[libribook.com] Traumatic Scar Tissue Management 1st Edition

Clinical Consideration
Acute and chronic or persistent pain present as different clinical entities.
Acute pain, provoked by a specific disease or injury, serves a useful
biologic purpose and is self-limited, lasting less than 6 months. The
therapy of acute pain is aimed at treating the underlying cause and
interrupting the nociceptive signals. The therapy of chronic pain must rely
on a multidisciplinary approach and should involve more than one
therapeutic modality (Grichnik & Ferrante 1991).
Fasciagenic pain: because fascia has been largely overlooked as a potential pain
generator and because scarring impacts fascia, specific consideration is given
here. Fascia contains type C nociceptors and some of the free nerve endings in
fascia are substance P-containing receptors, commonly assumed to be
nociceptive and rendering fascia a potential pain generator (Tesarz 2009). And,
as previously noted, neurofascial coverings are innervated by nervi nervorum.
Hyperalgesia: heightened pain sensation from a stimulus that normally
provokes pain, a consequence of hyperexcitation involving peripheral or central
sensitization or both.
• Primary hyperalgesia: occurs at the site of injury, associated with increased
sensitivity of peripheral receptors (e.g. local nocis activated by substances
released as a result of injured tissue).
• Secondary hyperalgesia: occurs in tissue outside the site of injury, associated
with central sensitization (e.g. changes in spinal cord glial and satellite cells
and voltage spiking pattern changes).
• Opioid-induced hyperalgesia: sensitization associated with long-term use of
exogenous opioids (e.g. heroin, oxycodone).
Neuropathic pain: pain that arises as a consequence of injury or disease
affecting the somatosensory NS (Treede et al. 2008, Correa-Illanes et al. 2010).
Neuropathic pain may occur as a manifestation of various conditions that cause
nerve damage, such as viral infections (postherpetic neuralgia), metabolic