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Erasmus Mundus Program
European Union
Gda
ń
sk Sport University
Gda
ń
sk, Poland
Leipzig University
Leip zig, Germa ny
Queen’ s Par k Massage Ther apy
Vancouver, Canada
THE BRAIN BEHIND MYOFASCIAL
TRIGGER POINTS
Paul Valdemar Sulżycki,
RMT, BSc
Department of Physical Education & Sport Sciences
University of Thessaly, Trikala, Greece
April 4th, 2018
⋅ i ⋅
Declaration & Acknowledgements: This thesis is submitted in final fulfillment of the requirements
for a joint Master of Science in Sport
&
Exercise Psychology from the University of Thessaly and
Leipzig University on April 4th, 2018. The study was completed May 1st, 2015, and the thesis
presented under the working title
Imagery Effectiveness in Trigger Point Treatment
to a supervising
committee of Profs. Marios Goudas, Antonis Hatzigeorgiadis, and Athanasios Papaioannou
June
24th, 2015. A copy resides on spmx.ca/trp, including summary and trigger point release videos.
This thesis is my original work with no material jointly-authored, previously published or used for
other studies, with all contributions and references clearly cited. It is the result of work I carried
out since diving into this topic during my master’s studies in early 2015. The resulting synthesis
contains much inference, upon which I hope other researchers build. I acknowledge that copies
of this thesis must be lodged at the University of Thessaly library, and that copyright of all material
in it resides with its original holders. Otherwise, this full work is released under the CC0 license,
with all rights waived and further work stemming from it actively encouraged.
I must thank my sister, Joanna Sulzycki, for modeling in the
Methods
section, and my colleagues,
Lois Reyes and Jana Konkin, for acting in my trigger point treatment video and for the “melting”
script, respectively. I am indebted to Vassilis Bouglas at the University of Thessaly library for his
truly above-and-beyond help in my research, and to my practicum supervisor, Marek Graczyk,
and the physiotherapy department director, Małgorzata Kawa, at Gdańsk Sport University who
gave me the means and participants to run my study on campus, as well as Agnieszka Lasota
and Dagmara Budnik-Przybylska, for helping recruit further participants from local actors and
neighbouring Gdańsk University sport science students. Most importantly, however, were the
finances that made all this possible through my working a
very
irregular schedule at Queen’s Park
Massage Therapy in New Westminster just outside Vancouver, something the owners, Kelly Baxter
and Sharon Nagle, not only allowed but actively supported.
Lastly, to my fellow students from this program and from the many conferences we attended
abroad, thank you for your energy and curiosity, enthusiastically reflecting my own as we tumbled
through this unforgettable master’s degree. And to my good friend, Lukas, always a phone call
(and a time zone or two) away with a quick quip and a laugh as contagious as my own, never
forgetting to wish me safe flights every trip. And to my girlfriend, Brigitte, for her gentle, patient
smiles, and for teaching me so many things I never knew I never knew, things that were paradigm-
⋅ ii ⋅
shifting then but that are so clear and obvious now. And to my family — extended throughout
Europe (mostly Poland) and Canada (mostly Hamilton): knowing that you are always there with
a warm meal, a place to sleep, a hot shower, and a drive to the station is a godsend… a sincere
thank-you to my aunt, Lucy, for inspiring me to become a massage therapist, my uncle, Wojtek,
for driving me to massage college ~100km from Hamilton to Toronto for months on end, rain or
shine, and my cousins Ewa, Mateusz, and Piotruś, for all the love in Gdańsk, providing airport
rides, restful nights, and everything in between. This security was what really freed me to focus
on these studies. And particularly my mother, Barbara, for always being there. Always. We never
wanted for anything because of her now calloused hands. And my father, Janusz, for coaching
our minds and bodies, for introducing me to sport, to philosophy, and to ethology — leading to
biology studies that ultimately started me on this privileged path of learning. And to my inspiring
sisters, Magdalene, the other half of my mind, and Joanna, the other half of my smile. I love you
all. So very,
very
much. There is a piece of each and every one of you in this paper. I do not have
room enough for a proper outpouring of thanks and emotion for all the good that has met me in
life, but here’s hoping this paper pays some of that forward by reducing pain for others. And in
closing, of course, an exceptional thank-you to the stoic face of patience itself that was my
supervisor, Marios. He waited his while to receive this completed document, but now has, in his
own words, a “good thesis”.
I thank you all for your support and especially space to think while I sometimes chipped,
sometimes hacked, sometimes stumbled but always fell forward in this scope creep of a
Sisyphean effort.
Ideas need space. This one, not anymore.
Thank you.
Hamilton, Canada
April 4th, 2018
⋅ iii ⋅
ABSTRACT
Despite imagery’s regular use in massage therapy there are few studies examining its
effectiveness. This experimental study examined the effect of imagery on manual trigger point
release. Forty individuals (11 male and 29 female), aged 19-51 (
M
= 26.13,
SD
= 8.05) were divided
into two groups; one focusing on deep, diaphragmatic breathing and the second on a rich imagery
script, imagining their trigger point being a “ball of butter melting”. Manual trigger point release
was applied four successively deeper times to the same point in the dominant upper trapezius
muscle following the common “searching for 7” pain scale protocol. Significant differences were
found in self-reported pain tolerance scores for participants using the breathing (
M
= 2/10, SD =
1.8/10) versus imagery scripts (
M
= 1/10, SD = 1.2/10), t(37) = 2.10,
p
= .043. A trend only
approaching statistical significance was observed between treatments in both average press
release (imagery:
M
= 25.6 s,
SD
= 15.5 s, breathing:
M
= 30.0 s,
SD
= 27.3 s,
t
(38) = 0.62,
p
= .540)
and total treatment time (imagery:
M
= 2:15 m,
SD
= 1:08 m, breathing:
M
= 2:36 m,
SD
= 2:04 m,
t
(38) = 0.67,
p
= .507), with largest differences in the final two presses.
However, analyzing the above while taking local
v.
referred pain presence into account showed
significant main effects of pain on the first press (local/breathing:
M
= 43.2 s,
SD
= 24.8 s;
local/imagery:
M
= 31.5 s,
SD
= 16.1 s; referred/breathing:
M
= 23.2 s,
SD
= 12.5 s, referred/imagery:
M
= 28.1 s,
SD
= 12.2 s;
F
1,30 = 4.53,
p
= .042) and significant interaction effects of both pain and
treatment type on total treatment time (local/breathing:
M
= 3:32 m,
SD
= 2:34 m; local/imagery:
M
= 2:07 m,
SD
= 1:12 m; referred/breathing:
M
= 1:50 m,
SD
= 1:11 m, referred/imagery:
M
= 2:22
m, SD = 1:08 m;
F
1,30 = 4.64,
p
= .039). Based on this study, therapists should include breathing
techniques in manual trigger point release for patients experiencing referred pain and imagery
scripts for patients experiencing only local pain.
Keywords:
massage therapy, myofascial trigger point, imagery, PETTLEP, gate control, neuromatrix,
neural modulation, sensitization, referred pain, pain, muscle, neurology
CONTENTS
DECLARATION
&
ACKNOWLEDGEMENTS............................................................................................................................................................ i
ABSTRACT .............................................................................................................................................................................................................. iii
INTRODUCTION ........................................................................................................................................................................................................ 1
Background
........................................................................................................................................................................................................ 1
Problem
............................................................................................................................................................................................................... 3
Hypot hesis
......................................................................................................................................................................................................... 4
LITERATURE REVIEW .............................................................................................................................................................................................. 5
Massage therapy, psychology, and pain
................................................................................................................................................. 5
Pain: sensation, modulation, and perception
....................................................................................................................................... 6
Ascending modulation
................................................................................................................................................................................... 7
Referred pain
............................................................................................................................................................................................. 7
Gate control theory
................................................................................................................................................................................. 8
Descending modulation
............................................................................................................................................................................... 10
Neuromatrix theory
............................................................................................................................................................................... 12
Trigger point pathophysiology
.................................................................................................................................................................. 12
Formation
................................................................................................................................................................................................. 12
Anatomy
.................................................................................................................................................................................................... 13
As different from acupuncture points
............................................................................................................................................ 14
As different fr om muscle “knots”
.................................................................................................................................................... 15
As different fr om healthy muscle
..................................................................................................................................................... 15
Trigger point treat ment
............................................................................................................................................................................... 15
Hot and cold therapy
............................................................................................................................................................................ 16
Other approaches
.................................................................................................................................................................................. 16
Imagery neuroanatomy
............................................................................................................................................................................... 17
Perception
................................................................................................................................................................................................. 17
Imagery
...................................................................................................................................................................................................... 18
Imagery in rehabilitation
............................................................................................................................................................................ 19
The PETTLEP model
................................................................................................................................................................................. 20
Physiological effects of imagery
............................................................................................................................................................... 21
METHODS .............................................................................................................................................................................................................. 22
Population
........................................................................................................................................................................................................ 22
Groups and scripts assigned
..................................................................................................................................................................... 22
Positioning and treatment
......................................................................................................................................................................... 23
Data collection
............................................................................................................................................................................................... 25
CONTENTS (cont'd)
RESULTS ................................................................................................................................................................................................................. 26
Main findings
.................................................................................................................................................................................................. 26
Referred versus local pain
.......................................................................................................................................................................... 27
Individual variance
........................................................................................................................................................................................ 28
Focus ability and distractibility
................................................................................................................................................................ 29
Pain tolerance
................................................................................................................................................................................................. 30
Trigger point symptoms
.............................................................................................................................................................................. 31
Exceptional treatments
............................................................................................................................................................................... 31
DISCUSSION ........................................................................................................................................................................................................... 32
Summarizing ascending modulation: referred pain and massage
............................................................................................... 32
Summarizing descending modulation: pain in the brain
................................................................................................................ 33
Moving towards a comprehensive, neurologica l trigger point model
......................................................................................... 35
Explaining pain
............................................................................................................................................................................................... 36
Local pain and imagery
........................................................................................................................................................................ 36
Local pain and breathing
.................................................................................................................................................................... 37
Referred pain, breathing, and ima gery
........................................................................................................................................... 37
Caveat emptor
......................................................................................................................................................................................... 37
Study limitations
........................................................................................................................................................................................... 37
Directions for future research
................................................................................................................................................................... 39
How these findings have changed my practice
................................................................................................................................... 41
CONCLUSION ......................................................................................................................................................................................................... 43
The brain behind myofascial trigger points
......................................................................................................................................... 43
Applications
.................................................................................................................................................................................................... 44
REFERENCES .......................................................................................................................................................................................................... 45
APPENDICES .......................................................................................................................................................................................................... 60
Informed consent form
................................................................................................................................................................................ 61
Breathing script
............................................................................................................................................................................................. 63
Imagery script
................................................................................................................................................................................................. 65
Post-t reatment questionnaire
................................................................................................................................................................... 67
LISTS OF FIGURES
&
TABLES
Figure 1: Upper trap ezius referred pain
...................................................................................................................................................... 3
Figure 2: Main pain theories in context
...................................................................................................................................................... 6
Figure 3: Referred pain
...................................................................................................................................................................................... 7
Figure 4: Ga te control theory
.......................................................................................................................................................................... 8
Figure 5: Original pain model
.......................................................................................................................................................................... 9
Figure 6: Afferent nerve compar ison
............................................................................................................................................................ 9
Figure 7: Pain timeline
...................................................................................................................................................................................... 9
Figure 8: Descending modulation
................................................................................................................................................................ 10
Figure 9: Pain in the brain
............................................................................................................................................................................. 11
Figure 10: Trigger point formation
.............................................................................................................................................................. 13
Figure 11: Proposed trigger point anatomy
............................................................................................................................................. 14
Figure 12: Trigger point therapy and ice
................................................................................................................................................... 16
Figure 13: Perception neuroana tomy
......................................................................................................................................................... 17
Figure 14: Decoding brain imagery
.............................................................................................................................................................. 18
Figure 15: Decoding dreams
.......................................................................................................................................................................... 18
Figure 16: Ima gery neuroana tomyted.
....................................................................................................................................................... 19
Figure 17: Participant positioning
............................................................................................................................................................... 23
Figure 18: Various point-press techniques
............................................................................................................................................... 24
Figure 19: Main results
.................................................................................................................................................................................... 27
Figure 20: Treatment efficacy: referred versus local pa in
................................................................................................................... 28
Figure 21: Individual variance
....................................................................................................................................................................... 29
Figure 22: Focus and distractibility
............................................................................................................................................................. 29
Figure 23: Pain tolerance
................................................................................................................................................................................ 30
Figure 24: Ascending modulation
................................................................................................................................................................ 32
Figure 25: Descending modulation
.............................................................................................................................................................. 34
Figure 26: Pain release tr endlines across presses
................................................................................................................................. 35
Figure 27: Original pain r elease t ime differences between groups
.................................................................................................. 36
Figure 28: Trigger point posters
................................................................................................................................................................... 39
Figure 29: Referred pain pattern evolution
.............................................................................................................................................. 40
Figure 30: The brain behind myofascial trigger points
......................................................................................................................... 43
Table 1: Result summary
................................................................................................................................................................................ 26
Table 2: Results summary: referred v. local pain groups
................................................................................................................... 27
Table 3: Participant focus throughout treatment
.................................................................................................................................. 30
Table 4: Trigger point pain distribution among subjects
.................................................................................................................... 31
Table 5: Exceptional trea tment s
.................................................................................................................................................................. 31
⋅ 1 ⋅
⇑
INTRODUCTION
Background
Massage therapists across Canada often use psychological techniques during treatment, even if
they are rarely labelled as such. From a warm clinic decor to the hushed tones and gentle music
used in treatment, the field is constantly seeking new ways of fostering mind-body harmony. The
process begins in school with an introduction to the “principles of massage”: a set of gold
standards outlining a slow, progressive approach to treatment.1 These are to be followed
regardless of technique or style with few exceptions, ensuring an easy, supportive progression
that builds trust and confidence into the vital patient-therapist relationship. The ultimate goal, of
course, is the delivery of a treatment that is maximally effective and long-lasting… something that
is nearly impossible unless the patient is relaxed. It is logical, therefore, that certain psychological
elements would have seeped into common massage therapy practice, from reframing pain, to
goal-setting across treatment plans, to even harnessing imagery during the more painful moments
in treatment. It is on this last tendency that this paper focuses.
As massage therapy develops formal protocols, a common sense/no-harm philosophy with little
scientific backing has prevailed, kept alive through misunderstanding and uncertainty. A good
example is the fear that massage may metastasize cancer in patients through increasing blood
flow and thereby physically “moving” the cancer to other body regions. In fact the opposite is
⋅ 2 ⋅
↑
⇑
true: massage boosts the immune system through upping the production of NK cells, known for
combating cancer.2
Since rigorous, peer-reviewed studies on the mechanisms and efficacy of massage are still few
and far between2-4 — with those exploring trigger point pathology rarer still5,6 — interdisciplinary
research is a good springboard for key findings to emerge. Sport psychology has much to offer in
this regard, especially considering its strong history of training perception to reach certain
performance levels. Because of all this, research for this paper extended beyond the traditional
literature or even media. It drew on web forums, conversations with therapists, university tutorials
and course notes, and several clinicians’ videos explaining various phenomena for their patients
and students. For this reason, what is presented is more a launchpad into the area straddling
sport psychology and massage therapy than it is any definitive text on either subject. It is also
why it begins with a series of separate concepts that only reach full synthesis in the discussion.
Even so, this paper is an attempt at bridging these fields beyond the usual anecdotal, “common
sense” approach criticized earlier. Recent calls have been made for closer psychosomatic
collaboration from both physiological7,8 and psychological4,9-12 fronts. Benefits of such integration
include increased professional growth for therapists as well as improved treatment effectiveness
for patients.4 Clear applications of massage have already been found in improving anxiety,
depression,4 perception/sensation, sleep, learning, and alertness.10,13 Indeed, connecting
psychology with massage therapy is not only recommended14 but required when it comes to the
phenomenon of pain, which is modulated by both physiological and psychological
processes.7,8,11,12,15-26 There currently exist some manual treatment modalities tying psychological
theories into their application4,27-30 and some forays have already been made to integrate massage
therapy into psychotherapy sessions — with great effect.31 What were once purely anecdotal cases
tying these fields together are quickly gaining traction as scientifically-sound research.32-35 Further,
since pain is both a sensory and emotional experience, it makes sense to use both pathways in
dealing with such a complex phenomenon.36 Past studies have linked both massage therapy and
imagery with muscle pain relief;37,38 it is the aim of this paper to continue building upon these
psychosomatic connections in the field of rehabilitative therapy.
⋅ 3 ⋅
↑
⇑
Problem
Imagery use has naturally evolved alongside massage therapy’s development into a serious health
profession worldwide. Therapists often create scripts spontaneously when working through
particularly stubborn muscle knots; generally simple, relatable, relaxing themes rooted in local
culture. These are inevitably shared throughout clinics, naturally paired with anecdotal stories of
their effectiveness. I have worked over a decade as a massage therapist in spas and in
chiropractic, physiotherapy, massage, and sports medicine clinics in five distinct regions across
Canada. Each of these was set on vast bodies of water: Toronto (Great Lakes), Cape Breton
(Atlantic Ocean), Yellowknife (Great Slave Lake), Vancouver (Pacific Ocean) and Montreal (St.
Lawrence River). During this time, I would often note therapists using imagery scripts with
coastlines and water as main themes (eg: “undulating waves hugging the shore”, “golden sand
baking in the sun”, “the call of seagulls and the swells of approaching tides”).
Though nice and relaxing, I wanted to know what
imagery’s actual effectiveness was in treatment,
specifically regarding trigger point release. Should it
prove to be ineffectual, then it could be abandoned
and we could shift our focus to other, better
techniques for pain relief. However, should the
opposite be true then imagery could be officially
incorporated into the trigger point treatment
protocol slowly being developed in physical therapy
clinics worldwide. A second reason I was interested
in this topic was the complete absence of any
comprehensive theory explaining the mysterious
trigger point referred pain phenomenon I would deal
with almost daily in clinic. This pain didn’t seem to
follow any known neural routes… so where was it
coming from?
The muscle chosen for this study was the upper
trapezius since it is here that trigger points are most
often found,39 causing what is probably the most
Figure
1: Upper trapezius referred pain.
Classic
“question mark” pain brought about through
pressing its trigger point (
X).39
⋅ 4 ⋅
↑
⇑
classic of all muscle tension headaches: a “question mark” pain referral looping around the
ipsilateral ear, starting at the neck and mastoid process up to the temple and even sometimes
including the jaw below (
Figure 1
).40-42 Headaches of this type have a very high incidence rate,
ranking along with migraines as the world’s 8th most burdensome health issue (ahead of diabetes,
heart disease, cancer, and malaria),22 with 30-40% of the global population experiencing at least
one annually43,44 (though rates do vary across cultures),45 and costing billions of dollars in
combined employee inefficiency and outright absence.46 As shorter healing times have direct
implications for a nation’s health and economy, and as myofascial disorders like tension
headaches consistently rank as one of the most prevalent conditions in the world,47-53 the results
from this study present applications for a large segment of the world population.39,54
The main theoretical framework used in this study is Melzack and Wall’s gate control model of
pain perception (
Figure 4
).55 This theory is the one most frequently taught in Canadian massage
colleges to explain why massage is so effective in alleviating pain.2,56 Further, according to the
gate control theory, negative cognitions such as expectations or worries have the power to
intensify pain perception while positive cognitions like distraction, relaxation, and positivity have
the power to lessen or even completely deactivate pain perception.55,57,58 Since imagery delivers
these very positive cognitions,59 it seemed a logical addition to the otherwise purely mechanical
trigger point treatment.
Hypothesis
Based on the following literature review and on my own clinical experience, including anecdotal
evidence from many physiotherapists, chiropractors, and other massage therapists along the way,
releasing trigger points with traditional massage therapy combined with a relaxing imagery script
was expected to result in faster and more effective treatment times than would coupling the
treatment with a generic breathing script.
⋅ 5 ⋅
⇑
LITERATURE REVIEW
Massage therapy, psychology, and pain
In addition to the many studies written on the physiological effects of massage therapy, there
have been several on the psychological and behavioural effects it has on patients. Findings relate
a wide variety of improvements: reductions in stress, anxiety, depression, cortisol levels, ADHD
symptoms, and pain, as well as in activity limitations caused by pain. Further, massage improves
mood, sleeping, eating habits, body image perception, relaxation, performance, alertness, and
concentration.2,4,10,56,60-62 But this is not without reproach. Criticism always returns to inconsistent
findings, methodological flaws, and to a simple lack of studies in the field.2,61
However, the main gap this paper fills compared to the studies mentioned is that nearly each
studied the unidirectional effects of massage on a person’s psychology; rarely was the reverse
ever examined. Indeed, this has been the main stance of Western medicine since the scientific
revolution: that the body affects the mind is clear. The reverse pathway is coming to light in
mainstream science only as of recently.63 Articles on the psychology of trigger point treatment
were even scarcer, despite the treatment having clear psychological ties regarding pain perception
and despite this therapy being one of the most painful and most prevalent massage modalities
currently used in across Canada.14
Current theories explaining why massage alleviates pain focus primarily on physiological
phenomena, including its increasing blood and decreasing cortisol circulation, its activation of the
parasympathetic nervous system via relaxation, and its modulation of incoming nerve signals as
⋅ 6 ⋅
↑
⇑
outlined in the gate control model (
Figure 4
). In addition to all these factors, there also exist the
hypotheses that massage improves affect via social support and touch,3 and that people’s
personalities — broadly described as pain-adaptive or -nonadaptive — can predict pain response
(with the former inherently dealing better with managing pain than the latter).20,21,64 Such
integrated, personalized treatment is already underway for low back pain, with patients being
reliably divided into several subgroups based on psychosocial risk factors for specialized
treatment instead of treating every incidence of the condition as part of a single batch
phenomenon.65
Pain: sensation, modulation, and perception
Pain is particular among sensations in two ways. First, it is not always subject to habituation.
Indeed, it often undergoes the opposite, intensifying with increased or maintained stimuli in what
is called “sensitization”.22,23,66-70 Secondly, it has an emotional element: unpleasantness,
consisting first of sensation and then only sometimes perception (
Figure 7
). This first is the
reception of all the physical elements — pressure, registration of touch,
etc
. The second is the
cerebral labeling of these as unpleasant, and is heavily dependent on the modulation the
nociceptive signal undergoes from peripheral stimulation to cerebral processing.71
Figure
2: Main pain theories in context. Image 1
contextualizes cerebrospinal neuroanatomy, zooming in on a C3/4
transverse section where many trapezius nerves enter and exit the spinal cord.
Image 2
zooms in on the spinal cord,
showing the pain stimulus (
X), the site of referred pain (ʔ), and all pain
modulation models outlined in this paper:
original ascending pain (
red), potential modulation (blue, including referred pain (a), gate control (b
), and descending
modulation (spinal:
c, cerebral neuromatrix: d)), as well as the resulting signal perceived (purple).
1 2
d
c
a
b
⋅ 7 ⋅
↑
⇑
Modulation happens in a few spots along pain’s path to the brain, where it may intensify or
diminish, or even disappear altogether,23,57,67,72 explaining why pain may occur without injury (
eg
:
phantom limb pain), may remain long after an injury has healed, or may even not occur at all
when expected (
eg
: battle wounds). Pain is a bidirectional process, undergoing modulation
through both ascending and descending pathways (
Figure 2
). Ascending modulation occurs when
pain is modified by a competing signal arriving from the periphery or by an interneuronal signal
still in the spinal cord, as with referred pain (
Figure 3
) or in the gate control model (
Figure 4
).
Descending modulation occurs in the spinal cord where a cerebral signal modulates peripheral
pain (
Figure 8
) as in the pain-tension cycle67,73 or inside the brain as per the neuromatrix
theory16,72,74,75 through release of analgesic neurotransmitters (
eg
: serotonin).76
Ascending modulation
Referred pain
The most pertinent diagnostic tool for this study was the
referred pain pattern elicited through point compression of the
tender trigger point (
Figures 1 & 18
).77 Though not following
any known nerve pathways or myotomes,78,79 these patterns
are very consistent across patients.5 Because of this, when a
patient is experiencing referred pain in a known pattern, their
therapist can often quickly deduce which muscle is behind
it.39,46,78,80-82 These patterns are especially prevalent in muscle
tension headaches (muscular in origin and characterized by
their gradual onset, accompanying sensations of pressure and
tension, and sustained triggering of generally unconscious
contractions in head and neck musculature),57,83 while also
being an important factor in the etiology and maintenance of
chronic migraines.84 However, there is no one clear mechanism
yet explaining their phenomenon completely.85
The current model posits pain as converging at spinal synapses,78,86 a process identified over fifty
years ago and consisting of “convergent projection” —
ie
. spinal nerve neural overlap of the injury
and referral zones — and “central sensitization” — increased spinal neuron response with repeated
peripheral neuron stimulation, enabling smaller and stimuli to trigger a response (
Figure 3
).87-101
Figure
3: Referred pain.
Trigger point
(
red) and referral pain (blue
) nerves
converging as pain (
purple
) “felt” at
both injury (
X) and referral (ʔ) sites.39
⋅ 8 ⋅
↑
⇑
This happens over several stages. First, a muscle suffers a mild injury (
eg
: repetitive stress in
sustained poor posture as in
Figure 10
), sending painful neural signals to the spinal cord. These
are ignored by the brain owing to their mildness, but converge with signals arriving from unrelated
nerves, perhaps even synapsing with them over time. If this is the case, chemicals released from
the first nerve could activate several nonproblematic nerves nearby, making it seem to the brain
as if these nerves are now delivering painful signals as well.46,74,89-91,102 These convergence and
sensitization processes would strengthen over time, allowing less intense stimuli of the injury
site to result in the same or even more intensified referred pain responses,39,67,102 similar to the
phenomenon at the root of arm/chest/jaw referred pain common during a heart attack.103
Gate control theory
A second model explaining how massage releases both local and referred pain is that of “gate
control”.55,104 Pain was initially thought to correlate directly with the degree of injury (
ie
. being
objectively
painful, as in
Figure 5
).12,16,105 Gate control theory, however, showed that pain is not a
simple linear process starting with a stimulus and ending at perception. Rather, it is controlled
by “gates” modulated by competing nerve signals. This happens in the spinal cord where primary
sensory nerves synapse with interneurons, as well as in the brain itself, where sensation,
emotion, and memory combine with other cognitions to form perception (
Figure 4
).55,57,74,75
Figure
4: Gate control theory. Image 1 shows the neurology involved: peripheral sensory nerves (blue
), inhibitory
spinal interneurons (
green), and the projection neuron bringing final modulated signals to the brain (red).
Image 2
shows
Aδ
firing from a painful signal, stimulating pain directly as well as indirectly through inhibiting inhibitory
interneurons.
Image 3 shows Aβ
firing from pressure or motion. This stronger mechanical signal immediately
overrides
Aδ nociception via spinal int
erneurons, canceling the perception of pain. Pain cannot be perceived without
the activation of interneurons carrying this signal to neurons that ultimately arrive in the brain.
55,106-112
Aβ Aβ
Aδ, C Aδ
1 2 3
⋅ 9 ⋅
↑
⇑
This modulation is possible because different sensations travel along
different nerves at different speeds. Proprioception travels fastest,
through thick, myelinated Aα fibres, while touch travels more less
quickly through thinner, myelinated Aβ fibres. Sharp, acute pain
travels slowly through thin, myelinated Aδ fibres, and sustained,
“burning” pain travels slower still, through thin, unmyelinated C
fibres.46,106,114-116 To put this all in perspective, Aα signals travel at the
speed of a bullet train and Aβ almost as fast as Formula One racing
cars, while Aδ signals could only keep pace with fast cyclists and C
signals would fall behind even a brisk walker (
Figure 6
).36,67,117,118
The majority of Aδ signals (90%) quickly reach the brain, precisely locating the injury. However,
only about 10% of the C fibre signals do the same, making the source of this duller pain much
harder to locate, partially explaining why some chronic pain becomes very difficult to pinpoint.116
Aα: proprioception, 13-20 µm
80-120 m/s (avg. ~360 km/h)
Aβ: touch, 6-12 µm
35-75 m/s (avg. ~200 km/h)
Aδ: sharp pain, 1-5 µm
5-35 m/s (avg. ~70 km/h)
C: sustained pain, 0.2-1.5 µm
0.5-2.0 m/s (avg. ~5 km/h)
Figure
6: Afferent nerve comparison: diameter, perception, myelination (light blue), and conduction velocities.
These differences explain why acute injury subjects generally first
report an immediate shock — registering the sensation of touch —
followed by an almost-immediate jolt of intense, stabbing pain (“first”
pain), ending in a sustained, throbbing pain (“second” pain) that
appears slowly and remains for some time (
Figure 7
).
All these fibres converge in the spinal cord,55 from which pain travels to the brain from the Aδ
and C fibres unless inhibited through a much faster signal traveling via Aβ fibres, like pressure
or motion (
Figure 4
). Noxious thermal stimuli (>43°C or <25°C) may also override nociception: these
are registered by both Aδ and C fibres,114 with the latter likely being the primary afferent.119 This
ascending gate control modulation explains both why we reflexively rub, shake, and ice injuries
immediately, as well as why massage brings almost immediate pain relief to sore muscles.117,120
Figure
5
: Original pain model.
Descartes' 1664 pain pathway
is linear and unidirectional.
113
Figure 7: Pain timeline.72,
117
⋅ 10 ⋅
↑
⇑
Descending modulation
Nociception is also modulated via descending pathways through direct cortical or thalamic
neurotransmitter release (
eg
: serotonin, noradrenaline, endogenous opioids),67,76 through rapid,
cognition-induced brain activity (
eg
: beliefs, experiences, expectations, fear),55 and through
behavioural changes like increased sleep or exercise.12,18,26,36,55,121,122
Figure
8: Descending modulation. Images 1 and 2 are as in Figure 4
, with the focus now on modulatory nerves
(
purple) descending from the brain.16 Image 3 shows this modulation overriding Aδ
nociception, eliminating
pain.
55,57,74,107-109,114,123 Prescription opioids like morphine act similarly and so are used in cases of chronic pain.123
The brainstem bridges cognitions with top-down pain modulation (
Figure 8
). Nociception enters
the brain from the spinal cord (
Figure 9.3 violet track
) where some neurons — mostly Aδ116 —
transmit information on location and intensity to the somatosensory cortex via the thalamus124
(
Figure 9.3 red track
). This branch meets with descending analgesic tracts in the midbrain’s
periaqueductal grey matter,125,126 modulating pain based on fear, attention, and
expectation,11,123,127,128 and in the rostroventral medulla oblongata’s nucleus raphe magnus
(NRM)114,123 is close to the retrotrapezoid nucleus which itself regulates breathing,129-131 perhaps
explaining why focused breathing consistently delivers analgesic effects.132-135 Other neurons
travel to the cingulate and insular cortices via the pons’ parabrachial nucleus and the amygdala,
modulating pain through emotion (
Figure 9.3 yellow track
). The amygdala fires more in situations
involving fear136 while the insular cortex serves to identify pain magnitude122 and is more active
with visual input,137 even if imagined (as is true for the anterior cingulate cortex).136 This anatomy
explains why cognitions like anxiety, worry, depression, and focusing on pain could “open” the
gate mentioned earlier, while distraction, relaxation, and positive emotions could “close” it.11,57,104
Aδ, C Aδ
1 2 3
⋅ 11 ⋅
↑
⇑
Figure
9: Pain in the brain. Images 1 and 2
show the brainstem’s medulla oblongata, pons and midbrain; the
amygdala and the cingulate, insular and somatosensory cortices; and the thalamus and hypothalamus. Nociception
ascends (
red) in Image 3, and is modulated by cerebral affects (yellow) and direct brainstem input (violet
), perhaps
via the medulla oblongata’s nucleus raphe magnus and the midbrain’s periaqueductal grey matter.
23,30,114,123,138,139
Clinicians are now teaching patients to fear pain less and to not catastrophize their state or
future,16-26,140 while also teaching them to better deal with day-to-day occupational, mood, and
social stressors, knowing that mastering these leads to more effective pain resolution.21,23,138,140
The detrimental mind-body feedback loop of a physical injury causing psychological stress — itself
increasing risk of re-injury — has been extensively studied.69 Tension, anxiety, and panic cause
muscle spasms, vasoconstriction, and blood flow shunting from the extremities to the core,
causing a drop in oxygen availability and bringing alertness as well as muscle and brain activity
down with it. Once this loop is understood — as well as the patient’s own power over it — the
patient is better able to put a stop to it and take an active role in their own recovery, reducing
anxiety and thereby allowing for healing to begin.68,73
Of special importance to this paper is that trigger points worsen with psychological stressors. In
one study, trigger point activity was shown to increase with both expressed and inhibited anger,
with significant correlation with the latter in particular.141 This may be due to muscle guarding141
or to sympathetic neurological involvement at muscle spindles (capsular sensory receptors
embedded in muscle bellies)142 seen in pharmacological studies showing decreased
electromyographic activity in the trigger point with sympathetic neuron blockers but not with
1 2 3
⋅ 12 ⋅
↑
⇑
motor neuron blockers.143 Other studies showed that recalling emotional events increased trigger
point activation144 while relaxation techniques did the opposite.145,146 Ties were later found
between individuals with internalizing traits (high worry, fear of criticism, low assertiveness) and
feeling more pain in trigger points than individuals without these traits.144 Lastly, biopsychosocial
interventions — physiological interventions with psychsocial support systems — have been found
to decrease the overall experience of chronic pain,14 while a lack of social support relates to a
marked increase in its perception.3,12,21 Therefore, interventions including muscle relaxation,
biofeedback, social support, and imagery are recommended as a major goal of treatment.147
Neuromatrix theory
All this is being distilled into a theory that it is a widespread cerebral network — a “neuromatrix”
— that perceives pain,72,74,75,104 modulating its sensation starting with cognitions that were
traditionally written off as mere reactions (
eg
: apprehension, fear).74,75 It shows pain to be a very
complex process governed by a convergence of influences, including genetic determinants,
cognitive events, and somatosensory input.67,75 It underlines that pain management may be more
effective when cognitive processes are taken into account, explaining why cognitions like imagery
have mitigated pain consistently in both the literature as well as in clinical practice.148
Trigger point pathophysiology
Trigger points were described as early as the 16th century and have remained a very controversial
topic since their rediscovery in the 20th,84 with even their very existence currently being
questioned.149-153 That said, the focus of this paper isn’t so much on their physiology or etiology
as it is on the mediation of the pain they cause, both locally and via referral, which is very real
indeed. Still, their commonly-accepted pathogenesis follows for context.
Formation
From the seminal text on the subject, a trigger point is a hyperirritable spot in skeletal muscle
often palpable as a nodule in a taut band.39,84,86,154,155 It forms when performance intensity
outmatches the body’s normal ability to sustain it and normal recovery is prevented.5,156-160 This
can be the result of sudden muscle load increases, as with intense movements or trauma (
eg
:
whiplash, muscle strain),84 of slowly-mounting strains as in repetitive stress injuries (chronically
sustained, submaximal contractions),5,6,46,84,161,162 or even of the mere addition of biomechanical
stress to cooled muscles (these are less supple and therefore more prone to tearing).102
⋅ 13 ⋅
↑
⇑
Trigger points occur in 20-70% of the general population,39,53,163-165 most often in, again, the upper
trapezius muscle.39 This is likely due to its frequent flexion, both in the classic shoulder-hunching,
defensive posture typical in response to stress, as well as in sedentary postures increasingly
prevalent throughout society (
eg
: anterior head carriage and accompanying shoulder rounding
characteristic of Upper Crossed Syndrome, as in
Figure 10
). Our head weighs 10 lbs, with another
10 lbs of stress added to our neck musculature every inch it moves forward of the midline (the
upper trapezius being a key player).166,167 It is not surprising, therefore, that these muscles may
respond with injury over time, potentially causing trigger point formation.
Figure
10: Trigger point formation. Posture-
induced via anterior head carriage and muscle guarding: as the head
leans forward, tension on the upper trapezius muscle increases with its fibres hardening in response.
46,166-168
Key to this study is the emotional activation of trigger points. Intense emotions sustain muscle
tension via “muscle guarding”,160 reducing tension via muscle shortening in the short-term but
creating a chronic pain-spasm-pain cycle in the long run (
Figure 10
).169,170 This tension decreases
blood flow and distorts posture, further exacerbating the condition and its associated pain.78,80,86
Anatomy
Trigger points are often found near the point of motor innervation in muscle, with excessive nerve
activity in — or direct stress or trauma to — this area triggering irritation (
ie
. flexing, stretching,
or pressing it).80 When a series of such hyperirritable loci remain contracted within a muscle, they
form a raised, palpable nodule — a trigger point — while pulling the rest of their fibres into a taut
band (
Figure 11
). This sustained contraction could be the result of excessive acetylcholine release.5
⋅ 14 ⋅
↑
⇑
Figure
11: Proposed trigger point anatomy. Normal (left) v. tense (right
) muscle fibres show the formation of nodules
and their associated taut bands.
86 A trigger point is hypothesized to be a concentration of such nodules (X).5,154,171-
173
The increase in energy consumption this causes, and its associated reduced energy supply via
severe local hypoxia due to sustained muscle contraction, creates an energy crisis that further
contributes to the trigger point pain cycle.86,102,174 The point may be painful locally and can elicit
predictable referred pain or muscle twitch responses into otherwise unassociated muscles
(
Figures 1
& 3
).77,175 These are distal effects are suspected of being mediated by mechanisms in
the spinal cord.86 Additional symptoms may include limited, painful range of motion as well as
weakness in the affected muscle. Further, a trigger point may be active — currently producing
pain, or latent — asymptotic until activated (again: flexed, stretched, or pressed).39,47,53,84,158
As different from acupuncture points
Due to their similarity, a distinction must be made between trigger and acupuncture points. The
first are a muscular pathology and can occur anywhere inside the muscle belly,164 though usually
at large groupings of dysfunctional neuromuscular junctions.102 Conversely, the second seem to
lack any uniform morphology86 and occur only on predefined lines throughout the body, termed
“meridians” or “energy flows”. These are based on traditional Chinese medicine and have no
clear biomedical basis thus far.85,160 Interestingly, one study found a 71% overlap between the
⋅ 15 ⋅
↑
⇑
two in their distribution and referred pain.176 Both phenomena also present with local twitch
responses as well as possible spinal cord mechanisms,86 suggesting they share at least some
underlying physiological underpinnings.160,176
As different from muscle “knots”
In a similar vein, trigger points are not “muscle knots”, a very common confusion. Just noting
muscle tension is not grounds enough to suspect trigger point presence.152,153 First, bony
prominences (
eg
: ribs, hips) and tendinous muscle attachment sites (
eg
: levator scapulæ) are
often mistaken for “knotted” muscle. Secondly, some muscles are naturally stiffer owing to
consistent use in posture (
eg
: solei, erector spinæ). Lastly, even when a muscle is tight or hard,
it is not always painful itself or referring pain anywhere else. In one study of the trapezius muscle
almost 30% of tender sites did not share comorbidity with tissue hardness.6
As different from healthy muscle
Lastly, trigger points have been shown to differ biochemically from healthy muscle177-179 and to
undergo thermal180 and biochemical181 changes when released. However, a lack of agreement
regarding accepted diagnostic criteria has been a serious handicap in both recognizing myofascial
trigger point pain as a distinct phenomenon and in studying the topic and comparing treatment
effectiveness across different techniques.39,53,85,157,165,182-184 That said, treatment
standardization,53,185,186 increased clinical experience,187 and improved technological diagnostic
tools180,188,189 have already started clearing these issues up.
Trigger point treatment
As explained by the gate control model (
Figure 4
), individuals often shake and then rub affected
areas immediately following injury.115 Similar reactions are found in people suffering from trigger
points: there is a common tendency to self-massage or stretch the area of referred pain.158 This
is ineffective as the pain’s source — the trigger point — is almost always elsewhere. However,
compressing this point, once found, is one of the most effective, non-invasive ways of resolving
the issue,84,156,190,191 with its application becoming something of a specialty in itself.157
Common protocol includes first massaging the referral site to increase the patient’s confidence
in the procedure and to harness any placebo effect possible. This is followed by pressing the
trigger point, recreating the pain (referred and/or local) and holding the pressure until the pain
disappears or diminishes greatly, then “flushing out” the area through general massage. Though
⋅ 16 ⋅
↑
⇑
deep finger pressure was advocated early on, current protocol suggests a gentler approach, first
focusing on accurately locating and confirming the trigger point and then pressing it gently, going
deeper to match the patient’s subjective rate of pain relief. This takes into account that trigger
points are hypoxic, energy-crisis zones, where adding deeper pressure could potentially
exacerbate the problem. Pressure treatment should be followed by a stretch resolving any
remaining neuromuscular junction contractures.102 Slow, regular breathing is an effective method
of continuing chronic pain management,135 especially breathing “into” the trigger point during
release.158 Again, since regions in the medulla are both responsible for breathing (the respiratory
centre) as well as for pain modulation (the nucleus raphe magnus),127,128 activation of the first
system could also have effects on the second (
Figure 9
).
Hot and cold therapy
Icing referred pain provides a strong signal along Aδ and C
fibres,192 possibly overriding the sensitized “false” pain signal at
the spinal convergence115 (
Figure 12
). Heat at the trigger point
eliminates pain and brings in blood via vasodilation, resolving
any energy crises. It also relaxes the area through facilitating
release of any unconscious muscle guarding.
Homecare includes stretching and applying heat to the trigger
point zone to release any remaining adhesions and flush it of any
biochemical aftereffects.158 Flare-ups are dealt with by icing the
referred pain zone while applying heat to the trigger point
(
Figures 24 & 30
). Relief lasts at least a few weeks following
treatment,186 if not several months or until the next stressor.
Other approaches
Needling has been very successful,155,193-195 especially if a local twitch response is elicited before
the needle is applied.86,175 It functions through mechanically disrupting the point itself,156 though
it is important to, again, distinguish trigger point needling from acupuncture.85 A stretch-and-
spray technique pioneered by Travell is also effective, stretching the affected muscle while
spraying it with a coolant and distracting the patient from the sudden pain.38,39 Chiropractic
cervical spine adjustments have also met with success,196,197 possibly through unblocking spinal
nerve pathways or through the reflexive muscle relaxation process such adjustments naturally
Figure
12
: Trigger point therapy
and ice.
How cooling may override
spinal sensitization.
39,115
⋅ 17 ⋅
↑
⇑
produce.161 Other treatments include ultrasound,198-202 transcutaneous electrical nerve stimulation
(TENS)38 and low level laser therapy,203 various injections,204 and even mud bath or magnetic field
immersion. It is not yet certain how effective these last approaches are.47,156
Imagery neuroanatomy
Perception
Figure
13: Perception neuroanatomy. Image 1 shows visual cortex image arrival (blue
) and dorsoventral splitting
into action
- (green) and description-oriented (violet) streams. Image 2
shows macaque visual cortex retinotopic
organization its field of vision (
box) and corresponding cortex activity (slice, from blue
section of macaque head
inset).
205,206 Image 3 shows the corresponding human anatomy (a-b), visual field (c), and visual cortical map (d).207
To understand imagery, it helps to first understand perception. When eyes see, neural signals
reach the brain’s posterior visual centre, retinotopically mapping the stimulus to resemble the
visual field.205 This is seen with eerie accuracy in a macaque’s occipitocerebral energy (glucose)
consumption in its visual cortex matching its visual field (
Figure 13.2
). Compartmentalization
continues as the brain processes an image, passing signals further ventrally and dorsally to
memory, emotion, and sensation centres, making sense of what is being seen.
Imagery
Imagery differs from perception in that it recreates the same without visual input,208,209 bridging
high-level information (thoughts, emotions, memories) with low-level sensations.210 All this
1 2
3 a b c d
⋅ 18 ⋅
↑
⇑
information is processed in occipital visual centres,209,211-224 then emerging through two major
nerve bundles: the superior and inferior longitudinal fasciculi. The first carry spatial, action-
oriented details dorsally through the parietal and frontal lobes (
eg
: where an object is, how to
use it), while the second carry description-oriented object details ventrally and into the temporal
lobe (
ie
. what an object is).209,225-229
Figure
14: Decoding brain imagery. Video snippets seen (top) and then reconstructed via fMRI (bottom).230,231
Certain objects or details have distinct representations along these streams, with their imagery
evoking very clear neural signatures. Surfaces, faces, outdoor scenes, houses, chairs, animals,
and tools all light up unique patterns along the ventral stream,209,232 with characteristics like
image vividness acting to further distinguish the signature.233 Recent studies have even been able
to decode what a person is seeing or imagining through retinotopic reconstruction of ventral
stream activity (
Figures 13.3 & 14
),230,234-237 and are now decoding even technique now decoding
even dreams (
Figure 15
).231,235,238-241
Left
: “… There was
something like a
writing paper for
composing an
essay, and I was
looking at the
characters from the
essay…”
Left
: “… ther e were
persons, about 3
persons, inside some
sort of hall. There
was a male, a
female, and maybe
like a child… a boy,
a girl, and mother…”
Figure
15: Decoding dreams.
Video stills of reconstructed dreams and descriptor keywords chosen by the computer,
alongside participant descriptions of their dreams immediately upon awakening.
238,239,242
⋅ 19 ⋅
↑
⇑
Virtually all pathways traveling between visual areas are
bidirectional.215,243,244 Parieto- and temporo-occipital
regions are especially active during imagery,211,219,245-251
with regions in the frontal and parietal cortex activated
during both imagery and perception,252-254 particularly in
the left precuneus209,255 and other structures in the left
hemisphere nearby,254,256-258 underlining their importance
in creating and maintaining mental images.209 Perception
also receives input from memory259 so imagery may have
some ties to temporal memory areas,209,218,254,260,261
providing a reason for this bidirectionality (
Figure 16
).
However, the phenomena differ in key ways262 (
eg
:
perception activates posteroanteriorly along the ventral
stream while imagery does the reverse,234 suppressing
primary sensory regions263 and hinting at memory input).
Imagery in rehabilitation
Past literature has showed imagery’s effectiveness in improving conditions as varied as cancer,264
psoriasis,265 stress,266 ulcers, paraplegia, fractures, hip disarticulations, intraabdominal lesions,267
phantom limb pain,268 and chronic pain.269 It has also been successful in injury rehabilitation,
resulting both in faster recovery times270 as well as in improved pain management associated
with healing.59,267,271-275 It is unsurprising therefore, that many imagery scripts have been
developed over the years to treat a wide array of conditions, often emerging from the fields of
psychiatry and psychotherapy.63 In the case of injury, imagery scripts are most effective when
they are clear, accurate, strong, positive, and meaningful to the patient, and if the patient
understands and can accurately imagine the entire healing process (
eg
: anatomy, treatment
modality, end goal).59 Such detailed imagery requires the patient to be relaxed, facilitating
enhanced mental reception and muscle relaxation. Only then can proper healing take place.270
Injury imagery has three main focuses: pleasant imagining (comfort-inducing, reducing
sympathetic nervous activity and muscle tension, useful especially in early stages of
rehabilitation), pain acknowledgement (assigning pain physical properties for later mental
manipulation) and dramatized coping (reframing, where pain is now part of the challenge of goal
Figure
16: Imagery neuroanatomy.
Areas
associated with imagery forming and storage
(
yellow
, including left precuneus), as well as
parieto
- and temporo-
occipital regions and the
reverse ventral stream (
orange) highlighted.
⋅ 20 ⋅
↑
⇑
achievement). Injury imagery may also take one of two directions: associative or dissociative —
focusing “towards” or “away from” the pain. Dissociative imagery tends to be more effective,
though associative approaches are useful in reducing pain while providing the athlete with a
sense of control over their condition.59 Lastly, imagery may be motivational (energizing), cognitive
(helping first plan and then practice a technique or strategy),276 or healing (visualizing positive,
healthy physiological processes or imaging oneself in a state of health).273,277 Initially, motivational
imagery was suspected as being used more often in athletic rehabilitation, particularly with elite
athletes.278 A follow-up study, however, showed athletes in rehabilitation using all forms of
imagery mentioned, only in lower amounts than those in training or competition.7,277 Healing
imagery on its own was found to increase athletes’ satisfaction in the rehabilitation process,
though without decreasing the time required to return to sport.279 Its application generally lapsed
in the beginning until a few days post-injury because athletes needed to let their minds clear of
negativity. Healing and cognitive (but not motivational) imagery was then generally applied until
the injury had healed.280,281
The PETTLEP model
One effective approach for rich, relevant imagery is the PETTLEP model,282 traditionally used for
motor imagery (
ie
. the mental rehearsal of an action). This was one of the first approaches backed
by neuroimaging technology and providing a concrete, comprehensive method for systematically
enriching imagery. It states that imagery ought to be physical (
eg
: done while wearing a game-
day uniform, or in the arena where the imagined performance will take place), take place in the
same environment as the upcoming event, and revolve around details relevant to the task in real-
time (
eg
: appropriate skill level, matching personal preferences). It should also be re-learned as
needed and be packed with the same emotions felt as when performing the task imagined. Lastly,
it can take one of two perspectives: first-person is recommended for open-skilled tasks with a
focus on timing (
eg
: karate) while third-person is recommended for aesthetic tasks where form
and positioning are important (
eg
: surfing). Such rich imagery results in fewer distractions,
though, should these hit, the patient should focus first on re-establishing imagery through the
senses they respond to most easily (generally visual), which quickly sweeps in with it other, less-
used senses. Looking at images of natural settings beforehand clears the mind well, and for those
who tend to verbalize what they see, it is recommended to spend a few minutes before treatment
letting their gaze wander the room, consciously not putting a label to anything spotted.63
⋅ 21 ⋅
↑
⇑
Physiological effects of imagery
Other studies have also shown imagery to change the body’s physiology, from causing similar
brain activity as performing the imagined motion would,283 to raising heart and respiration rates,284
to increasing muscle strength,285-287 activation,288,289 and relaxation — this last both at the motor
neuron level290 as well as via fatigue induced through depleted self-control.291 It has also been
found that personalised, emotion-laden imagery scripts result in increased muscle activity, likely
because of the increased image vividness brought about with this approach.292 Of specific
importance to this study, imagery has been helpful in resolving most major classifications of
headaches,293,294 with hand-warming biofeedback exercises showing particular effectiveness and
widespread use.295-301 Other studies showed that imagery can be used to increase skin
temperature,302 of which a key one showed that focusing skin-warming imagery to trigger point
sites — in combination with implementing a general relaxation and thermal biofeedback training
program — increased skin temperature and muscle relaxation at these sites while also decreasing
subjects’ overall pain sensitivity.303 A potential explanatory mechanism for all these physiological
changes is that imagery eliminates the stressful, destructive, vasoconstriction-causing mental
images.304
⋅ 22 ⋅
⇑
METHODS
Population
Forty participants, 11 male and 29 female, were recruited from Gdańsk University and Gdańsk
Sport University on the Baltic coast in northern Poland. Thirty were students or their friends and
ten were professors or their friends, aged 19-51 (M = 26.13, SD = 8.05). There were no exclusion
criteria. Testing took place in Polish at Gdańsk Sport University’s sport psychology office with a
massage table from the physiotherapy department and with the Smart Voice Recorder app on an
LG Nexus 4 cell phone recording audio throughout treatment. Only the therapist and the current
study participant were in the room during testing.
Groups and scripts assigned
On entering treatment participants freely consented to participate in the study (
Appendix
), were
then randomly assigned into control or imagery groups, and then were read the treatment
protocol, trigger point description, rating measures,305 and their group-specific script. The control
group (n = 20) was given a breathing-focused relaxation script, below, then had it demonstrated
and tried it prior to treatment (
Appendix
):
“Concentrate on breathing, first filling up your stomach, then your ribs from the sides, and
finally your chest. Exhale in the reverse order. Breathe in with your nose an