Pain and Disability Clinical, Behavioral, and Public Policy Perspectives (1987) / Chapter Skim
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7. The Anatomy and Physiology of Pain
7. The Anatomy and Physiology of Pain
Pages 121-145
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From page 123... ...
The primary afferent nociceptor contacts second-order pain-transmission neurons in the spinal cord. The secondorder cells relay the message through well-defined pathways to higher centers, including the brain stem reticular formation, thalarnus, somatosensory cortex, and limbic system.
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From page 124... ...
Thus, while experimental studies provide fairly good models for acute pain, they are poor models for clinical syndromes of chronic pain. Not only do they provide little information about the muscles, joints, and tendons that are most often affected by chronically painful conditions, but they do not address the vast array of psychosocial factors that influence the pain experience profoundly.
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From page 125... ...
, in which a noxious stimulus produces nerve impulses in the primary adherent nociceptor. These impulses are conducted to the spinal cord, where the primary afferent nociceptors contact the central paintransmission cells.
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From page 126... ...
In practice, such assays are not available to clinicians. It should be pointed out that most of our knowledge of primary afferent nociceptors is derived from studies of cutaneous nerves.
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From page 127... ...
Its peripheral process runs in peripheral nerves, and its peripheral terminals are present In most body structures These terminals are sensitive to noxious heat, mechanical stimulation, end or pain-producing chemicals. The central process enters the spinal cord via the dorsal root and terminates on central paintransmission cells that relay the info~-l~ation to higher centers.
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From page 128... ...
40 45 50 TEMPERATURE (°C) c,, 20 15 an to o Pai: _4 1 2 3 4 5 6 SUBJECTIVE INTENSITY FIGURE 7-3 The relation of discharge frequency in primary aiferent nociceptors to subjective pain intensity in human subjects.
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From page 129... ...
For this reason the method of recording primary afferent nociceptors could be used to confirm the presence of an input, but it could not be used to prove that pain was not present. Besides these theoretical limitations of trying to assess subjective pain intensity by recording primary afferent nociceptors, there are important practical problems in measuring either pain-producing substances or primary afferent nociceptor activity.
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From page 130... ...
3. According to the convergence-projection hypothesis, a single nerve cell in the spinal cord receives nociceptive input both from the internal organs and from nociceptors coming from the skin and muscles.
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From page 131... ...
Pain Pathways in the Central Nervous System Primary afferent nociceptors transmit impulses into the spinal cord (or if they arise from the head, into the medulla oblongata of the brain stem)
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From page 132... ...
Neurons in the ventrocaudal thalamus project directly to the somatosensory cortex (Willis, 19851. The medial thalamus receives some indirect input from the spinal cord, but in addition, it receives a major input from the region of the brain stem reticular formation to which the nociceptive spinoreticular neurons project.
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From page 133... ...
Focusing on the sensory aspects, a person might describe his or her pain as a mild burning pain located on the back of the hand. In contrast, the affective or unpleasantness aspect of pain correlates with the aversive drive to terminate the noxious stimulus and is described by terms that are not specifically tied to a sensory experience, for example, nagging, uncomfortable, or excruciating.
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From page 134... ...
Modulation The abovementioned processes were discussed in terms of a highly reliable pain-transmission system, the assumption being that pain intensity is a direct function of nociceptor activity. In fact, the excellent correlation among stimulus intensity, impulses in primary afferent nociceptors, and reported pain intensity demonstrated in human subjects under experimental conditions often does not apply to the clinical situation.
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From page 135... ...
SPA can be elicited from well-clefined brain stem sites. A body of evidence now indicates that SPA is mediated by a discrete neuronal network running from the midbrain to the medulla and then to the spinal cord (Figure 7-1)
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From page 136... ...
Sensitization Tissue damage initiates a variety of processes that sustain and amplify pain. With repeated stimuli, the thresholds of primary afferent nociceptors progressively decrease, so that normally innocuous stimuli become painful (Campbell et al., 1979; Gybels et al., 1979; LaMotte et al., 19833.
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From page 137... ...
This condition, called reflex sympathetic dystrophy, usually responds to sympathetic blocks and physical therapy (De Takats, 1937; Livingston, 1943; Procacci et al., 19751. Physiological studies in animals indicate that the sympathetic outflow can induce discharge of primary afferent nociceptors.
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From page 138... ...
Muscle Contraction Nociceptor activity results in sustained contraction in muscles. In limbs, this muscle contraction produces flexion, a form of primitive withdrawal that is presumably a protective movement.
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From page 139... ...
was the first to emphasize the clinical importance of these positive feedback loops; that is, the pain produces muscle contraction and sympathetic outflow that in turn activate nociceptors, which produce more sympathetic outflow and muscle contraction, and so on (Figure 7-41. The point is that painful injuries set in motion secondary processes, not associated with tissue damage, that cause a prolongation and spread of nociceptive input and may contribute to chronicity.
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From page 140... ...
Acute Versus Chronic Pain Is there any physiological basis for differentiating between acute and chronic pain? Little is known about the effects of prolonged pain on the central nervous system.
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From page 141... ...
It is technically possible to measure the chemicals released at spinal synapses by primary afferent nociceptors. If the concentration of such chemicals in the cerebrospinal fluid could be shown to correlate with either the activity of the primary afferent nociceptors or with the severity of clinical pain, this could provide evidence similar to that derived from recording the activity of the primary afferents.
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From page 142... ...
Indirect measures, such as those of sympathetic nervous system activity (skin temperature or skin resistance) or of muscle contraction in painful areas might be helpful in providing objective evidence of sustained nociceptive input.
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From page 143... ...
Effects of mechanical and chemical stimulation of fine muscle afferents upon primate spinothalamic tract cells. Journal of Physiology 286:21~231, 1979.
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From page 144... ...
Markus, H., Pomeranz, B., and Krushelnycky, D Spread of saphenous somatotropic projection map in spinal cord and hypersensitivity of the foot after chronic sciatic denervation in adult rat.
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From page 145... ...
Torebdork, H.E., and Hallin, R.G. Perceptual changes accompanying controlled preferential blocking of a and c fibre responses in intact human skin nerves.
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