MEDICAL BACKGROUD

MUSCLE PAIN SYNDROME

INTRODUCTION

Classifications and identifications :

1. Primary fibromyalgia syndrome(PFS)

-fibrositis, diffuse myofascial pain
syndrome, or primary diffuse fibrositis
syndrome
2. Myofascial Pain Syndrome (MPS)
-specific myofascial pain syndrome
3. Temporomandibular pain and
dysfunction syndrome (TMPSD)

Definition of Terms
a. Trigger Point
-a hyperirritable spot in skeletal muscle that is
associated with a hypersensitive palpable nodule in
a taut band.
b.

Taut band
-The group of tense muscle fibers extending from
a trigger point to the muscle attachments
c.

Local twitch response

-A transient contraction of a group of tense
muscle fibers (taut band) that traverse a trigger
point.

d.

Snapping Palpation
-A fingertip is placed against the tense band
of muscle at right angles to the direction of
the band and suddenly presses down while
the examiner draws the finger back so as to
roll the underlying fibers under the finger.
e.

f.

Algology
-Study of pain

Referred Pain
-Occurs when spontaneous pain is referred
to remote sites from an MTrP.

g.

Essential Pain Zone (Area)

-The region of referred pain (indicated by solid red
areas in pain pattern figures) that is present in nearly
every patient when the trigger point is active.
h.

Flat Palpation
-Examination by finger pressure that proceeds
across the muscle fibers at a right angle to their
length, while compressing them against a firm
underlying structure, such as bone.
i.

Pincer Palpation
-examination of a part by holding it in a pincer grasp
between the thumb and fingers.

 EPIDEMIOLOGY

 Sex
-Commonly seen in women
Age
-20-50 y/o
Work
-Sedentary jobs and lifestyle than in those who engage in regular physical
activity.
Race
-No racial differences in the incidence of myofascial pain.
Personality
-typical is that of a worrier who has many real or perceived responsibilies and
who has difficulty getting relaxed.
-patients have lost or perhaps never had the biofeedback loop needed to
prevent their muscle from being unnecessarily tense. This causes their muscle to
be chronically tense, resulting in painful metabolic and structural changes in the
muscles.

 Anatomy,
Physiology,
Kinesiology of
Muscles

 STRUCTURE AND FINE STRUCTURE

Muscle fibers: the length of the muscle fibers can be up to 40 cm, although
they are usually shorter than 10 cm.

Each muscle fiber is surrounded by :
Epimysium ( outside the muscle)
is an overcoat of dense irregular connective tissue that surrounds the whole muscle

Perimysium and fascicles

Within each skeletal muscle, the muscle fibers are grouped into fascicles
(bundles) that resemble bundles of sticks.
Surrounding each fascicle is a layer of fibrous connective tissue called
perimysium (around the muscle [fascicles]).
Endomysium ( within the muscle)
is a wispy sheath of connective tissue that surrounds each individual muscle fiber. It
consists of fine areolar connective tissue.

THE MUSCLE FIBERS ARE ARANGE AS FOLLOWS:

pennate muscles
Muscles whose fibers run obliquely to the line of pull (they
resemble a feather)
unipennate muscle
the tendon lies along one side of the muscle and the muscle fibers
pass obliquely to it (e.g., extensor digitorum longus).
bipennate muscle
is one in which the tendon lies in the center of the muscle and the
muscle fibers pass to it from two sides (e.g., rectus femoris).
multipennate muscle
arranged as a series of bipennate muscles lying alongside one
another (e.g., acromial fibers of the deltoid)

FINE STRUCTURE
Myofibrils:
myofibrils are the contractile units of the muscle fibers.
consist of chains of sarcomeres.
the length of a sarcomere is about 1.5-2.2 m.
sarcomere comprise more than 1500 thick myosin and 300 thin
actin filaments.
The individual myofibrils are surrounded by sarcoplasm.

Myosin filament:
myosin is a long thin protein with a head on it.
myosin proteins are linked together in a bundle, also forming a
filament, , called thick filament with the heads pointing out.

 Actin filament
is a round protein shaped roughly like a ball.
actin molecules are linked together in a long chain to
form a filament, called thin filament.
composed of two helical strands of F-actin molecules
and two strands of tropomyosin molecules that fit in the
grooves between the actin strands. Attached to one end
of each tropomyosin molecule is a troponin complex that
initiates contraction.

STRIATION OF THE
SARCOMERES:
A-striation is formed by the myosin filaments
arrange in parallel,
Z-striation is the linking zone of the actin
filaments
H-striation is the area in the middle of the Astriation, which consists only of myosin filaments;
right in the middle it is therefore called M-striation,
I-striation consists of actin filaments and borders
on the Z-striation.
The arrangement of the striation in the sarcomere
always takes place in the sequence Z-I-A-H-A-I-Z.

Sliding filament theory

1. A myofiber , together with all of its myofibrils , shortens by
movement of the insertion towards the origin of the muscle .
2. shortening of the myofibrils is caused by shortening of the
sarcomere (The distance between Z lines is reduced) .
3. shortening of the sarcomere is accomplished by each
filament remains the same during contraction .
4. sliding is produced by power strokes of myosin cross bridges ,
which pull the thin actin over the thick myosin .
5. The A band remains the same length during contraction , but
are pulled toward the origin of the muscle .
6. Adjacent A bands are pulled closer together as the I bands
between them shorten .
7. The H band shorten during contraction as the thin filaments
on the sides of the sarcomeres are pulled towards the middle .

MUSCLE FIBER TYPES:

Type I fibers (red fibers)
are rich in myoglobin.
Functionally, they are capable of persistent contractile activity.
On activation there is a slow twitch of 75 ms duration (slow-twitch fibers).
The high level of oxidative enzymes, low level of phosphorylases, small amount of
glycogen storage and capacity for resistance to tiredness are remarkable.
Type I fibers are numerous in postural muscles.

Type IIB fibers (white fibers)

contain less myoglobin than type I fibers.
Functionally they are designed for rapid contractions.
On activation there is a fast twitch of 25 ms duration (fast-twitch glycolytic fibers).
Type II fibers are rich in phosphorylase and glycogen.
The very high number of mitochondria is histologically remarkable.
They participate in short, fast movements.

 Type IIA fibers (mixed type)

favour aerobic oxidative energy metabolism
as well as glycolysis (fast-twitch oxidative
glycolytic)
they possess a moderate resistance to
tiredness.

TYPES OF MUSCULAR
ACTIVATION

Concentric activation
-Occurs as a muscle produces an active force and simultaneously shortens, as
aresult, the muscle decreases the distance between its proximal and distal
attachments.
During a concentric contraction the internal torque produced by the muscle is
greater than the external torque produces by an outside force.

Eccentric activation
-Occurs as a muscle produces an active force-attempts to contract- but is
simultaneously pulled to a longer length by more dominant external force.
-During eccentric muscular activation, the external torque often generated by
gravity, exceeds the internal torque produced by muscle.
-Most often gravity or a held weight is allowed to win effectively lengthening
the muscle in a controlled manner.

Isometric activation
-Occurs when a muscle generates an active force while remaining at a
constant length.
This occurs when the muscle generates an internal torque equal to the external
torque as a consequence, there is no motion and so no change in joint angle.

MUSCLE HEALING AFTER INJURY

TYPES OF INJURY:
Cutting injury:
the fibers and covering fascia of the
muscle rupture as a result of direct
trauma or tear.

Close injury:
only the fibers are damaged; this injury
frequently occurs after repeated
eccentric strain or after injection of LA.

MUSCLE REGENERATION AFTER

INJURY OCCURS:
Non-inflammatory degenerative phase:
-the Z-layers react most sensitive to injury cause by
exercise. Autolysis occurs as a result of the
interruption of Ca2- homeostasis. The first regeneration
processes have been observed 4-8 hr after injury.
Inflammatory degenerative phase:
-start of phagocytosis due to immigrating
macrophages. These eliminate damaged fiber
residues. Introduce by increased proteolysis of the
extracellular matrix, an increase in neutrophil
concentration takes place within homeostasis. The first
regeneration processes have been observed 4-8 hrs.
after injury.

 Regenerative phase:
-Takes place quicker with closed injuries. It begins with
the activation of satellite cells if the basal lamina are
intact. Growth factors originating from fibroblasts and
blood platelets are involved.
Maturation phase:
-the differentiation of the satellite cells is stimulated by
somatomedin (insulin-like growth factor (IGF)I). Gene
expression is altered is the meantime by the fusion of the
cells so that formation of muscle-specific proteins begins.
Myogenesis goes through the stages of embryonic
myosin filaments. Slow-twitch myosin is produced from
innervation that leads to slow twitch muscle; creatinine
kinase activity also increases.


CONSEQUENCES OF REDUCED MUSCLE TRAINING

MUSCLE FIBRE DISTRIBUTION

Ending stamina training leads to a shift from HA to HB fibers.
Ending strength training leads to an increase in type I fibers.

MUSCLE DIAMETER
Stopping short-term training causes a reduction in muscle diameter, which is
mainly due to a reduction in the diameter of IIA fibers. This results mostly in a loss
of muscle strength compared to stamina.
A long-term pause of training in athletes causes a reduction in the diameter of fast
and slow-twitch fibers. There is also reduction in the ratio of fast to slow-twitch
fibers.
Stopping training decreases enzyme activity in athletes: reduction in oxygen
capacity by 30-40%, daily loss of aerobic capacity (VO 2max) of 0.9%
Decrease in muscle strength as a result of immobilization of 3-8 weeks. The muscle
diameter decreases by about 20%. This leads to a reduction in the rest frequency
of the motor neurons. Motor areas in the cerebral cortex are reorganized. A
reduction in the size of the areas associated with muscle activity takes place.


Etiology

CAUSATIVE FACTORS OF ACUTE

MYOFASCIAL PAIN
Blunt muscle trauma
Pulled muscle
Torn muscle
Sprain or dislocation of joints
Increase isometric muscle contraction
Shortening of the muscle
Increase in muscle tension caused by climate
Change in muscle tension of psychogenic cause
Slight muscular strain due to prior condtions

CAUSATIVE FACTORS OF
DELAYED MYOFASCIAL PAIN

Chronic strain
Continued use of the muscles on one side.
Too many demands mad on the muscle.
Being forced into an awkward position.
Advanced functional disorders (blockade of segments of vertebral column).
Lack of coordination/poor exercise technique.
Poor posture.
Deformity of vertebral column or joints.
Irritation of the roots of the peripheral nerves.
Entrapment of the peripheral nerves.

Psychogenic factors
Depression
Anxiety
Stress

PERPETUATING FACTORS OF
MYOFASCIAL PAIN
Poor posture of deformity of incorrect position (segments of the
vertebral column) of the skeletal system of the locomotor
apparatus.
Constant functional disorders of the locomotor apparatus.
Poor diet (alcohol, minerals, vitamins, smoking).
Anaemia and hypoxia affecting the muscles (hyperuricaemia,
hypoglycaemia, thyroid disorders).
Underlying medical, urological or glynaecological diseases via
the reflex arcs.
Sleep disorders, irritations caused by lifestyle (stress,
relaxation).
Psychogenic factors such as inability to express ones own
feelings, stress, depression, anger/annoyance, lack of
challenge and anxiety.

CHRONIFICATION OF
MYOFASCIAL PAIN
biological factors are
peripheral and central
sensitizing mechanisms.
neurogenic inflammatory selfperpetuating
cascades
neuronal reconstruction
processes and the expression
of transcription factor genes
with resulting new receptors
and ion channels (neuronal
plasticity) at the level of the
spinal cord
changed neuronal pain
defence system,
genetic factors

Psychological chronification
factors.
-lack of internal conviction
-feelings of helplessness
-impending catastrophe
-excessive protective
-avoidance behavior
-rigidly carrying on without considering
the personal stress.
Other factors:
-an excessive amount learning
-secondary or tertiary illness,
conditioning
-inadequately dealing with feelings
and psychological tension.
- Poor processing of stress and
increased likelihood of psychological or
psychological reactions can also play a
part in an illness becoming chronic.

Social factors
stress or dissatisfaction at work
bullying
the negative influence of long-term proceedings for damage
claims
surveys and reports
retirement
family,
conflict
social isolation
low level of education
a feeling of insufficient recompense for performance
lack of recognition
elements in the health system that can promote illness.
With many chronic pain diseases there is also a poor quality of
life or a lack of a life plan and this may be an expression of only
a simple spirituality.

 PATHOPHYSIOLOGY / MECAHNISM OF
INJURY / PATHOLOGY

 Clinical Signs and Symptoms /

physical disabilities / impairments

Signs/Symptoms:

Pain in muscles
Limited range of motion
Fatigue
Local pain
Referred pain
Headache
Nodule
Taut band
Tenderness
Spasms
Local twitch response
Weakness

Another clinical sign and

symptoms includes :
pain in neck and posterior
shoulder, with pain or unusual
feelings in upper extremity
sleep disturbance
trigger points in upper
trapezius: stiffness of the neck
pain
inhibition of function causing
the appearance of upper
extremity weakness and
sclerotomal pain
visual disturbances
vague neck pain that is difficult
to
localize
autonomic disturbances
nausea
vomiting
fainting.


To make the clinical diagnosis of myofascial
pain syndrome, the findings should include
five major criteria and at least one of three
minor criteria include the following:

1. Regional pain complaint.

2. Pain complaint or altered sensation in the
expected distribution of referred pain from a
myofascial trigger point.
3. Taut band palpable in an accessible muscle.
4. Exquisite spot tenderness at one point
along the length of the taut band.
5. Some degree of restricted range of motion,
when measurable.

The three minor criteria include the following:

1. Reproduction of clinical pain complaint, or
altered sensation, by pressure on the
tender
spot.
2. Elicitation of a local twitch response by
transverse snapping palpation at the tender spot or
by needle insertion into the tender spot in the taut
band.
3. Pain alleviated by elongating(stretching) the
muscle or by injecting the tender spot (trigger point).

Diagnostic tools / procedure

or test

PALPABLE TENDER NODULE AND

TAUT BAND:
Flat palpation
-refers to the use of a fingertip that employs the
mobility of the subcutaneous tissue to slide the patient's
skin across the muscle fibers. This movement permits
detection of changes in the underlying structures
Pincer palpation
-is used when opposite sides of the muscle are
accessible and the belly of the muscle can be grasped
between the digits
Deep or probing palpation
must be used for deep muscles with considerable tissue
between them and the

Differentail diagnosis
conditions
Myofascial Pain
Syndrome
Trigger Points
Localized
musculoskeletal
conditions
No associated sign
and symptoms
Etiology: overuse,
repetitive motions;
reduced muscle
activity

Fibromyalgia
Syndrome
Tender Points
Systemic Conditions

Wide array of
associated signs and
symptoms
Etiology:
neurohormonal
imbalance; autonomic
nervous system
dysfunction

management

Pharmacological Management