbance may make it even more unpleasant. This kind of ablative surgery is rarely, if ever, indicated for back pain.

There may also be neurophysiologic changes in chronic pain. The CNS is not a set of rigid electrical circuits, but is plastic in nature. We are all familiar with axon injury and regrowth, but there is little evidence of structural nerve damage in most cases of ordinary backache. Rather, chronic pain may involve more functional changes in the nervous system (Devor 1996, Doubell et al 1999, Ren & Dubner 2002). Tissue damage or inflammation can cause peripheral sensitization of peripheral nociceptors, so that normal stimuli produce pain. Sensory neurones can become hyperexcitable and cause neuropathic pain. Central sensitization may occur in the spinal cord and higher levels of the CNS. But, crucially, in many normal people the

CNS seems to adapt to continued pain and reduce its sensitivity. Chemical and morphologic changes in the dorsal horn of the spinal cord may either raise or lower receptor thresholds. Summation or habituation may occur in the spinal cord. There may be changes in the electrical and chemical activity of the spinal cord and the brain itself. Neural networks and their function can change and may be altered by neural activity itself over time. There is experimental evidence for all of these events. These changes may be lasting, which could explain how pain may persist after the original stimulus has stopped. They could also account for spread, so that pain seems to affect a wider area. Many pain lectures give the impression that these neurophysiologic changes are irreversible, but that is untrue, as shown by the relief of chronic pain after joint replacement.

Yet even the best neurophysiology cannot fully explain human pain. Neurophysiology is about the CNS, even the brain, but it is not the mind. Neurophysiology can only explain the physiologic mechanisms, the bodily substrate, or electrochemical correlates of mental events. Clinical pain is a complex and subtle experience in a thinking, feeling human being. To understand the pain experience fully we must also look at emotions, psychology, and human behavior. We might draw an analogy with grand prix racing. Of course we depend on the internal combustion engine and the chemistry of high-octane fuel to compete, but we need much more than that if we are to win the race.

Neurophysiology and psychology are not alternatives: they go together. Pain is not only filtered and modulated through the nervous system. Pain is also filtered and modulated though the individual's genetic make-up, previous experience, and learning. And through current physiological status, emotional state, and sociocultural environment (Turk 2002). Sensitization may be both neurophysiologic and psychological (Eriksen & Ursin 2002). The major advance of modern neurophysiology is to offer an explanation for how physiologic and psychological events interact to influence afferent input and the pain we feel, our suffering and pain behavior (Villemure & Bushnell 2002).

At this point it is worth revisiting Descartes. Earlier, we looked at the Cartesian model, which is a very mechanistic and biologic view of pain. It reflects Descartes' earlier writing and his distinction between the physical substance of the body and the non-physical aspects of thought and mind. It is the famous mind-body dichotomy. But Descartes was a philosopher, whose concern was with the soul and the meaning of life. He was not a scientist. His biology reflected knowledge in the 17th century, and no one uses him as a scientific authority. So why did 19th- and 20th-century medicine adopt that model so enthusiastically? Perhaps that tells us more about "modern" medicine with its focus on disease and physical treatment than it tells us about Descartes. Philosophically, Descartes took a much more holistic approach. Philosophers since Socrates have stressed the importance of mind and Descartes agreed. "I think, therefore I am." Descartes spent the last decade of his life insisting on the interdependence of body and mind to form a complete human being (Cottingham 2000). He described feelings of pain as a prime example of "confused perceptions" that must not be referred to the body alone or the mind alone. Pain arises from "the close and intimate union of the mind with the body" (Cottingham 1993).

Pat Wall devoted his life to neurophysiology, yet Devor (2001) suggested that Wall's last message was that pain is a function of the complex human organism and we must not lose sight of the mind. In the final analysis, neurophysiology and philosophy agree!

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