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ORIGINAL: rwillcott

When dealing with a patient that may be centrally sensistized it's importnat to note that proprioceptors are also involved in the tranmission of painful stimuli to the brain.  There are dormant intersynapes between nociceptors and proprioceptors that become activated in patients who are centrally sensitized.  These intersynapses become activated and allow proprioception to be misinterpreted as noxious stimuli.  In this case there need not be chemical irritants or tissue damage present.  Simple movement can be interpreted as pain in various areas of the brain.

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ORIGINAL: Jon Newman

See here and here

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When dealing with a patient that may be centrally sensistized it's importnat to note that proprioceptors are also involved in the tranmission of painful stimuli to the brain. There are dormant intersynapes between nociceptors and proprioceptors that become activated in patients who are centrally sensitized. These intersynapses become activated and allow proprioception to be misinterpreted as noxious stimuli

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A rudimentary understanding
of Quantum Physics clearly demonstrates that there is
NO OBJECTIVITY.

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I found that
my patient’s fascial system
was full of life, memories,
emotions and consciousness!

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Traditional therapy missed a key component for effectiveness, the
treatment of the Myofascial system, the conduit of consciousness.

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Trauma and inflammatory responses create
myofascial restrictions that can produce pressures of approximately
2,000 pounds per square inch on pain sensitive structures
that do not show up in any of the standard tests (x-rays, MRI’s,
myelograms, CAT scans, electromyography, etc.). This enormous
pressure acts like a “straightjacket” on muscles, nerves, blood
vessels and osseous structures producing the symptoms of pain,
headaches, and restriction of motion, and disease.

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ORIGINAL: Sebastian Asselbergs

I have not seen any study, article, or research that addresses the actual testing of fascia as a source of a complaint from a patient. There is no definition of what "dysfunctional" fascia is.
And yes, Rod, I know you are not asking me....But I thought I'd answer anyway

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BTW, I am not at all in agreement that the brain is aware of fascia. As far as I have been able to find, there is not one book, article, or study showing a specific representation in the brain (akin to our "fuzzy homonunculus") of "the" fascia. No conscious brain "map" of the fascia. No discrete specificity of fascial awareness.

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So, if we do not have specific awareness of fascia, there are no specific tests for fascia, the patient has no way of indicating their complaint is related to fascia, there is no way to disconnect the fascia from the skin (at least, allowed by the laws governing my clinic) for testing or treating....Need I go on?

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In other words, - releasing the fascia - according to Barnes, or anyone else - is a non-event and should not be promoted as a manual treatment technique in a evidence based profession.

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(And before those MFR-ers pipe in and say: "But I feel the release - and so does my patient!" - I say: both are perceiving something quite normal, constructed by their brain, but explain it in a Cirque De Soleil convoluted way).

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Distribution of Nociceptor Peripheral Endings

* free nerve endings are to be found throughout the body, mainly in the adventitia of small blood vessels, in outer and inner epithelia, in connective tissue capsules, and in the periosteum

* are most densely arranged in the cornea, dental pulp, skin and mucosa of the head, skin of the fingers, parietal pleura, and peritoneum.


SKIN:

* two main types of nociceptors in the skin are Aδ mechanical and C polymodal nociceptors (Willis and Westlund 2004), although other types of nociceptors have also been described (Davis et al. 1993).

* Within the dermis, the afferent fiber gives off several branches that penetrate the basal lamina and extend into the
epidermis.

* As a rule, the myelin sheath ends within the dermis.

* Most large axons lose their myelin sheaths and perineurium before reaching the papillary layer of the dermis, with the exception of the axons innervating Merkel cells, although those also become unmyelinated before penetrating the epidermis (Iggo and Muir 1969; Kruger et al. 1981; Halata et al. 2003).

* Cauna (1973) described an elaborate cluster of unmyelinated fibers entering the papillary layer of human hairy skin as a free “penicillate ending”.

* Terminals that penetrate the epidermis for a considerable distance (to the stratum granulosum) have been reported in studies, utilizing methylene blue or silver stainings (Woolard 1935).

* In the beginnings of ultrastructural examination, numerous reports on the electron microscopic image of the skin receptors appeared (Halata 1975; Andres and von Düring 1973; Cauna 1973, 1980; Chouchkov 1978; Kruger et al. 1981).

* Even in recent papers (Kruger 1996; Kruger and Halata 1996;Messlinger 1996; Kruger et al. 2003a, b) the authors are careful in the description of the intraepithelial run of the free nerve endings.

* As the axon-Schwann cell complex approaches the basal epidermis, the thin Schwann cell basal lamina merges with the thicker epidermal basal lamina.

* The axon penetrating the epidermis is accompanied by thin Schwann cell processes which follow its course until a single axonal profile is completely enveloped by keratinocytes, without junctional specializations (Kruger et al. 1981, 2003b).

* The Meissner corpuscles are widely regarded as low-threshold mechanoreceptors.

* However, Pare et al. (2001) showed that Meissner corpuscles are multiafferented receptor organs that may have also nociceptive capabilities.

* In the Meissner corpuscles of glabrous skin of monkey digits they found that the Aα-β-fibers are closely intertwined with endings of peptidergic C-fibers (SP and CGRP).

* These intertwined endings are segregated into zones containing nonpeptidergic C-fibers expressing immunoreactivity for vanilloid receptor 1.


CORNEA

* The enormous number of free nerve endings in the cornea and the lack of any encapsulated receptors were demonstrated by Ramon y Cajal as early as 1909.

* The innervation density is 300–600 times that of the skin (Rozsa and Beuerman 1982).

* The number of PA neurons in the TG, that send their peripheral processes in the ophthalmic nerve is modest (La Vail et al. 1993); however, a single corneal sensory neuron in the rabbit support approximately 3,000 individual nerve endings (Marfurt et al. 1989; Belmonte and Gallar 1996; Müller et al. 2003).

* Both myelinated Aδ and unmyelinated C-fibers are present in the peripheral cornea but the central cornea is innervated by unmyelinated fibers.

* The latter penetrate Bowman’s membrane and terminate between the epithelial cells (Müller et al. 2003; Waite and Ashwell 2004; Guthoff et al. 2005).


TEETH

* Human premolars receive about 2,300 axons at the root apex, and 87% of these fibers are unmyelinated.
* Most apical myelinated axons are fast conducting Aδ-fibers with their receptive fields located at the pulpal periphery and inner dentin.

* These fibers are probably activated by a hydrodynamic mechanism and conduct impulses that are perceived as a short, well-localized sharp pain.

* Most C-fibers are slow-conducting fine afferents with their receptive fields located in the pulp and transmit impulses that are experienced as dull, poorly localized and lingering pain (Nair 1995;Waite and Ashwell 2004).

* Free nerve endings inmature teeth are found in the peripheral plexus of Rashkow, the odontoblastic layer, the predentin, and

the dentin.

* The endings are most numerous in the regions near the tip of the pulp horn,where more than 40% of the dentinal tubules can be innervated (Byers 1984).

* Endings can extend for up to 200 μm into the dentinal tubules in both monkey and human teeth, particularly near the cusps of the crown (Byers and Dong 1983; Waite and Ashwell 2004).

* The periodontal ligament is rich in free nerve endings.

* The periodontal pain is usually well localized and exacerbated by pressure (Waite and Ashwell 2004).


MUSCLE

* In the muscles, the free nerve endings are found in the adventitia of the blood vessels, but also between muscle fibers, in the connective tissue of the muscle and in the tendons (Andres et al. 1985).

* The small myelinated afferent fibers in the muscles have conduction velocities from 2.5–20 m/s, and the unmyelinated fibers less than 2.5 m/s.

* Of all of the small myelinated and unmyelinated fibers, approximately 40% were believed to be nociceptors (Marchettini et al. 1996; Mense 1996).


BONE

* Bone has a rich sensory innervation; the density of nociceptors in the periosteum is high, whereas nerve fibers in the mineralized portion of the bone are less concentrated and are associated with blood vessels in Volkman and Haversian canals (Bjurholm et al. 1988; Hill and Elde 1991; Hukkanen et al. 1992; Mach et al. 2002).


JOINT

* Nociceptors in the joint are located in the capsule, ligaments, bone, articular fat pads, and perivascular sites, but not in the joint cartilage (Heppelmann et al. 1990;Hukkanen et al. 1992; Halata et al. 1999).

* The free nerve endings in the cruciate ligaments are found subsynovially, and are seen also between collagen fibers, close to blood vessels.

* However, at least part of the latter fibers appear to be efferent sympathetic fibers and not nociceptors (Halata et al. 1999).

* The branched, terminal tree of the unmyelinated fibers has a “string of beads” appearance which probably represent multiple receptive sites in the nerve ending (Heppelmann et al. 1990; Schmidt 1996).


DISC

* In the healthy back, only the outer third of the annulus fibrosus of the intervertebral disk is innervated (see Coppes et al. 1990, 1997; Freemont et al. 1997).

* Lower back pain was studied in diseased lumbar intervertebral discs and was for the first time reported to be related to ingrowth of nociceptive fibers by Coppes et al. (1990, 1997).

* This finding was confirmed in 46 samples of diseased intervertebral disks (Freemont et al. 1997).

* Both groups characterized this ingrowth and extension of the neuronal disk network by the nociceptive neurotransmitter substance P.

* It is now well established that a change of the innervation of the disk is the morphological substrate for discogenic pain.


VISCERA

* There are two classes of nociceptors in viscera (Cervero 1994). The first class is composed of “high-threshold” receptors that respond to mechanical stimuli within the noxious range.

* Such are found within different organs: gastrointestinal tract, lungs, ureters and urinary bladder, and heart (Cervero 1996; Gebhart 1996).

* The second class has a low threshold to natural stimuli and encodes the stimulus intensity in the magnitude of their discharges: “intensity-encoding” receptors.

* Both receptor types are concerned mainly with mechanical stimuli (stretch) and are involved in peripheral encoding of noxious stimuli in the organs (Cervero and Jänig 1992).

* The cardiac receptors are the peripheral processes of the pseudounipolar PA neurons, located in the SG and the ganglion inferius n. vagi.

* The sympathetic afferents are considered solely responsible for the conduction of pain arising in the heart.

* However, Meller and Gebhart (1992) suggest that afferent fibers of the vagus nerve might also contribute to the cardiac pain.

* The vagus nerve is largely responsible for the pain conduction arising in the lung.

* Klassen et al. (1951) demonstrated that the burning sensation caused by an endobronchial catheter can be abolished by vagal block.

* In general, solid organs are least sensitive, whereas the serous membranes, covering the viscera are most sensitive to nociceptive stimuli (Giamberardino and Vecchiet 1996).


IN GENERAL

* Except for avascular structures, such as cornea, skin, and mucosa epithelia, nociceptors are adjacent to capillaries and mast cells (Kruger et al. 1985; Dalsgaardet al. 1989; Heppelmann et al. 1995;Messlinger 1996).

* This triad is a functional nociceptive response unit, which is sensitive to tissue damage (Kruger 1996;McHughand McHugh 2000).

* The firing of nociceptors at the site of tissue injury causes release of vesicles containing the peptides SP, NKA, and CGRP, which act in an autocrine and paracrine manner to sensitize the nociceptor and increase its rate of firing (Holzer 1992; Donnerer et al. 1993; Dray 1995; Kruger 1996; Cao et al. 1998; Holzer and Maggi 1998; Millan 1999; McHugh and McHugh 2000).

* Cellular damage and inflammation increase concentrations of chemical mediators such as histamine, bradykinin, and prostaglandins in the area surrounding functional pain units.

* These additional mediators act synergistically to augment the transmission of nociceptive impulses along sensory afferent fibers (McHugh and McHugh 2000).

* In addition to familiar inflammatory mediators, such as prostaglandins and bradykinin, potentially important, pronociceptive roles have been proposed for a variety of “exotic” species, including protons, purinergic transmitters, cytokines, neurotrophins (growth factors), and NO (Mannion et al. 1999; Millan 1999; Boddeke 2001;Willis 2001;Mantyh et al. 2002; Scholz andWoolf 2002).

* Physiological pain starts in the peripheral terminals of nociceptors with the activation of nociceptive transducer receptor/ion channel complexes inducing changes in receptor potential, which generate depolarizing currents in response to noxious stimuli (Woolf and Salter 2000).

* In PA neurons, the transducer proteins that respond to extrinsic or intrinsic irritant chemical stimuli are selectively expressed (McCleskey and Gold 1999; and references therein).

* The noxious heat transducers include the vanilloid receptors VR1 and VRL1 (Caterina et al. 1997, 1999; Tominaga et al. 1998; Guo et al. 1999;Welch et al. 2000; Caterina and Julius 2001; Michael and Priestly 1999; Valtschanoff et al. 2001; Hwang et al. 2003).

* VR1 are on the terminals of many unmyelinated and some finely myelinated nociceptors and respond to capsaicin, heat, and low pH (Holzer 1991; Caterina et al. 1997, 2000; Helliwell et al. 1998; Tominaga et al. 1998).

* On the other hand, VRL1 are on PAs with myelinated axons, have a high heat threshold, and do not respond to capsaicin and low pH (Caterina et al. 1999).

* mRNA for VR1 has been shown to be widely distributed in the brains of both rats and humans (Mezey et al. 2000), so that the role of these receptors in response to painful stimuli may bemuch more complex than previously thought.


SILENT NOCICEPTORS

* There are nociceptors that under normal circumstances are inactive and rather unresponsive. Such nociceptors were first detected in the knee joint and were called “silent” or “sleeping” by Schaible and Schmidt (1983a, b).

* Inflammation leads to sensitization of these fibers, they “awaken” and become much more sensitive to peripheral stimulation (Schaible and Schmidt 1985, 1988; Segond von Banchet et al. 2000).

* Later, “silent” nociceptors were described also in cutaneous and visceral nerves (Davis et al. 1993; McMahon and Koltzenberg 1994; Schmidt et al. 1995, 2000; Snider and McMahon 1998; Petruska et al. 2002).