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diffuse and Well or poorly localized radiating Quality Sharp, pricking, or burning Usually dull or aching, Deep aching or sharp stabbing sensation cramping pain, which is often referred to cutaneous sites Associated symptoms Cutaneous tenderness, Tenderness, reflex muscle Malaise, nausea, vomiting, and signs hyperalgesia hyperesthesia, spasm, and sympathetic sweating, tenderness, reflex muscle allodynia hyperactivityb spasm Clinical examples Sunburn, chemical or Arthritis pain, tendonitis, Colic, appendicitis, pancreatitis, thermal burns, cuts and myofascial pain peptic ulcer disease, bladder contusions of the skin distension Sources: References 22-24 and 88-89. aVisceral organs include the heart, lungs, gastrointestinal tract, pancreas, liver, gallbladder, kidneys, and bladder. bSymptoms and signs of sympathetic (autonomic) nervous system hyperactivity include increased heart rate, blood pressure, and respiratory rate; sweating; pallor; dilated pupils; nausea; vomiting; dry mouth; and increased muscle tension. gData from animal studies suggest that the following changes may contribute to neuropathic pain: 1) generation of spontaneous ectopic activity, 2) loss of normal inhibitory mechanisms in the dorsal horn (i.e., central disinhibition), 3) altered primary afferent neuron phenotypes, and 4) sprouting of nerve fibers (i.e., altered neural connections).27,63-91-95 Collectively, these changes cause abnormal nerve impulse firing and/or abnormal signal amplification.48 in origin.96 Painful peripheral mononeuropathy and polyneuropathy, deafferentation pain, sympathetically maintained pain, and central pain are subdivisions of these categories. Neuropathic pain is sometimes called “pathologic” pain because it serves no purpose.81 A chronic pain state may occur when pathophysiologic changes become independent of the inciting event.46 Sensitization plays an important role in this process (see I.B.7-8). Although central sensitization is relatively short lived in the absence of continuing noxious input, nerve injury triggers changes in the CNS that can persist indefinitely.48 Thus, central sensitization explains why neuropathic pain is often disproportionate to the stimulus (e.g., hyperalgesia, allodynia) or occurs when no identifiable stimulus exists (e.g., persistent pain, pain spread). Neuropathic pain may be continuous or episodic and is perceived in many ways (e.g., burning, tingling, prickling, shooting, electric shock-like, jabbing, squeezing, deep aching, spasm, or cold).97 Table 2 summarizes examples and characteristics of neuropathic pain. C. C LASSIFICATION O F PAIN Although pain classes are not diagnoses, categorizing pain helps guide treatment. Multiple systems for classifying pain exist. These include multidimensional classification systems, such as the IASP Classification of Chronic Pain,19 and a variety of systems based on a single dimension of the pain experience. Of the latter systems, those 10 Pain: Current Understanding of Assessment, Management, and Treatments Section I: Background and Significance Table 2. Examples and Characteristics of Neuropathic Pain Painful Mononeuropathies and Sympathetically Polyneuropathies Deafferentation Pain Maintained Paina Central Pain Definition Pain along the distribution of Pain that is due to a loss Pain that is maintained Pain caused by a one or multiple peripheral of afferent input by sympathetic nervous primary lesion or nerve(s) caused by damage to system activity dysfunction of the CNS the affected nerve(s) Pain Three main types: • Quality: burning, • Quality: burning, • Quality: burning, characteristics • Continuous, deep, cramping, crushing, throbbing, pressing, numbing, tingling, and associated burning, aching or bruised pain aching, stabbing, or shooting shooting symptoms • Paroxysmal lancinating or shooting • Allodynia • Spontaneous and (shock-like) pain • Hyperalgesia • Hyperalgesia steady or evoked • Abnormal skin sensitivity • Hyperpathia • Associated ANS • +/- sensory loss • Dysesthesia dysregulation and • Allodynia • Other abnormal trophic changesb • Hyperalgesia sensations Sources • Metabolic disorders • Damage to a • Peripheral nerve • Ischemia (e.g., stroke) (e.g., diabetes) peripheral nerve, damage (e.g., CRPS II) • Tumors • Toxins (e.g., alcohol ganglion, or • Sympathetic efferent • Trauma (e.g., spinal chemotherapy agents) plexus (motor) innervation cord injury) • Infection (e.g., HIV, • CNS disease or • Stimulation of nerves • Syrinx herpes zoster) injury (occasional) by circulating • Demyelination • Trauma catecholamines • Compressive (nerve entrapment) • Autoimmune and hereditary diseases Clinical • Diabetic neuropathy • Phantom limb pain • CRPS • Post-stroke pain examples • Alcoholic neuropathy • Post-mastectomy pain • Phantom limb pain • Some cancer pain • Postherpetic neuralgia • Postherpetic neuralgia • Pain associated with • Carpal tunnel syndrome • Some metabolic multiple sclerosis neuropathies Sources: References 22-23, 87, and 97a-97d. aSympathetically maintained pain is a pain mechanism, not a diagnosis. It is associated with several types of pain, but it also may exist as a single entity.97c bFocal autonomic dysregulation can manifest with signs and symptoms such as swelling, pallor, erythema (redness), sweating, and temperature changes. Trophic changes include thinning of the skin,
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