CLINICAL AND PSYCHOLOGIC ASPECTS OF PAIN

Terminology Several terms related to the experience of altered sensations and pain are often used interchangeably, but each has specific meaning. Hyperesthesia is a general term for heightened cutaneous sensitivity. The term hyperalgesia refers to an increased sensitivity and a lowered threshold to painful stimuli. Inflammation and burns of the skin are common causes of hyperalgesia. The term hypalgesia, or hypoalgesia, refers to the opposite state—i.e., a decreased sensitivity and a raised threshold to painful stimuli. A demonstrable defect in pain perception (i.e., an elevated threshold) in the affected part, associated with an increased reaction to the stimulus once it is perceived, is sometimes referred to as hyperpathia (subtly different from hyperalgesia). In this circumstance there is an excessive reaction to all stimuli, even those (such as light touch) that normally do not evoke pain, a symptom termed allodynia. The elicited allodynic pain may have unusual features, being diffuse, modifiable by fatigue, emotion, etc., and often mixed with other sensations. The mechanism of these abnormalities is not clear, but both hyperpathia and allodynia are common features of neuropathic or neurogenic pain, i.e., pain generated by peripheral neuropathy. These features are exemplified by causalgia, a special type of burning pain that results from interruption of a peripheral nerve (see page 1438).
Skin Pain and Deep Sensibility As indicated earlier, the nerve endings in each tissue are activated by different mechanisms, and the pain that results is characterized by its quality, locale, and temporal attributes. Skin pain is of two types: a pricking pain, evoked immediately on penetration of the skin by a needle point, and a stinging or burning pain, which follows in a second or two. Together they constitute the “double response” of Lewis. Both types of dermal pain can be localized with precision. Ischemia of nerve by the application of a tourniquet to a limb abolishes pricking pain before burning pain. The first (fast) pain is thought to be transmitted by the larger (A-d) fibers and the second (slow) pain, which is somewhat more diffuse and longer-lasting, by the thinner, unmyelinated C fibers.
Deep pain from visceral and skeletomuscular structures is basically aching in quality; if intense, it may be sharp and penetrating (knife-like). Occasionally there is a burning type of pain, as in the “heartburn” of esophageal irritation and rarely in angina pectoris. The pain is felt as being deep to the body surface. The pain is diffuse and poorly localized, and the margins of the painful zone are not well delineated, presumably because of the relative paucity of nerve endings in viscera.
Referred Pain The localization of deep pain raises a number of problems. Although deep pain has indefinite boundaries, its location always bears a fixed relationship to the skeletal or visceral structure that is involved. It tends to be referred not to the skin overlying the viscera of origin but to other areas of skin innervated by the same spinal segment (or segments). This pain, projected to some fixed site at a distance from the source, is called referred pain. Small-caliber pain afferents from deep structures project to a wide range of lamina V neurons in the dorsal horn, as do cutaneous afferents. The convergence of deep and cutaneous afferents on the same dorsal horn cells, coupled with the fact that cutaneous afferents are far more numerous than visceral afferents and have direct connections with the thalamus, probably explains the phenomenon of referred pain.
Since the nociceptive receptors and nerves of any given visceral or skeletal structure may project upon the dorsal horns of several adjacent spinal or brainstem segments, the pain may be fairly widely distributed. For example, afferent pain fibers from cardiac structures, distributed through segments T1 to T4, may be projected superficially to the inner side of the arm and the ulnar border of the hand and arm (T1 and T2) as well as the precordium (T3 and T4). Once this pool of sensory neurons in the dorsal horns of the spinal cord is activated, additional noxious stimuli may heighten the activity in the whole sensory field ipsilaterally and, to a lesser extent, contralaterally.
Another peculiarity of localization is aberrant reference, explained by an alteration of the physiologic status of the pools of neurons in adjacent segments of the spinal cord. For example, cervical arthritis or gallbladder disease, causing low-grade discomfort by constantly activating their particular segmental neurons, may induce a shift of cardiac pain cephalad or caudad from its usual locale. Any pain, once it becomes chronic, may spread quite widely in a vertical direction on one side of the body. On the other hand, painful stimuli arising from a distant site exert an inhibitory effect upon segmental nociceptive flexion reflexes in the leg (DeBroucker et al). Yet another clinical peculiarity of segmental pain is the reduction in power of muscle contraction that it may cause (reflex paralysis, or algesic weakness).
In an injured nerve, the unmyelinated sprouts of A-d and C fibers become capable of spontaneous ectopic excitation and afterdischarge and susceptible to ephaptic activation (Rasminsky). They are also sensitive to locally applied or intravenous catecholamines because there are adrenergic receptors on the regenerating fibers. Either this mechanism or ephapsis (nerve-to-nerve cross-activation) is thought to be the basis of causalgia and other forms of reflex sympathetic dystrophy; either mechanism would explain the relief afforded by sympathetic block. This subject is discussed in greater detail in relation to peripheral nerve injuries (see page 1438).
Central sensory structures, e.g., sensory neurons in the dorsal horns of the spinal cord or thalamus, if chronically bombarded with pain impulses, may become autonomously overactive (being maintained in this state perhaps by excitatory amino acids) and may remain so after the peripheral pathways have been interrupted. Peripheral nerve lesions have been shown to induce enduring derangements of central (spinal cord) processing (Fruhstorfer and Lindblom). Avulsion of nerves or nerve roots may cause chronic pain even in analgesic zones (anesthesia dolorosa or “deafferentation pain”). In experimentally deafferented animals, neurons of lamina V begin to discharge irregularly in the absence of stimulation. Later the abnormal discharge subsides in the spinal cord but can still be recorded in the thalamus. Hence, painful states such as causalgia, spinal cord pain, and phantom pain are not abolished simply by cutting spinal nerves or spinal tracts.
Pain has several other singular attributes. It does not appear to be subject to negative adaptation—i.e., pain may persist as long as the stimulus is operative—whereas other somatic stimuli, if applied continuously, soon cease to be effective. Furthermore, prolonged stimulation of pain receptors sensitizes them, so that they become responsive to even low grades of stimulation, such as touch (allodynia). Another remarkable characteristic of pain is the strong feeling or affect with which it is endowed, nearly always unpleasant. Since pain has this affective element, psychologic conditions assume great importance in all persistent painful states. It is of interest that despite this strong affective aspect of pain, it is difficult to recall precisely, or to re-experience from memory, a previously experienced acute pain. Also, the patient's tolerance of pain and capacity to experience it without verbalization are influenced by race, culture, and religion. Some individuals—by virtue of training, habit, and phlegmatic temperament—remain stoic in the face of pain, and others react in an opposite fashion. Pain may be the presenting or predominant symptom in a depressive illness (Chap. 57).
Finally, a comment should be made about the devastating behavioral effects of chronic pain. To quote from Ambroise Paré, a sixteenth-century French surgeon, “There is nothing that abateth so much the strength as paine.” Continuous pain increases irritability and fatigue, disturbs sleep, and impairs appetite. Ordinarily strong persons can be reduced to a whimpering, pitiable state that may arouse the scorn of healthy observers. Patients in pain may seem irrational about their illness and make unreasonable demands on family and physician. Characteristic also is an unwillingness to engage in or continue any activity that might enhance their pain. They withdraw from the main current of daily affairs. Their thoughts and speech come to be dominated by the pain. Once a person is subjected to the tyranny of chronic pain, depressive symptoms are practically always added. The demand for and dependence on narcotics often complicate the clinical problem.