The threshold for perception of pain, that is, the lowest intensity of a stimulus recognized as pain, is approximately the same in all persons. Inflammation lowers the threshold for perception of pain by a process called sensitization. The pain threshold is, of course, raised by local anesthetics, centrally acting analgesic drugs, and by certain lesions of the nervous system. Mechanisms other than lowering or raising the pain threshold are important as well. Placebos reduce pain in about one-third of patients in which such effects have been studied (see further on for discussion of placebo). Distraction and suggestion, by turning attention away from the source of pain, reduce the awareness of and response to pain but not the threshold for its perception. Strong emotion (fear or rage) suppresses pain, presumably by activation of the above-described descending noradrenergic system. The experience of pain appears to be lessened in manic states and enhanced in depression. Anxious 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 briefly or casually if at all. Some of the terminology pertaining to abnormal pain perception is discussed below.
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. It was believed 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 evolved to 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. It is also likely that the cortex can suppress or otherwise modify the perception of pain; for example, it has been shown that central transmission in the spinothalamic tract can be inhibited by stimulation of the sensorimotor areas of the cerebral cortex. As indicated above, a number of descending fiber systems have been traced to the dorsal horn laminae from which this tract originates.
The functional imaging studies by Wager and coworkers have given insights into the ensemble of brain regions that are activated by painful stimuli. In addition to the expected thalamic and parietal sensory regions, the hypothalamus, and both insular and cingulate cortices, are prominently involved, in proportion to the intensity of the stimulus. These investigators have sought to develop an imaging “pain signature” that could, in the future, objectively measure the human pain response. Moreover, physical pain in their experiments could be differentiated from social and emotional pain.