Carolyn R. McMakin, MA, DC,1 and James L. Oschman, PhD2
Frequency-specific microcurrent (FSM) is an emerging technique for treating many health conditions. Pairs of
frequencies of microampere-level electrical stimulation are applied to particular places on the skin of a patient
via combinations of conductive graphite gloves, moistened towels, or gel electrode patches. A consistent finding
is a profound and palpable tissue softening and warming within seconds of applying frequencies appropriate for
treating particular conditions. Similar phenomena are often observed with successful acupuncture, cranialsacral, and other energy-based techniques. This article explores possible mechanisms involved in tissue softening. In the 1970s, neuroscientist and osteopathic researcher Irvin Korr developed a ‘‘c-loop hypothesis’’ to
explain the persistence of increased systemic muscle tone associated with various somatic dysfunctions. This
article summarizes how physiologists, neuroscientists, osteopaths, chiropractors, and fascial researchers have
expanded on Korr’s ideas by exploring various mechanisms by which injury or disease increase local muscle
tension or systemic muscle tone. Following on Korr’s hypothesis, it is suggested that most patients actually
present with elevated muscle tone or tense areas due to prior traumas or other disorders, and that tissue
softening indicates that FSM or other methods are affecting the cause of their pathophysiology. The authors
believe this concept and the research it has led to will be of interest to a wide range of energetic, bodywork, and
Electricity has long been used to stimulate healing; the
recorded history dates from 2750 bc when sick people
were exposed to electric eels.1 In 1812, Dr. John Birch in
London healed a nonunion of the tibia with electric currents
passed through needles surgically implanted in the fracture
region.2 By the mid 1800s, this had become the preferred
method for treating slow-healing bone fractures. However,
the Flexner Report and the Pure Food and Drug Act of 1906
led to the abolition of electricity for healing3 until the 1980s,
when careful research confirmed the effectiveness of electrical
currents for stimulating bone healing. It was then discovered
that coils could be used to noninvasively induce current flows
through fracture sites.4 This is known as pulsing electromagnetic field (PEMF) therapy. Following on this success,
other investigators have successfully applied PEMF to a variety of other tissues, with each tissue respond
magnetic fields in the surrounding space (Ampe`re’s Law,
1820),10 and moving magnetic fields induce currents to flow
through conductors (Faraday’s Law, 1831).11 Electromagnetic fields arise when charges accelerate.12 Hence, when
oscillating or pulsing microcurrents are applied to the human body for therapeutic purposes, there is the possibility
that beneficial effects may be due to the microcurrents
themselves, to the magnetic fields induced in conductive
tissues by charge movements, or to electromagnetic fields.
Energy medicine and bioelectromagnetics recognize the
importance of resonance—the tendency of objects such as
atomic nuclei, electrons, or molecules to vibrate strongly at
certain frequencies and for these vibrations to be coupled
through space to other objects with similar resonant frequencies. Magnetic resonance imaging, for example, is based
on resonant interactions between magnetic and electromagnetic fields and protons in tissues. The high degree of frequency specificity of frequency-specific microcurrent (FSM)
indicates that resonance is probably involved in the mechanism of action, in which the applied current is resonating
with charged particles or dipoles in the tissues.
FSM has emerged over the last decade as a reproducible
treatment for various somatic and visceral conditions including fibromyalgia, chronic fatigue, and myofascial and
neuropathic pain. Recent publications13,14,15 summarize the
origins, possible mechanisms, applications, and practical
details of FSM. The technique is based on pairs of frequencies, low-level micro-amperage currents, and the principles
of biologic resonance. The publications describe protocols for
treating various health complaints; multicenter clinical case
reports documenting successful applications; and review
condition pathophysiology, differential diagnosis, and current research. A study of delayed-onset muscle soreness
summarizes the history of FSM, including the history of the
discovery of effective frequencies and frequency combinations.16
FSM practitioners consistently observe a profound and
easily palpable change in tissue texture within seconds of
applying frequencies appropriate for a particular disorder.
This ‘‘state change’’ can usually be detected anywhere on the
body when one has found the correct frequencies and
placements of the conductors (conductive graphite gloves,
gloves wrapped in moist cloth, or gel electrode patches) (Fig.
1), provided the patient is hydrated. The softening is not
superficial, as in the epidermal layer, but is in the deeper
Tissue softening provides rapid feedback when one is
optimizing a protocol for a condition not previously treated
with FSM. Since so many variables are involved—two separate frequencies, signal intensities and waveforms, positioning of the conductive materials, and the patient’s
condition—tissue softening facilitates the determination of
the best combinations.
The purpose of this report is to explore the possible causes
of changes in muscle tension and muscle tone* during the
therapeutic encounter. The report is not about muscle testing
and applied kinesiology, although the information presented
may be relevant to those controversial subjects.**
Specific changes include the following:
The tissue rapidly and profoundly softens within seconds.
Usually tissue all over the body softens when a beneficial frequency combination is applied anywhere on the
body for any condition—likely a change in systemwide
Sometimes there are unresponsive regions that stand
out amid the softened tissue—apparently due to localized muscle tension. These areas can be addressed with
additional frequency choices and locations of the conductors.
Muscle tissue that is hard, tough, scarred, firm, rigid,
‘‘gnarly,’’ or stiff begins to soften and within minutes
feels ‘‘smooshy,’’ like pudding in a plastic sack.
The tissue becomes warm. This can be felt through the
conductive gloves. Some sensitive practitioners can feel
the warming with their hand several inches away from
The patient may become somewhat dreamy or ‘‘spaced
For example, place a hand on an arm muscle while testing
the eight possible frequency combinations previously identified for treating sinus conditions, with the microcurrent
applied via conductive gloves inserted in warm moistened
towels placed on the neck and forehead (Fig. 1A). One or
more of the frequency combinations will result in profound
softening of the arm muscle as the sinus condition begins to
resolve. Figures 1B and 1C show the use of the conductive
gloves and gel electrode patches, respectively.
Side-Effect or Causal Relationship
There are two contrasting perspectives on tissue softening
with FSM. One is that it is a ‘‘side-effect’’ of the application of
therapeutic frequencies, and has no physiologic significance.
Another is that injuries, physical or emotional traumas, or
other pathologic conditions can increase bodywide muscle
*The terms ‘‘muscle tone’’ or ‘‘residual muscle tension’’ or ‘‘muscle
tonus’’ refer to the continuous and passive partial contraction of the
resting skeletal muscles, or the muscle’s resistance to passive stretch
while in the resting state, as opposed to active contraction. Physical
disorders, injuries, and stress can result in abnormally low (hypotonia) or high (hypertonia) muscle tone throughout the body. In contrast, muscle tension refers to a condition in which particular muscles
remain chronically semicontracted. Muscle tension is typically a response to stress, overuse, or injury to a particular part of the body.
Stress can also lead to sympathetically mediated constriction of
blood vessels, reducing the flow of oxygen and nutrients to muscles,
tendons, and nerves, often referred to as ischemia. This can lead to
the local or systemic buildup of metabolic waste products, resulting
in muscle tension, spasm, and pain. FSM is effective at normalizing
both bodywide muscle tone and localized muscle tension, and at
ameliorating their consequences.
**Muscle testing or applied kinesiology uses muscle relaxation as
an indicator of a biologic response. The method has been used at
various stages in the development of methods that involve ‘‘listening’’ to obtain feedback on the functional status of the body and
appropriateness of various interventions. Examples of therapists
who use muscle testing include chiropractors, naturopaths, medical
doctors, dentists, nutritionists, physical therapists, massage therapists, nurse practitioners, practitioners of BodyTalk, Holographic or
Resonance Repatterning, and many others.
2 MCMAKIN AND OSCHMAN
tone or local muscle tension, and that tissue softening indicates that the pathophysiology is being addressed. On the
basis of the work of Irvin Korr and others to be described
below, it is suggested that patients often have some degree of
elevated muscle tone or tension stemming from the trauma,
disease, injury, or other condition that brought them to the
physician’s office, and that tissue softening indicates that
treatment is progressing.
Many patients experiencing a traumatic event go on with
their lives without lasting negative effects; others have reactions that lead to chronic physical and/or emotional issues. For example, psychologic factors have been associated
with primary fibromyalgia syndrome,17 and Mines suggests
that most people are ‘‘in shock’’ from old traumatic experiences.18 Musculoskeletal pain, for example, can have multiple causes, and some patients benefit from therapies that
‘‘unwind’’ old traumas.19
Physiologists, neuroscientists, osteopaths, chiropractors,
and fascial researchers have explored various mechanisms
by which injury or disease increases local or systemic muscle
tension or tone. They have described a variety of connections
between pain, injury, disease, and impaired movement, on
the one hand, and palpable muscle tone or tension on the
other. Their goal has been to find ways of resolving the
causes of pathophysiologies of all kinds. Often distinctions
have been made between visceral (organ) pathologies and
somatic (body wall or musculoskeletal system, in contrast to
the viscera) pathologies. As with reductionist ‘‘mind–body’’
distinctions, the holistic perspective teaches that we must be
cautious about such separations, as they may have little
relevance to how the human body actually responds in
health and disease. For example, the distinction between
electrical conduction ‘‘outside’’ and ‘‘inside’’ is blurred because the skin surface is anatomically continuous via the
nose, nasal cavities, and bronchial tree, extending into
the thin alveolar membranes separating the air space and
the blood. A similar anatomically continuous outside–inside
pathway connects to the body interior via the mouth and
mucous membranes of the digestive tract.
A Web of Interactions
secondary disorders or diseases involving segmentally related visceral organs. For a detailed introduction, see Morris24 and Simons and Travell,25 who devoted a chapter to the
abdominal muscles and their associated somatovisceral and
visceralsomatic reflexes. For example, they associated trigger
points in the oblique abdominals with diarrhea, belching,
dysmenorrhea, or nausea. Simons and Travell also reported
that a specific trigger point in the pectoralis major is associated with a type of ectopic cardiac arrhythmia and that
elimination of this trigger point immediately restored normal
While these ideas are widely taught, there is much doubt
and controversy. In a thoughtful review, Nansel and Szlazk
explore the concept that somatic therapies can treat the
causes of visceral (organ) disorders by removing blockages at
particular segments of the spinal cord. After review of some
350 articles published over a period of about 75 years, Nansel
and Szlazk concluded that misalignment in the vertebral
column can cause symptoms that can be mistaken for, or
mimic, visceral diseases, but that there is no substantial scientific evidence that segmental misalignment can actually
cause true visceral disease. Nansel and Szlazak continued to
be open to a segmental theory of visceral disease, but were
simply unable to find objective evidence for it. They emphasized that ‘‘afferent convergence’’ can create somatic
signs and symptoms that are virtually indistinguishable from
those produced by organ malfunctions.26 This brought into
question the widely taught concepts of somatovisceral and
visceralsomatic pathways. The resulting arguments were
summarized by Seaman.27
Convergence of visceral and somatic afferents continues to
be a topic of neurophysiologic research. For example, noxious stimuli in the esophagus can cause pain that is referred
to the anterior chest wall because of convergence of visceral
and somatic afferents within the spinal cord.28
These discussions are relevant to this report both because
FSM provides clinically verifiable relief from both somatic
and visceral issues, and because there is still widespread
acceptance that visceral dysfunctions can elevate somatic
muscle tension. For example, flank muscle hypertonicity can
arise secondary to renal dysfunction, and trigger points can
be activated in acute appendicitis, peptic ulcer, ulcerative
colitis, and diverticulitis.29 FSM, acupuncture, and other
energy medicine techniques document interactions between
the epidermis and internal organs. Whether these interactions are best referred to as somatovisceral reflexes is an open
question. Certainly relationships between somatic and visceral systems can be described in terms of chemistry (metabolic imbalances in the periphery might impact organ
functions and vice versa); in terms of neurology, such as the
convergence of visceral and somatic afferent nerves; in terms
of structural or fascial relationships between peripheral
structures and organs; in terms related to the endocrine
system and lymphatic drainage (Chapman’s Points)30,31; and
in terms of energetic pathways between the skin and internal
organs, as theorized, for example, in acupuncture. The
questions arising from these ideas are profound and are of
major medical significance.
Several inter-related hypotheses have therefore been explored in order to provide a perspective on tissue softening
with FSM. The concepts are presented in historical sequence,
without favoring any one of them. The goal is to provide a
background for further theoretical, clinical and applied research, recognizing that aspects of several of these mechanisms may be involved simultaneously.
The Vicious Cycle Relating Muscle Spasm
and Pain (1940s)
A ‘‘vicious cycle’’ hypothesis of pain and increased muscle
tension was proposed in 1942:
Limitation of motion is primarily a reaction to pain
rather than the result of structural lesion. If muscle
spasm causes pain, and pain reflexively produces
muscle spasm, a self-perpetuating cycle might be established.32
While this concept is still widely held, controlled studies
have shown no significant difference in resting electromyographic activity when painful and nonpainful muscles are
compared.33,34,35 A painful inflamed muscle can actually
have lower-than-normal tension.36
The Vascular Autonomic Signal (1950s)
The vascular autonomic signal (VAS) is an instantaneous
change in the tone of the walls of all arteries, mediated by the
autonomic nervous system.37 Changes are palpable at the
radial or carotid arteries. The VAS is thought to be a sensitive
indicator of autonomic changes from a variety of external or
internal factors, and was first used to study the effects of
auricular (ear) acupuncture. It is unlikely that the momentary shift in arterial pressure observed in the VAS explains
tissue softening with FSM, which has a slower onset and
persists for the duration of a treatment.
The c-Loop Hypothesis (1970s)
In 1975 and 1978 Irvin Korr introduced a ‘‘c-loop hypothesis’’ to explain the persistence of increased local or
systemic muscle contractions associated with various somatic and/or visceral dysfunctions.38,39 The hypothesis
states that such dysfunctions lead to increased resting muscle
contractions mediated by the autonomic nervous system and
by the c efferent loops regulating local muscle tension or
global muscle tone.* Appropriate FSM treatments targeting
specific conditions may therefore restore normal autonomic
function and/or shift the ‘‘c gain’’ regulating muscle tone or
tension. Autonomic effects could also account for circulatory
changes (tissue warming) and effects on consciousness (the
dreamy or ‘‘spaced out’’ condition often observed in FSM).
Perhaps resetting the c gain and lowering resting tonus of the
musculature causes a transient drop in blood pressure (indicated by the VAS) from reduced muscular compression on
the vasculature. The carotid sinus and aortic baroreceptor
*The c loops consist of efferent neurons (neurons from the central
nervous system to the periphery, such as motor neurons) and afferent neurons (neurons from the periphery to the central nervous
system, such as sensory nerves). Gamma (c) motor neurons are the
efferent component of the fusimotor system that controls and
modifies the sensitivity of muscle spindles. The muscle spindles
provide proprioceptive feedback for the movement, position and
extension of muscles. Gamma (c) motor neurons are located in the
brainstem and spinal cord and are smaller than their a-motoneuron
counterparts, which stimulate contractions of the skeletal muscles.
4 MCMAKIN AND OSCHMAN
feedback loops40 would quickly restore blood volume and
pressure, explaining why the VAS is a transient change arterial pressure.
Korr pointed out that there is a large though scattered
body of clinical and experimental literature describing
chronic hyperactivity of sympathetic pathways in many
clinical conditions, involving a variety of organs and tissues.
He suggested that this widely shared feature of local, regional, or segmental sympathetic hyperactivity is overlooked
because of barriers created by specialization: The ophthalmologist is not ordinarily exposed to the gastroenterologic
literature, the gastroenterologist to the cardiologic, and so
on. Each discoverer of a sympathetic component seems to
regard it as peculiar to this or that disease, rather than as part
of a general theme. Korr referred to this hypothesis and its
consequences as sustained sympatheticotonia.39
Sympathetic activation can have both local and systemic
effects on cardiac output, distribution of blood flow, heat
dissipation through the skin, release of stored metabolites,
local muscle tension or systemic skeletal muscle tone, range
of motion, and emotional affect.41 In other words, any injury
or inflammation or any somatic or visceral dysfunction
anywhere in the body can elevate muscle tone throughout
the musculoskeletal system, or increase skeletal muscle tension in selected areas, depending on the myotome, dermatome, or sclerotome involved.*
Korr’s hypothesis of sustained sympatheticotonia may
apply to FSM, since a consistent observation is that application of the correct treatment frequencies leads to a palpable
local or bodywide tissue softening and warming, which is
often associated with vasodilation. Frequency effects on the
autonomic nervous system have been noted before (e.g.,
McKay et al., 2006).42 FSM may actually reset c gain and
sympathetic tone, with beneficial local and/or systemic
consequences on resting muscle tone and visceral functioning.** How specific frequencies may cause such changes remains an open question.
The Johansson/Sojka Hypothesis (1990s)
In 1991, Swedish physiologists H. Johansson and P. Sojka
developed a model to help explain why chronic musculoskeletal pain syndromes such as those encountered with industrial injuries have a tendency to perpetuate themselves
and spread from one muscle to another.43 The hypothesis is
that metabolites produced by static or chronic muscle contractions stimulate muscle afferents, activating the c-motor
neurons, increasing muscle stiffness, leading to further production of metabolites, thereby creating a ‘‘built-in’’ positive
feedback loop or ‘‘vicious cycle’’ that perpetuates and
spreads the hypertonicity from muscle to muscle. While the
model is popular, it is not clinically proven to operate in
humans.33 More recently, studies on humans demonstrated
that acute activation of muscle or skin nociceptors*** does not
cause a reflexive increase in c gain.44
The Facilitated Segment Theory (2003)
Chiropractic researchers extended Korr’s work and developed a facilitated segment theory: chronic, repetitive, and
abnormal segmental input creates referred segmental pain
and tenderness, hypertonicity of key muscles, and even
secondary soft-tissue changes within the girdles and limbs. A
facilitated segment can maintain a disturbed state from impulses of endogenous origin entering the corresponding
dorsal root ganglion. All somatic and visceral structures receiving efferent nerve fibers from that segment are potentially exposed to excessive excitation or inhibition.45
Impulses of endogenous origin include autonomic and c efferent fibers to muscle.
Following up on Korr’s concepts and the Johansson and
Sojka hypothesis, in 2003 chiropractic researchers Knutson
and Owens reviewed the complexities of skeletal muscle in
regard to anatomy, active and passive tone, detection of
muscle tone, neurophysiology, and how muscle function fits
into a variety of subluxation/joint dysfunction models.46,47
(The Association of Chiropractic Colleges defines subluxation as a complex of functional and/or structural and/or
pathologic articular changes that compromise neural integrity and that may influence organ system function and
general health.)45 Part II of the Knutson and Owens report
discusses the extensive literature on how the various degrees
of elevated muscle tone and their causes can help clinicians
find underlying sources of neuromusculoskeletal problems
and select appropriate interventions.47 All of these concepts
Tension and Softening of Connective Tissue/Fascia
(Beginning in 2004)
Fascia is the bodywide structural and tensional component of the musculoskeletal system and has extensions to all
of the viscera. In the past there has been uncertainty as to
which kinds of connective tissue should be included under
the term ‘‘fascia’’—superficial fascia, endomysium, perineurium, visceral membranes, aponeuroses, retinaculae, tendons, ligaments, or joint/organ capsules. At the 1st
International Fascia Research Congress, held at Harvard
Medical School in 2007, it was proposed that all collagenous
connective tissues whose morphology is shaped primarily by
tensional loading and that is part of the interconnected tensional network that extends throughout the body could be
considered ‘‘fascial tissues.’’49
Fascia has usually been viewed as a passive material that
simply transmits forces exerted by muscles and gravity.
However, a series of reports by Robert Schleip and colleagues, beginning in 2004, confirmed earlier suggestions
that fascia may have both sensory and contractile properties.
They showed that lumbar fascia, plantar fascia, and the fascia
lata contain myofibroblast cells that stain for a-smoothmuscle actin.50 Further in vitro research showed that smooth
muscle-like contractions can be both induced and inhibited
pharmacologically.51 Schleip and colleagues recognized that
*The terms, myotomes, dermatomes and sclerotomes refer to tissues that develop from particular masses of embryonic mesoderm.
Dermatomes develop into dermis, myotomes develop into skeletal
muscle, and sclerotomes develop into vertebrae and most of the skull
bones. The terms ‘‘myotome’’ and ‘‘dermatome’’ also respectively
describe the muscles and skin areas served by a single nerve root.
**There is histological evidence that muscle spindles are innervated by sympathetic nerves, but little is known about their function.
***Nociceptors or pain receptors are lightly myelinated or unmyelinated afferent sensory neurons that are found in any area of the
body that can sense pain caused by mechanical, thermal, or chemical
stimuli that are strong enough to damage tissues.
TISSUE SOFTENING WITH FREQUENCY-SPECIFIC MICROCURRENT 5
contractility of intramuscular connective tissue could be a
significant component of passive muscle stiffness, which is
also referred to as passive elasticity, passive muscular compliance, passive extensibility, resting tension, or passive
These important findings have implications for visceral
and somatic disorders or dysfunctions, and could also be a
component of the elevated tissue stiffness discussed here.
The observed time-course of fascial lengthening is probably
too slow to account for the tissue softening taking place
during FSM, but could be a component of the longer-term
healing responses triggered by FSM.
The main hypothesis of this report is that tissue softening
noted when a therapeutic frequency is applied to the body is
accounted for by the fact that most patients actually present
with elevated muscle tone or tense areas related to previous
traumatic or disease experiences, as originally proposed by
Irvin Korr. Several possible mechanisms have been discussed
by which trauma and disease lead to elevated muscle tone or
tense areas. The most recent research has shown that fascia
has both sensory and contractile properties that can influence
passive muscle stiffness, elasticity, compliance, extensibility,
resting tension, and muscle tone. This new work was unknown to the earlier investigators cited here.
The fascial network is pervasive, extending to the capsules
and interiors of organs, and could therefore be involved in
both the origin and resolution of both somatic and visceral
disorders. A recent report by Finando and Finando suggests
that fascia is the medium involved in the effects of acupuncture, including effects on organ pathology.53 When the
body is injured, stressed, or traumatized, fascia responds by
laying down new fibers to provide support for the injured
area (Wolff’s Law for bone,54 and Davis’s Law for soft tissues) and by ‘‘gluing’’ adjacent muscles to each other.
Thickening and gluing of fascial layers can persist long after
an injury has healed and leave behind dense pockets or
nonresilient bands that can be felt deep in the tissues.55 These
palpable densities may correspond to the trigger points and
taut bands described by Simons and Travell56 and/or to the
inflammatory pockets described by Selye.57 Residual local
tensions and gluing in the fascial network can give rise to
compensating tensions extending throughout the musculoskeletal system. Such compensations can disturb more distant structures, leading to compromised movement patterns
that leave the body vulnerable to further injury.
Because of its anatomical pervasiveness, the fascia is involved in every aspect of physiology. Hence, the fascia
constitutes a medium by which superficial injuries or contractions or constrictions might influence internal organs,
and by which organ pathologies might be expressed in the
periphery. Recent research has indicated that fibrosis created
by a superficial injury can extend into the viscera to create socalled fibrocontractive diseases.58,59,60,61 These concepts
provide a possible fascial basis for the so-called somatovisceral and visceralsomatic reflexes. The review of Nansel
and Szlazak26 cast doubt on the existence of such reflex
pathways as they were described in the earlier literature.
However, such reflexes could have an anatomical and energetic basis in the form of specific pathways through the
fascial network. The tissue softening taking place with FSM
renews interest in the possible relations between somatic and
The second author ( JLO) has received lecture honoraria
and consulting fees from Frequency Specific Seminars Inc. in
Vancouver, Washington for the research and writing of this
1. Kellaway P. The part played by electric fish in the early
history of bioelectricity and electrotherapy. Bull History
2. Becker RO, Seldon G. The Body Electric: Electromagnetism
and the Foundation of Life. New York: William and Morrow
Company, Inc., 1985:172.
3. Oschman JL. Energy Medicine: The Scientific Basis.
Churchill Livingstone/Harcourt Brace, 2000:15. Edinburgh,
4. Bassett CAL. Bioelectromagnetics in the service of medicine.
In: Blank M, ed. Electromagnetic Fields: Biological Interactions and Mechanisms. Advances in Chemistry Series 250.
Washington, DC: American Chemical Society, 1995:265–275.
5. Siskin BF, Walker J. Therapeutic aspects of electromagnetic
for soft-tissue healing. In: Blank M, ed. Electromagnetic
Fields: Biological Interactions and Mechanisms. Advances in
Chemistry Series 250. Washington, DC: American Chemical
6. Strauch B, Patel MK, Rosen DJ, et al. Pulsed magnetic field
therapy increases tensile strength in a rat Achilles’ tendon
repair model. J Hand Surg Am 2006;31:1131–1135.
7. Soda A, Ikehara T, Kinouchi Y, Yoshizaki K. Effect of exposure to an extremely low frequency-electromagnetic field
on the cellular collagen with respect to signaling pathways
in osteoblast-like cells. J Med Invest 2008;55:267–278.
8. Cundy PJ, Paterson DC. A ten-year review of treatment of
delayed union and nonunion with an implanted bone
growth stimulator. Clin Orthop Relat Res 1990;259:216–222.
9. Melzack R. Prolonged relief of pain by brief, intense transcutaneous somatic stimulation. Pain 1975;1:357–373.
10. Ampe`re A-M. Me´moire pre´sente´ a` l’Acade´mie royale des
sciences. In: Annales de Chimie et de Physique XV, Paris,
France: V. Masson, 1820. Submission presented to the Royal
Academy of Sciences [in French]
11. Faraday M. First report on magneto-electric induction, read
before the Royal Society on the 24th of November, 1831.
12. Boulware DG. Radiation from a uniformly accelerated
charge. Ann Phys 1980;124:169–188.
13. McMakin C. Frequency Specific Microcurrent in Pain
Management. Edinburgh: Churchill Livingstone/Elsevier,
14. McMakin C. Qi in chronic fatigue and fibromyalgia. In:
Mayor D, Micozzi M, eds. Energy Medicine East and
West. Edinburgh: Churchill Livingstone/Elsevier, 2011:
15. McMakin C. Microcurrent therapy in the treatment of fibromyalgia. In: Chaitow L, ed. Fibromyalgia Syndrome: A
Practitioner’s Guide to Treatment. Edinburgh: Churchill Livingstone, 2003;179–206.
6 MCMAKIN AND OSCHMAN
16. Curtis D, Fallows S, Morris M, McMakin C. The efficacy of
frequency specific microcurrent therapy on delayed onset
muscle soreness. J Bodywork Move Ther 2010;14:272–279.
17. Antes TA, Yunus MB, Ritey SD, et al. Psychological factors
associated with primary fibromyalgia syndrome. Arthritis
18. Mines S. We Are All in Shock. How Overwhelming Experiences Shatter You.and What You Can Do About It.
Franklin Lakes, NJ: New Page Books, 2003.
19. Barnes JF. Healing Ancient Wounds: The Renegade’s Wisdom. Sedona, AZ: MFR Treatment Centers and Seminars,
June 1, 2000.
20. Willis WD. The somatosensory system, with emphasis
on structures important for pain. Brain Res Rev 2007;55:
21. Gamsa A. The role of psychological factors in chronic pain: I.
A half century of study. Pain 1994;57:5–15.
22. Apkarian AV, Bushnell MC, Treede RD, Zubieta JK. Human
brain mechanisms of pain perception and regulation in
health and disease. Eur J Pain 2005;9:463–484.
23. Kokebie R, Aggarwal R, Kahn S, Kartz RS. Muscle tension is
increased in fibromyalgia: Use of a pressure gauge. Abstract
1935, American College of Rheumatology 2008 Annual
Scientific Meeting, October 24–29, 2008, San Francisco,
24. Morris C. Low Back Syndromes: Integrated Clinical Management. New York: McGraw-Hill Medical, 2005.
25. Simons DG, Travell JG. Travell & Simons’ Myofascial Pain
and Dysfunction: The Trigger Point Manual. Baltimore:
Williams & Wilkins, 1999:660.
26. Nansel D, Szlazak M. Somatic dysfunction and the phenomenon of visceral disease simulation: A probable explanation for the apparent effectiveness of somatic therapy in
patients presumed to be suffering from true visceral disease.
J Manip Physiol Ther 1995;18:379–397.
27. Seaman D. Chiropractic care and visceral disorders: What is
the neurological link? Dynamic Chiropractic, 1996;14:Issue
24. Online document at: www.dynamicchiropractic.com/
mpacms/dc/article.php?id = 39453 Accessed December
28. Hobson AR, Chizh B, Hicks K, et al. Neurophysiological
evaluation of convergent afferents innervating the human
esophagus and area of referred pain on the anterior chest
wall. Am J Physiol Gastrointest Liver Physiol 2010;298:
29. Morris CE. Low Back Syndromes: Integrated Clinical Management. New York: McGraw-Hill, 2005:267.
30. Owens C. An Endocrine Explanation for Chapman’s Reflexes, 2nd ed. Indianapolis, IN: Academy for Applied Osteopathy, 1963.
31. Washington K, Mosiello R, Venditto M, et al. Presence of
Chapman reflex points in hospitalized patients with pneumonia. J Osteopath Assoc 2003;103:479–483.
32. Travell J, Rinzter S, Herman M. Pain and disability of the
shoulder and arm. JAMA 1942;120:417–422.
33. Knutson G. The role of the c-motor system in increasing
muscle tone and muscle pain syndromes: A review of the
Johansson/Sojka hypothesis. J Manip Physiol Ther 2000;
34. Matre DA, Sinkjaer T, Svensson P. Arendt-Nielsen L. Experimental muscle pain increases the human stretch reflex.
35. Mense S. Pathophysiologic basis of muscle pain syndromes.
Phys Med Rehab Clin N Am 1997;8:23–53.
36. Mense S, Skeppar P. Discharge behavior of feline gamma
motorneurons following induction of an artificial myositis.
37. Ackerman JM. The Biophysics of the Vascular Autonomic
Signal and Healing: Frontier Perspectives. Philadelphia:
Temple University, 2001:10:9–15.
38. Korr IM. Proprioceptors and somatic dysfunction. J Am
Osteopath Assoc 1975;74:638–650.
39. Korr IM. Sustained sympathicotonia as a factor in disease.
In: Korr IM, ed. The Neurobiologic Mechanisms in Manipulative Therapy. New York: Plenum Press, 1978.
40. Stanfield CL, Germann WJ. Principles of Human Physiology, 3rd ed. New York: Pearson Benjamin Cummings,
41. Robertson D, et al., eds. Primer on the Autonomic Nervous
System, 3rd ed. New York: Academic Press, 2011.
42. McKay KC, Prato FS, Thomas AW. A literature review: The
effects of magnetic field exposure on blood flow and blood
vessels in the microvasculature. Bioelectromagnetics 2007;
43. Johansson H, Sojka P. Pathophysiological mechanisms
involved in genesis and spread of muscular tension in
occupational muscle pain and in chronic musculoskeletal
pain syndromes: A hypothesis. Med Hypoth 1991;35:
44. Birznieks I, Burton AR, Macefield VG. The effects of experimental muscle and skin pain on the static stretch sensitivity
of human muscle spindles in relaxed leg muscles. J Physiol
45. Pettman E. The facilitated segment. The North American
Institute of Orthopædic Manual Therapy. 2005;IX:issue 5.
Online document at: www.naiomt.com/www.naiomt.com/
articles/05Oct.pdf Accessed July 4, 2011.
46. Knutson GA, Owens EF. Active and passive characteristics
of muscle tone and their relationship models of subluxation/
joint dysfunction: Part I. J Can Chiopr Assoc 2003;47:
47. Knutson GA, Owens EF. Active and passive characteristics
of muscle tone and their relationship models of subluxation/
joint dysfunction. Part II. J Can Chiopr Assoc 2003;47:
48. Seaman D. Chiropractic Care and Visceral Disorders: What
Is the Neurological Link? Online document at: www.cpdo
.net/res/page15.html Accessed January 19, 2012.
49. Findley TW, Schleip R, eds. Fascia Research: Basic Science
and Implications for Conventional and Complementary
Health Care. Munich: Elsevier GmbH, 2007.
50. Schleip R, Klingler W, Lehmann-Horn F. Active contraction
of the thoracolumbar fascia: Indications of a new factor in
low back pain research with implications for manual therapy. Presented at: 5th Interdisciplinary World Congress on
Low Back & Pelvic Pain, Melbourne, November 2004.
51. Schleip R, Klingler W, Lehmann-Horn F. Fascia is able to
contract in a smooth muscle-like manner and thereby influence musculoskeletal mechanics. Presented at: 5th World
Congress of Biomechanics, Munich, Germany, July 29–
August 4, 2006.
52. Schleip R, Naylor IL, Ursu D, et al. Passive muscle stiffness
may be influenced by active contractility of intramuscular
connective tissue. Med Hypotheses 2006;66:66–71.
53. Finando S, Finando D. Fascia and the mechanism of acupuncture. J Bodywork Movement Ther 2011;15:168–176.
54. Wolff J. The Law of Bone Remodeling. Translation of the
1892 German edition. Berlin: Springer, 1986.
TISSUE SOFTENING WITH FREQUENCY-SPECIFIC MICROCURRENT 7
55. Rolf IP. Rolfing. Reestablishing the Natural Alignment and
Structural Integration of Human Body for Vitality and WellBeing. Rochester, VT: Healing Arts Press, 1989:129.
56. Simons DG, Travell JG. Travell & Simons’ Myofascial Pain
and Dysfunction: The Trigger Point Manual, 2nd ed. Baltimore: Williams & Wilkins, 1999:8–9.
57. Selye H. The Stress of Life. New York: McGraw-Hill Book
Company, 1956, Plate 3, or revised edition, 1984:219.
58. Hinz B. Masters and servants of the force: The role of matrix
adhesions in myofibroblast force perception and transmission. Eur J Cell Biol 2006;85:175–181.
59. Tomasek J, et al. Myofibroblasts and mechano-regulation of
connective tissue remodeling. Nat Rev Mol Cell Biol 2002;3:
60. Gabbiani G. The myofibroblast in wound healing and fibrocontractive diseases. J Pathol 2003;200:500–503.
61. Desmoulie`re A, Badid C, Bochaton-Piallat ML, Gabbiani G.
Apoptosis during wound healing, fibrocontractive diseases and
vascular wall injury. Int J Biochem Cell Biol 1997;29:19–30.
Address correspondence to:
Carolyn R. McMakin, MA, DC
Fibromyalgia and Myofascial Pain Clinic of Portland
819 SE Morrison
Portland, OR 97214