Fwd: WHAT IS PAIN?

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Terminology

Acute pain and chronic pain differ in their etiology,

pathophysiology, diagnosis and treatment. Acute pain is self–limiting

and serves a protective biological function by acting as a warning of

on–going tissue damage. It is a symptom of a disease process

experienced in or around the injured or diseased tissue. Associated

psychological symptoms are minimal and are usually limited to mild

anxiety.

Acute pain is nociceptive in nature, and occurs secondary to

chemical, mechanical and thermal stimulation of A–delta and C–

polymodal pain receptors.Chronic pain, on the other hand, serves no

protective biological function. Rather than being the symptom of a

disease process, chronic pain is itself a disease process. Chronic

pain is unrelenting and not self–limiting and as stated earlier, can

persist for years and even decades after the initial injury. Chronic

pain can be refractory to multiple treatment modalities. If chronic

pain is inadequately treated, associated symptoms can include chronic

anxiety, fear, depression, sleeplessness and impairment of social

interaction. Chronic, non–malignant pain is predominately neuropathic

in nature and involves damage either to the peripheral or central

nervous systems.Nociceptive and neuropathic pain are caused by

different neuro–physiological processes, and therefore tend to

respond to different treatment modalities.

Nociceptive pain is mediated by receptors on A–delta and C–fibers

which are located in skin, bone, connective tissue, muscle and

viscera. These receptors serve a biologically useful role at

localizing noxious chemical, thermal and mechanical stimuli.

Nociceptive pain can be somatic or visceral in nature. Somatic pain

tends to be well localized, constant pain that is described as sharp,

aching, throbbing, or gnawing. Visceral pain, on the other hand,

tends to be vague in distribution, paroxysmal in nature and is

usually described as deep, aching, squeezing and colicky in nature.

Examples of nociceptive pain include: post–operative pain, pain

associated with trauma, and the chronic pain of arthritis.

Nociceptive pain usually responds to opioids and non–steroidal anti–

inflammatories (NSAIDS).Neuropathic pain, in contrast to nociceptive

pain, is described as " burning " , " electric " , " tingling " ,

and " shooting " in nature. It can be continuous or paroxysmal in

presentation. Whereas nociceptive pain is caused by the stimulation

of peripheral of A–delta and C–polymodal pain receptors, by

algogenic

substances (eg. histamine bradykinin, substance P, etc.) neuropathic

pain is produced by damage to, or pathological changes in the

peripheral or central nervous systems.Examples of pathological

changes include prolonged peripheral or central neuronal

sensitization, central sensitization related damage to nervous system

inhibitory functions, and abnormal interactions between the somatic

and sympathetic nervous systems.

The hallmarks of neuropathic pain are chronic allodynia and

hyperalgesia. Allodynia is defined as pain resulting from a stimulus

that ordinarily does not elicit a painful response (eg. light touch).

Hyperalgesia is defined as an increased sensitivity to a normally

painful stimuli. Primary hyperalgesia, caused by sensitization of C–

fibers, occurs immediately within the area of the injury. Secondary

hyperalgesia, caused by sensitization of dorsal horn neurons, occurs

in the undamaged area surrounding the injury.

Examples of neuropathic pain include: monoradiculopathies, trigeminal

neuralgia, postherpetic neuralgia, phantom limb pain, complex

regional pain syndromes and the various peripheral neuropathies.

Neuropathic pain tends to be only partially responsive to opioid

therapy.