Observations on the mechanical sensitivity of sympathetic and other types of small-diameter nerve fibers

Neuromuscular strain as a contributor to cognitive and other symptoms in chronic fatigue syndrome: hypothesis and conceptual model

“…A series of observations over the last several decades—by Brieg, Sunderland, and others (Lindquist et al, 1973; Brieg, 1978; Sunderland, 1978; Butler, 1991, 2000; Kornberg and McCarthy, 1992; Shacklock, 1995; Slater and Wright, 1995; Elvey, 1997; Rempel et al, 1999; Orlin et al, 2005; Topp and Boyd, 2006)—has focused attention on the ability of the nervous system to undergo accommodative changes in length in response to the range of limb and trunk movements carried out during daily activity. The interaction of nerve mechanics and function has been termed neurodynamics.…”

“…If that ability to elongate is impaired—due to movement restrictions in tissues adjacent to the median nerve and its branches, or due to swelling or adhesions within the median nerve itself—the result is an increase in mechanical tension within the nerve. This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides (Lindquist et al, 1973; Kornberg and McCarthy, 1992; Shacklock, 1995; Slater and Wright, 1995; Balster and Jull, 1997; Van der Heide et al, 2001; Kobayashi et al, 2003; Orlin et al, 2005). It is now well-established that manual stretch of nerves is capable of evoking increased sweating and alterations of blood flow in peripheral tissues, providing evidence of electrophysiologic activity in sympathetic nerve fibers (Lindquist et al, 1973; Kornberg and McCarthy, 1992; Slater and Wright, 1995; Orlin et al, 2005).…”

“…This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides (Lindquist et al, 1973; Kornberg and McCarthy, 1992; Shacklock, 1995; Slater and Wright, 1995; Balster and Jull, 1997; Van der Heide et al, 2001; Kobayashi et al, 2003; Orlin et al, 2005). It is now well-established that manual stretch of nerves is capable of evoking increased sweating and alterations of blood flow in peripheral tissues, providing evidence of electrophysiologic activity in sympathetic nerve fibers (Lindquist et al, 1973; Kornberg and McCarthy, 1992; Slater and Wright, 1995; Orlin et al, 2005). Conversely, treatment of areas of adverse neural tension (for example in carpal tunnel syndrome, cervico-brachial pain, and osteoarthritis) leads to improved functional outcomes (Rozmaryn et al, 1998; Deyle et al, 2000; Tal-Akabi and Rushton, 2000; Akalin et al, 2002; Allison et al, 2002).…”

General neuropathodynamics

“…High intensity force evokes much activity in undamaged axons and this is more significant in injured nerves (Gray & Richie 1954;Lindquist et al 1973;Howe et al1976, 1977BurchielI984). The first is that nerves are never mechanosensitive and therefore could not be a source of pain.…”