Page 114 - Canine Lameness

86 6 The Myofascial Examination

The taut band is a localized, linear, discrete band of hardened muscle within the softer,
homogeneous muscle that runs parallel to muscle fibers. The MTP is located within the taut
band and is what distinguishes it from other painful areas within muscle. The contractile
properties of this group of taut fibers is not the result of alpha motor neuron initiating activ-
ity at the motor endplate (like in muscle spasm), but rather due to intrinsic causes. Taut
bands result in muscle shortening and reduced joint range of motion.
The local twitch response is an additional motor component of the MTP. It is a unique
spinal cord reflex resulting in a rapid contraction of the taut band following manual stimu-
lation via direct palpation or insertion of a needle (Gerwin 2010). The presence of a local
twitch response can serve as validation of the presence of a MTP.
Weakness is recognized in muscles with MTPs. This weakness is without muscle atrophy
and is not related to neuropathy or myopathy. Weakness is often rapidly reversed following
inactivation of the MTP suggesting that weakness from MTPs is due to inhibition of muscle
activation. A MTP in one muscle can also inhibit effort or contractile forces in another mus-
cle, suggesting a central inhibition process (Gerwin 2010). Additional motor or muscle dys-
function from MTPs is the result of disordered muscle recruitment or activation patterns in
muscles during movement or specific action.
In people, several conditions such as coryza, lacrimation, salivation, changes in skin tem-
perature, piloerection, and erythema have been identified as autonomic manifestations of
myofascial pain (Lavelle et al. 2007). However, such conditions remain difficult to observe
in the canine patient.

6.3 Etiology and Pathophysiology of Myofascial Trigger Points

The etiology as to the formation of the taut bands and MTPs is unknown. However, the Integrated
Trigger Point Hypothesis postulates that muscle injury leads to motor end plate dysfunction and
excessive release of acetylcholine. This excessive release of acetylcholine results in extended
release of calcium from the sarcolemma resulting in sarcomere shortening and sustained muscle
fiber contraction (Gerwin 2010; Wall 2014). This sarcomere shortening has been observed histo-
pathologically (Simons and Stolov 1976).
More recently the role of fascia and hyaluronic acid in the pathophysiology of MTPs has been
theorized. The muscle fascia receives innervation with both mechanoreceptors that detect changes
in length and tension as well as nociception. Hyaluronic acid is present in abundance in the body’s
connective tissues and serves as a lubricant and reservoir for electrolytes and nutrients. However,
alterations in the conformation of hyaluronic acid can result in adhesion rather than lubrication.
It has been proposed that increased temperature and massage may allow reversal of the pathologic
configurations of hyaluronic acid (Stecco et al. 2013).
Other possible mechanisms that have been suggested to cause muscle injury and the develop-
ment of MTPs and MPS are thought to be related to muscle overload or stress due to direct trauma,
unaccustomed eccentric contractions, eccentric contractions in unconditioned muscle, or maxi-
mal or submaximal concentric contractions (Wall 2014; Gerwin 2016). MTPs can be observed in
limbs that are not primarily affected as well as in muscles of the affected limb that are overused.
An example would be the formation of MTPs in the coxofemoral flexors of the affected limb in
dogs that are non‐weight‐bearing due to cranial cruciate ligament rupture. These dogs maintain
the non‐weight‐bearing posture by continuous flexion of the coxofemoral joint. The muscles that