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Perception of Pain
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The threshold for perception of pain, ie, the lowest intensity of a stimulus recognized as pain, is approximately the same in all persons In ammation lowers the threshold for perception of pain by a process called sensitization This process allows ordinarily innocuous stimuli to produce pain in sensitized tissues The pain threshold is, of course, raised by local anesthetics and by certain lesions of the nervous system as well as by centrally acting analgesic drugs Mechanisms other than lowering or raising the pain threshold are important as well Placebos reduce pain in about onethird of the groups of patients in which such effects have been recorded Acupuncture at sites anatomically remote from painful operative elds apparently reduces the pain in some individuals Distraction and suggestion, by turning attention away from the painful part, reduce the awareness of and response to pain Strong emotion (fear or rage) suppresses pain, presumably by activation of the above-described descending adrenergic system The experience of pain appears to be lessened in manic states and enhanced in depression Neurotic patients in general have the same pain threshold as normal subjects, but their reaction may be excessive or abnormal The pain thresholds of frontal lobotomized subjects are also unchanged, but they react to painful stimuli only brie y or casually if at all The degrees of emotional reaction and verbalization also vary with the personality and character of the patient The conscious awareness or perception of pain occurs only when pain impulses reach the thalamocortical level The precise roles of the thalamus and cortical sensory areas in this mental process are not fully understood, however For many years it was taught that the recognition of a noxious stimulus as such is a function of the thalamus and that the parietal cortex is necessary for appreciation of the intensity, localization, and other discriminatory aspects of sensation This traditional separation of sensation (in this instance awareness of pain) and perception (awareness of the nature of the painful stimulus) has been abandoned in favor of the view that sensation, perception, and the various conscious and unconscious responses to a pain stimulus comprise an indivisible process That the cerebral cortex governs the patient s reaction to pain cannot be doubted, however It is also likely that the cortex can sup-
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cerned with pain transmission, perhaps providing a rationale for the use of certain antidepression medications that are serotonin agonists in patients with chronic pain
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PRIMARY SENSORY NEURON Enkephalin Receptors
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Terminology (Table 8-2) Several terms related to the experience of altered sensations and pain are Enkephalin often used interchangeably, but each has speci c Substance P Receptors meaning Hyperesthesia is a general term for heightened cutaneous sensitivity The term hyperSPINAL INTERNEURON algesia refers to an increased sensitivity and a lowered threshold to painful stimuli In ammation and burns of the skin are common causes of hyRECEPTOR NEURON peralgesia The term hypalgesia, or hypoalgesia, refers to the opposite state ie, a decreased sensitivity and a raised threshold to painful stimuli A demonstrable reduction in pain perception (ie, an elevated threshold, associated with an increased reFigure 8-4 Mechanism of action of enkephalin (endorphin) and morphine in the transmission action to the stimulus once it is perceived, is someof pain impulses from the periphery to the CNS Spinal interneurons containing enkephalin times referred to as hyperpathia (subtly different synapse with the terminals of pain bers and inhibit the release of the presumptive transmitter, from hyperalgesia) In this circumstance there is an substance P As a result, the receptor neuron in the dorsal horn receives less excitatory (pain) impulses and transmits fewer pain impulses to the brain Morphine binds to unoccupied en- excessive reaction to all stimuli, even those (such kephalin receptors, mimicking the pain-suppressing effects of the endogenous opiate enkeph- as light touch) that normally do not evoke pain, a symptom termed allodynia The elicited allodynic alin pain may have unusual features, outlasting the stimulus and being diffuse, modi able by fatigue and emotion, and often being mixed with other sensations The mechSoon after the discovery of speci c opiate receptors in the anism of these abnormalities is not clear, but both hyperpathia and central nervous system (CNS), several naturally occurring peptides, allodynia are common features of neuropathic or neurogenic pain, which proved to have a potent analgesic effect and to bind specifie, pain generated by peripheral neuropathy These features are ically to opiate receptors, were identi ed (see Hughes et al for a exempli ed by causalgia, a special type of burning pain that results summary of these substances) These endogenous, morphine-like from interruption of a peripheral nerve (see page 121) compounds are generically referred to as endorphins, meaning the morphines within The most widely studied are -endorphin, a Table 8-2 peptide sequence of the pituitary hormone -lipotropin, and two Nomenclature in the description of pain and abnormal other peptides, enkephalin and dynorphin They are found in greatsensation (see also Table 9-1) est concentration in relation to opiate receptors in the midbrain At the level of the spinal cord, exclusively enkephalin receptors are Dysesthesia: Any abnormal sensation described as unpleasant by found A theoretical construct of the roles of enkephalin (and subthe patient stance P) at the point of entry of pain bers into the spinal cord is Hyperalgesia: Exaggerated pain response from a normally illustrated in Fig 8-4 A subgroup of dorsal horn interneurons also painful stimulus; usually includes aspects of summation with contains enkephalin; they are in contact with spinothalamic tract repeated stimulus of constant intensity and aftersensation neurons Hyperpathia: Abnormally painful and exaggerated reaction to a Thus it would appear that the central effects of a painful conpainful stimulus; related to hyperalgesia dition are determined by many ascending and descending systems Hyperesthesia (hypesthesia): Exaggerated perception of touch utilizing a variety of transmitters A de ciency in a particular restimulus gion would explain persistent or excessive pain Some aspects of Allodynia: Abnormal perception of pain from a normally opiate addiction and also the discomfort that follows withdrawal nonpainful mechanical or thermal stimulus; usually has of the drug might conceivably be accounted for in this way Indeed, elements of delay in perception and of aftersensation it is known that some of these peptides not only relieve pain but Hypoalgesia (hypalgesia): Decreased sensitivity and raised suppress withdrawal symptoms threshold to painful stimuli Finally it should be noted that the descending pain-control Anesthesia: Reduced perception of all sensation, mainly touch systems contain noradrenergic and serotonergic as well as opiate Analgesia: Reduced perception of pain stimulus links A descending norepinephrine-containing pathway, as menParesthesia: Mainly spontaneous abnormal sensation that is not tioned, has been traced from the dorsolateral pons to the spinal unpleasant; usually described as pins and needles cord, and its activation blocks spinal nociceptive neurons The rosCausalgia: Buring pain in the distribution of one or more troventral medulla contains a large number of serotonergic neurons peripheral nerves Descending bers from the latter site inhibit dorsal horn cells con-
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