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-
-
-Trigger point
-
-
NOCICEPTORS–
NC
SKIN NOCICEPTORS
JOINT NOCICEPTORS
VISCERAL NOCICEPTORS
Mechanoreceptor
Thermo receptor
Chemo receptor
Polymodal receptor
SKIN NOCICEPTORS
SKIN NOCICEPTORS
(Silent NC)
Golgi Tendon organ
Muscle spindle
Chemo receptorNeuropeptides, Substance P, CGRP*
Polymodal receptor
JOINT NOCICEPTORS
*CGRP: Calcitonin gene-related peptide
PROPRIOCEPTION
JOINT NOCICEPTORS
VISCERAL NOCICEPTORS
VISCERAL NOCICEPTORS
THE PATHWAYS
SOMATOSENSORY CORTEX
Penfield Homunculus (1951)
Ascending pathwaysDescending pathways
Detection
Deduction
Transduction
Modulation
Perception
Pain Modulation
)
Morphine receptors
(Brain and digestive tract)
Dynorphin, Endorphine,
Endomorphine, Nociceptine
-
-
-
-
-
-
-
-
-
-
-
-
Pain location Prev
HEADACHE 40%
ABDOMINAL 23%
BACK 39%
NECK 31%
SHOULDER 29%
HAND/WRIST 23%
HIP/KNEE 28%
ANKLE/FOOT 17%
Windt et al. 2008
-
.1
.2
.3
.4
.1
-
-
Merskey 1979; Merskey and Bogduk 1994; van Tulder et al. 1997
MYOFASCIAL TRIGGER POINT
Janet G. Travell – 1942
Clinical definition
MYOFASCIAL TRIGGER POINT
Janet G. Travell – 1942
Taut band–
Etiological definition
MYOFASCIAL TRIGGER POINT
Central Tp’Satellite Myofascial Tp’
(secondary Tp’)
MYOFASCIAL TRIGGER POINT
Dry Needling
-Central Tp’
Shah et al.– Dry needling for MTrp’ - 2008
.1–
.2–
-Fast twitch
Cell damage * Vasodilatation  Edema
** Hyperalgesia  Muscle contraction  Ischemia
* Cell damage  Arachidonic acid + Cycloxygenase (COX) = Prostaglandin
INFLAMMATION
**Prostaglandin = PAIN
* Cell damage  Arachidonic acid + Cycloxygenase (COX) = Prostaglandin
**Prostaglandin = PAIN
COX 1
–
COX 2
PARACETAMOL (Acetaminophen
Analgetics
Acamol, Dexamol, Paramol, Aldolor
IBUPROFEN
Nsaid’s / non selective COX
COX inhibitor
-COX
Neurofen, Adex, Advil, Artofen, Diclofenac
ETORICOXIB
Nsaid’s / non selective COX
COX 2 inhibitor
-COX 2
Etodolac, Etopan
ETODOLAC
Nsaid’s / selective COX
COX 2 inhibitor
-COX 2
Arcoxia, VIOXX (Rofecoxib)
-
-–
--
-

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