Pruritus (dermo-epidermal junction, pathophysiology)

The origin of itch can be

• peripheral
  • cutaneous (‘pruritoceptive’) - e.g. dermatitis
  • neuropathic - e.g. multiple sclerosis
• central
  • neurogenic - e.g. cholestasis
  • mixed - e.g. uraemia
  • psychogenic (1)

The dermo-epidermal junction is a key site in the genesis of the sensation of pruritus due to the high concentration of free nerve endings. Also, from this vantage, not only is there ready access to external antigenic stimuli, but the dermal blood supply is in close proximity.

Rapidly-conducting myelinated A-type neuronal fibres are the mediators of the quick stabbing or stinging sensation that heralds the attack. This is followed by the signal carried by non-myelinated C-type fibres which is intense and burning.

Although both itch and pain impulses are transmitted through a common neural pathway (from dorsal horn of the spinal cord through the spinothalamic tract to the thalamus, and finally to the somatosensory cortex), C type fibers which carry itch impulse are functionally different from the fibers which carry pain (1).

These afferent C-fibers are sensitive to many pruritogens which includes histamine, acetylcholine, serotonin and prostaglandins (1).

Reference:

• (1) Twycross R et al. Itch: scratching more than the surface. Q J Med 2003; 96: 7-26