Pathophysiology 17 (2010) 19–28

Myofascial syndrome and pain: A neurophysiological approach

Juhani V. Partanen a,∗ , Tuula A. Ojala b , Jari P.A. Arokoski c
a University and University Hospital of Helsinki, Department of Clinical Neurophysiology, Jorvi Hospital, P.O. Box 800, FIN-00029 HUS, Finland
b University Hospital of Kuopio, Department of Clinical Neurophysiology, FIN-70200 Kuopio, Finland
c University Hospital of Kuopio, Department of Physical Medicine and Rehabilitation, FIN-70200 Kuopio, Finland

Received 7 December 2008; received in revised form 26 March 2009; accepted 7 May 2009

Abstract
It has been debated whether muscle spindles have a role in myofascial pain or not. We present a number of arguments for the former
hypothesis. It was hypothesized that firing of intrafusal muscle fibres, i.e. fusimotor activity can be observed as “end plate spikes” (EPSs)
in electromyography (EMG). The EPSs may be found in local active spots of muscle, often associated with miniature end plate potentials
(MEPPs). Insertion of EMG needle electrodes into an active spot is painful, indicating nociception in the muscle spindle. Myofascial syndrome
patients have taut bands with active trigger points (TrPs) in painful muscles.
End plate activity (EPSs and MEPPs) is a significantly more common finding in TrPs of myofascial pain than in control points of the muscle,
indicating the presence of muscle spindles. However, some control sites may show EPSs of normal muscle spindles. Increased amount of
inflammatory metabolites have been observed in active TrPs.
Muscle spindle is a capsulated gel-filled container, where inflammatory and contraction metabolites may be heavily concentrated during
sustained fusimotor activation. Thus the intrafusal chemosensitive pain mediating III- and IV-afferents are sensitized and activated. Intrafusal
inflammation causes further reflex activation of the fusimotor and skeletofusimotor systems via sensitized III- and IV-afferents. The taut band
itself may be a contracture (rigor) of local skeletofusimotor (beta) units caused by sustained reflex drive by the given muscle spindles. In
EMG this may be seen as complex repetitive discharges. We conclude that TrPs of myofascial pain are related to painful muscle spindles in
taut bands.
© 2009 Elsevier Ireland Ltd. All rights reserved.

Keywords: Myofascial syndrome; Gamma and beta motor units; Muscle spindle; Muscle III- and IV-afferent; Electromyography

1. Introduction muscle involved. The latent TrP is a focal area of tenderness

Myofascial syndrome is a muscular pain syndrome [1]
with regional symptoms [2]. It is common with a prevalence
rate of 30% in the internal medicine practice [3] and cause
much disability and inability to work [4]. Typical clinical
findings in symptomatic muscles are taut bands with active
trigger points (TrPs) of myofascial pain [2]. Latent TrPs are
common even in non-symptomatic individuals. They have
been detected in the shoulder girdle musculature in nearly
half of a group of young, asymptomatic military personnel
[5].
The active TrP is defined to cause spontaneous pain at rest,
with an increase in pain on contraction or stretching of the
∗ Corresponding author.
E-mail address: juhani.v.partanen@hus.fi (J.V. Partanen).
and tightness in a muscle that does not result in spontaneous
pain [6]. The main characteristic criteria of the myofascial
syndrome are as follows: 1. regional pain complaint, 2. pain
or paraesthesia in the typical distribution of the TrP, 3. a taut
band in the muscle, 4. exquisite tenderness found in that taut
band, 5. a local twitch response within the band of muscle
on plucking palpation across the fibres, and 6. a restricted
range of motion in the affected muscle [2,7–11]. There are
maps describing the typical locations of TrPs and referred
pain areas [12]. Mapping of the infraspinatus muscle showed
that most, but not all active TrPs are at midfiber region in the
painful side [13]. Functional complaints include decreased
work tolerance, fatigue, and weakness [14]. Myofascial syn-
drome may be activated by recent muscle injury or chronic
overload (repetitive strain) of muscles [6]. Works which need
repetitive movements demanding precision or repetitive light

0928-4680/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.pathophys.2009.05.001
20 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
lifting may cause myofascial pain especially in the shoulder
and neck region [4]. It has also been suggested that anx-
iety, muscle wasting by malignant disease or neurological
disorders, muscle ischemia, visceral disease, radiculopathic
compression of motor nerves or climatic causes may be pos-
sible reasons for myofascial pain [2].
2. Hypotheses on the origin of myofascial pain
Kellgren [15] was the first to study human muscular pain
experimentally by injecting hypertonic saline into muscles,
and he also turned his attention to patients with muscle pain.
The reason for muscular pain syndromes has, however, been
a matter of debate for a longer time. Muscular strain is one
of the reasons for myofascial syndrome [2]. There are sur-
prisingly sparse histological alterations either in the muscle
or in the TrPs, although mitochondrial changes have been
described [16]. Thus muscle trauma or lesion does not seem
to be the primary cause [1]. There may be an increase of
reticular or elastic fibres which are absent in normal muscle
[17]. Local muscle pain might be related to local, temporary
hypoxia causing a limited energy crisis within the muscle
fibres [16,18]. Reduced blood flow was observed in Trapez-
ius myalgia and it correlated with the intensity of pain [16].
Muscle biopsies of tender points show that there were abnor-
malities in high energy phosphate metabolites, but there
were no abnormalities in the non-tender muscle [19]. An
“integrated hypothesis” was presented; muscular ischaemia,
energy crisis, and increased leakage of acetylcholine into
neuromuscular junction cause TrPs in taut bands [12].
There is a sustained electrically silent contracture (rigor)
of muscle fibres in taut bands [20]. A role of fusimotor
reflexes evoked by muscular III- and IV-afferent activation
in the evolution of muscle pain and stiffness has also been
suggested [21–23]. However, no electrophysiological signs
of spasticity in these patients have been confirmed [9,24].
The muscle contraction of a local twitch response following
a direct mechanical stimulation of a myofascial TrP appears
to occur only within the taut band with latency consistent
with a polysynaptic reflex [25]. Recently, using the micro-
dialysis method an increase of a number of inflammatory and
algesic metabolites and decrease of pH has been observed in
active myofascial TrPs with local twitch response, compared
to normal muscle [26,27]. This explains pain and pressure
sensitivity by inflammation in TrPs.
3. Nociception of a muscle is mainly in “active spots”
with end plate activity
3.1. Hypothesis for the origins of end plate activity
Every electromyographer sometimes observes end plate
activity in the muscle studied. These minuscule sites are
called “active spots” or “active areas” of the muscle [28].
End plate activity arises in two forms: 1. end plate noise or
miniature end plate potentials (MEPPs) [28–31] and 2. end
plate spikes (EPSs), which have a characteristic irregular fir-
ing pattern [29,32,33]. MEPPs and several sequences of EPSs
are usually activated together [34]. The firing pattern [35–39]
and wave form [38] of EPSs is distinctly different from other
potentials in electromyography (EMG). If a concentric nee-
dle electrode is inserted through an active spot, the cannula
potentials representing EPSs are seen as sputtering positive
potentials in EMG. These potentials are converted to EPSs
as the electrode is withdrawn [40].
In needle EMG the insertion of needle through skin and
fascia is felt as sharp transient pain, but further advancement
is painless [41]. However, there are local spots in the muscle
which often are exquisitely painful when inserted with an
EMG needle. The hallmark of these spots is end plate activity
in EMG [29,32,34,41] (Fig. 1). Occasionally a brief twitch
of a strip of a muscle is seen as the recording needle enters an
active area [28], i.e. a local myotatic response may be seen
in the active spot.
MEPPs are considered to be local postsynaptic non-
propagated potentials caused by spontaneous vesicular
exocytosis of acetylcholine from the nerve terminal mem-
brane into the neuromuscular synaptic cleft [31]. The
initiating factor in EPS generation is believed to be the needle
electrode “irritating” mechanically the terminal motor nerve
or endplate connected to a muscle fibre. The EPSs are then
recorded postsynaptically with the same needle electrode
[30,42,43].
However, there is some concern with the prevailing
hypothesis of the origin of EPSs. Experienced neurophys-
iologists have not observed prolonged injury discharges in
nerve fibres. If a peripheral nerve is cut across, the muscle
is seen to twitch but contraction does not continue. This is
evidence that large myelinated motor axons generate nerve
impulses on section, but the discharge is brief [44]. Insertion
of microelectrode into nerve fascicles may cause spontaneous
activity, brief bursts of two to five spikes. Short-term damage
to the nerve fibre may result in the generation of spontaneous
repetitive discharges. They appear mainly as rhythmic single
potentials or rhythmic bursts, “crazy units” [45], i.e. with fir-
ing patterns different from that of EPSs [38]. Spontaneously
active units could not be influenced by mechanical stimu-
lation within the fascicular innervation territory, nor could
units recorded from motor fascicles be influenced by volun-
tary effort [45], contrary to the behaviour of EPSs [33,34,38].
Ectopic potentials of peripheral branches of motor axons
spread to both directions from the site of origin, causing motor
unit potentials or fasciculations, not EPSs. There is no exper-
imental data pointing out that mechanical manipulation of
a nerve terminal might cause sustained postsynaptic action
potentials in the muscle fibre, even if increased concentration
of potassium ions accelerates the MEPP frequency [46].
Another theory was presented for EPSs: they are action
potentials of intrafusal nuclear chain and nuclear bag muscle
fibres [34]. This theory was based on observed EPS reactions
 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
Fig. 1. Typical end plate spikes (EPSs) as seen in needle electromyography in an active spot of a relaxed gastrocnemius muscle. Note the occurrence of EPSs
with a negative onset (upwards) and others with a positive onset (downwards) as well (arrows, inset). There is end plate noise (MEPPs) in the background.
to a number of gamma efferent activating and non-activating
procedures. Due to arguments against this theory [47], new
needle EMG recordings with several electrodes in active spots
(with EPSs) and parallel silent sites (non-active areas) of the
given muscle were performed [38]. The results were in accor-
dance with the local intrafusal origin of EPSs. Thus it seems
to be possible to record EMG activity (MEPPs and EPSs) of
intrafusal muscle fibres with needle EMG [38], as well as with
microelectrodes [48]. Indeed, intrafusal muscle fibres are not
very small in diameter (mean 16.7 ␮m for bag and 8.4 ␮m for
chain fibres), compared to the diameter of extrafusal muscle
fibres and in the extracapsular C region the diameter of a
bag fibre may resemble that of small extrafusal fibre [49].
The topographical localization of motor endplates of a mus-
cle is usually restricted and confined to the midfibre region
(endplate zone) [50]. The MEPPs and EPSs may be recorded
both inside and outside of the endplate zone for example in
the brachial biceps muscle [38,41,51]. Muscle spindles are
concentrated in the region of nerve entry and around the sub-
divisions of the intramuscular nerves, preferentially among
extrafusal fibres with a high proportion of oxidative and fast
oxidative-glykolytic types [49,52]. This corresponds to the
observation of MEPPs and EPSs both in motor point and
non-motor point sites (83% in motor point sites and 34% in
non-motor point sites) [41].
3.2. End plate spikes and intrafusal nociceptors
According to the present hypothesis only MEPPs, not
EPSs could be recorded from the extrafusal neuromuscu-
lar junctions, whereas MEPPs and EPSs together derive
21
from intrafusal neuromuscular junctions together with action
potentials of the intrafusal muscle fibres under fusimotor
drive. MEPPs are the hallmark of neuromuscular junction
in alpha motor unit [28]. However, intrafusal MEPPs (“spon-
taneous miniature potentials”) have also been observed in
microelectrode recording of intrafusal muscle fibre close to
motor terminals [48]. Most EPSs are local but there are
also irregularly firing EPSs which propagate for a greater
length than a muscle spindle, resembling a motor unit terri-
tory, and these are probably derived from skeletofusimotor
(beta) units [38]. Irregular firing and frequent short interpo-
tential intervals in sequences of EPSs [38] could be caused by
lack or rarity of recurrent inhibition of gamma-motoneurones
[52]. The lack of recurrent inhibition is surprising since
gamma-motoneurones are smaller than even the smallest
alpha-motoneurones which have widespread and powerful
recurrent inhibition via Renshaw cells [53] and thus long
interpotential intervals and a relatively regular firing pattern.
Nociceptors of the muscle seem in EMG to be concen-
trated in active spots which thus have the EMG characteristics
of muscle spindles [38]. There are several descriptions of
spontaneous EMG activity either in active spots [32–34] or
TrPs of muscular pain syndromes [12,24,54–57]. Recently is
has been established that EMG activity in myofascial TrPs
indeed is typical end plate activity [58,59]. Thus TrPs also
have the EMG characteristics of muscle spindles. However,
myofascial TrP spindles do not represent all muscle spin-
dles of a painful muscle and thus it is conceivable that end
plate activity with spikes (of normal muscle spindles) can also
be observed in control points outside the TrP, or in control
muscles, although with a lower incidence. Another, distinctly
22 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
different form of spontaneous activity in myofascial TrPs is
the complex repetitive discharge, which is not as common
finding as EPSs [24]. Spontaneous end plate activity may
eventually become a gold standard against which the bed-
side diagnostic criteria for myofascial pain syndrome can be
validated [60].
4. Afferent and efferent systems of the muscle and
muscle spindle
Muscle spindle consists of static and dynamic intra-
fusal motor units which adjust the sensitivity of Ia and II
mechanoreceptors to change and rate of change of the mus-
cle length. These mechanoreceptors are situated in the nuclear
chain and nuclear bag intrafusal muscle fibres; Ia receptors
in the equatorial region and II receptors close to Ia receptors
between the equatorial and polar regions of the spindle [48].
The reflex effects of these receptors differ. Ia-afferents acti-
vate alpha motor neurons and cause increase of the muscle
tension. II-afferents have only weak monosynaptic excitation
of homonymous alpha motor neurons. II-afferents activate
mainly gamma motor neurons, affecting the sensitivity of
the muscle spindle [61,62]. A part of muscle spindles receive
also autonomic axons that are in non-selective neuroeffective
association with the intrafusal muscle fibres [63,64].
There are also thin somatic sensory nerve fibres in the
muscle [64]. These afferents may be either mechanosen-
sitive or chemosensitive. There is evidence that thinly
myelinated III-afferents are sensitive to pressure and other
group III receptors respond to chemical changes within the
muscle [66]. Unmyelinated IV-afferents are high-threshold
mechanoreceptors, and also sensitive to pain-producing sub-
stances [67–69]. III- and IV-afferents are structurally A␦ and
C nerve fibres. However, the finding that the (extrafusal)
muscle fibres proper are not supplied with neuropeptide-
containing free nerve endings may relate to the clinical
experience that muscle cell death – even on a large scale,
such as may occur during muscular dystrophy, polymyositis,
or dermatomyositis – usually is not painful [70,71]. The evi-
dence so far available suggests that receptors with group III
and IV axons play a particular role in nociception and also
subserve a wide range of sensory modalities [1,66–68,72].
The efferent system on muscle spindle consists of static
and dynamic gamma efferents [53]. Dynamic gamma effer-
ents innervate intrafusal nuclear bag I muscle fibres and
static gamma efferents innervate intrafusal nuclear bag II and
nuclear chain fibres [49]. There are also some non-selective
fusimotor axons [73]. Activated nuclear bag fibres have junc-
tion potentials (“local responses”) which do not propagate
from the end plate area of the muscle fibre. Junction potentials
spread electrotonically, i.e. are seen as synchronous negative-
onset waves in electrodes along a minute distance of the
nuclear bag fibre [74,75]. Nuclear chain fibres have prop-
agated action potentials [74,75]. Propagation is seen in the
form of positive component before the main spike compo-
nent of the action potential of the muscle fibre, correlated
to the distance of the recording site from the neuromuscular
junction [76]. However, the action potential propagation is
confined to the polar region and does not happen over the
equatorial region of muscle spindle, where the Ia-afferent
receptors are situated [49]. Thus the fusimotor innervation
of the polar regions of a muscle fibre takes place selectively.
The great majority of fusimotor axons produce activity at one
spindle pole only [73]. One third of the responses to stimu-
lation of static fusimotor axons are action potentials and the
rest are junction potentials [75]. The figures are in concert
with EPSs having a short initial positive deflection (sign of a
propagated potential, 36%) and EPSs having a negative onset
(local response, 64%) in EMG [38]. There may be some spon-
taneous fusimotor activity in relaxed muscle but spontaneous
skeletofusimotor activity is lacking [53,77].
5. Effects of sustained muscle contraction on III- and
IV-afferents
Sustained muscle contraction and fatigue cause gradual
decrease of the firing rate of motor units but excitation of
group III and IV muscle afferents [78], most of which have
high threshold of firing [79]. This excitation may be medi-
ated by ischemic contraction, lactic acid (acidosis), and also
by algesic metabolites, such as bradykinin, serotonin, and
arachidonic acid [23,69,80–82], which may be concentrated
in exhausted muscle [23]. Excitation of group III- and IV-
afferents evokes reflex activation of gamma-efferent system
in the same and also neighbouring muscles [72,80,83], but
it may inhibit alpha motor neurones [68,84]. The gamma
and beta efferent axons show both convergence (4–5 dif-
ferent axons innervate the poles of a muscle spindle) [73]
and divergence (each gamma or beta axon innervates several
spindles, but in a selective manner) [49], which explains the
spread of evoked gamma and beta activation within a mus-
cle. If the muscle overload continues for a long time, there
may even be neurogenic inflammation and sensitization of
III- and IV-afferent receptors [85], and even afferents which
under normal conditions have a high threshold for excitation
[79].
6. Hypothesis: intrafusal III- and IV-afferents and
their activation in the muscle spindle play a part in
myofascial pain
The single largest group of sensory fibres leaving skele-
tal muscles are small myelinated or unmyelinated (groups III
and IV) fibres [68]. Successively smaller nerve fibres are pro-
duced by branching. Eventually they leave the nerve trunks
to end freely in the muscle. Free nerve endings are present
in virtually every tissue of the muscle with the exception
of capillaries. Free nerve endings are found in the blood
vessels, connective tissue adjacent ligaments, between extra-
 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
Fig. 2. A schema illustrating the sensory innervation of the muscle spindle.
In addition to the Ia and II afferents the presence of III- and IV-afferents with
free nerve endings was observed.
fusal and intrafusal muscle fibres, and in the adventitia of
arterioles and venules [23,65,68,86]. Considering the mus-
cle spindle, muscle spindle capsule has free nerve endings
[87] and unmyelinated somatic C-nerve fibre (IV-afferent)
was observed inside the muscle spindle (which are the first
to degenerate after section of the somatic nerve) [88]. A few
group III axons serve spindle secondary endings, other are
widely distributed in skeletal muscle [66]. The presence of
one or two very small-diameter (less than 0.5 ␮m) unmyeli-
nated nerve fibres in the human muscle spindle without any
endings were observed and considered sympathetic [89].
They show varicosities [63,90]. Somatic unmyelinated IV-
afferents may also exist as thin varicose nerve fibres [91]
(Fig. 2). Stacey [65] describes the difficulty to observe C-
fibres with light microscope; electron microscope reveals a
four-fold increase of non-myelinated fibres present in the
muscle nerve over that seen with the light microscope. It
is not possible to determine the nature of thin axon ter-
minals in silver preparations [63]. Autonomic fibres were
observed by the subsequent use of fluorescence microscopy
[63]. Neurogenic inflammation is caused by release of neu-
ropeptides, for example substance P from the terminals of
primary nociceptive neurons [92] via an axon reflex. Thus
there are varicosities and exocytosis also in these nocicep-
tive afferent neurons. Novel studies of somatic C-fibres of
the muscle spindle, especially neuropeptide-containing ones,
are evidently needed with the modern immunohistochemical
staining and electron microscopic methods.
The capsulated part of muscle spindle is isolated from
the extrafusal tissue. Tight junctions between capsular sheet
cells act as barrier to the diffusion of substances into the
periaxial space. There is some leakage in the poles through
the open end of each capsular sleeve. There is a transcapsular
potential of −15 mV due in part to a relatively high K+ in the
periaxial fluid, especially after sustained fusimotor activity
[49,53]. This may contribute to the increased excitability of
the sensory endings [49].
Extrafusal and intrafusal capillaries are different. The
spindle capillaries, as capillaries supplying intramuscular
nerves do not leak as capillaries supplying extrafusal mus-
23
cle. A blood/nervous system barrier therefore, obtains in both
endoneurial and intrafusal periaxial spaces [93,94]. There are
few or no capillaries in the periaxial space [95]. This cap-
sular barrier and vascular arrangement may predispose the
accumulation of lactic acid, potassium ions, algogenic and
inflammatory agents (“inflammatory soup”) in the periaxial
space over the intrafusal sensory terminals during sustained
fusimotor or skeletofusimotor activation. Muscle spindle is
a container with thick membrane and tight sleeves. The
periaxial space is full of highly viscous gel containing gly-
cosaminoglycan hyaluronate [96]. Thus the accumulation
of “inflammatory soup” may be stronger intrafusally than
extrafusally. Those facts also slow down the evacuation of
“inflammatory soup” from the intrafusal periaxial space,
compared to the well perfused extrafusal muscle tissue.
Algesic substances like bradykinin, 5-HT, histamine,
TNF␣, interleukin 8, potassium, or hypertonic sodium
chloride stimulate chemosensitive III- and IV-afferents
[27,66,67,97]. The activation of III- and IV-afferents cause
fusimotor reflex activation which may readily reach other
spindles of the same and even neighbour muscles [22]. It is
more difficult to distinguish a local intrafusal inflammation
than a widespread inflammation in extrafusal muscle tissue.
Sensitization of intrafusal III- and IV-afferents may lead to
spontaneous firing and neuropathic pain, intensified by local
pressure. Chronic nociceptor firing is reflected for instance
in elevated substance P levels in the cerebrospinal fluid. Sub-
stance P is a peptide involved in the neurotransmission of pain
from the periphery to the central nervous system [98]. The
development of central hyperexitability may ensue [6,99].
Reflex effects of intrafusal III- and IV-afferent activa-
tion may cause also activation of extrafusal muscle fibres
of the skeletofusimotor (beta) motor units. There is histo-
chemical evidence for the existence of beta innervation in
the primate [100]. There is histological and electrophysio-
logical evidence for beta motor units in man [38,101,102].
There is evidence that sustained isometric muscle contrac-
tion in man causes muscle spindle excitation on hard-wired
basis via static skeletofusimotor (beta) units [102]. A large
number of intrafusal P1 plates are observed in feline hind-
limb muscles and also in man. P1 plates are the probable
sign of beta innervation. Extrafusal beta fibres are widely
distributed within a muscle fascicle. There are both dynamic
and static beta axons. The high density of beta innervation
suggests that the beta system may be as important in con-
trolling muscle spindle sensitivity as the separate fusimotor
system [103].
During postural stresses, precision work or sustained over-
load of the muscle there is an increase in the fusimotor and
skeletofusimotor drive, which causes accumulation of inflam-
matory and algesic agents into the capsular region (periaxial
space) of the muscle spindle. These agents cause activation
and sensitization of intrafusal III- and IV-afferents, which
further increase gamma and beta efferent drive via reflex
pathway (a positive feedback loop). Reflex activation of beta
motor units associated with a given muscle spindle may cause
24 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28

Fig. 3. A complex repetitive discharge (40 Hz) recorded from a painful trigger point in the levator scapulae muscle of a patient with myofascial syndrome.
There were no signs of peripheral neuropathy in this patient.

fatigue, energy crisis and finally silent contracture of the
extrafusal muscle fibres of these beta motor units, observed
clinically as a palpable taut band. Complex repetitive dis-
charges [24] may represent this short-living EMG pattern of
the ongoing development of a taut band, which finally leads to
exhaustion and silent contracture (rigor) of the muscle fibres
involved (Fig. 3). There is also a spread of the fusimotor drive
to less active muscle spindles [22,104], and thus a taut band
may even be formed by a number of neighbour beta units
(Fig. 4). It should again be emphasized that there is no EMG
evidence of general increase of the muscle tension (alpha
motor unit activity) in these patients [24].

Fig. 4. A schema illustrating the taut band. Striped muscle fibres are extrafusal beta muscle fibres in silent contracture. The inflamed muscle spindles are red.
The divergent beta innervation (illustrated from the right side of the figure) to several muscle spindles as well as to extrafusal beta fibres forms the pathway for
concomitant III- and IV-afferent reflex drive (positive feedback loop) to both of them. Light grey muscle fibres are innervated by alpha motor neurons at the
end plate zone (not illustrated) and they are capable to produce the local twitch response of the taut band when Ia afferents are stimulated.
 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
6.1. The nature of the vicious cycle in myofascial
syndrome
Considering the intrafusal localization of sensitized III-
and IV-afferents to activate the gamma and beta efferent
system it is not surprising, that small intramuscular injec-
tions of hypertonic saline do not cause increased fusimotor
drive [105]. The explanation is that a small extrafusal bolus
of hypertonic saline does not penetrate to the well capsu-
lated muscle spindles. A longer infusion caused the stretch
reflex response to increase. However, the H-reflex did not
change and thus the excitability of the alpha motoneurone
pool was unchanged [106] and thus the extrafusally orig-
inated vicious cycle model [21] was not supported. If the
intramuscular injection of hypertonic saline is very large
compared to the volume of the muscle studied, the muscle
spindles are affected and the afferent effects of injections are
significant [107]. It is hypothetized that an intrafusal vicious
cycle exists but it originates from the sensitized III- and IV-
afferents of the inflamed muscle spindles. It activates the
gamma and beta efferent system of the same and neighbour
muscle spindles via the spinal reflex pathway. The reflection
of this kind of vicious cycle could be the complex repeti-
tive discharges in EMG, as observed in myofascial syndrome
patients [24]. Complex repetitive discharges were observed
in partially denervated muscles [108] but also in some healthy
muscles [109]. Thus the activation of a reflex loop (intrafusal
III- or IV-afferent to beta efferent) is possible in myofascial
syndrome.
7. Therapy
Numerous therapy methods have been employed in
myofascial pain. Prevention of muscle overload with effi-
cient work ergonomy has been recommended, although there
is little scientific data to support this [14]. Fusimotor drive is
largely dependent on subject’s internal attitude toward partic-
ular tasks and contexts [77,110], and thus short pauses during
precision work may decrease intrafusal overload and help to
restore the homeostasis. The same holds true for tasks caus-
ing fatigue, which activates muscle III- and IV-afferents and
gamma efferent activity [111]. There are relatively few spin-
dles in the shoulder-girdle muscles [49]. This may increase
the proprioceptive burden of muscle spindles in these mus-
cles, especially during precision work, leading to myofascial
syndrome and TrPs.
Stretching exercise is considered to be one of the basic
treatments of myofascial pain because the muscles involved
in this syndrome are shortened [6,14]. There are several dif-
ferent stretching techniques such as reciprocal inhibition and
post-isometric relaxation techniques. It has been suggested
that focal muscle contractions result in prolonged ATP con-
sumption and that the restoration of a muscle to its full stretch
length breaks the link between the energy crisis and contrac-
tion of sarcomeric unit [6]. It can also be speculated that
25
massage and stretching may mechanically improve perfu-
sion of the muscle spindles and empty the “inflammatory
soup” from the periaxial space via open sleeves of the spindle
capsule and thus relieve neurogenic inflammation. Condition-
ing programme may also facilitate increased aerobic capacity
and increased muscle strength may alleviate the symptoms
[10,112].
Anti-inflammatory agents have been used to inhibit
prostaglandin E2 accumulation [69]. TrP injections by preci-
sion needling and local anaesthetic and anti-inflammatory
agents reduce pain [6]. The technique involves mechani-
cal disruption of the TrP and by the present hypothesis the
effect is due to disruption of the spindle capsules, which
empties the intrafusal “inflammatory soup” to the well per-
fused extrafusal muscle tissue, from which it is soon carried
away. Dry needling may do the same. Due to the possible
excessive release of acetylcholine from the dysfunctional
motor endplates in myofascial pain [113,114], it could be
considered rational to use therapeutic agents, which target
this undesirable neurotransmitter release. Because botulinum
toxin acts to prevent the presynaptic release of acetylcholine
from cholinergic nerve terminals, it could be considered that
injections of botulinum toxin may be used to treat myofas-
cial pain. Although botulinum toxin was beneficial in some
patients [115], the current evidence does not support the
use of botulinum toxin injection for TrPs in myofascial pain
[116,117].
8. Conclusion
A number of hypotheses has been presented in this review,
not always in concert with the prevailing ones. However,
every consideration is based on published data. The main
points for the neurophysiological hypothesis for myofascial
syndrome are the following:
1. The motor end plates are confined to a strip in the
midfibre area of a muscle, the endplate area. 2. However,
the muscular distribution of “active spots” with EPSs in
EMG, TrPs of myofascial syndrome, and muscle spindles
are not confined to the endplate area. 3. MEPPs and EPSs
in “active spot” in EMG are supposed to derive from intra-
fusal end plates and muscle fibres under fusimotor drive.
4. The exquisite pain caused by EMG needle electrode in
“active spots” of muscle and exquisite pain of TrPs in myofas-
cial syndrome, which also often show end plate spikes,
reflect the nociceptive role of muscle spindles. 5. A taut
band in myofascial syndrome is caused by inflammation
of muscle spindles and consequent III- and IV-afferent-
driven skeletofusimotor activity and contracture of extrafusal
muscle fibres of beta units. The active stage is reflected
as complex repetitive discharges in EMG. 6. The local
twitch response of a taut band is caused by activation of
local Ia afferents and consequent reflex response of alpha
motor neurones (a local myotatic reflex) and it indicates the
presence of muscle spindles. We hope that these hypothe-
26 J.V. Partanen et al. / Pathophysiology 17 (2010) 19–28
ses give impetus for further studies of EPSs and muscle
pain.
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