Pain is the most common reason for medical appointments, resulting in an estimated 40 million visits annually and costing an estimated $100 billion each year in healthcare and lost productivity. According to the American Pain Foundation, one in three Americans lose more than 20 h of sleep each month due to pain. In addition, over 26 million people between the ages of 20 and 64 experience frequent back pain and two-thirds of Americans will have back pain during their lifetime. Furthermore, only an estimated one in four people with pain receive proper treatment.

Drugs for the treatment of pain, or analgesics, have been historically placed into one of two general categories: (1) opioids (narcotics) such as morphine, codeine, and fentanyl; and (2) non-opioid inhibitors of cyclooxygenase (COX), like aspirin, ibuprofen, and celecoxib. Both opioid and non-opioid analgesics are efficacious and widely used (e.g., sales exceeded $8 billion in the US alone in 2004), although unwanted effects can limit their use. Accordingly, development of analgesics with novel mechanisms and improved side-effect profiles remains a high priority.

Acute pain (pricks, cuts, and burns), postoperative pain, and many chronic pains are initiated by activation of a nociceptor. Nociceptors are the sensory receptors in the periphery that respond to stimuli termed 'noxious' and that commonly give rise to pain. Nociceptors are present in all tissues. Nociceptors in skin respond to stimuli that damage or threaten damage to skin (cutting, crushing, burning, etc.), but the adequate noxious stimuli that activate nociceptors in muscle, joints, and the viscera differ from those in skin. For example, chemical mediators in muscle (e.g., lactic acid) and distension of hollow organs are noxious in those tissues.

Technically, nociceptors are the end-organs that transduce noxious stimulus energy (mechanical, thermal, and chemical) into electrical signals that travel along an axon to pass on information to a second-order neuron, typically in the spinal cord. Conventionally, however, the term 'nociceptor' is commonly applied to the sensory neuron in which the nociceptor is embedded. The peripheral terminals of nociceptors in all tissues are very fine and typically without a defining structure (i.e., there is no encapsulated end-organ and nociceptors are often characterized as 'free' nerve endings).

The mechanisms by which opioid and non-opioid analgesics work are well understood, but neither class of drugs is ideal as either an analgesic or antihyperalgesic. Accordingly, considerable effort continues to be directed at improved understanding of nociceptor function and development of selective analgesics that do not have unwanted effects, such as associated with opioid and non-opioid analgesics. Recent focus has turned to a variety of ion channels or receptors that respond to changes in the chemical milieu in which the nociceptor resides. These include, but are not limited to:

• the transient receptor potential vanilloid (TRPV1), or capsaicin, receptor;

• acid-sensing ion channels (ASICs);

Back Pain Relief

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