Chapter 4. Definitions and Classification of Pain

“For all the happiness

Mankind can gain;

Is not in pleasure,

But in rest from pain.”

John Dryden (1631–1701)

Relief of pain is one of the great objectives of medicine. Pain is the most common symptom reported to physicians; more than 80% of all patients who see physicians do so because of pain. It has been a predominant concern of humankind since the beginning of recorded history. Chronic pain affects hundreds of millions of people worldwide, altering their physical and emotional functioning, decreasing their quality of life, and impairing the ability to work. It affects general health, psychological health, and social and economic well-being. Patients in chronic pain use health services up to five times more frequently than the rest of the population. The cost of unrelieved chronic pain in the United States is more than $50 billion per year (more than $80 billion per year if lost wages from work are counted) and in the age of steady cost-cutting in a managed care environment, we can no longer afford it. More than 550 million workdays are lost every year because of chronic pain. Yet 40% of all cancer patients, 50% of nursing home patients, 55% of postoperative patients, and 70% of patients with acquired immunodeficiency syndrome (AIDS) have unrelieved or inadequately relieved pain.

In October 2000, the 106th U.S. Congress passed HR 3244, which was then signed into law. Title VI, Sec. 1603, provides for the “Decade of Pain Control and Research,” to begin January 2001. It follows the “Decade of the Brain” and is only the second congressionally declared, medically related decade. Pain is now designated as a public health problem of national significance. Beginning in 2001, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) implemented new standards to assess and treat pain. To qualify for accreditation, all facilities, including rehabilitation centers, outpatient surgical centers, hospitals, and nursing homes, must recognize the right of patients to appropriate assessment and management of pain. All health care facilities must identify pain in patients during initial assessment and, where required, during ongoing periodic assessments and must educate patients and their families about pain management.

The word pain is derived from the Latin poena, meaning punishment. The International Association for the Study of Pain (IASP) defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”1 This definition may appear somewhat convoluted, but it clearly states that pain is subjective. It is both a physiologic sensation and an emotional reaction to that sensation. Viewed from an evolutionary prospective, pain is perceived as a threat or damage to one’s biological integrity and has three components: sensory-discriminative, motivational-affective, and cognitive-evaluative.

The concepts of pain and suffering are frequently mixed and sometimes confused in the dialogue between patient and physician, especially because pain is commonly used as if it were synonymous with suffering. However, pain and suffering are distinct phenomena. Suffering is loosely defined as a “state of severe distress associated with events that threaten the intactness of person.” Not all pain causes suffering, and not all suffering expressed as pain or coexisting with pain, stems from pain.

Pain has a protective role. It warns us of imminent or actual tissue damage. If tissue damage is unavoidable, a set of excitability changes in the peripheral and central nervous systems establish profound but reversible pain hypersensitivity in inflamed and surrounding tissue. This process avoids further damage until wound healing has occurred. In contrast, chronic pain syndromes offer no biologic advantage and cause suffering and distress.

Acute pain

Acute pain signifies the presence of a noxious stimulus that produces actual tissue damage or possesses the potential to do so. The presence of acute pain implies the presence of an intact nervous system and is associated with autonomic hyperactivity: hypertension, tachycardia, sweating, and vasoconstriction. A common definition of acute pain is “the normal, predicted physiologic response to an adverse chemical, thermal, or mechanical stimulus . . associated with surgery, trauma, and acute illness.” Acute pain is short lived.

Allodynia

Implies pain caused by a stimulus, which does not normally provoke pain. Allo means “other” in Greek and is a common prefix for medical conditions that diverge from the expected. Odynia is derived from the Greek word “odune” or “odyne,” which is used in “pleurodynia” and “coccydynia” and is similar in meaning to the root from which we derive words with –algia or –algesia in them. Allodynia is common in many neuropathic conditions, such as postherpetic neuralgia, chronic regional pain syndromes, and certain peripheral neuropathies. Allodynia can be produced in two ways: by the action of low-threshold myelinated Aβ fibers on an altered central nervous system, and by a reduction in the threshold of nociceptor terminals in the periphery. As allodynia is used in the terms of clinical diagnosis, it can be also used to subclassify the broader symptoms of hyperalgesia, which may help identify the mechanisms causing it.

Analgesia

Implies absence of pain in response to stimulation, which would normally be painful. Analgesia can be produced peripherally (at the site of tissue damage, receptor, or nerve) or centrally (in the spinal cord or brain).

Anesthesia dolorosa

Implies pain in an area or region, which is anesthetic. Anesthesia dolorosa is more common after lesions that totally denervate a region. It is most commonly noted after surgery for atypical facial pain but can occur after surgery for tic douloureux or after traumatic nerve injury.

Central pain

Pain initiated or caused by a primary lesion or dysfunction in the central nervous system. Any type of vascular, demyelinating, infectious, inflammatory, or traumatic lesion in the brain or spinal cord can produce central pain syndrome.

Chronic pain

Defining when a pain becomes chronic is always difficult. Pain that is unlikely to resolve or pain that lasts longer than the usual healing time is defined as chronic pain. From a temporal perspective, pain is deemed to be chronic when it persists beyond 3 months. Function of the nervous system becomes reorganized (neuroplasticity) with the potential for spontaneous and atopic nerve excitation.

Complex regional pain syndrome

Used to describe the painful syndromes that formerly were described under the title of reflex sympathetic dystrophy and causalgia. The term reflex sympathetic dystrophy was a misnomer, because not all cases have sympathetically maintained pain and not all were dystrophic. Thus, in 1993, a consensus group of pain medicine experts (a special consensus workshop of the IASP) gathered with the task of redefining causalgia and reflex sympathetic dystrophy. The diagnostic criteria proposed are purely clinical, with no laboratory test or diagnostic blocks. The consensus group divided the disorders based on the type of injury that initiated the disorder: type I, following a soft tissue injury, similar to reflex sympathy dystrophy (RSD), and type II, following well-defined nerve injury.

The criteria for complex regional pain syndrome, type I, are as follows:

• 1. The presence of an initiating noxious event or a cause for immobilization.
• 2. Continuing pain, allodynia, or hyperalgesia in which the pain is disproportionate to any known or inciting event.
• 3. Evidence at some time of edema, changes in the skin blood flow, or abnormal sudomotor activity in the region of pain.
• 4. The diagnosis is excluded by the existence of other conditions that would otherwise account for the degree of dysfunction.

Complex regional pain syndrome, type II, has the same clinical features as type I except for the clinical signs and history consistent with a specific nerve injury.

Dysesthesia

An unpleasant abnormal sensation, whether spontaneous or evoked. Examples include the burning feet that may be felt in alcoholic neuropathy.

Hyperalgesia

An increased response to a stimulus that is normally painful. It is the result of abnormal processing of nociceptor input. Stimulus-evoked hyperalgesias are commonly classified into subgroups on the basis of modality (i.e., mechanical, thermal, or chemical). Mechanical hyperalgesias are further classified as brush-evoked (dynamic), pressure-evoked (static), and punctuate hyperalgesia. Brush-evoked (dynamic) hyperalgesia is a consequence of increased central response to Aβ fiber input.

Hyperesthesia

Increased sensitivity to stimulation, excluding special senses.

Hyperpathia

A painful syndrome characterized by an abnormally explosive painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold. Faulty identification and localization of the stimulus, delay, radiating sensation, and after sensation may occur.

Hypoalgesia

Diminished response to a normally painful stimulus.

Hypoesthesia

Decreased sensitivity to stimulation, excluding the special senses.

Neuralgia

Pain in the distribution of a peripheral nerve, typically described as lancinating or electric shock–like sensation

Neuritis

A special type of neuropathy; the term is reserved primarily for describing inflammatory process affecting nerves.

Neurogenic pain

Pain initiated or caused by a primary lesion or dysfunction, or by transitory perturbation in the peripheral or central nervous system.

Neuropathic pain

Pain initiated or caused by a primary lesion or dysfunction in the nervous system. Neuropathic pain syndromes can originate at any point or points along the somatosensory pathways, from the most distal nerve endings in the skin to the somatosensory cortex in the parietal lobe.

Neuropathy

A disturbance of function or pathologic change in nerves. It may be in a single nerve (mononeuropathy), in several nerves (mononeuropathy multiplex), or symmetric and bilateral (polyneuropathy).

Nociceptor

A receptor preferentially sensitive to a noxious stimulus or to a stimulus that would become noxious if prolonged.

Noxious stimulus

A stimulus that is damaging to normal tissues.

Pain threshold

The least experience of pain that a subject can recognize.

Pain tolerance level

The greatest level of pain a subject is prepared to tolerate.

Paresthesia

An abnormal sensation, whether spontaneous or evoked. The most common paresthesia is the sense of “pins and needles.”

Peripheral neurogenic pain

Pain initiated or caused by a primary lesion or dysfunction, or by transitory perturbation in the peripheral nervous system.

Peripheral neuropathic pain

Pain initiated or caused by a primary lesion or dysfunction in the peripheral nervous system.

Phantom pain

Pain in a part of the body that has been surgically removed or is congenitally absent. Although best described after limb amputations, phantom pain can occur after a wide variety of amputations, including mastectomy, dental extraction, and removal of visceral organs such as the rectum.

Referred pain

Pain localized not to the site of its cause but to an area that may be adjacent to or at a distance from such a site. An example is shoulder pain caused by diaphragmatic irritation.

The most recognized categories of classification are based on neurophysiologic mechanism, temporal aspects, etiology, or region affected.

Neurophysiologic

The neurophysiologic classification is based on inferred mechanism of pain. There are essentially two types of pain: nociceptive pain and non-nociceptive pain.

The term nociceptive is applied to pain that is presumed to be maintained by continual tissue injury. Nociceptive pain results from the activation or sensitization of nociceptors in the periphery, which transduce noxious stimulus into electrochemical impulses. These impulses are then transmitted to the spinal cord and higher rostral centers within the central nervous system. Arthritic, acute postoperative, and postoperative pain fall into this category.

Nociceptive pain is further subdivided into somatic and visceral pain, which can be distinguished by the quality of the pain and associated clinical features. Somatic pain results from excitation and sensitization of nociceptors in tissues such as bone, periarticular soft tissue, joints, and muscles. Four physiologic processes are involved in the somatic nociception: (1) transduction, (2) transmission, (3) modulation, and (4) perception. Somatic pain is characterized as being well localized topographically, intermittent, or constant and is described as “aching, stabbing, gnawing, or throbbing.”

Visceral pain has five important clinical characteristics:

• 1. It is not evoked from all visceral organs, such as liver; kidney, most solid viscera, and lung parenchyma are not sensitive to pain.
• 2. It is not always linked to visceral injury (cutting the intestine causes no pain, whereas stretching of the bladder causes pain).
• 3. It is diffuse and poorly localized, owing to organization of visceral nociceptive pathways in the central nervous system, particularly the absence of a separate visceral sensory pathway and the low proportion of the visceral afferent nerve fibers.
• 4. It is referred to other locations.
• 5. It is accompanied by motor and autonomic reflexes, such as the nausea, vomiting, and lower back muscle tension that occur in renal colic. Discrete nociceptors in the cardiovascular, respiratory, gastrointestinal, and genitourinary systems mediate visceral pain. Although its neural pathways are less well defined than those of somatic pain, the visceral pathways share some of the features with somatic pathways. Visceral pain is less topographically distinct and is described as diffuse. It may be intermittent or constant and is often described as “dull, colicky, or squeezing.”

Non-nociceptive pain can be subdivided into neuropathic and idiopathic pain. Neuropathic pain results from injury to neural structures within the peripheral or central nervous system. It is believed to be sustained by aberrant somatosensory processing in the periphery or central nervous system. Neuropathic pain is typically described as “sharp or burning.” There are three subsets of neuropathic pain. Peripherally generated neuropathic pain involves such entities as cervical or lumbar radiculopathy, spinal nerve lesions, and brachial or lumbosacral plexopathies. Centrally generated pain involves injury to the central nervous system at the level of the spinal cord or above. Sympathetically maintained pain may be generated peripherally or centrally and is characterized by localized autonomic dysregulation in the affected area, with vasomotor or sudomotor changes, edema, sweating, and atrophy. It is referred to as reflex sympathetic dystrophy, causalgia, or, more recently, complex regional pain syndrome.

The term idiopathic pain has been used interchangeably with the term psychogenic pain. Idiopathic pain is probably the more appropriate term because it implies a wider spectrum of poorly understood pain states. Myofascial pain syndrome and somatoform pain disorder are examples of idiopathic pain. In some patients, there is no evidence of an associated organic cause, whereas in others, pain and associated symptoms are grossly out of proportion to identifiable organic pathology.

Finally, it is worth emphasizing that all pain has a psychological component. Psychological factors, which are often not obvious, as well as cultural and environmental factors, must be taken into consideration when evaluating a patient with chronic pain. For example, emotional arousal can enhance nociception at the periphery. Heightened sympathetic activity with the release of norepinephrine at the sympathetic terminals can sensitize or directly activate nociceptors; similarly, reflex muscle spasm caused by anxiety can contribute to a positive feedback loop in which nociception fosters increased muscle tone in the area near the site of injury, eventually activating the muscle nociceptors. Patients in clinical practice often exhibit more than one type of pain. One example is patients with cancer pain who may have neuropathic, nociceptive, and myofascial pain.

Temporal

The temporal classification is based on the duration of symptoms and is usually divided into acute and chronic categories. The major shortcoming is that distinction between acute and chronic is arbitrary. Cancer pain includes pain associated with the disease progression, treatment, and concurrent conditions. Hence, the pain associated with cancer may be acute or chronic. Some clinicians advocate cancer pain as a third category, distinct from acute and chronic pain.

Mechanism-Based

In 1998, Woolf and his colleagues suggested implementation of a mechanism-based classification of pain. They believed it could have profound implications: drugs could be developed that target distinct mechanisms, basic scientists could have new guidelines for experimental design, and clinicians could be armed with more reliable and valid diagnostic tools for treatment and clinical investigation.

Etiologic

The etiologic classification pays more attention to the primary disease process in which the pain occurs, rather than to the neurophysiologic basis. Examples include cancer pain, arthritis pain, and pain in sickle cell disease. Therapeutically, it is less useful than the neurophysiologic classification.

Regional

The regional classification is strictly topographic and does not infer pathophysiology or etiology. It is defined by the part of the body affected.

Multiaxial

An alternative to the one-dimensional approach is the multidimensional approach. The IASP has published an expert-based multiaxial classification of chronic pain with the goals of standardization and provision of a point of reference. The published taxonomy classifies chronic pain patients according to five axes based on the best-published information and consensus:

• a. Region of the body affected (axis I)

• b. System whose abnormal functioning could conceivably produce pain (axis II)

• c. Temporal characteristics of pain and pattern of occurrence (axis III)

• d. Patient’s statement of intensity and time since the onset of pain (axis IV)

• e. Presumed etiology (axis V)

Pain management is a rapidly advancing field. Many concepts and terminologies that were a source of confusion in the past have now been more clearly defined. However, more work clearly needs to be done in classification and taxonomy to simplify the communication and meet the objectives of basic scientists, researchers, and clinicians providing patient care.