PAIN PHYSIOLOGY

“Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”
Why feel pain?
Gives conscious awareness of tissue damage
Protection:
Remove body from danger
Promote healing by preventing further damage
Avoid noxious stimuli
Elicits behavioural and emotional responses
Nociceptors

free nerve endings in skin respond to noxious stimuli

Nociceptors are special receptors that respond only to noxious stimuli and generate nerve impulses which the brain interprets as "pain".

Nociopectors

Adequate Stimulation
Temperature
Mechanical damage
Chemicals (released from damaged tissue)
Bradykinin, serotonin, histamine, K+, acids, acetylcholine, and proteolytic enzymes can excite the chemical type of pain.
Prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them.

Hyperalgesia:
The skin, joints, or muscles that have already been damaged are unusually sensitive. A light touch to a damaged area may elicit excruciating pain;

Primary hyperalgesia occurs within the area of damaged tissue;
Secondary hyperalgesia occurs within the tissues surrounding a damaged area.

. Localization of Pain
Superficial Somatic Pain arises from skin areas
Deep Somatic Pain arises from muscle, joints, tendons & fascia
Visceral Pain arises from receptors in visceral organs
localized damage (cutting) intestines causes no pain
diffuse visceral stimulation can be severe
distension of a bile duct from a gallstone
distension of the ureter from a kidney stone

Fast and Slow Pain
Most pain sensation is a combination of the two types of message.
If you prick your finger you first feel a sharp pain which is conducted by the A fibres,
and this is followed by a dull pain conveyed along C fibres
Fast pain (acute)
occurs rapidly after stimuli (.1 second)
sharp pain like needle puncture or cut
not felt in deeper tissues
larger A nerve fibers
Slow pain (chronic)
begins more slowly & increases in intensity
in both superficial and deeper tissues
smaller C nerve fibers
Impulses transmitted to spinal cord by
Myelinated Aδ nerves: fast pain (80 m/s)
Unmyelinated C nerves: slow pain (0.4 m/s)

Notable features of visceral pain:
Often accompanied by strong autonomic and/or somatic reflexes
Poorly localized;
may be “referred”
Mostly caused by distension of hollow organs or ischemia (localized mechanical trauma may be painless)

Referred Pain
Pain originating from organs perceived as coming from skin

Site of pain may be distant from organ
This type of referred pain occurs because both visceral and somatic afferents often converge on the same interneurons in the pain pathways.

Excitation of the somatic afferent fibers is the more usual source of afferent discharge,

so we “refer” the location of visceral receptor activation to the somatic source even though in the case of visceral pain.

The perception is incorrect.

Pain Gate” Theory

Melzack & Wall (1965)

A gate, where pain impulses can be “gated”

The synaptic junctions between the peripheral nociceptor fiber and the dorsal horn cells in the spinal cord are the sites of considerable plasticity.

A “gate” can stop pain signals arriving at the spinal cord from being passed to the brain

Reduced pain sensation
Natural pain relief (analgesia)
Applications of pain gate
Stimulation of touch fibres for pain relief:
TENS (transcutaneous electrical nerve stimulation)
Acupuncture
Massage

Release of natural opioids
Hypnosis
Natural childbirth techniques
Pain Relief
Aspirin and ibuprofen block formation of prostaglandins that stimulate nociceptors
Novocain blocks conduction of nerve impulses along pain fibers
Morphine lessen the perception of pain in the brain.