Page 52 - Journal of Special Operations Medicine - Winter 2016

the context of SOF deployments). Each session lasted 45 in the treated shoulder compared with the untreated
minutes and consisted of deep dry needling with elec- shoulder. Patients had remarkably reduced pain on the
trical stimulation to the lumbar musculature. The dry treated side and little or no change in pain levels on the
needling to the patient’s right upper leg was without untreated side. These subjective changes in pain levels
4
electrical stimulation. Following 1–2 days of soreness in are further supported by changes in regional biochemi-
the area that was treated, the Soldier’s pain was unno- cal factors around MTrPs.
ticeable. This pain-free period lasted approximately 3–4
weeks, at which point the pain gradually reappeared. Much of the current literature on TrP-DN is based on
case studies and even many of the randomized placebo-
controlled trials are considered to have inadequate pla-
Scientific Research
cebo controls or sample size too small for verifiable
SOF personnel are subject to physically stressful job re- quantitative results. The number of published studies
quirements, often consisting of repetitive movements. of the effectiveness of TrP-DN, therefore, are limited.
Moving long distances under heavy load and remaining Although our study, too, is case-based, we believe that
completely stationary for days on end are both neces- SOF could also potentially be a driver of a large ran-
sary SOF skills and cause an extreme amount of physi- domized controlled trial, given the common use of TrP-
cal stress on the body. There is a consensus that muscle DN among THOR3 physical therapists. Furthermore,
overuse or direct trauma to the muscle can cause the for- there is growing evidence in support of the hypothetical
mation of MTrPs. Myofascial pain syndrome (MPS) is pathophysiology of MTrPs, as well as the physiologic
14
a common complication of musculoskeletal injuries. effect of TrP-DN therapy, by using ultrasound shear-
1–4
MPS is characterized by regional pain and the presence wave elastography and invasive analysis of inflamma-
of MTrPs. These MTrP nodules are hyperirritable, are tory markers in soft tissue.
14
located in taut bands of skeletal muscle fibers, and con-
tain contraction knots theorized to be caused by exces- In a study conducted at the National Institutes of Health,
sive acetylcholine (ACh) and other biochemical markers researchers were able to invasively monitor inflammatory
at the motor endplate. MTrPs can be further subdi- markers and the biochemical environment surrounding
1,2
vided into latent and active MTrPs. Latent MTrPs do MTrPs before and after an LTR. The study used micro-
not cause spontaneous pain but may cause unfamiliar analysis of needle insertions around active and latent
pain and inhibit full ROM or strength, whereas active MTrPs, as well as areas determined to be normal in the
MTrPs cause familiar pain or local and referred pain at upper trapezius muscle, to explore the biochemical en-
rest. Evidence suggests that these referred pain patterns vironment of MTrPs before treatment, during the treat-
may be characteristic of specific muscles and not any ment and the LTR, and after TrP-DN was performed.
anatomic location of the MTrP. 1 They found statistically significant changes in the bio-
chemical environment of MTrPs, including changes in
The goal of TrP-DN is to elicit an LTR, which is a spinal levels of inflammatory markers, catecholamines, neuro-
reflex that causes an involuntary spasm of the taut muscle peptides, and cytokines. These chemicals were viewed in

fibers. It is believed that the LTR is the primary thera- patients with active and latent MTrPs, as well as those
15
peutic effect of TrP-DN and that it resolves the MTrP; al- without MTrPs. This study “confirmed that biochemi-

though the mechanism is still largely theoretical. Evidence cals associated with pain and inflammation are elevated
2
has shown that “LTRs can normalize the chemical envi- in soft tissue in the vicinity of active MTPs.” 2
ronment of active MTrPs and diminish endplate noise as-
sociated with MTrPs in rabbits nearly instantaneously” ; The contracted sarcomeres involved in an MTrP create
1
however, more research is needed to fully understand both local hypoxia and ischemia from compromised circula-
the physiology behind MTrPs and the mechanism of TrP- tion and an increased metabolic demand. This would
2
DN effectiveness. It is also conjectured that an effectively explain the increased concentrations of these inflamma-
1
placed needle may stretch the contracted sarcomeres and tory and pain-sensitizing chemicals near MTrPs. The
2
allow them to resume their resting length by reducing the increased levels of inflammatory markers and other bio-
actin and myosin filament overlap. 1 chemicals around an MTrP create the chronic nature of
the MTrP life cycle as it develops from latent to active.
A study conducted at the Department of Physical therapy After treatment, these biochemical levels decrease as a
at Hungkuang University, Taiwan, used TrP-DN on 14 result of either direct nerve stimulation or a local in-
patients with bilateral shoulder pain and active MTrPs. crease in blood flow. 2
A single shoulder was dry needled, and the shoulder
pain intensity, ROM, and pressure pain threshold of the These findings reinforce the theories of another pioneer
MTrPs were measured before and after treatment. There of TrP-DN, David G. Simons. Simons created the “inte-
were significant improvements in pain levels and ROMs grated hypothesis of MTrP,” which postulates that the

36 Journal of Special Operations Medicine Volume 16, Edition 4/Winter 2016