(ĐTĐ) - Pain is purely subjective, difficult to define, and often hard to characterize or interpret. It is currently defined as an unpleasant sensory and emotional response to a stimulus associated with actual or potential tissue damage or described in terms of such damage (3–5).


However, pain has never been shown to be a simple function of the amount of physical injury; it is extensively influenced by anxiety, depression, expectation, and other psychological and physiological variables. It is a multifaceted experience, an interweaving of the physical characteristics of the stimulus with the individual’s motivational, affective, and cognitive functions. The pain experience is in part behavior based on an interpretation of the event, influenced by present and past experiences.

Acute pain

Acute pain is a biologic symptom of an apparent nociceptive stimulus, such as tissue damage that is due to disease or trauma that persists only as long as the tissue pathology itself persists. The pain may be highly localized or may radiate. Acute somatic pain may be well localized, aching, and sharp, whereas acute visceral pain may be burning, cramping, and radiating. It is usually associated with upregulated sympathetic activity, tachycardia, hypertension, tachypnea, increased metabolic rate, and hypercoagulability. Acute pain is generally self-limiting, and as the nociceptive stimulus lessens, the pain decreases. Acute pain usually lasts a few days to a few weeks (4). If it is not effectively treated, it may progress to a chronic form.

Chronic pain

Chronic pain is a disease process in which the pain is a persistent symptom of an autonomous disorder with neurologic, psychological, and physiologic components. Differing significantly from acute pain, it is defined as pain lasting longer than anticipated (greater than 3 months) within the context of the usual course of an acute disease or injury. The pain may be associated with continued pathology or may persist after recovery from a disease or injury. Due to the complex nature of chronic pain, many other definitions have been proposed. Some include factors such as the persistence of pain despite extraordinary measures in a nonacute setting or pain that is without apparent biological value (6). Operational definitions include aspects such as pain sensation, pain behavior, functional status, emotion, and somatic preoccupation (6). As with acute pain, treatable chronic pain that is due to organic disease is managed by effectively treating the underlying disorder; however, no such identifiable organic disease may be evident. Chronic pain can mimic the qualities of acute pain except that associated signs of autonomic nervous system response may be absent, and the patient may appear exhausted, listless, depressed, and withdrawn. Chronic pain can have exacerbations that are triggered by progression of organic pathology, physiologic stress, or worsening emotional, social, and psychiatric problems. As these problems subside, the pain may improve. Chronic pain may also be highly persistent and reported as severe for years without remission. Proper management of pain requires an understanding of its complexity and knowledge of the nonneurologic factors that determine its individual expression. The treatment of pain with physical modalities is as ancient as the history of humanity, but the use of interdisciplinary rehabilitation techniques has gained acceptance only within the past few decades.

Epidemiology

Nearly everyone experiences acute pain. Its incidence approximates the cumulative total of all acute diseases, trauma, and surgical procedures. In studies of the general population, patients have identified the head and lower limbs as the most common sites of acute pain and have identified the back as the most common site of chronic pain (7). Chronic pain is less frequently experienced but is reaching epidemic proportions in the United States. There are more than 36 million individuals with arthritis, 70 million with episodic back pain, 20 million with migraine headaches, and additional millions with pain that is due to gout, myofascial pain syndromes, phantom limb pain, and complex regional pain syndromes (CRPS) (8–11). The pain resulting from cancer afflicts approximately 1 million Americans and 20 million individuals worldwide. Moderate to severe pain occurs in about 40% of patients with intermediate-stage cancer and in 60% to 80% of patients with advanced cancer (12–14). Back pain, as a general condition, episodically affects nearly 75% of the population in most industrialized nations. It is estimated that at least 10% to 15% of the working population of industrialized nations are affected by back pain each year (9,10).

Genetics and Pain

The genetic determinants have been evaluated in humans with clinical pain (47). The variability in pain syndromes has been associated with inherited genetic factors in back pain (48), fibromyalgia (FM) (49), menstrual pain (50), and migraine (51). Family and twin heritability estimates indicate genetic as well as significant environmental factors modulating pain (52,53). Polymorphic pain genes have been associated with congenital insensitivity to pain (54), drug metabolism due to cytochrome P450 (55), familial hemiplegic migraine (52,56), FM (57), and reflex sympathetic dystrophy (58).

Gene therapy and other advances in molecular medicine may offer a means of enhancing antinociceptive receptors ( cannaboid—1 and 2, acetylcholine—m and n, opioid—m and k, adrenergic—a2) or blocking pronociceptive receptors (neurokinin—1-a-amino-3-hydroxy-5-methyl-4-isoazoleproprionate [AMPA], n-methyl-d-aspartate [NMDA]); acting directly on the calcium channels of pain fibers; or acting directly on membrane receptors, protein C-GAMA, or other areas of the central nervous system involved in the transmission of pain (59,60). Definitive applications of gene intervention in pain control remain to be developed.

Resolution of Pain

Acute pain is frequently the result of tissue damage in which the initial pain leads to an increase in anxiety, which magnifies the pain experience. The amount of anxiety generated and possibly the level of pain seem to be more influenced by the setting in which the pain develops rather than personality variables. With the healing process comes a reduction or termination of the anxiety and acute pain perception. When acute pain, which functions as a warning signal, fails to respond to treatment with conventional medical therapies, illness behavior and chronic pain develop. The anxiety characteristic of acute pain is replaced by depression with hopelessness, helplessness, and despair. When pain relief fails, physical activities decrease and suffering and depression increase.

Acute pain usually resolves when the source of nociception is removed or cured and resolves quickly with application of appropriate pharmacologic or regional analgesic therapy. The cause of acute pain can be documented by physical examination findings and diagnostic procedures. When indicated, appropriate operative intervention can be performed on the basis of these findings. A short course of analgesic medication usually controls postoperative pain, and a return to full, painless function can be anticipated in a matter of weeks. Acute pain control requires the administration of an efficacious analgesic dosage. Too little analgesia promotes suffering and anxiety, thus defeating the purpose of prescribing medications. Fear of drug addiction contributes to the underutilization of analgesic medications, and physicians tend to undermedicate in terms of frequency and dosage of pain medications (61,62). By prescribing low oral doses of opioids at infrequent intervals, physicians inadvertently force patients to adopt pain behavior in order to obtain adequate opioid analgesia. Pain behavior is characterized by high verbalization of pain, dependency, and the inability to work. Addiction in the acute pain situation is very rare, approximating less than 0.1% (63,64).

Unfortunately, a significant minority of acute pain patients continues to experience pain, which may progress into a more complex disease entity. Pain, a symptom of physiologic malfunction, now becomes the disease itself. Chronic pain represents a complex interaction of physical, psychological, and social factors in which the pain complaint is a socially acceptable manifestation of the disease. The etiology of chronic pain may be persistent nociceptive input, such as arthritis or terminal cancer; psychological disorders, such an anxiety, depression, and learned behavior; or social factors, such as job loss, divorce, and secondary gain.

The optimal treatment for chronic pain is prevention. Once the disease state of chronic pain commences, reinforcers such as monetary compensation, presence of job-related problems, manipulation of the environment to satisfy unmet needs, and retirement from the competitive world obstruct complete disease resolution. Therapies designed for acute pain are often contraindicated for chronic pain.

Prevention of chronic pain requires identifying contributing factors and resolving them early in the acute stage. Aspects worthy of attention include psychological stress, drug or alcohol abuse, and poor posture or muscle tone, as well as significant psychological and operant pain mechanisms. Physicians should set a reasonable timeframe for the resolution of the acute pain process. Patients should be advised when the pain medication will no longer be needed and that those medications that are no longer effective will not be continued. The patient’s attention should be directed to a gradual return of full activity on a prescribed schedule. Follow-up appointments should be planned at specified intervals so that the patient does not need to justify a visit. Work intolerance and job conflicts should be resolved.

Pain-Reinforcing Factors

Chronic pain syndrome is a learned behavior pattern reinforced by multiple factors. These behaviors are frequently found in individuals who are depressed, are inactive, and lack the skills or opportunity to compete in the community. These environmental factors promote pain behavior, regardless of the etiology of the pain, thereby distinguishing the patient with chronic pain from the population at large. Patients often develop a new self-image and see themselves as disabled by their pain. This self-perceived disability justifies their inactivity and manipulation of others and attempts to collect compensation. The typical patient often has been unemployed, has low job satisfaction, or has been on sick leave for long periods of time (65–68). Our data indicate that individuals who have been removed from the labor market because of pain for less than 6 months have a 90% chance of returning to full employment; those removed from the labor force because of pain for more than 1 year have less than a 10% chance of return to full employment (66). Individuals with chronic pain syndrome receive gains from their pain behavior; hence, they continue this behavior to maintain those positive reinforcers. Physicians reinforce the pain behaviors by lacking knowledge of this chronic disease process, failing to identify the chronic pain behavior and prolonging prescription of inappropriate medications, inactivity, and work limitations. The physician’s failure to acknowledge and direct the patient toward recovery tends to validate the chronic pain syndrome by providing an undiagnosable and untreatable problem. Family members also frequently reinforce the chronic pain behavior. They allow the individual to become inactive and cater to the patient’s requests and needs over prolonged periods of time. In some instances, patients with chronic pain provide role models for pain or disability behavior for other family members (69,70).

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