Download Sarcopenia

‫‪Musculoskeletal medicine‬‬
‫ד"ר ריטה משוב‬
‫מומחית ברפואת משפחה‬
‫מרכזת תחום כאב‬
‫מחוז צפון‬
‫מיני קורס כאב שרר‪-‬שלד‬
‫‪18.11.2015‬‬
Musculoskeletal medicine
• Joints
Injuries or pain
• Ligaments/ Tendons
•Muscles
•Nerves
•Fascia
Structures that support limbs, neck and back
Musculoskeletal medicine
Degenerative
diseases
Inflammatory
conditions
Abrasions,
• Contusions,
• Fractures
•
that cause pain
and impair normal
activities
A muscle fiber is composed of many fibrils, which
give the cell its striated appearance.
A skeletal muscle
fiber is surrounded
by a plasma
membrane:
Sarcolemma
which contains
Sarcoplasm, the cytoplasm of muscle cells.
•Each I band has a dense line running vertically through
the middle called a Z disc or Z line.
•The Z discs mark the border of units called sarcomeres,
which are the functional units of skeletal muscle.
.
One sarcomere is the space between two consecutive Z
discs and contains one entire A band and
two halves of an I band, one on either side of the A band
Sarcomeres are the smallest functional unit of skeletal muscle
and are composed of two protein filaments;
actin and myosin.
Actin is a thin filament and myosin is a thick filament, and it is
the interaction between these two filaments that causes a
muscle to contract and shorten.
The action potential
reaches the axon
terminal
This binding
causes ion
channels
to open.
Voltage-dependent calcium
gates open, allowing calcium
to enter the axon terminal
Neurotransmitter vesicles fuse with
the presynaptic membrane and (ACh)
acetylcholine is released into the
synaptic cleft via exocytosis
The Neuromuscular Junction
If enough acetylcholine is released, the sarcolemma becomes
temporarily more permeable to sodium ions (Na+ ), which rush into the
muscle cell and to potassium ions (K+ ) which diffuse out of the cell.
More Na+ enters than K + leaves.
The cell interior an excess of positive ions, which reverses the electrical
conditions of the sarcolemma and opens more channels that allow Na+
entry only.+
This “upset” generates an electrical current called an action potential.
Once begun, the action potential is unstoppable. The result is contraction
of the muscle cell.
“The Integrated Trigger Point Hypothesis”
• The presence of excessive acetylcholine (ACh) at the
neuromuscular junction
– stimulates voltage-gated sodium channels of the
sarcoplasmic reticulum
– continuously increases intracellular Ca2+ levels.
• This results in ongoing activation of
– Nebulin
– Troponin
– Tropomyosin
• Causes persistent muscle contractures consistent with
myofascial trigger points.
TrP Pathology
• The contractures resulting from excessive Ach may cause
myosin filaments to get stuck in sticky titin gel at the Z-line,
thereby damaging the sarcomere assembly.
Wang K, Yu L. Emerging concepts of muscle contraction and clinical implications
for myofascial pain syndrome [abstract]. Focus on Pain, 2000; Mesa AZ. Janet G. Travell, MD, Seminar Series
• Persistent contractures will compromise local
blood vessels
– reducing the local oxygen supply
– hypoxia, a lowered pH, and hypoperfusion
muscle pain and dysfunction
Maekawa K, Clark GT, Kuboki T. Intramuscular hypoperfusion, adrenergic
receptors, and chronic muscle pain. J Pain 2002;3(4):251-260.
Myofascial pain is a common, though poorly
understood, source of discomfort and
disability for many patients.
Myofascial pain and
dysfunction
Janet Travell & David
Saimons
Janet Travell, MD, developed the concept of
myofascial pain syndrome in the 1950s.
According to Simons and Travell, the syndrome is
defined by the presence of trigger points.
A trigger point are sensitive, painful area in the
muscle or the junction of the muscle and fascia
Trigger Point
A focal hyperirritable spot in skeletal muscle
associated with a palpable nodule in a taut
band:
painful on compression and can give rise to
characteristic referred pain; tenderness;
motor dysfunction and autonomic
phenomena (Simons et al., 1999).
INTEGRATED TRIGGER POINT HYPOTHESIS
Reduced O2
levels in
myofascial
TrPs
Muscle
contractures
local shortage
of ATP
•Failure of Ca2+ pump
•Increased ACh release
increased
metabolic
demand
local energy
shortage
INTEGRATED TRIGGER POINT HYPOTHESIS
• Increased concentration of acethylcholine
(Ach) in the synaptic cleft,
• Release of substances from damaged muscle:
adenosine triphosphate (ATP) [2], bradykinin
(BK), 5-hydroxytryptamin (5-HT, serotonin),
prostaglandins, and potassium (K+), and from
the extracellular fluid around the TrP, such as
protons (H+), from the acidic milieu, which
occurs in ischemia and in exercise
INTEGRATED TRIGGER POINT HYPOTHESIS
Released substances
• Activate muscle nociceptors
pain
• Induce to release calcitonin gene - related
peptide (CGRP) from the muscle nociceptors
and from the motor nerve terminal which
increases motor end plate activity.
Early Observations - Kellgren
Examined the effects of injecting hypertonic saline into muscles
Kellgren JH 1938 Observations on referred pain arising from muscle Clinical Science 3: 175-190
Early Observations - Kellgren
• Referred pain distant from
stimulated point
• May be felt in joints, teeth,
scrotum
• Follows spinal segmental
pattern
• Does not correspond with
sensory segmental patterns
Early Observations - Kellgren
Correlated clinical muscular
pain with tender
points on palpation
Referred pain area not
usually tender
Injection of novocain 1%
abolished pain,
sometimes completely
Kellgren JH. 1938. A preliminary account of referred pain arising from muscle. BMJ 1:325-327
Trigger points
Taut bands of muscle
fibers are "ropy" and
tender to the touch and,
when palpated, create a
local twitch response (also
known as a "jump sign")
that is an involuntary
shortening of the fibrous
muscle band).
CAUSES
• Sudden stress on shortened muscles or on
musculoskeletal tissues (muscles, ligaments, tendons,
bursae)
• Leg length discrepancies
• Skeletal asymentry
• Repetative motions
• Muscle strain due to over activity
• Poor posture
• Assumption of a static position for a long period of
time (eg, a broken arm in a sling)
CAUSES
• Generalize fatigue
• Systemic conditions (eg, gall
bladder inflammation, heart
attack, appendicitis, stomach
irritation)
• Nutritional deficiencies
• Hormonal changes (eg, trigger
point development during PMS
or menopause)
• Nervous tension or stress
• Chilling of areas of the body (eg
sitting under an air conditioning
duct; sleeping in front of an air
conditioner).
Types of trigger points
• Active
Active trigger points
cause
ongoing, persistent
pain
• Latent
Latent trigger points
are silent until
palpated
Active trigger points can activate
"satellite,“
or secondary trigger points in the
reference zone that respond because
of the increased stress to the
involved muscle groups .
Soleus muscle
Sends pain to the calf
and heel(“joggers
heel”).
APPEARS IN THE SACRO-ILIAC
JOINT
REAPPEARS IN THE FACE AND
JAW
Sternocleidomastoid
TMJ, tinnitus, "sinus", and toothache
Dizziness, nausea,
"migraine" and "sinus"
Masseter
Scalenes
Thoracic outlet" and
"carpal tunnel"
syndromes This is one of the
reasons why carpal tunnel
surgery is so ineffective.
is easily confused with
angina
contribute to severe
tension headache
Pectoralis Major
Muscle
Why? When? How?
Overuse
Result of repetitive micro-trauma
to the
Repetitive strain
tendons,
Repeated exposure to
bones
force or
Vibration
and joints.
Overuse/ Overload injury
Exercise
bones, muscles, tendons, and
ligaments get stronger and
more functional
Remodeling
The break down occurs
more rapidly than build up
The balance between
breakdown and build
up of tissue
Chronic Passive Overload - posture
Adding to the “Injury Pool”
Chronic Active Overload
Tensegrity Model
Buckminster Fuller
Architect
Kenneth Snelson
Sculptor
Geodesic Domes
Tensegrity Model
Tensegrity Model
Compression
elements
Tension
elements
Tensegrity Models
Anatomy Trains
‫‪SARCOPENIA‬‬
‫‪ – PENIA /SARX‬בשר ‪/‬עוני‬
‫אובדן במסת שרר השלד כחלק‬
‫מתהליך הזדקנות‬
‫• בכל שנה מעל גיל ‪ 25‬מאבד גו האד בי ‪0.5%‬‬
‫‪ 1%‬ממסת שריר השלד‪.‬‬
‫• שכחות סרקופניה היא ‪ 30%‬בקרב אנשי מעל‬
‫גיל ‪60‬‬
‫•‬
Sarcopenia
Sarcopenia
• Overall, from age 30 to age 80,
muscle mass decreases in relation
to body weight by about 30-40%.
• Te loss is not linear; it accelerates
with increasing age
• Sarcopenia is characterized first
by a muscle atrophy (a decrease
in the size of the muscle), along
with a reduction in muscle tissue
quality
Sarcopenia
Sarcopenia
•
•
•
•
•
Replacement of muscle fibers with fat
An increase in fibrosis
Changes in muscle metabolism
Oxidative stress
Degeneration of the neuromuscular junction
• Progressive loss of muscle function and
Frailty
Sarcopenia- European Consensus
European Society on Clinician Nutrition and Metabolism
(ESPEN)
• Low muscle mass
DXA >2 standard deviations below that mean
measured in young adults (aged 18–39 years)
of the same sex and ethnic background
• Low gait speed
e.g. a walking speed below 0.8 m/s in the
4-m walking test
Sarcopenia - Frailty
• Low muscle mass
• Low muscle strength
• Low physical performance
Linda Fried / Johns Hopkins Frailty
Criteria
• unintentional weight loss,
• exhaustion,
• muscle weakness,
• slowness while walking, and
• low levels of activity
Management of Sarcopenia