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. According to an Institute of Medicine report released in 2011, one in three Americans experiences chronic pain—more than the total affected by heart disease, cancer, and diabetes combined. In Europe, the prevalence of chronic pain is 25% to 30%. It affects general health, psychological health, and social and economic well-being. Pain as a symptom—now considered the fifth vital sign—accounts for approximately 80% of physician visits and is estimated to cause $650 billion (in U.S. dollars) annually between health care expenditures and lost productivity percentage. More than 550 million workdays are lost every year because of chronic pain.

In October 2000, the 106th U.S. Congress passed HR 3244, which was then signed into law. Title VI, Section 1603, provides for the “Decade of Pain Control and Research,” to begin in 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.” 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: 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: Pain in response to a non-nociceptive stimulus. 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.

Catastrophizing: A distinct phenomenon characterized by feelings of helplessness, active rumination, and excessive magnification of cognitions and feelings toward the painful situation. Pain catastrophizing has been shown to be an important predictor of response to both acute and chronic pain.

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 (CRPS): CRPS is a syndrome characterized by a continuing (spontaneous and/or evoked) regional pain that is seemingly disproportionate in time or degree to the usual course of any known trauma or other lesion. The pain is regional (not in a specific nerve territory or dermatome) and usually has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor, and/or trophic findings. The syndrome shows variable progression over time. 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 sympathetic dystrophy (RSD), and type II, following well-defined nerve injury.

IASP criteria are as follows:

CRPS I

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.

CRPS II

1. 
   

   Type II is a syndrome that develops after nerve injury. Spontaneous pain or allodynia/hyperalgesia occurs and is not necessarily limited to the territory of the injured nerve.

   
   
2. 
   

   There is or has been evidence of edema, skin blood flow abnormality, or abnormal sudomotor activity in the region of the pain since the inciting event.

   
   
3. 
   

   This diagnosis is excluded by the existence of the conditions that would otherwise account for the degree of pain and dysfunction.

Ten years after the IASP conference, new diagnostic criteria were defined by the Budapest task force in a consensus conference. Also, there is more recent evidence that both CRPS type I and CRPS type II may be associated with nerve injury, and CRPS I may represent a small fiber predominant mono- or oligoneuropathy that is initiated by limb trauma.

The IASP criteria as written (i.e., criteria can be met by either self-reported symptoms or objective signs) were highly sensitive but had poor specificity.

Budapest clinical diagnostic criteria:

1. 
   

   Continuing pain, which is disproportionate to any inciting event

   
   
2. 
   

   Must report at least one symptom in three of the four following categories:

   
   
   
   
   • 
     

     Sensory: reports of hyperesthesia and/or allodynia

     
     
   • 
     

     Vasomotor: reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry

     
     
   • 
     

     Sudomotor/edema: reports of edema and/or sweating changes and/or sweating asymmetry

     
     
   • 
     

     Motor/trophic: reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)

   
   
3. 
   

   Must display at least one sign at time of evaluation in two or more of the following categories:

   
   
   
   
   • 
     

     Sensory: evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement)

     
     
   • 
     

     Vasomotor: evidence of temperature asymmetry and/or skin color changes and/or asymmetry

     
     
   • 
     

     Sudomotor/edema: evidence of edema and/or sweating changes and/or sweating asymmetry

     
     
   • 
     

     Motor/trophic: evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)

   
   
4. 
   

   There is no other diagnosis that better explains the signs and symptoms

Deafferentation pain: Pathological pain condition associated with a partial or complete loss of sensory input from a part of the body after lesions in somatosensory pathways, often as a result of reorganization in the central nervous system.