The physiology of pain (Proceedings)

The physiology of pain (Proceedings)

Apr 01, 2009

What is pain?

• Pain is a complex sensory and emotional experience that can be associated with actual or potential tissue damage. Despite its importance, it is often overlooked. It wasn't until the year 2000 that it was recognized as the 5th vital sign in human medicine along side temperature, pulse, respiration and blood pressure. In 2003, AAHA made the assessment of pain the 4th vital sign (temp, pulse, resp, pain = TPRP)


• Nociception

o Nervous system activity produced by a noxious stimulus

• Noxious stimulus

o A stimulus capable of producing pain; can be chemical, mechanical or thermal

• Nociceptor

o A receptor that detects painful stimuli, they are found throughout the body

• Can detect either one type of noxious stimuli, or all three

• Allodynia

o Pain produced by a stimulus that is not typically painful

• Hyperalgesia

o An increased or exaggerated response to a painful stimulus at he site of injury or nearby

• Hyperesthesia

o Increased sensitivity to stimuli that is not considered painful

• Peripheral pain

o Visceral (abdominal or thoracic organs); poorly localized, may be referred and seem cutaneous in origin

o Somatic (superficial- skin; deep- tendons, joints, muscle, periosteum); easily localized

• Neuropathic pain

o Pain resulting in damage to peripheral nerves or spinal cord. Often difficult to treat.

Factors affecting pain

• Stress

o Can exacerbate pain through nervous system modifications in response to tension.

o Can result from pain or external stressors like environment or internal like disease

• Anxiety

o Can also exacerbate pain and make it difficult to recognize

o Low dose anxiolytics may be used in combination with analgesic when pain is suspected

• High doses of a sedative/tranquilizer may mask pain without alleviating it, this is inhumane.

• Wind-up

o Noxious stimuli can sensitize the nervous systems response to subsequent stimuli

o Patients who experience unrelenting pain release an increased amount of a neurotransmitter called glutamate. This increase activates the NMDA receptor (normally inactive) which then activates an intracellular cascade that increases the membranes sensitivity to subsequent stimuli. This "central sensitization" can last for hours to days or even longer.

The pain pathway

• Transduction

o A painful stimulus becomes a chemical signal (release of inflammatory mediators secondary to cellular injury) that is translated into electrical activity at the sight of injury

o That energy is converted into a signal that the nervous system can understand

• Transmission

o Pain signal is transmitted through the peripheral nervous system to the spinal cord via nerve fibers

• A-delta (small, myelinated, fast; acute pain)

• C-fibers (large, unmyelinated, slow; chronic pain)

• Modulation