Pain

Classification

In 1994, responding to the need for a more useful system for describing chronic pain, the International Association for the Study of Pain (IASP) classified pain according to specific characteristics:

1. region of the body involved (e.g. abdomen, lower limbs),
2. system whose dysfunction may be causing the pain (e.g., nervous, gastrointestinal),
3. duration and pattern of occurrence,
4. intensity and time since onset, and
5. cause

However, this system has been criticized by Clifford J. Woolf and others as inadequate for guiding research and treatment. Woolf suggests three classes of pain:

1. nociceptive pain,
2. inflammatory pain which is associated with tissue damage and the infiltration of immune cells, and
3. pathological pain which is a disease state caused by damage to the nervous system or by its abnormal function (e.g. fibromyalgia, peripheral neuropathy, tension type headache, etc.).

Duration

Pain is usually transitory, lasting only until the noxious stimulus is removed or the underlying damage or pathology has healed, but some painful conditions, such as rheumatoid arthritis, peripheral neuropathy, cancer and idiopathic pain, may persist for years. Pain that lasts a long time is called chronic or persistent, and pain that resolves quickly is called acute. Traditionally, the distinction between acute and chronic pain has relied upon an arbitrary interval of time from onset; the two most commonly used markers being 3 months and 6 months since the onset of pain, though some theorists and researchers have placed the transition from acute to chronic pain at 12 months. Others apply acute to pain that lasts less than 30 days, chronic to pain of more than six months' duration, and subacute to pain that lasts from one to six months. A popular alternative definition of chronic pain, involving no arbitrarily fixed durations, is "pain that extends beyond the expected period of healing". Chronic pain may be classified as cancer pain or else as benign.

Nociceptive

Nociceptive pain is caused by stimulation of sensory nerve fibers that respond to stimuli approaching or exceeding harmful intensity (nociceptors), and may be classified according to the mode of noxious stimulation. The most common categories are "thermal" (e.g. heat or cold), "mechanical" (e.g. crushing, tearing, shearing, etc.) and "chemical" (e.g. iodine in a cut or chemicals released during inflammation). Some nociceptors respond to more than one of these modalities and are consequently designated polymodal.

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.

Neuropathic

Neuropathic pain is caused by damage or disease affecting any part of the nervous system involved in bodily feelings (the somatosensory system). Peripheral neuropathic pain is often described as "burning", "tingling", "electrical", "stabbing", or "pins and needles". Bumping the "funny bone" elicits acute peripheral neuropathic pain.

Phantom

Phantom pain is pain felt in a part of the body that has been lost or from which the brain no longer receives signals. It is a type of neuropathic pain. Phantom limb pain is a common experience of amputees.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb. Phantom limb pain may accompany urination or defecation.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Mirror box therapy produces the illusion of movement and touch in a phantom limb which in turn may cause a reduction in pain.

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Psychogenic

Psychogenic pain, also called psychalgia or somatoform pain, is pain caused, increased, or prolonged by mental, emotional, or behavioral factors. Headache, back pain, and stomach pain are sometimes diagnosed as psychogenic. Sufferers are often stigmatized, because both medical professionals and the general public tend to think that pain from a psychological source is not "real". However, specialists consider that it is no less actual or hurtful than pain from any other source.

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

The term 'psychogenic' assumes that medical diagnosis is so perfect that all organic causes of pain can be detected; regrettably, we are far from such infallibility... All too often, the diagnosis of neurosis as the cause of pain hides our ignorance of many aspects of pain medicine.

Breakthrough pain

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's regular pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

Incident pain

Incident pain is pain that arises as a result of activity, such as movement of an arthritic joint, stretching a wound, etc.

Pain asymbolia and insensitivity

The ability to experience pain is essential for protection from injury, and recognition of the presence of injury. Episodic analgesia may occur under special circumstances, such as in the excitement of sport or war: a soldier on the battlefield may feel no pain for many hours from a traumatic amputation or other severe injury.

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Insensitivity to pain may also result from abnormalities in the nervous system. This is usually the result of acquired damage to the nerves, such as spinal cord injury, diabetes mellitus (diabetic neuropathy), or leprosy in countries where that disease is prevalent. These individuals are at risk of tissue damage and infection due to undiscovered injuries. People with diabetes-related nerve damage, for instance, sustain poorly-healing foot ulcers as a result of decreased sensation.

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy. Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Na_v1.7) necessary in conducting pain nerve stimuli.

Effect on functioning

Experimental subjects challenged by acute pain and patients in chronic pain experience impairments in attention control, working memory, mental flexibility, problem solving, and information processing speed. Acute and chronic pain are also associated with increased depression, anxiety, fear, and anger.

If I have matters right, the consequences of pain will include direct physical distress, unemployment, financial difficulties, marital disharmony, and difficulties in concentration and attention…

Historical theories

Before the relatively recent discovery of neurons and their role in pain, various different body functions were proposed to account for pain. There were several competing early theories of pain among the ancient Greeks: Hippocrates believed that it was due to an imbalance in vital fluids. In the 11th century, Avicenna theorized that there were a number of feeling senses including touch, pain and titillation.

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt.

Three dimensions of pain

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

Theory today

Wilhelm Erb's (1874) "intensive" theory, that a pain signal can be generated by intense enough stimulation of any sensory receptor, has been soundly disproved. Some sensory fibers do not differentiate between noxious and non-noxious stimuli, while others, nociceptors, respond only to noxious, high intensity stimuli. At the peripheral end of the nociceptor, noxious stimuli generate currents that, above a given threshold, send signals along the nerve fiber to the spinal cord. The "specificity" (whether it responds to thermal, chemical or mechanical features of its environment) of a nociceptor is determined by which ion channels it expresses at its peripheral end. Dozens of different types of nociceptor ion channels have so far been identified, and their exact functions are still being determined.

The pain signal travels from the periphery to the spinal cord along an A-delta or C fiber. Because the A-delta fiber is thicker than the C fiber, and is thinly sheathed in an electrically insulating material (myelin), it carries its signal faster (5–30 m/s) than the unmyelinated C fiber (0.5–2 m/s). Pain evoked by the A-delta fibers is described as sharp and is felt first. This is followed by a duller pain, often described as burning, carried by the C fibers. These "first order" neurons enter the spinal cord via Lissauer's tract.

These A-delta and C fibers connect with "second order" nerve fibers in the central gelatinous substance of the spinal cord (laminae II and III of the dorsal horns). The second order fibers then cross the cord via the anterior white commissure and ascend in the spinothalamic tract. Before reaching the brain, the spinothalamic tract splits into the lateral, neospinothalamic tract and the medial, paleospinothalamic tract.

Second order neospinothalamic tract neurons carry information from A-delta fibers and terminate at the ventral posterolateral nucleus of the thalamus, where they connect with third order neurons of the somatosensory cortex. Paleospinothalamic neurons carry information from C fibers and terminate throughout the brain stem, a tenth of them in the thalamus and the rest in the medulla, pons and periaqueductal gray matter.

Second order, spinal cord fibers dedicated to carrying A-delta fiber pain signals, and others that carry both A-delta and C fiber pain signals to the thalamus have been identified. Other spinal cord fibers, known as wide dynamic range neurons, respond to A-delta and C fibers, but also to the large A-beta fibers that carry touch, pressure and vibration signals. Pain-related activity in the thalamus spreads to the insular cortex (thought to embody, among other things, the feeling that distinguishes pain from other homeostatic emotions such as itch and nausea) and anterior cingulate cortex (thought to embody, among other things, the affective/motivational element, the unpleasantness of pain). Pain that is distinctly located also activates primary and secondary somatosensory cortex.

Evolutionary and behavioral role

Pain is part of the body's defense system, producing a reflexive retraction from the painful stimulus, and tendencies to protect the affected body part while it heals, and avoid that harmful situation in the future. It is an important part of animal life, vital to healthy survival. People with congenital insensitivity to pain have reduced life expectancy.

In his book, The Greatest Show on Earth: The Evidence for Evolution, biologist Richard Dawkins grapples with the question of why pain has to be so very painful. He describes the alternative as a simple, mental raising of a "red flag". To argue why that red flag might be insufficient, Dawkins explains that drives must compete with each other within living beings. The most fit creature would be the one whose pains are well balanced. Those pains which mean certain death when ignored will become the most powerfully felt. The relative intensities of pain, then, may resemble the relative importance of that risk to our ancestors (lack of food, too much cold, or serious injuries are felt as agony, whereas minor damage is felt as mere discomfort). This resemblance will not be perfect, however, because natural selection can be a poor designer. The result is often glitches in animals, including supernormal stimuli. Such glitches help explain pains which are not, or at least no longer directly adaptive (e.g. perhaps some forms of toothache, or injury to fingernails).

Idiopathic pain (pain that persists after the trauma or pathology has healed, or that arises without any apparent cause), may be an exception to the idea that pain is helpful to survival, although some psychodynamic psychologists argue that such pain is psychogenic, enlisted as a protective distraction to keep dangerous emotions unconscious.

Thresholds

In pain science, thresholds are measured by gradually increasing the intensity of a stimulus such as electric current or heat applied to the body. The pain perception threshold is the point at which the stimulus begins to hurt, and the pain tolerance threshold is reached when the subject acts to stop the pain.

Differences in pain perception and tolerance thresholds are associated with, among other factors, ethnicity, genetics, and sex. People of Mediterranean origin report as painful some radiant heat intensities that northern Europeans describe as nonpainful. And Italian women tolerate less intense electric shock than Jewish or Native American women. Some individuals in all cultures have significantly higher than normal pain perception and tolerance thresholds. For instance, patients who experience painless heart attacks have higher pain thresholds for electric shock, muscle cramp and heat.

Assessment

A person's self-report is the most reliable measure of pain. Some health care professionals may to underestimate severity. A definition of pain widely employed in nursing, emphasizing its subjective nature and the importance of believing patient reports, was introduced by Margo McCaffery in 1968: "Pain is whatever the experiencing person says it is, existing whenever he says it does". To assess intensity, the patient may be asked to locate their pain on a scale of 0 to 10, with 0 being no pain at all, and 10 the worst pain they have ever felt. Quality can be established by having the patient complete the McGill Pain Questionnaire indicating which words best describe their pain.

Multidimensional pain inventory

The Multidimensional Pain Inventory (MPI) is a questionnaire designed to assess the psychosocial state of a person with chronic pain. Analysis of MPI results by Turk and Rudy (1988) found three classes of chronic pain patient: "(a) dysfunctional, people who perceived the severity of their pain to be high, reported that pain interfered with much of their lives, reported a higher degree of psychological distress caused by pain, and reported low levels of activity; (b) interpersonally distressed, people with a common perception that significant others were not very supportive of their pain problems; and (c) adaptive copers, patients who reported high levels of