The plantar fascia connects the hind foot to the fore foot, providing stabilization important for stance and gait. When tension increases during the heel-off phase, the plantar fascia stores potential energy and converts that stored tension into kinetic energy as it passively contracts during toe-off, imparting foot acceleration. Because of this windlass effect, the plantar fascia contributes more to the mechanical support of the arch than the spring ligament in gait. Cadaver studies reveal that dissecting the plantar fascia weakens the medial longitudinal support of the arch and increases the tensile forces in other ligaments and the posterior tibial tendon. The pain in refractory plantar fasciitis may be to the result of one or more of the following mechanisms:
1. Irritation of pain fibers by repeated trauma and/or chronic pressure from a thickened plantar fascia (2).
2. Ischemic pain from chronic pressure of thickened fascia against digital vessels.
From: Therapeutic Uses of Botulinum Toxin Edited by: G. Cooper © Humana Press Inc., Totowa, NJ
3. Enhanced effect of local pain neurotransmitters/chemicals such as substance P or glutamate (3), which are shown to accumulate at the site of local trauma.
4. Increased nociceptor sensitivity secondary to inflammation.
Furthermore, in any chronic painful condition, a cascade of events typically occurs, leading to a vicious cycle of pain maintenance (4). These may include central sensitization after peripheral injury in which non-nociceptive spinal cord neurons perceive non-nociceptive peripheral stimuli as painful and sympathetically maintained pain in which an overgrowth of sympathetic nerve fibers occurs into the dorsal root ganglia resulting in persistent pain transmission (5).
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